Hairstyling Practices to Prevent Hair Damage and Alopecia in Women of African Descent

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Hairstyling Practices to Prevent Hair Damage and Alopecia in Women of African Descent

Central centrifugal cicatricial alopecia (CCCA), traction alopecia, and acquired proximal trichorrhexis nodosa are 3 forms of alopecia that disproportionately affect women of African descent.1 Central centrifugal cicatricial alopecia is characterized by a shiny smooth patch of hair loss over the vertex of the scalp that spreads centrifugally (Figure 1).1-4 Traction alopecia results from prolonged or repeated tension on the hair root that causes mechanical damage, hair loss, and shortening of hairs along the frontotemporal line (the so-called fringe sign)(Figure 2).1,3,5 Acquired proximal trichorrhexis nodosa, a result of trauma, is identified by a substantial number of hairs breaking off midshaft during a hair pull test.1 By understanding the unique structural properties and grooming methods of hair in women of African descent, physicians can better manage and stop the progression of hair loss before it becomes permanent.1,4,5

Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp
FIGURE 1. A and B, Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp.

The characterization of hair between and within ethnic groups is challenging and lies on a spectrum.6,7 Many early studies broadly differentiated hair in 3 ethnic subgroups: African, Asian, and Caucasian6-8; older descriptions of hair texture also included terms such as straight, wavy, curly, and kinky.6 However, defining hair texture should be based on an approach that is more objective than an inaccurate ethnicity-based classification or the use of subjective, ill-defined, and overlapping descriptive terms.7 The segmentation tree analysis method (STAM) is an objective classification system that, when applied to hair, yields 8 curl-type groups (I=straight; VIII=tightly curly) based on curve diameter, curl index, number of waves, and twists.6-9 (We discuss the “tightly coiled” [group VII] through “tight, interwoven small curls” [group VIII] groups in the STAM classification of hair.)

A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia
FIGURE 2. A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia.

Highly textured hair has been found to be more susceptible to breakage than other hair types because of an increased percentage of spirals and relatively fewer elastic fibers anchoring hair follicles to the dermis.1-4,10,11 In a cross-section, the hair shaft of individuals of African descent tends to be more elliptical and kidney shaped than the hair shaft of Asian individuals, which is round and has a large diameter, and the hair shaft of Caucasian individuals, which structurally lies between African and Asian hair.1,2,4,11 This axial asymmetry and section size contributes to points of lower tensile strength and increased fragility, which are exacerbated by everyday combing and grooming. Curvature of the hair follicle leads to the characteristic curly and spiral nature of African hair, which can lead to increased knotting.2,4

Practice Gap

Among women of African descent, a variety of hairstyles and hair treatments frequently are employed to allow for ease of management and self-expression.1 Many of these practices have been implicated as risk factors for alopecia. Simply advising patients to avoid tight hairstyles is ineffective because tension is subjective and difficult to quantify.5 Furthermore, it might be unreasonable to ask a patient to discontinue a hairstyle or treatment when they are unaware of less damaging alternatives.3,5

We provide an overview of hairstyles for patients who have highly textured hair so that physicians can better identify high-risk hairstyles and provide individualized recommendations for safer alternatives.1,3,5

Techniques for Hair Straightening

Traditional thermal straightening uses a hot comb or flat iron1,2,4,12 to temporarily disrupt hydrogen bonds within the hair shafts, which is reversible with exposure to moisture.1,2,4,5 Patients repeat this process every 1 or 2 weeks to offset the effects of normal perspiration and environmental humidity.5,12 Thermal straightening techniques can lead to increased fragility of the hair shaft and loss of tensile strength.11

Alternate methods of hair straightening use lye (sodium hydroxide) or nonlye (lithium and guanidine hydroxide) “relaxers” to permanently disrupt hydrogen and disulfide bonds in the hair shaft, which can damage and weaken hair.1-5,11,12 Touch-ups to the roots often are performed every 6 to 8 weeks.1,2

 

 

Chemical relaxers historically have been associated with CCCA but have not been definitively implicated as causative.2,3,4,13 Most studies have not demonstrated a statistically significant association between chemical relaxers and CCCA because, with a few exceptions,13 studies have either been based on surveys or have not employed trichoscopy or scalp biopsy. In one of those studies, patients with CCCA were determined to be 12.37 times more likely to have used a chemical relaxer in the past (P<.001).13 In another study of 39 women in Nigeria, those who had frequent and prolonged use of a chemical relaxer developed scarring alopecia more often than those who did not use a chemical relaxer (P<.0001). However, it is now known that the pathogenesis of CCCA may be related to an upregulation in genes implicated in fibroproliferative disorders (FPDs), a group of conditions characterized by aberrant wound healing, low-grade inflammation and irritation, and excessive fibrosis.14 They include systemic sclerosis, keloids, atherosclerosis, and uterine fibroids. The risk for certain FPDs is increased in individuals of African descent, and this increased risk is thought to be secondary to the protective effect that profibrotic alleles offer against helminths found in sub-Saharan Africa. A study of 5 patients with biopsy-proven CCCA found that there was increased expression of platelet-derived growth factor gene, PDGF; collagen I gene, COL I; collagen III gene, COL III; matrix metallopeptidase 1 gene, MMP1; matrix metallopeptidase 2 gene, MMP2; matrix metallopeptidase 7 gene, MMP7; and matrix metallopeptidase 9 gene, MMP9, in an affected scalp compared with an unaffected scalp.14 Still, chemical relaxers weaken the hair shaft and follicle structure, increasing the possibility of hair breakage and allowing for inflammation and trauma to render negative follicular effects.3,13

The following interventions can be recommended to patients who thermally or chemically treat their hair to prevent hair damage:

  • Decrease the frequency of thermal straightening.
  • Use lower heat settings on flat irons and blow-dryers.
  • Thermally straighten only clean dry hair.
  • Regularly trim split ends.
  • Use moisturizing shampoos and conditioners.
  • Have a trained professional apply a chemical relaxer, if affordable.
  • Consider decreasing (1) the frequency of chemical relaxer touch-up (to every 8 to 10 weeks) and (2) the overall manipulation of hair. There is a fine balance between not treating often enough and treating too often: The transition point between chemically processed hair and grown-out roots is a high-tension breakage point.
  • Apply a thick protective emollient (known as scalp basing) to the scalp before applying a relaxer1,5; this protects the scalp from irritation.

Techniques for Braids, Weaves, and Twists

Braids and cornrows, sewn-in or glued-on extensions and weaves, and twists are popular hairstyles. When applied improperly, however, they also can lead to alopecia.1-5,11,12 When braids are too tight, the patient might complain of headache. Characteristic tenting—hair pulled so tight that the scalp is raised—might be observed.3,5 Twists are achieved by interlocking 2 pieces of hair, which are held together by styling gel.1,4 When twists remain over many months, hair eventually knots or tangles into a permanent locking pattern (also known as dreadlocks, dreads, or locs).1,2,4 In some cases, the persistent weight of dreadlocks results in hair breakage.1,3,5

The following recommendations can be made to patients who style their hair with braids or cornrows, extensions or weaves, twists, or dreadlocks:

  • Apply these styles with as little traction as possible.
  • Change the direction in which braids and cornrows are styled frequently to avoid constant tension over the same areas.
  • Opt for larger-diameter braids and twists.
  • Leave these styles in place no longer than 2 or 3 months; consider removing extensions and weaves every 3 or 4 weeks.
  • Remove extensions and weaves if they cause pain or irritation.
  • Avoid the use of glue; opt for loosely sewn-in extensions and weaves.
  • Consider the alternative of crochet braiding; this is a protective way to apply extensions to hair and can be worn straight, curly, braided, or twisted.5,12

Techniques for Other Hairstyling Practices

Low-hanging ponytails or buns, wigs, and natural hairstyles generally are considered safe when applied correctly.1,5 The following recommendations can be made to patients who have a low-hanging ponytail, bun, wig, or other natural hairstyle:

  • Before a wig is applied, hold the hair against the scalp with a cotton, nylon, or satin wig cap and with clips, tapes, or bonds. Because satin does not cause constant friction or absorb moisture, it is the safest material for a wig cap.5
  • Achieve a natural hairstyle by cutting off chemically processed hair and allowing hair to grow out.5
  • Hair that has not been thermally or chemically processed better withstands the stresses of traction, pulling, and brushing.5
  • For women with natural hair, wash hair at least every 2 weeks and moisturize frequently.5,12
  • Caution patients that adding synthetic or human hair (ie, extensions, weaves) to any hairstyle to increase volume or length using glue or sewing techniques1-4,11 can cause problems. The extra weight and tension of extensions and weaves can lead to alopecia. Glue can trigger an irritant or allergic reaction, especially in women who have a latex allergy.1,4,5,11

Practice Implications

Women of African descent might be more susceptible to alopecia because of the distinctive structural properties of their hair and the various hair treatments and styles they often employ. Physicians should be knowledgeable when counseling these patients on their hair care practices. It also is important to understand that it might not be feasible for a patient to completely discontinue a hair treatment or style. In that situation, be prepared to make recommendations for safer hairstyling practices.

References
  1. Callender VD, McMichael AJ, Cohen GF. Medical and surgical therapies for alopecias in black women. Dermatol Ther. 2004;17:164-176. doi:10.1111/j.1396-0296.2004.04017.x
  2. Herskovitz I, Miteva M. Central centrifugal cicatricial alopecia: challenges and solutions. Clin Cosmet Investig Dermatol. 2016;9:175-181. doi:10.2147/CCID.S100816
  3. Tanus A, Oliveira CCC, Villarreal DJ, et al. Black women’s hair: the main scalp dermatoses and aesthetic practices in women of African ethnicity. An Bras Dermatol. 2015;90:450-465. doi:10.1590/abd1806-4841.20152845
  4. Gathers RC, Lim HW. Central centrifugal cicatricial alopecia: past, present, and future. J Am Acad Dermatol. 2009;60:660-668. doi:10.1016/j.jaad.2008.09.066
  5. Haskin A, Aguh C. All hairstyles are not created equal: what the dermatologist needs to know about black hairstyling practices and the risk of traction alopecia (TA). J Am Acad Dermatol. 2016;75:606-611. doi:10.1016/j.jaad.2016.02.1162
  6. Loussouarn G, Garcel A-L, Lozano I, et al. Worldwide diversity of hair curliness: a new method of assessment. Int J Dermatol. 2007;46(suppl 1):2-6. doi:10.1111/j.1365-4632.2007.03453.x
  7. De la Mettrie R, Saint-Léger D, Loussouarn G, et al. Shape variability and classification of human hair: a worldwide approach. Hum Biol. 2007;79:265-281. doi:10.1353/hub.2007.0045
  8. Takahashi T. Unique hair properties that emerge from combinations of multiple races. Cosmetics. 2019;6:36. https://doi.org/10.3390/cosmetics6020036
  9. Cloete E, Khumalo NP, Ngoepe MN. The what, why and how of curly hair: a review. Proc Math Phys Eng Sci. 2019;475:20190516. doi:10.1098/rspa.2019.0516
  10. Westgate GE, Ginger RS, Green MR. The biology and genetics of curly hair. Exp Dermatol. 2017;26:483-490. doi:10.1111/exd.13347
  11. McMichael AJ. Ethnic hair update: past and present. J Am Acad Dermatol. 2003;48(6 suppl):S127-S133. doi:10.1067/mjd.2003.278
  12. Roseborough IE, McMichael AJ. Hair care practices in African-American patients. Semin Cutan Med Surg. 2009;28:103-108. doi:10.1016/j.sder.2009.04.007
  13. Narasimman M, De Bedout V, Castillo DE, et al. Increased association between previous pregnancies and use of chemical relaxers in 74 women with central centrifugal cicatricial alopecia. Int J Trichology. 2020;12:176-181. doi:10.4103/ijt.ijt_37_20
  14. Aguh C, Dina Y, Talbot CC Jr, et al. Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2018;79:904-912.e901. doi:10.1016/j.jaad.2018.05.1257
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Ms. Geisler is from The CUNY School of Medicine, New York, New York. Drs. Oyerinde and Scott are from the Department of Dermatology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts.

The authors report no conflict of interest.

Correspondence: Amaris N. Geisler, BS, The CUNY School of Medicine, 160 Convent Ave, New York, NY 10031 ([email protected]).

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Ms. Geisler is from The CUNY School of Medicine, New York, New York. Drs. Oyerinde and Scott are from the Department of Dermatology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts.

The authors report no conflict of interest.

Correspondence: Amaris N. Geisler, BS, The CUNY School of Medicine, 160 Convent Ave, New York, NY 10031 ([email protected]).

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Ms. Geisler is from The CUNY School of Medicine, New York, New York. Drs. Oyerinde and Scott are from the Department of Dermatology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts.

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Correspondence: Amaris N. Geisler, BS, The CUNY School of Medicine, 160 Convent Ave, New York, NY 10031 ([email protected]).

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Central centrifugal cicatricial alopecia (CCCA), traction alopecia, and acquired proximal trichorrhexis nodosa are 3 forms of alopecia that disproportionately affect women of African descent.1 Central centrifugal cicatricial alopecia is characterized by a shiny smooth patch of hair loss over the vertex of the scalp that spreads centrifugally (Figure 1).1-4 Traction alopecia results from prolonged or repeated tension on the hair root that causes mechanical damage, hair loss, and shortening of hairs along the frontotemporal line (the so-called fringe sign)(Figure 2).1,3,5 Acquired proximal trichorrhexis nodosa, a result of trauma, is identified by a substantial number of hairs breaking off midshaft during a hair pull test.1 By understanding the unique structural properties and grooming methods of hair in women of African descent, physicians can better manage and stop the progression of hair loss before it becomes permanent.1,4,5

Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp
FIGURE 1. A and B, Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp.

The characterization of hair between and within ethnic groups is challenging and lies on a spectrum.6,7 Many early studies broadly differentiated hair in 3 ethnic subgroups: African, Asian, and Caucasian6-8; older descriptions of hair texture also included terms such as straight, wavy, curly, and kinky.6 However, defining hair texture should be based on an approach that is more objective than an inaccurate ethnicity-based classification or the use of subjective, ill-defined, and overlapping descriptive terms.7 The segmentation tree analysis method (STAM) is an objective classification system that, when applied to hair, yields 8 curl-type groups (I=straight; VIII=tightly curly) based on curve diameter, curl index, number of waves, and twists.6-9 (We discuss the “tightly coiled” [group VII] through “tight, interwoven small curls” [group VIII] groups in the STAM classification of hair.)

A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia
FIGURE 2. A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia.

Highly textured hair has been found to be more susceptible to breakage than other hair types because of an increased percentage of spirals and relatively fewer elastic fibers anchoring hair follicles to the dermis.1-4,10,11 In a cross-section, the hair shaft of individuals of African descent tends to be more elliptical and kidney shaped than the hair shaft of Asian individuals, which is round and has a large diameter, and the hair shaft of Caucasian individuals, which structurally lies between African and Asian hair.1,2,4,11 This axial asymmetry and section size contributes to points of lower tensile strength and increased fragility, which are exacerbated by everyday combing and grooming. Curvature of the hair follicle leads to the characteristic curly and spiral nature of African hair, which can lead to increased knotting.2,4

Practice Gap

Among women of African descent, a variety of hairstyles and hair treatments frequently are employed to allow for ease of management and self-expression.1 Many of these practices have been implicated as risk factors for alopecia. Simply advising patients to avoid tight hairstyles is ineffective because tension is subjective and difficult to quantify.5 Furthermore, it might be unreasonable to ask a patient to discontinue a hairstyle or treatment when they are unaware of less damaging alternatives.3,5

We provide an overview of hairstyles for patients who have highly textured hair so that physicians can better identify high-risk hairstyles and provide individualized recommendations for safer alternatives.1,3,5

Techniques for Hair Straightening

Traditional thermal straightening uses a hot comb or flat iron1,2,4,12 to temporarily disrupt hydrogen bonds within the hair shafts, which is reversible with exposure to moisture.1,2,4,5 Patients repeat this process every 1 or 2 weeks to offset the effects of normal perspiration and environmental humidity.5,12 Thermal straightening techniques can lead to increased fragility of the hair shaft and loss of tensile strength.11

Alternate methods of hair straightening use lye (sodium hydroxide) or nonlye (lithium and guanidine hydroxide) “relaxers” to permanently disrupt hydrogen and disulfide bonds in the hair shaft, which can damage and weaken hair.1-5,11,12 Touch-ups to the roots often are performed every 6 to 8 weeks.1,2

 

 

Chemical relaxers historically have been associated with CCCA but have not been definitively implicated as causative.2,3,4,13 Most studies have not demonstrated a statistically significant association between chemical relaxers and CCCA because, with a few exceptions,13 studies have either been based on surveys or have not employed trichoscopy or scalp biopsy. In one of those studies, patients with CCCA were determined to be 12.37 times more likely to have used a chemical relaxer in the past (P<.001).13 In another study of 39 women in Nigeria, those who had frequent and prolonged use of a chemical relaxer developed scarring alopecia more often than those who did not use a chemical relaxer (P<.0001). However, it is now known that the pathogenesis of CCCA may be related to an upregulation in genes implicated in fibroproliferative disorders (FPDs), a group of conditions characterized by aberrant wound healing, low-grade inflammation and irritation, and excessive fibrosis.14 They include systemic sclerosis, keloids, atherosclerosis, and uterine fibroids. The risk for certain FPDs is increased in individuals of African descent, and this increased risk is thought to be secondary to the protective effect that profibrotic alleles offer against helminths found in sub-Saharan Africa. A study of 5 patients with biopsy-proven CCCA found that there was increased expression of platelet-derived growth factor gene, PDGF; collagen I gene, COL I; collagen III gene, COL III; matrix metallopeptidase 1 gene, MMP1; matrix metallopeptidase 2 gene, MMP2; matrix metallopeptidase 7 gene, MMP7; and matrix metallopeptidase 9 gene, MMP9, in an affected scalp compared with an unaffected scalp.14 Still, chemical relaxers weaken the hair shaft and follicle structure, increasing the possibility of hair breakage and allowing for inflammation and trauma to render negative follicular effects.3,13

The following interventions can be recommended to patients who thermally or chemically treat their hair to prevent hair damage:

  • Decrease the frequency of thermal straightening.
  • Use lower heat settings on flat irons and blow-dryers.
  • Thermally straighten only clean dry hair.
  • Regularly trim split ends.
  • Use moisturizing shampoos and conditioners.
  • Have a trained professional apply a chemical relaxer, if affordable.
  • Consider decreasing (1) the frequency of chemical relaxer touch-up (to every 8 to 10 weeks) and (2) the overall manipulation of hair. There is a fine balance between not treating often enough and treating too often: The transition point between chemically processed hair and grown-out roots is a high-tension breakage point.
  • Apply a thick protective emollient (known as scalp basing) to the scalp before applying a relaxer1,5; this protects the scalp from irritation.

Techniques for Braids, Weaves, and Twists

Braids and cornrows, sewn-in or glued-on extensions and weaves, and twists are popular hairstyles. When applied improperly, however, they also can lead to alopecia.1-5,11,12 When braids are too tight, the patient might complain of headache. Characteristic tenting—hair pulled so tight that the scalp is raised—might be observed.3,5 Twists are achieved by interlocking 2 pieces of hair, which are held together by styling gel.1,4 When twists remain over many months, hair eventually knots or tangles into a permanent locking pattern (also known as dreadlocks, dreads, or locs).1,2,4 In some cases, the persistent weight of dreadlocks results in hair breakage.1,3,5

The following recommendations can be made to patients who style their hair with braids or cornrows, extensions or weaves, twists, or dreadlocks:

  • Apply these styles with as little traction as possible.
  • Change the direction in which braids and cornrows are styled frequently to avoid constant tension over the same areas.
  • Opt for larger-diameter braids and twists.
  • Leave these styles in place no longer than 2 or 3 months; consider removing extensions and weaves every 3 or 4 weeks.
  • Remove extensions and weaves if they cause pain or irritation.
  • Avoid the use of glue; opt for loosely sewn-in extensions and weaves.
  • Consider the alternative of crochet braiding; this is a protective way to apply extensions to hair and can be worn straight, curly, braided, or twisted.5,12

Techniques for Other Hairstyling Practices

Low-hanging ponytails or buns, wigs, and natural hairstyles generally are considered safe when applied correctly.1,5 The following recommendations can be made to patients who have a low-hanging ponytail, bun, wig, or other natural hairstyle:

  • Before a wig is applied, hold the hair against the scalp with a cotton, nylon, or satin wig cap and with clips, tapes, or bonds. Because satin does not cause constant friction or absorb moisture, it is the safest material for a wig cap.5
  • Achieve a natural hairstyle by cutting off chemically processed hair and allowing hair to grow out.5
  • Hair that has not been thermally or chemically processed better withstands the stresses of traction, pulling, and brushing.5
  • For women with natural hair, wash hair at least every 2 weeks and moisturize frequently.5,12
  • Caution patients that adding synthetic or human hair (ie, extensions, weaves) to any hairstyle to increase volume or length using glue or sewing techniques1-4,11 can cause problems. The extra weight and tension of extensions and weaves can lead to alopecia. Glue can trigger an irritant or allergic reaction, especially in women who have a latex allergy.1,4,5,11

Practice Implications

Women of African descent might be more susceptible to alopecia because of the distinctive structural properties of their hair and the various hair treatments and styles they often employ. Physicians should be knowledgeable when counseling these patients on their hair care practices. It also is important to understand that it might not be feasible for a patient to completely discontinue a hair treatment or style. In that situation, be prepared to make recommendations for safer hairstyling practices.

Central centrifugal cicatricial alopecia (CCCA), traction alopecia, and acquired proximal trichorrhexis nodosa are 3 forms of alopecia that disproportionately affect women of African descent.1 Central centrifugal cicatricial alopecia is characterized by a shiny smooth patch of hair loss over the vertex of the scalp that spreads centrifugally (Figure 1).1-4 Traction alopecia results from prolonged or repeated tension on the hair root that causes mechanical damage, hair loss, and shortening of hairs along the frontotemporal line (the so-called fringe sign)(Figure 2).1,3,5 Acquired proximal trichorrhexis nodosa, a result of trauma, is identified by a substantial number of hairs breaking off midshaft during a hair pull test.1 By understanding the unique structural properties and grooming methods of hair in women of African descent, physicians can better manage and stop the progression of hair loss before it becomes permanent.1,4,5

Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp
FIGURE 1. A and B, Central centrifugal cicatricial alopecia presenting as a shiny smooth patch of hair loss over the vertex of the scalp.

The characterization of hair between and within ethnic groups is challenging and lies on a spectrum.6,7 Many early studies broadly differentiated hair in 3 ethnic subgroups: African, Asian, and Caucasian6-8; older descriptions of hair texture also included terms such as straight, wavy, curly, and kinky.6 However, defining hair texture should be based on an approach that is more objective than an inaccurate ethnicity-based classification or the use of subjective, ill-defined, and overlapping descriptive terms.7 The segmentation tree analysis method (STAM) is an objective classification system that, when applied to hair, yields 8 curl-type groups (I=straight; VIII=tightly curly) based on curve diameter, curl index, number of waves, and twists.6-9 (We discuss the “tightly coiled” [group VII] through “tight, interwoven small curls” [group VIII] groups in the STAM classification of hair.)

A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia
FIGURE 2. A, Fringe sign in traction alopecia. B, Clinical presentation of traction alopecia.

Highly textured hair has been found to be more susceptible to breakage than other hair types because of an increased percentage of spirals and relatively fewer elastic fibers anchoring hair follicles to the dermis.1-4,10,11 In a cross-section, the hair shaft of individuals of African descent tends to be more elliptical and kidney shaped than the hair shaft of Asian individuals, which is round and has a large diameter, and the hair shaft of Caucasian individuals, which structurally lies between African and Asian hair.1,2,4,11 This axial asymmetry and section size contributes to points of lower tensile strength and increased fragility, which are exacerbated by everyday combing and grooming. Curvature of the hair follicle leads to the characteristic curly and spiral nature of African hair, which can lead to increased knotting.2,4

Practice Gap

Among women of African descent, a variety of hairstyles and hair treatments frequently are employed to allow for ease of management and self-expression.1 Many of these practices have been implicated as risk factors for alopecia. Simply advising patients to avoid tight hairstyles is ineffective because tension is subjective and difficult to quantify.5 Furthermore, it might be unreasonable to ask a patient to discontinue a hairstyle or treatment when they are unaware of less damaging alternatives.3,5

We provide an overview of hairstyles for patients who have highly textured hair so that physicians can better identify high-risk hairstyles and provide individualized recommendations for safer alternatives.1,3,5

Techniques for Hair Straightening

Traditional thermal straightening uses a hot comb or flat iron1,2,4,12 to temporarily disrupt hydrogen bonds within the hair shafts, which is reversible with exposure to moisture.1,2,4,5 Patients repeat this process every 1 or 2 weeks to offset the effects of normal perspiration and environmental humidity.5,12 Thermal straightening techniques can lead to increased fragility of the hair shaft and loss of tensile strength.11

Alternate methods of hair straightening use lye (sodium hydroxide) or nonlye (lithium and guanidine hydroxide) “relaxers” to permanently disrupt hydrogen and disulfide bonds in the hair shaft, which can damage and weaken hair.1-5,11,12 Touch-ups to the roots often are performed every 6 to 8 weeks.1,2

 

 

Chemical relaxers historically have been associated with CCCA but have not been definitively implicated as causative.2,3,4,13 Most studies have not demonstrated a statistically significant association between chemical relaxers and CCCA because, with a few exceptions,13 studies have either been based on surveys or have not employed trichoscopy or scalp biopsy. In one of those studies, patients with CCCA were determined to be 12.37 times more likely to have used a chemical relaxer in the past (P<.001).13 In another study of 39 women in Nigeria, those who had frequent and prolonged use of a chemical relaxer developed scarring alopecia more often than those who did not use a chemical relaxer (P<.0001). However, it is now known that the pathogenesis of CCCA may be related to an upregulation in genes implicated in fibroproliferative disorders (FPDs), a group of conditions characterized by aberrant wound healing, low-grade inflammation and irritation, and excessive fibrosis.14 They include systemic sclerosis, keloids, atherosclerosis, and uterine fibroids. The risk for certain FPDs is increased in individuals of African descent, and this increased risk is thought to be secondary to the protective effect that profibrotic alleles offer against helminths found in sub-Saharan Africa. A study of 5 patients with biopsy-proven CCCA found that there was increased expression of platelet-derived growth factor gene, PDGF; collagen I gene, COL I; collagen III gene, COL III; matrix metallopeptidase 1 gene, MMP1; matrix metallopeptidase 2 gene, MMP2; matrix metallopeptidase 7 gene, MMP7; and matrix metallopeptidase 9 gene, MMP9, in an affected scalp compared with an unaffected scalp.14 Still, chemical relaxers weaken the hair shaft and follicle structure, increasing the possibility of hair breakage and allowing for inflammation and trauma to render negative follicular effects.3,13

The following interventions can be recommended to patients who thermally or chemically treat their hair to prevent hair damage:

  • Decrease the frequency of thermal straightening.
  • Use lower heat settings on flat irons and blow-dryers.
  • Thermally straighten only clean dry hair.
  • Regularly trim split ends.
  • Use moisturizing shampoos and conditioners.
  • Have a trained professional apply a chemical relaxer, if affordable.
  • Consider decreasing (1) the frequency of chemical relaxer touch-up (to every 8 to 10 weeks) and (2) the overall manipulation of hair. There is a fine balance between not treating often enough and treating too often: The transition point between chemically processed hair and grown-out roots is a high-tension breakage point.
  • Apply a thick protective emollient (known as scalp basing) to the scalp before applying a relaxer1,5; this protects the scalp from irritation.

Techniques for Braids, Weaves, and Twists

Braids and cornrows, sewn-in or glued-on extensions and weaves, and twists are popular hairstyles. When applied improperly, however, they also can lead to alopecia.1-5,11,12 When braids are too tight, the patient might complain of headache. Characteristic tenting—hair pulled so tight that the scalp is raised—might be observed.3,5 Twists are achieved by interlocking 2 pieces of hair, which are held together by styling gel.1,4 When twists remain over many months, hair eventually knots or tangles into a permanent locking pattern (also known as dreadlocks, dreads, or locs).1,2,4 In some cases, the persistent weight of dreadlocks results in hair breakage.1,3,5

The following recommendations can be made to patients who style their hair with braids or cornrows, extensions or weaves, twists, or dreadlocks:

  • Apply these styles with as little traction as possible.
  • Change the direction in which braids and cornrows are styled frequently to avoid constant tension over the same areas.
  • Opt for larger-diameter braids and twists.
  • Leave these styles in place no longer than 2 or 3 months; consider removing extensions and weaves every 3 or 4 weeks.
  • Remove extensions and weaves if they cause pain or irritation.
  • Avoid the use of glue; opt for loosely sewn-in extensions and weaves.
  • Consider the alternative of crochet braiding; this is a protective way to apply extensions to hair and can be worn straight, curly, braided, or twisted.5,12

Techniques for Other Hairstyling Practices

Low-hanging ponytails or buns, wigs, and natural hairstyles generally are considered safe when applied correctly.1,5 The following recommendations can be made to patients who have a low-hanging ponytail, bun, wig, or other natural hairstyle:

  • Before a wig is applied, hold the hair against the scalp with a cotton, nylon, or satin wig cap and with clips, tapes, or bonds. Because satin does not cause constant friction or absorb moisture, it is the safest material for a wig cap.5
  • Achieve a natural hairstyle by cutting off chemically processed hair and allowing hair to grow out.5
  • Hair that has not been thermally or chemically processed better withstands the stresses of traction, pulling, and brushing.5
  • For women with natural hair, wash hair at least every 2 weeks and moisturize frequently.5,12
  • Caution patients that adding synthetic or human hair (ie, extensions, weaves) to any hairstyle to increase volume or length using glue or sewing techniques1-4,11 can cause problems. The extra weight and tension of extensions and weaves can lead to alopecia. Glue can trigger an irritant or allergic reaction, especially in women who have a latex allergy.1,4,5,11

Practice Implications

Women of African descent might be more susceptible to alopecia because of the distinctive structural properties of their hair and the various hair treatments and styles they often employ. Physicians should be knowledgeable when counseling these patients on their hair care practices. It also is important to understand that it might not be feasible for a patient to completely discontinue a hair treatment or style. In that situation, be prepared to make recommendations for safer hairstyling practices.

References
  1. Callender VD, McMichael AJ, Cohen GF. Medical and surgical therapies for alopecias in black women. Dermatol Ther. 2004;17:164-176. doi:10.1111/j.1396-0296.2004.04017.x
  2. Herskovitz I, Miteva M. Central centrifugal cicatricial alopecia: challenges and solutions. Clin Cosmet Investig Dermatol. 2016;9:175-181. doi:10.2147/CCID.S100816
  3. Tanus A, Oliveira CCC, Villarreal DJ, et al. Black women’s hair: the main scalp dermatoses and aesthetic practices in women of African ethnicity. An Bras Dermatol. 2015;90:450-465. doi:10.1590/abd1806-4841.20152845
  4. Gathers RC, Lim HW. Central centrifugal cicatricial alopecia: past, present, and future. J Am Acad Dermatol. 2009;60:660-668. doi:10.1016/j.jaad.2008.09.066
  5. Haskin A, Aguh C. All hairstyles are not created equal: what the dermatologist needs to know about black hairstyling practices and the risk of traction alopecia (TA). J Am Acad Dermatol. 2016;75:606-611. doi:10.1016/j.jaad.2016.02.1162
  6. Loussouarn G, Garcel A-L, Lozano I, et al. Worldwide diversity of hair curliness: a new method of assessment. Int J Dermatol. 2007;46(suppl 1):2-6. doi:10.1111/j.1365-4632.2007.03453.x
  7. De la Mettrie R, Saint-Léger D, Loussouarn G, et al. Shape variability and classification of human hair: a worldwide approach. Hum Biol. 2007;79:265-281. doi:10.1353/hub.2007.0045
  8. Takahashi T. Unique hair properties that emerge from combinations of multiple races. Cosmetics. 2019;6:36. https://doi.org/10.3390/cosmetics6020036
  9. Cloete E, Khumalo NP, Ngoepe MN. The what, why and how of curly hair: a review. Proc Math Phys Eng Sci. 2019;475:20190516. doi:10.1098/rspa.2019.0516
  10. Westgate GE, Ginger RS, Green MR. The biology and genetics of curly hair. Exp Dermatol. 2017;26:483-490. doi:10.1111/exd.13347
  11. McMichael AJ. Ethnic hair update: past and present. J Am Acad Dermatol. 2003;48(6 suppl):S127-S133. doi:10.1067/mjd.2003.278
  12. Roseborough IE, McMichael AJ. Hair care practices in African-American patients. Semin Cutan Med Surg. 2009;28:103-108. doi:10.1016/j.sder.2009.04.007
  13. Narasimman M, De Bedout V, Castillo DE, et al. Increased association between previous pregnancies and use of chemical relaxers in 74 women with central centrifugal cicatricial alopecia. Int J Trichology. 2020;12:176-181. doi:10.4103/ijt.ijt_37_20
  14. Aguh C, Dina Y, Talbot CC Jr, et al. Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2018;79:904-912.e901. doi:10.1016/j.jaad.2018.05.1257
References
  1. Callender VD, McMichael AJ, Cohen GF. Medical and surgical therapies for alopecias in black women. Dermatol Ther. 2004;17:164-176. doi:10.1111/j.1396-0296.2004.04017.x
  2. Herskovitz I, Miteva M. Central centrifugal cicatricial alopecia: challenges and solutions. Clin Cosmet Investig Dermatol. 2016;9:175-181. doi:10.2147/CCID.S100816
  3. Tanus A, Oliveira CCC, Villarreal DJ, et al. Black women’s hair: the main scalp dermatoses and aesthetic practices in women of African ethnicity. An Bras Dermatol. 2015;90:450-465. doi:10.1590/abd1806-4841.20152845
  4. Gathers RC, Lim HW. Central centrifugal cicatricial alopecia: past, present, and future. J Am Acad Dermatol. 2009;60:660-668. doi:10.1016/j.jaad.2008.09.066
  5. Haskin A, Aguh C. All hairstyles are not created equal: what the dermatologist needs to know about black hairstyling practices and the risk of traction alopecia (TA). J Am Acad Dermatol. 2016;75:606-611. doi:10.1016/j.jaad.2016.02.1162
  6. Loussouarn G, Garcel A-L, Lozano I, et al. Worldwide diversity of hair curliness: a new method of assessment. Int J Dermatol. 2007;46(suppl 1):2-6. doi:10.1111/j.1365-4632.2007.03453.x
  7. De la Mettrie R, Saint-Léger D, Loussouarn G, et al. Shape variability and classification of human hair: a worldwide approach. Hum Biol. 2007;79:265-281. doi:10.1353/hub.2007.0045
  8. Takahashi T. Unique hair properties that emerge from combinations of multiple races. Cosmetics. 2019;6:36. https://doi.org/10.3390/cosmetics6020036
  9. Cloete E, Khumalo NP, Ngoepe MN. The what, why and how of curly hair: a review. Proc Math Phys Eng Sci. 2019;475:20190516. doi:10.1098/rspa.2019.0516
  10. Westgate GE, Ginger RS, Green MR. The biology and genetics of curly hair. Exp Dermatol. 2017;26:483-490. doi:10.1111/exd.13347
  11. McMichael AJ. Ethnic hair update: past and present. J Am Acad Dermatol. 2003;48(6 suppl):S127-S133. doi:10.1067/mjd.2003.278
  12. Roseborough IE, McMichael AJ. Hair care practices in African-American patients. Semin Cutan Med Surg. 2009;28:103-108. doi:10.1016/j.sder.2009.04.007
  13. Narasimman M, De Bedout V, Castillo DE, et al. Increased association between previous pregnancies and use of chemical relaxers in 74 women with central centrifugal cicatricial alopecia. Int J Trichology. 2020;12:176-181. doi:10.4103/ijt.ijt_37_20
  14. Aguh C, Dina Y, Talbot CC Jr, et al. Fibroproliferative genes are preferentially expressed in central centrifugal cicatricial alopecia. J Am Acad Dermatol. 2018;79:904-912.e901. doi:10.1016/j.jaad.2018.05.1257
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Chewing xylitol gum may modestly reduce preterm birth

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Fri, 02/04/2022 - 09:27

In the country with one of the highest rates of preterm birth in the world, these early deliveries dropped by 24% with a simple intervention: chewing gum with xylitol during pregnancy. The decrease in preterm births was linked to improvement in oral health, according to research presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Although the findings, from a randomized controlled trial of women in Malawi, barely reached statistical significance, the researchers also documented a reduction in periodontitis (gum disease) that appears to correlate with the reduction in early deliveries, according to Kjersti Aagaard, MD, PhD, of Baylor College of Medicine and Texas Children’s Hospital, both in Houston.

Dr. Ilina Pluym

“For a while, we have known about the association with poor oral health and preterm birth but I am not aware of a study of this magnitude suggesting a simple and effective treatment option,” said Ilina Pluym, MD, an assistant professor in maternal fetal medicine at the University of California, Los Angeles, who attended the presentation. Dr. Pluym called the new data “compelling” and said the study “adds to our possible strategies to treat a condition that causes a significant burden of disease worldwide.” The findings must be replicated, ideally in countries with lower rates of preterm birth and periodontal disease to see if the effect is similar, before broadly implementing this cheap and simple intervention.

Preterm birth is a leading cause of infant mortality and a major underlying cause of health problems in children under 5 worldwide. As many as 42% of children born preterm have a health condition related to their prematurity or do not survive childhood.

About one in five babies in Malawi are born between 26 and 37 weeks, about double the U.S. rate of 10.8% preterm births, which in this country is considered births that occur between 23 and 37 weeks’ gestation. Researchers also chose Malawi for the trial because residents there see preterm birth as a widespread problem that must be addressed, Dr. Aagaard said.

Multiple previous studies have found a link between periodontal disease and deliveries that are preterm or low birth weight, Dr. Aagaard told attendees. However, 11 randomized controlled trials that involved treating periodontal disease did not reduce preterm birth despite improving periodontitis and oral health.

Dr. Aagaard’s team decided to test the effectiveness of xylitol – a natural prebiotic found in fruits, vegetables, and bran – because harmful oral bacteria cannot metabolize the substance, and regular use of xylitol reduces the number of harmful mouth bacteria while increasing the number of good microbes in the mouth. In addition, a study in 2006 found that children up to 4 years old had fewer cavities and ear infections when their mothers chewed gum containing xylitol and other compounds. Dr. Aagaard noted that gums without xylitol do not appear to produce the same improvements in oral health.

Before beginning the trial, Dr. Aagaard’s group spent 3 years doing a “run-in” study to ensure a larger, longer-term trial in Malawi was feasible. That initial study found a reduction in tooth decay and periodontal inflammation with use of xylitol. The researchers also learned that participants preferred gum over lozenges or lollipops. Nearly all the participants (92%) chewed the gum twice daily.

Dr. Kjersti Aagaard

Among 10,069 women who enrolled in the trial, 96% remained in it until the end. Of the initial total, 4,029 participants underwent an oral health assessment at the start of the study, and 920 had a follow-up oral health assessment.

Of the 4,349 women who chewed xylitol gum, 12.6% gave birth before 37 weeks, compared with 16.5% preterm births among the 5,321 women in the control group – a 24% reduction (P = .045). The 16.5% rate among women not chewing gum was still lower than the national rate of 19.6%, possibly related to the education the participants received, according to the researchers.

No statistically significant reduction occurred for births at less than 34 weeks, but the reduction in late preterm births – babies born between 34 and 37 weeks – was also borderline in statistical significance (P = .049). Only 9.9% of women chewing xylitol gum had a late preterm birth compared to 13.5% of women who only received health education.

The researchers estimated it would take 26 pregnant women chewing xylitol gum to prevent one preterm birth. At a cost of $24-$29 per pregnancy for the gum, preventing each preterm birth in a community would cost $623-$754.

The researchers also observed a 30% reduction in newborns weighing less than 2,500 g (5.5 pounds), with 8.9% of low-birth-weight babies born to moms chewing gum and 12.9% of low-birth-weight babies born to those not provided gum (P = .046). They attributed this reduction in low birth weight to the lower proportion of late preterm births. The groups showed no significant differences in stillbirths or newborn deaths.

The researchers did, however, find a significant reduction in periodontitis among the women who chewed xylitol gum who came for follow-up dental visits. The prevalence of periodontal disease dropped from 31% to 27% in those not chewing gum but from 31% to 21% in gum chewers (P = .04).

“This cannot be attributed to overall oral health, as dental caries composite scores did not significantly differ while periodontitis measures did,” Dr. Aagaard said.

One limitation of the trial is that it was randomized by health centers instead by individual women, although the researchers tried to account for differences that might exist between the populations going to different facilities. Nor did the researchers assess how frequently the participants chewed gum – although the fact that the gum-chewing group had better oral health suggests they appear to have done so regularly.

Whether recommending xylitol chewing gum to pregnant women in other countries would affect rates of preterm birth is unclear. The ideal population for an intervention like this is one where the population has a high rate of periodontal disease or other preterm birth risk factors, Dr. Pluym said.

”Preterm birth is multifactorial,” she said. “There are often multiple risk factors and causes to the complex pathophysiological process and a quick fix is not the solution for everyone.”

The study was funded by the Thrasher Research Fund. Dr. Aagaard and Dr. Pluym reported no disclosures.

This story was updated on Feb. 4, 2022.

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In the country with one of the highest rates of preterm birth in the world, these early deliveries dropped by 24% with a simple intervention: chewing gum with xylitol during pregnancy. The decrease in preterm births was linked to improvement in oral health, according to research presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Although the findings, from a randomized controlled trial of women in Malawi, barely reached statistical significance, the researchers also documented a reduction in periodontitis (gum disease) that appears to correlate with the reduction in early deliveries, according to Kjersti Aagaard, MD, PhD, of Baylor College of Medicine and Texas Children’s Hospital, both in Houston.

Dr. Ilina Pluym

“For a while, we have known about the association with poor oral health and preterm birth but I am not aware of a study of this magnitude suggesting a simple and effective treatment option,” said Ilina Pluym, MD, an assistant professor in maternal fetal medicine at the University of California, Los Angeles, who attended the presentation. Dr. Pluym called the new data “compelling” and said the study “adds to our possible strategies to treat a condition that causes a significant burden of disease worldwide.” The findings must be replicated, ideally in countries with lower rates of preterm birth and periodontal disease to see if the effect is similar, before broadly implementing this cheap and simple intervention.

Preterm birth is a leading cause of infant mortality and a major underlying cause of health problems in children under 5 worldwide. As many as 42% of children born preterm have a health condition related to their prematurity or do not survive childhood.

About one in five babies in Malawi are born between 26 and 37 weeks, about double the U.S. rate of 10.8% preterm births, which in this country is considered births that occur between 23 and 37 weeks’ gestation. Researchers also chose Malawi for the trial because residents there see preterm birth as a widespread problem that must be addressed, Dr. Aagaard said.

Multiple previous studies have found a link between periodontal disease and deliveries that are preterm or low birth weight, Dr. Aagaard told attendees. However, 11 randomized controlled trials that involved treating periodontal disease did not reduce preterm birth despite improving periodontitis and oral health.

Dr. Aagaard’s team decided to test the effectiveness of xylitol – a natural prebiotic found in fruits, vegetables, and bran – because harmful oral bacteria cannot metabolize the substance, and regular use of xylitol reduces the number of harmful mouth bacteria while increasing the number of good microbes in the mouth. In addition, a study in 2006 found that children up to 4 years old had fewer cavities and ear infections when their mothers chewed gum containing xylitol and other compounds. Dr. Aagaard noted that gums without xylitol do not appear to produce the same improvements in oral health.

Before beginning the trial, Dr. Aagaard’s group spent 3 years doing a “run-in” study to ensure a larger, longer-term trial in Malawi was feasible. That initial study found a reduction in tooth decay and periodontal inflammation with use of xylitol. The researchers also learned that participants preferred gum over lozenges or lollipops. Nearly all the participants (92%) chewed the gum twice daily.

Dr. Kjersti Aagaard

Among 10,069 women who enrolled in the trial, 96% remained in it until the end. Of the initial total, 4,029 participants underwent an oral health assessment at the start of the study, and 920 had a follow-up oral health assessment.

Of the 4,349 women who chewed xylitol gum, 12.6% gave birth before 37 weeks, compared with 16.5% preterm births among the 5,321 women in the control group – a 24% reduction (P = .045). The 16.5% rate among women not chewing gum was still lower than the national rate of 19.6%, possibly related to the education the participants received, according to the researchers.

No statistically significant reduction occurred for births at less than 34 weeks, but the reduction in late preterm births – babies born between 34 and 37 weeks – was also borderline in statistical significance (P = .049). Only 9.9% of women chewing xylitol gum had a late preterm birth compared to 13.5% of women who only received health education.

The researchers estimated it would take 26 pregnant women chewing xylitol gum to prevent one preterm birth. At a cost of $24-$29 per pregnancy for the gum, preventing each preterm birth in a community would cost $623-$754.

The researchers also observed a 30% reduction in newborns weighing less than 2,500 g (5.5 pounds), with 8.9% of low-birth-weight babies born to moms chewing gum and 12.9% of low-birth-weight babies born to those not provided gum (P = .046). They attributed this reduction in low birth weight to the lower proportion of late preterm births. The groups showed no significant differences in stillbirths or newborn deaths.

The researchers did, however, find a significant reduction in periodontitis among the women who chewed xylitol gum who came for follow-up dental visits. The prevalence of periodontal disease dropped from 31% to 27% in those not chewing gum but from 31% to 21% in gum chewers (P = .04).

“This cannot be attributed to overall oral health, as dental caries composite scores did not significantly differ while periodontitis measures did,” Dr. Aagaard said.

One limitation of the trial is that it was randomized by health centers instead by individual women, although the researchers tried to account for differences that might exist between the populations going to different facilities. Nor did the researchers assess how frequently the participants chewed gum – although the fact that the gum-chewing group had better oral health suggests they appear to have done so regularly.

Whether recommending xylitol chewing gum to pregnant women in other countries would affect rates of preterm birth is unclear. The ideal population for an intervention like this is one where the population has a high rate of periodontal disease or other preterm birth risk factors, Dr. Pluym said.

”Preterm birth is multifactorial,” she said. “There are often multiple risk factors and causes to the complex pathophysiological process and a quick fix is not the solution for everyone.”

The study was funded by the Thrasher Research Fund. Dr. Aagaard and Dr. Pluym reported no disclosures.

This story was updated on Feb. 4, 2022.

In the country with one of the highest rates of preterm birth in the world, these early deliveries dropped by 24% with a simple intervention: chewing gum with xylitol during pregnancy. The decrease in preterm births was linked to improvement in oral health, according to research presented at the meeting sponsored by the Society for Maternal-Fetal Medicine.

Although the findings, from a randomized controlled trial of women in Malawi, barely reached statistical significance, the researchers also documented a reduction in periodontitis (gum disease) that appears to correlate with the reduction in early deliveries, according to Kjersti Aagaard, MD, PhD, of Baylor College of Medicine and Texas Children’s Hospital, both in Houston.

Dr. Ilina Pluym

“For a while, we have known about the association with poor oral health and preterm birth but I am not aware of a study of this magnitude suggesting a simple and effective treatment option,” said Ilina Pluym, MD, an assistant professor in maternal fetal medicine at the University of California, Los Angeles, who attended the presentation. Dr. Pluym called the new data “compelling” and said the study “adds to our possible strategies to treat a condition that causes a significant burden of disease worldwide.” The findings must be replicated, ideally in countries with lower rates of preterm birth and periodontal disease to see if the effect is similar, before broadly implementing this cheap and simple intervention.

Preterm birth is a leading cause of infant mortality and a major underlying cause of health problems in children under 5 worldwide. As many as 42% of children born preterm have a health condition related to their prematurity or do not survive childhood.

About one in five babies in Malawi are born between 26 and 37 weeks, about double the U.S. rate of 10.8% preterm births, which in this country is considered births that occur between 23 and 37 weeks’ gestation. Researchers also chose Malawi for the trial because residents there see preterm birth as a widespread problem that must be addressed, Dr. Aagaard said.

Multiple previous studies have found a link between periodontal disease and deliveries that are preterm or low birth weight, Dr. Aagaard told attendees. However, 11 randomized controlled trials that involved treating periodontal disease did not reduce preterm birth despite improving periodontitis and oral health.

Dr. Aagaard’s team decided to test the effectiveness of xylitol – a natural prebiotic found in fruits, vegetables, and bran – because harmful oral bacteria cannot metabolize the substance, and regular use of xylitol reduces the number of harmful mouth bacteria while increasing the number of good microbes in the mouth. In addition, a study in 2006 found that children up to 4 years old had fewer cavities and ear infections when their mothers chewed gum containing xylitol and other compounds. Dr. Aagaard noted that gums without xylitol do not appear to produce the same improvements in oral health.

Before beginning the trial, Dr. Aagaard’s group spent 3 years doing a “run-in” study to ensure a larger, longer-term trial in Malawi was feasible. That initial study found a reduction in tooth decay and periodontal inflammation with use of xylitol. The researchers also learned that participants preferred gum over lozenges or lollipops. Nearly all the participants (92%) chewed the gum twice daily.

Dr. Kjersti Aagaard

Among 10,069 women who enrolled in the trial, 96% remained in it until the end. Of the initial total, 4,029 participants underwent an oral health assessment at the start of the study, and 920 had a follow-up oral health assessment.

Of the 4,349 women who chewed xylitol gum, 12.6% gave birth before 37 weeks, compared with 16.5% preterm births among the 5,321 women in the control group – a 24% reduction (P = .045). The 16.5% rate among women not chewing gum was still lower than the national rate of 19.6%, possibly related to the education the participants received, according to the researchers.

No statistically significant reduction occurred for births at less than 34 weeks, but the reduction in late preterm births – babies born between 34 and 37 weeks – was also borderline in statistical significance (P = .049). Only 9.9% of women chewing xylitol gum had a late preterm birth compared to 13.5% of women who only received health education.

The researchers estimated it would take 26 pregnant women chewing xylitol gum to prevent one preterm birth. At a cost of $24-$29 per pregnancy for the gum, preventing each preterm birth in a community would cost $623-$754.

The researchers also observed a 30% reduction in newborns weighing less than 2,500 g (5.5 pounds), with 8.9% of low-birth-weight babies born to moms chewing gum and 12.9% of low-birth-weight babies born to those not provided gum (P = .046). They attributed this reduction in low birth weight to the lower proportion of late preterm births. The groups showed no significant differences in stillbirths or newborn deaths.

The researchers did, however, find a significant reduction in periodontitis among the women who chewed xylitol gum who came for follow-up dental visits. The prevalence of periodontal disease dropped from 31% to 27% in those not chewing gum but from 31% to 21% in gum chewers (P = .04).

“This cannot be attributed to overall oral health, as dental caries composite scores did not significantly differ while periodontitis measures did,” Dr. Aagaard said.

One limitation of the trial is that it was randomized by health centers instead by individual women, although the researchers tried to account for differences that might exist between the populations going to different facilities. Nor did the researchers assess how frequently the participants chewed gum – although the fact that the gum-chewing group had better oral health suggests they appear to have done so regularly.

Whether recommending xylitol chewing gum to pregnant women in other countries would affect rates of preterm birth is unclear. The ideal population for an intervention like this is one where the population has a high rate of periodontal disease or other preterm birth risk factors, Dr. Pluym said.

”Preterm birth is multifactorial,” she said. “There are often multiple risk factors and causes to the complex pathophysiological process and a quick fix is not the solution for everyone.”

The study was funded by the Thrasher Research Fund. Dr. Aagaard and Dr. Pluym reported no disclosures.

This story was updated on Feb. 4, 2022.

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The differences between IBS-C and CIC

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The Differences Between IBS-C and CIC

Lin Chang, MD, serves as the Co-Director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience at UCLA. She is also Program Director of the UCLA Gastroenterology Fellowship Program. Dr. Chang’s expertise is in disorders of gut-brain interaction (also known as functional gastrointestinal disorders), particularly irritable bowel syndrome (IBS). She has recently served as the Clinical Research Councilor of the AGA Governing Board. She previously served as President of the American Neurogastroenterology and Motility Society (ANMS) and is a member of the Rome Foundation Board of Directors.

 

As a gastroenterologist focused on the pathophysiology of IBS related to stress, sex differences, and neuroendocrine alterations, and the treatment of IBS, Dr. Chang, what exactly is IBS-C and how is CIC defined differently?

Dr. Chang: IBS-C is irritable bowel syndrome with predominantly constipation which is a type of IBS. IBS is a symptom-based diagnosis for a chronic or recurrent gastrointestinal condition where patients have abdominal pain that's associated with constipation, diarrhea, or both. IBS is subtyped by bowel habit predominance into IBS with constipation, IBS with diarrhea, and IBS with mixed bowel habits. With IBS-mixed, one of the subgroups of IBS, they have diarrhea as well as constipation.

Patients will present with abdominal pain for usually one day, a week or even more. Sometimes, a little less. But when they have pain, it's associated with a change in stool frequency, a change in stool form, and/or the pain is related to defecation, meaning that when a patient has a bowel movement, they'll either have more pain or they'll have some pain relief, which is more common.

Now, CIC is Chronic Idiopathic Constipation and that's the term used for chronic constipation where abdominal pain is not a predominant symptom. The main difference between IBS-C and CIC is that abdominal pain is not a predominant or frequent symptom.

Patients with CIC can occasionally get abdominal pain, particularly if they haven't had a bowel movement for a prolonged period of time. However, in patients with IBS-C, they can have some normalization of their bowel habits or their constipation with treatment, although they can still have abdominal pain and discomfort. So, these patients have an element of visceral hypersensitivity where the gut is more sensitive than usual.

Very interesting Dr. Chang, and are the causes of IBS-C and CIC different? And then if so, in what ways?

Dr. Chang: Well, IBS is a multifactorial disorder and is known as a functional GI disorder. It has been redefined as a disorder of gut-brain interaction, which is a term people are starting to use and hear more.

There's a lot of scientific evidence that has demonstrated that IBS and other similar conditions, including chronic constipation and functional dyspepsia, where there is no structural and biochemical abnormality that you can readily determine, but there's scientific evidence to support that there’s an alteration in the brain-gut communication associated with symptoms. Altered brain-gut interactions are manifested by one or more of the following, which is visceral hypersensitivity, immune function, gut microbiota, gut motility, and central nervous system processing of visceral information. So, this really is a true brain-gut disorder.

There are multiple risk factors when it comes to IBS. It could be infection, or it could be stressful life events, in childhood and/or as an adult. Evidence shows that there can be some familial or genetic predisposition. Food and stress are the main triggers of IBS. Whereas, CIC can be considered a brain-gut disorder, but there's been more focus on gut function, including abnormal motility and defecation. There are three main subtypes of chronic idiopathic constipation.

There are six signs or symptoms that are the diagnostic criteria for CIC and the patient, or the individual, must meet two out of the six criteria, which I ask patients who report having constipation.

The subtypes of CIC are slow transit constipation where the transit time of stool through the colon is slower than normal which can be measured. Then there's normal transit constipation where the transit time of stool through the colon is normal. This group has not been studied that well and it's not completely understood why these patients have constipation, but it could be that they have a greater perception of constipation even though the transit time of stool in the colon is not slow.

And then there's the third group--defecatory disorders. The transit time of stool through the colon of stool can be normal or slow, but coexisting with that, a patient can have a defecation disorder. A common one is called dyssynergic defecation where the pelvic floor and the anal sphincter muscles don't relax appropriately when trying to evacuate stool. In this case, the rectum cannot straighten as much, the pelvic floor doesn't relax and descend, and stool is not easily evacuated.

There are also other conditions such as a significant large rectocele and rectal prolapse. Those are examples of defecatory disorders. So, when you see a patient with CIC, you want to first rule out secondary constipation where another condition or medication is causing constipation, such as hypothyroidism, diabetes, or a neurodegenerative disorder, or medications like opioids or anticholinergics.

CIC means that there isn't another cause of constipation, that is it is not a secondary condition. It's a primary chronic idiopathic constipation.

Let’s talk about the symptoms you're looking for and how they present themselves differently for IBS-C and CIC, at different times, depending on the diagnosis.

Dr. Chang: Sure! I mentioned what the symptom criteria of IBS was, which is having pain of a certain frequency that is associated with altered bowel habits. To determine the bowel habit subtype of IBS, you must assess the predominant stool form. We use the Bristol Stool Form Scale which is a validated stool form scale that's well known. It's publicly available.

The investigators did a survey years ago and they looked at the general population and found that the description of stool really could be encompassed in seven types, and those seven types of stool form correlate with transit time through the bowel. There's type 1 to type 7. Type 1 and 2 are the constipation type stool form where there's harder, drier pellet-like stools and that's associated with slower transit time through the colon. Types 3, 4 and 5 are more within the normal range. Types 6 and 7 are the loose or watery stools are suggestive of faster stool transit and considered indicative of diarrhea.

In patients with IBS-C,  at least 25% of their bowel movements are the type 1 or 2, which is the harder, drier stool and less than 25% of bowel movements are loose watery. For diarrhea, it's opposite. IBS-mixed bowel habits, at least 25% of bowel movements are type 1 or 2 and at least 25% are type 6 or 7.

Now, to meet the diagnostic criteria of CIC, you must meet two out of the six criteria. All but one of the criteria must be present with at least 25% of bowel movements. There’s a straining, sensation of incomplete evacuation, use of manual maneuvers to help facilitate stool evacuation, sensation of anorectal blockage, and a Bristol Stool Form Scale of type 1 or 2. The remaining criterion is less than three bowel movements per week. If a patient reports, or endorses, at least two of those six symptoms and signs, then their symptoms meet criteria.

Both IBS-C and CIC are chronic conditions. For the diagnosis of both IBS-C and CIC, symptoms are present for at least three months and started at least six months ago.

What's interesting is that if you ask health care providers and physicians what constipation is and  what symptoms define constipation, most of them will say having less than three bowel movements per week or infrequent bowel movements. But it turns out that in chronic constipation patients, they'll report decreased bowel movement frequency. About only a third of them will report that. They'll report the other symptoms of a constipation.

They could have multiple symptoms, but straining is a very common symptom as is hard stools. Even after a bowel movement, they don't feel completely evacuated. That's called sensation of incomplete evacuation. In fact, patients will present with different types of symptoms.

Constipation is often considered a symptom and a diagnosis. And it's fine to use it as a diagnosis, but you really want to delve into what symptoms of constipation they’re experiencing. Are they experiencing straining? Hard stools? Are they not having a bowel movement frequently? That's really part of the history taking so you can determine what the patient perceives as constipation and which symptom are bothersome to them.

So once diagnosed, how different are the treatments for each of the diseases?

Dr. Chang: In both IBS-C and CIC, treatments can include diet, exercise or ambulating more. Often, I will make sure they're drinking plenty of fluids. Those are dietary recommendations such as increasing fiber with foods and/or fiber supplementation. When looking at the difference between IBS-C and CIC, the one thing I should say is that they really exist along a spectrum, so we shouldn't really think of them as two separate diagnoses.

This goes back to the idea we touched on earlier that patients can move back and forth between the different diagnoses. At one point, a patient could have frequent abdominal pain and constipation and the symptoms would meet the criteria for IBS-C. But in the future, the pain gets better or resolves, but there’s still constipation. Their symptoms are more indicative of CIC. So, these conditions really exist along a spectrum.

Because both patients will have constipation symptoms, medications or treatments that help improve constipation can be used for both IBS-C and CIC. The key difference with IBS-C is that in addition to having altered gut motility where they're not moving stool effectively through the bowel, they also have visceral hypersensitivity which manifests as abdominal pain, bloating, and discomfort. Although there may be a modest correlation with bowel habits and IBS, sometimes, they don't correlate that well.

There are some treatments that help pain and constipation and those are the treatments that you want to think about in those patients with IBS-C where they're reporting both pain and constipation.

Now, it's very reasonable to use similar treatments in patients with mild symptoms, whether it's IBS or CIC. But if someone's having more severe IBS-C and they're having a fair amount of pain associated with constipation, you really want to think about treatments that can help reduce pain and constipation and not just constipation.

Treatments can include fiber such as psyllium and osmotic laxatives like polyethylene glycol, which is called MiraLAX, and magnesium-based regimens. These help constipation symptoms, but they don't significantly relieve abdominal pain. If someone came to me with IBS-C and they said, well, I do have pain, but it is mild, maybe a 2 or 3 out of 10, I could probably give them any one of the treatments I just mentioned. But in patients who say that their pain is 8 out of 10 or that it is their predominant symptom, I wouldn't necessarily prescribe the same treatment and would more likely opt for a treatment that has been shown to effectively reduce abdominal pain and constipation.

When you’re looking at the data, are their studies that might show a focus on the treatments and how they might impact the patients differently for IBS-C compared to CIC?

Dr. Chang: Well, the primary study endpoints that are used to determine efficacy of treatment in clinical trials differ in studies of CIC and IBS-C. However, studies also assess individual gastrointestinal symptoms that can be similar in both studies.

So, I would say that treatments that have been shown to be efficacious both in IBS-C and CIC likely relieve constipation symptoms similarly in both groups assuming that the severity of symptoms is comparable. It's just that in the CIC patient population, abdominal pain is not evaluated as much as it is in IBS-C.

References

F. Mearin, B. E. Lacy, L. Chang, W. D. Chey, A. J. Lembo, M. Simren, et al. Gastroenterology 2016 Vol. 150 Pages 1393-1407. http://www.ncbi.nlm.nih.gov/pubmed/27144627

 

D. A. Drossman. Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features and Rome IV. Gastroenterology 2016  https://www.ncbi.nlm.nih.gov/pubmed/27144617

 

Chang L. How to Approach a Patient with Difficult-to-Treat IBS. Gastroenterology 2021 Accession Number: 34331916 DOI: S0016-5085(21)03285-6 [pii]

10.1053/j.gastro.2021.07.034 https://www.ncbi.nlm.nih.gov/pubmed/34331916

 

A. E. Bharucha and B. E. Lacy. Mechanisms, Evaluation, and Management of Chronic Constipation. Gastroenterology 2020 Vol. 158 Issue 5 Pages 1232-1249 e3

Accession Number: 31945360 PMCID: PMC7573977 DOI: S0016-5085(20)30080-9 [pii]10.1053/j.gastro.2019.12.034 https://www.ncbi.nlm.nih.gov/pubmed/31945360

Author and Disclosure Information

Lin Chang, MD is a Professor of Medicine and Vice-Chief of the Vatche and Tamar Manoukian Division of Digestive Diseases at the David Geffen School of Medicine at UCLA.

 

Dr. Chang serves on the scientific advisory boards or does consulting for Ironwood, Immunic, Mauna Kea Technologies and Trellus. She is a speaker for AbbVie. She receives research grants from Arena and Ironwood, and stock options from ModifyHealth and Trellus.

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Author and Disclosure Information

Lin Chang, MD is a Professor of Medicine and Vice-Chief of the Vatche and Tamar Manoukian Division of Digestive Diseases at the David Geffen School of Medicine at UCLA.

 

Dr. Chang serves on the scientific advisory boards or does consulting for Ironwood, Immunic, Mauna Kea Technologies and Trellus. She is a speaker for AbbVie. She receives research grants from Arena and Ironwood, and stock options from ModifyHealth and Trellus.

Author and Disclosure Information

Lin Chang, MD is a Professor of Medicine and Vice-Chief of the Vatche and Tamar Manoukian Division of Digestive Diseases at the David Geffen School of Medicine at UCLA.

 

Dr. Chang serves on the scientific advisory boards or does consulting for Ironwood, Immunic, Mauna Kea Technologies and Trellus. She is a speaker for AbbVie. She receives research grants from Arena and Ironwood, and stock options from ModifyHealth and Trellus.

Lin Chang, MD, serves as the Co-Director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience at UCLA. She is also Program Director of the UCLA Gastroenterology Fellowship Program. Dr. Chang’s expertise is in disorders of gut-brain interaction (also known as functional gastrointestinal disorders), particularly irritable bowel syndrome (IBS). She has recently served as the Clinical Research Councilor of the AGA Governing Board. She previously served as President of the American Neurogastroenterology and Motility Society (ANMS) and is a member of the Rome Foundation Board of Directors.

 

As a gastroenterologist focused on the pathophysiology of IBS related to stress, sex differences, and neuroendocrine alterations, and the treatment of IBS, Dr. Chang, what exactly is IBS-C and how is CIC defined differently?

Dr. Chang: IBS-C is irritable bowel syndrome with predominantly constipation which is a type of IBS. IBS is a symptom-based diagnosis for a chronic or recurrent gastrointestinal condition where patients have abdominal pain that's associated with constipation, diarrhea, or both. IBS is subtyped by bowel habit predominance into IBS with constipation, IBS with diarrhea, and IBS with mixed bowel habits. With IBS-mixed, one of the subgroups of IBS, they have diarrhea as well as constipation.

Patients will present with abdominal pain for usually one day, a week or even more. Sometimes, a little less. But when they have pain, it's associated with a change in stool frequency, a change in stool form, and/or the pain is related to defecation, meaning that when a patient has a bowel movement, they'll either have more pain or they'll have some pain relief, which is more common.

Now, CIC is Chronic Idiopathic Constipation and that's the term used for chronic constipation where abdominal pain is not a predominant symptom. The main difference between IBS-C and CIC is that abdominal pain is not a predominant or frequent symptom.

Patients with CIC can occasionally get abdominal pain, particularly if they haven't had a bowel movement for a prolonged period of time. However, in patients with IBS-C, they can have some normalization of their bowel habits or their constipation with treatment, although they can still have abdominal pain and discomfort. So, these patients have an element of visceral hypersensitivity where the gut is more sensitive than usual.

Very interesting Dr. Chang, and are the causes of IBS-C and CIC different? And then if so, in what ways?

Dr. Chang: Well, IBS is a multifactorial disorder and is known as a functional GI disorder. It has been redefined as a disorder of gut-brain interaction, which is a term people are starting to use and hear more.

There's a lot of scientific evidence that has demonstrated that IBS and other similar conditions, including chronic constipation and functional dyspepsia, where there is no structural and biochemical abnormality that you can readily determine, but there's scientific evidence to support that there’s an alteration in the brain-gut communication associated with symptoms. Altered brain-gut interactions are manifested by one or more of the following, which is visceral hypersensitivity, immune function, gut microbiota, gut motility, and central nervous system processing of visceral information. So, this really is a true brain-gut disorder.

There are multiple risk factors when it comes to IBS. It could be infection, or it could be stressful life events, in childhood and/or as an adult. Evidence shows that there can be some familial or genetic predisposition. Food and stress are the main triggers of IBS. Whereas, CIC can be considered a brain-gut disorder, but there's been more focus on gut function, including abnormal motility and defecation. There are three main subtypes of chronic idiopathic constipation.

There are six signs or symptoms that are the diagnostic criteria for CIC and the patient, or the individual, must meet two out of the six criteria, which I ask patients who report having constipation.

The subtypes of CIC are slow transit constipation where the transit time of stool through the colon is slower than normal which can be measured. Then there's normal transit constipation where the transit time of stool through the colon is normal. This group has not been studied that well and it's not completely understood why these patients have constipation, but it could be that they have a greater perception of constipation even though the transit time of stool in the colon is not slow.

And then there's the third group--defecatory disorders. The transit time of stool through the colon of stool can be normal or slow, but coexisting with that, a patient can have a defecation disorder. A common one is called dyssynergic defecation where the pelvic floor and the anal sphincter muscles don't relax appropriately when trying to evacuate stool. In this case, the rectum cannot straighten as much, the pelvic floor doesn't relax and descend, and stool is not easily evacuated.

There are also other conditions such as a significant large rectocele and rectal prolapse. Those are examples of defecatory disorders. So, when you see a patient with CIC, you want to first rule out secondary constipation where another condition or medication is causing constipation, such as hypothyroidism, diabetes, or a neurodegenerative disorder, or medications like opioids or anticholinergics.

CIC means that there isn't another cause of constipation, that is it is not a secondary condition. It's a primary chronic idiopathic constipation.

Let’s talk about the symptoms you're looking for and how they present themselves differently for IBS-C and CIC, at different times, depending on the diagnosis.

Dr. Chang: Sure! I mentioned what the symptom criteria of IBS was, which is having pain of a certain frequency that is associated with altered bowel habits. To determine the bowel habit subtype of IBS, you must assess the predominant stool form. We use the Bristol Stool Form Scale which is a validated stool form scale that's well known. It's publicly available.

The investigators did a survey years ago and they looked at the general population and found that the description of stool really could be encompassed in seven types, and those seven types of stool form correlate with transit time through the bowel. There's type 1 to type 7. Type 1 and 2 are the constipation type stool form where there's harder, drier pellet-like stools and that's associated with slower transit time through the colon. Types 3, 4 and 5 are more within the normal range. Types 6 and 7 are the loose or watery stools are suggestive of faster stool transit and considered indicative of diarrhea.

In patients with IBS-C,  at least 25% of their bowel movements are the type 1 or 2, which is the harder, drier stool and less than 25% of bowel movements are loose watery. For diarrhea, it's opposite. IBS-mixed bowel habits, at least 25% of bowel movements are type 1 or 2 and at least 25% are type 6 or 7.

Now, to meet the diagnostic criteria of CIC, you must meet two out of the six criteria. All but one of the criteria must be present with at least 25% of bowel movements. There’s a straining, sensation of incomplete evacuation, use of manual maneuvers to help facilitate stool evacuation, sensation of anorectal blockage, and a Bristol Stool Form Scale of type 1 or 2. The remaining criterion is less than three bowel movements per week. If a patient reports, or endorses, at least two of those six symptoms and signs, then their symptoms meet criteria.

Both IBS-C and CIC are chronic conditions. For the diagnosis of both IBS-C and CIC, symptoms are present for at least three months and started at least six months ago.

What's interesting is that if you ask health care providers and physicians what constipation is and  what symptoms define constipation, most of them will say having less than three bowel movements per week or infrequent bowel movements. But it turns out that in chronic constipation patients, they'll report decreased bowel movement frequency. About only a third of them will report that. They'll report the other symptoms of a constipation.

They could have multiple symptoms, but straining is a very common symptom as is hard stools. Even after a bowel movement, they don't feel completely evacuated. That's called sensation of incomplete evacuation. In fact, patients will present with different types of symptoms.

Constipation is often considered a symptom and a diagnosis. And it's fine to use it as a diagnosis, but you really want to delve into what symptoms of constipation they’re experiencing. Are they experiencing straining? Hard stools? Are they not having a bowel movement frequently? That's really part of the history taking so you can determine what the patient perceives as constipation and which symptom are bothersome to them.

So once diagnosed, how different are the treatments for each of the diseases?

Dr. Chang: In both IBS-C and CIC, treatments can include diet, exercise or ambulating more. Often, I will make sure they're drinking plenty of fluids. Those are dietary recommendations such as increasing fiber with foods and/or fiber supplementation. When looking at the difference between IBS-C and CIC, the one thing I should say is that they really exist along a spectrum, so we shouldn't really think of them as two separate diagnoses.

This goes back to the idea we touched on earlier that patients can move back and forth between the different diagnoses. At one point, a patient could have frequent abdominal pain and constipation and the symptoms would meet the criteria for IBS-C. But in the future, the pain gets better or resolves, but there’s still constipation. Their symptoms are more indicative of CIC. So, these conditions really exist along a spectrum.

Because both patients will have constipation symptoms, medications or treatments that help improve constipation can be used for both IBS-C and CIC. The key difference with IBS-C is that in addition to having altered gut motility where they're not moving stool effectively through the bowel, they also have visceral hypersensitivity which manifests as abdominal pain, bloating, and discomfort. Although there may be a modest correlation with bowel habits and IBS, sometimes, they don't correlate that well.

There are some treatments that help pain and constipation and those are the treatments that you want to think about in those patients with IBS-C where they're reporting both pain and constipation.

Now, it's very reasonable to use similar treatments in patients with mild symptoms, whether it's IBS or CIC. But if someone's having more severe IBS-C and they're having a fair amount of pain associated with constipation, you really want to think about treatments that can help reduce pain and constipation and not just constipation.

Treatments can include fiber such as psyllium and osmotic laxatives like polyethylene glycol, which is called MiraLAX, and magnesium-based regimens. These help constipation symptoms, but they don't significantly relieve abdominal pain. If someone came to me with IBS-C and they said, well, I do have pain, but it is mild, maybe a 2 or 3 out of 10, I could probably give them any one of the treatments I just mentioned. But in patients who say that their pain is 8 out of 10 or that it is their predominant symptom, I wouldn't necessarily prescribe the same treatment and would more likely opt for a treatment that has been shown to effectively reduce abdominal pain and constipation.

When you’re looking at the data, are their studies that might show a focus on the treatments and how they might impact the patients differently for IBS-C compared to CIC?

Dr. Chang: Well, the primary study endpoints that are used to determine efficacy of treatment in clinical trials differ in studies of CIC and IBS-C. However, studies also assess individual gastrointestinal symptoms that can be similar in both studies.

So, I would say that treatments that have been shown to be efficacious both in IBS-C and CIC likely relieve constipation symptoms similarly in both groups assuming that the severity of symptoms is comparable. It's just that in the CIC patient population, abdominal pain is not evaluated as much as it is in IBS-C.

Lin Chang, MD, serves as the Co-Director of the G. Oppenheimer Center for Neurobiology of Stress and Resilience at UCLA. She is also Program Director of the UCLA Gastroenterology Fellowship Program. Dr. Chang’s expertise is in disorders of gut-brain interaction (also known as functional gastrointestinal disorders), particularly irritable bowel syndrome (IBS). She has recently served as the Clinical Research Councilor of the AGA Governing Board. She previously served as President of the American Neurogastroenterology and Motility Society (ANMS) and is a member of the Rome Foundation Board of Directors.

 

As a gastroenterologist focused on the pathophysiology of IBS related to stress, sex differences, and neuroendocrine alterations, and the treatment of IBS, Dr. Chang, what exactly is IBS-C and how is CIC defined differently?

Dr. Chang: IBS-C is irritable bowel syndrome with predominantly constipation which is a type of IBS. IBS is a symptom-based diagnosis for a chronic or recurrent gastrointestinal condition where patients have abdominal pain that's associated with constipation, diarrhea, or both. IBS is subtyped by bowel habit predominance into IBS with constipation, IBS with diarrhea, and IBS with mixed bowel habits. With IBS-mixed, one of the subgroups of IBS, they have diarrhea as well as constipation.

Patients will present with abdominal pain for usually one day, a week or even more. Sometimes, a little less. But when they have pain, it's associated with a change in stool frequency, a change in stool form, and/or the pain is related to defecation, meaning that when a patient has a bowel movement, they'll either have more pain or they'll have some pain relief, which is more common.

Now, CIC is Chronic Idiopathic Constipation and that's the term used for chronic constipation where abdominal pain is not a predominant symptom. The main difference between IBS-C and CIC is that abdominal pain is not a predominant or frequent symptom.

Patients with CIC can occasionally get abdominal pain, particularly if they haven't had a bowel movement for a prolonged period of time. However, in patients with IBS-C, they can have some normalization of their bowel habits or their constipation with treatment, although they can still have abdominal pain and discomfort. So, these patients have an element of visceral hypersensitivity where the gut is more sensitive than usual.

Very interesting Dr. Chang, and are the causes of IBS-C and CIC different? And then if so, in what ways?

Dr. Chang: Well, IBS is a multifactorial disorder and is known as a functional GI disorder. It has been redefined as a disorder of gut-brain interaction, which is a term people are starting to use and hear more.

There's a lot of scientific evidence that has demonstrated that IBS and other similar conditions, including chronic constipation and functional dyspepsia, where there is no structural and biochemical abnormality that you can readily determine, but there's scientific evidence to support that there’s an alteration in the brain-gut communication associated with symptoms. Altered brain-gut interactions are manifested by one or more of the following, which is visceral hypersensitivity, immune function, gut microbiota, gut motility, and central nervous system processing of visceral information. So, this really is a true brain-gut disorder.

There are multiple risk factors when it comes to IBS. It could be infection, or it could be stressful life events, in childhood and/or as an adult. Evidence shows that there can be some familial or genetic predisposition. Food and stress are the main triggers of IBS. Whereas, CIC can be considered a brain-gut disorder, but there's been more focus on gut function, including abnormal motility and defecation. There are three main subtypes of chronic idiopathic constipation.

There are six signs or symptoms that are the diagnostic criteria for CIC and the patient, or the individual, must meet two out of the six criteria, which I ask patients who report having constipation.

The subtypes of CIC are slow transit constipation where the transit time of stool through the colon is slower than normal which can be measured. Then there's normal transit constipation where the transit time of stool through the colon is normal. This group has not been studied that well and it's not completely understood why these patients have constipation, but it could be that they have a greater perception of constipation even though the transit time of stool in the colon is not slow.

And then there's the third group--defecatory disorders. The transit time of stool through the colon of stool can be normal or slow, but coexisting with that, a patient can have a defecation disorder. A common one is called dyssynergic defecation where the pelvic floor and the anal sphincter muscles don't relax appropriately when trying to evacuate stool. In this case, the rectum cannot straighten as much, the pelvic floor doesn't relax and descend, and stool is not easily evacuated.

There are also other conditions such as a significant large rectocele and rectal prolapse. Those are examples of defecatory disorders. So, when you see a patient with CIC, you want to first rule out secondary constipation where another condition or medication is causing constipation, such as hypothyroidism, diabetes, or a neurodegenerative disorder, or medications like opioids or anticholinergics.

CIC means that there isn't another cause of constipation, that is it is not a secondary condition. It's a primary chronic idiopathic constipation.

Let’s talk about the symptoms you're looking for and how they present themselves differently for IBS-C and CIC, at different times, depending on the diagnosis.

Dr. Chang: Sure! I mentioned what the symptom criteria of IBS was, which is having pain of a certain frequency that is associated with altered bowel habits. To determine the bowel habit subtype of IBS, you must assess the predominant stool form. We use the Bristol Stool Form Scale which is a validated stool form scale that's well known. It's publicly available.

The investigators did a survey years ago and they looked at the general population and found that the description of stool really could be encompassed in seven types, and those seven types of stool form correlate with transit time through the bowel. There's type 1 to type 7. Type 1 and 2 are the constipation type stool form where there's harder, drier pellet-like stools and that's associated with slower transit time through the colon. Types 3, 4 and 5 are more within the normal range. Types 6 and 7 are the loose or watery stools are suggestive of faster stool transit and considered indicative of diarrhea.

In patients with IBS-C,  at least 25% of their bowel movements are the type 1 or 2, which is the harder, drier stool and less than 25% of bowel movements are loose watery. For diarrhea, it's opposite. IBS-mixed bowel habits, at least 25% of bowel movements are type 1 or 2 and at least 25% are type 6 or 7.

Now, to meet the diagnostic criteria of CIC, you must meet two out of the six criteria. All but one of the criteria must be present with at least 25% of bowel movements. There’s a straining, sensation of incomplete evacuation, use of manual maneuvers to help facilitate stool evacuation, sensation of anorectal blockage, and a Bristol Stool Form Scale of type 1 or 2. The remaining criterion is less than three bowel movements per week. If a patient reports, or endorses, at least two of those six symptoms and signs, then their symptoms meet criteria.

Both IBS-C and CIC are chronic conditions. For the diagnosis of both IBS-C and CIC, symptoms are present for at least three months and started at least six months ago.

What's interesting is that if you ask health care providers and physicians what constipation is and  what symptoms define constipation, most of them will say having less than three bowel movements per week or infrequent bowel movements. But it turns out that in chronic constipation patients, they'll report decreased bowel movement frequency. About only a third of them will report that. They'll report the other symptoms of a constipation.

They could have multiple symptoms, but straining is a very common symptom as is hard stools. Even after a bowel movement, they don't feel completely evacuated. That's called sensation of incomplete evacuation. In fact, patients will present with different types of symptoms.

Constipation is often considered a symptom and a diagnosis. And it's fine to use it as a diagnosis, but you really want to delve into what symptoms of constipation they’re experiencing. Are they experiencing straining? Hard stools? Are they not having a bowel movement frequently? That's really part of the history taking so you can determine what the patient perceives as constipation and which symptom are bothersome to them.

So once diagnosed, how different are the treatments for each of the diseases?

Dr. Chang: In both IBS-C and CIC, treatments can include diet, exercise or ambulating more. Often, I will make sure they're drinking plenty of fluids. Those are dietary recommendations such as increasing fiber with foods and/or fiber supplementation. When looking at the difference between IBS-C and CIC, the one thing I should say is that they really exist along a spectrum, so we shouldn't really think of them as two separate diagnoses.

This goes back to the idea we touched on earlier that patients can move back and forth between the different diagnoses. At one point, a patient could have frequent abdominal pain and constipation and the symptoms would meet the criteria for IBS-C. But in the future, the pain gets better or resolves, but there’s still constipation. Their symptoms are more indicative of CIC. So, these conditions really exist along a spectrum.

Because both patients will have constipation symptoms, medications or treatments that help improve constipation can be used for both IBS-C and CIC. The key difference with IBS-C is that in addition to having altered gut motility where they're not moving stool effectively through the bowel, they also have visceral hypersensitivity which manifests as abdominal pain, bloating, and discomfort. Although there may be a modest correlation with bowel habits and IBS, sometimes, they don't correlate that well.

There are some treatments that help pain and constipation and those are the treatments that you want to think about in those patients with IBS-C where they're reporting both pain and constipation.

Now, it's very reasonable to use similar treatments in patients with mild symptoms, whether it's IBS or CIC. But if someone's having more severe IBS-C and they're having a fair amount of pain associated with constipation, you really want to think about treatments that can help reduce pain and constipation and not just constipation.

Treatments can include fiber such as psyllium and osmotic laxatives like polyethylene glycol, which is called MiraLAX, and magnesium-based regimens. These help constipation symptoms, but they don't significantly relieve abdominal pain. If someone came to me with IBS-C and they said, well, I do have pain, but it is mild, maybe a 2 or 3 out of 10, I could probably give them any one of the treatments I just mentioned. But in patients who say that their pain is 8 out of 10 or that it is their predominant symptom, I wouldn't necessarily prescribe the same treatment and would more likely opt for a treatment that has been shown to effectively reduce abdominal pain and constipation.

When you’re looking at the data, are their studies that might show a focus on the treatments and how they might impact the patients differently for IBS-C compared to CIC?

Dr. Chang: Well, the primary study endpoints that are used to determine efficacy of treatment in clinical trials differ in studies of CIC and IBS-C. However, studies also assess individual gastrointestinal symptoms that can be similar in both studies.

So, I would say that treatments that have been shown to be efficacious both in IBS-C and CIC likely relieve constipation symptoms similarly in both groups assuming that the severity of symptoms is comparable. It's just that in the CIC patient population, abdominal pain is not evaluated as much as it is in IBS-C.

References

F. Mearin, B. E. Lacy, L. Chang, W. D. Chey, A. J. Lembo, M. Simren, et al. Gastroenterology 2016 Vol. 150 Pages 1393-1407. http://www.ncbi.nlm.nih.gov/pubmed/27144627

 

D. A. Drossman. Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features and Rome IV. Gastroenterology 2016  https://www.ncbi.nlm.nih.gov/pubmed/27144617

 

Chang L. How to Approach a Patient with Difficult-to-Treat IBS. Gastroenterology 2021 Accession Number: 34331916 DOI: S0016-5085(21)03285-6 [pii]

10.1053/j.gastro.2021.07.034 https://www.ncbi.nlm.nih.gov/pubmed/34331916

 

A. E. Bharucha and B. E. Lacy. Mechanisms, Evaluation, and Management of Chronic Constipation. Gastroenterology 2020 Vol. 158 Issue 5 Pages 1232-1249 e3

Accession Number: 31945360 PMCID: PMC7573977 DOI: S0016-5085(20)30080-9 [pii]10.1053/j.gastro.2019.12.034 https://www.ncbi.nlm.nih.gov/pubmed/31945360

References

F. Mearin, B. E. Lacy, L. Chang, W. D. Chey, A. J. Lembo, M. Simren, et al. Gastroenterology 2016 Vol. 150 Pages 1393-1407. http://www.ncbi.nlm.nih.gov/pubmed/27144627

 

D. A. Drossman. Functional Gastrointestinal Disorders: History, Pathophysiology, Clinical Features and Rome IV. Gastroenterology 2016  https://www.ncbi.nlm.nih.gov/pubmed/27144617

 

Chang L. How to Approach a Patient with Difficult-to-Treat IBS. Gastroenterology 2021 Accession Number: 34331916 DOI: S0016-5085(21)03285-6 [pii]

10.1053/j.gastro.2021.07.034 https://www.ncbi.nlm.nih.gov/pubmed/34331916

 

A. E. Bharucha and B. E. Lacy. Mechanisms, Evaluation, and Management of Chronic Constipation. Gastroenterology 2020 Vol. 158 Issue 5 Pages 1232-1249 e3

Accession Number: 31945360 PMCID: PMC7573977 DOI: S0016-5085(20)30080-9 [pii]10.1053/j.gastro.2019.12.034 https://www.ncbi.nlm.nih.gov/pubmed/31945360

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Lifestyle likely responsible for obesity in children, not mother’s BMI

Article Type
Changed
Mon, 02/07/2022 - 09:43

Lifestyle is more likely to affect a child’s body mass index than the weight of their mother before and during pregnancy say researchers who have found that a mother’s high BMI before and during pregnancy is not a major cause of high BMI in their offspring – indicating that childhood and teen obesity is more likely to be a result of lifestyle factors.

According to UK Government figures 9.9% of reception age children (age 4-5) are obese, with a further 13.1% overweight. At age 10-11 (year 6), 21.0% are obese and 14.1% overweight.

Research from the Centre for Longitudinal Studies (CLS) at the UCL Social Research Institute, published in December 2020, showed that one in five (21%) young people were obese at age 17, and a further one in seven (14%) were overweight.
 

Nature or nurture

Greater maternal BMI before or during pregnancy is known to be associated with higher BMI throughout childhood, but exactly how much a mother’s weight before or during pregnancy contributes to childhood obesity, or whether it is lifestyle and environmental factors that are responsible, remains unclear.

To investigate this question researchers from the University of Bristol (England) and Imperial College London used data from the “Children of the 90s” (also known as the Avon Longitudinal Study of Parents and Children), and data from the “Born in Bradford” longitudinal study.

For their study, published in BMC Medicine, researchers used Mendelian randomisation, measuring variation in genes to determine the effect of an exposure on an outcome, along with polygenic risk scores, to investigate if associations between before and during early pregnancy BMI, and a child’s BMI from birth to adolescence, are causal.

They looked at birth weight and BMI at age 1 and 4 years in both “Children of the 90s” and “Born in Bradford” participants, and then also BMI at age 10 and 15 years in just the Children of the 90s participants.

Since the effects being explored may differ by ethnicity the authors reported that they limited analyses to two ethnic groups – White European and South Asian.
 

Interventions targeting everyone needed

The researchers found that there was a moderate causal effect between maternal BMI and the birth weight of children, however they said they “found no strong evidence for a causal effect of maternal BMI on offspring adiposity beyond birth”.

Tom Bond, MSc, senior research associate at the University of Bristol, explained: “We found that if women are heavier at the start of pregnancy this isn’t a strong cause of their children being heavier as teenagers.”

The authors wrote that their results suggested that “higher maternal pre-/early-pregnancy BMI is not a key driver of higher adiposity in the next generation,” something that Mr. Bond said was “important to know”.

The authors concluded that their findings “support interventions that target the whole population for reducing overweight and obesity, rather than a specific focus on women of reproductive age”.

Mr. Bond pointed out that “it isn’t enough to just focus on women entering pregnancy.” However, “there is good evidence that maternal obesity causes other health problems for mothers and babies, so prospective mothers should still be encouraged and supported to maintain a healthy weight.”

A version of this article first appeared on Medscape UK.

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Lifestyle is more likely to affect a child’s body mass index than the weight of their mother before and during pregnancy say researchers who have found that a mother’s high BMI before and during pregnancy is not a major cause of high BMI in their offspring – indicating that childhood and teen obesity is more likely to be a result of lifestyle factors.

According to UK Government figures 9.9% of reception age children (age 4-5) are obese, with a further 13.1% overweight. At age 10-11 (year 6), 21.0% are obese and 14.1% overweight.

Research from the Centre for Longitudinal Studies (CLS) at the UCL Social Research Institute, published in December 2020, showed that one in five (21%) young people were obese at age 17, and a further one in seven (14%) were overweight.
 

Nature or nurture

Greater maternal BMI before or during pregnancy is known to be associated with higher BMI throughout childhood, but exactly how much a mother’s weight before or during pregnancy contributes to childhood obesity, or whether it is lifestyle and environmental factors that are responsible, remains unclear.

To investigate this question researchers from the University of Bristol (England) and Imperial College London used data from the “Children of the 90s” (also known as the Avon Longitudinal Study of Parents and Children), and data from the “Born in Bradford” longitudinal study.

For their study, published in BMC Medicine, researchers used Mendelian randomisation, measuring variation in genes to determine the effect of an exposure on an outcome, along with polygenic risk scores, to investigate if associations between before and during early pregnancy BMI, and a child’s BMI from birth to adolescence, are causal.

They looked at birth weight and BMI at age 1 and 4 years in both “Children of the 90s” and “Born in Bradford” participants, and then also BMI at age 10 and 15 years in just the Children of the 90s participants.

Since the effects being explored may differ by ethnicity the authors reported that they limited analyses to two ethnic groups – White European and South Asian.
 

Interventions targeting everyone needed

The researchers found that there was a moderate causal effect between maternal BMI and the birth weight of children, however they said they “found no strong evidence for a causal effect of maternal BMI on offspring adiposity beyond birth”.

Tom Bond, MSc, senior research associate at the University of Bristol, explained: “We found that if women are heavier at the start of pregnancy this isn’t a strong cause of their children being heavier as teenagers.”

The authors wrote that their results suggested that “higher maternal pre-/early-pregnancy BMI is not a key driver of higher adiposity in the next generation,” something that Mr. Bond said was “important to know”.

The authors concluded that their findings “support interventions that target the whole population for reducing overweight and obesity, rather than a specific focus on women of reproductive age”.

Mr. Bond pointed out that “it isn’t enough to just focus on women entering pregnancy.” However, “there is good evidence that maternal obesity causes other health problems for mothers and babies, so prospective mothers should still be encouraged and supported to maintain a healthy weight.”

A version of this article first appeared on Medscape UK.

Lifestyle is more likely to affect a child’s body mass index than the weight of their mother before and during pregnancy say researchers who have found that a mother’s high BMI before and during pregnancy is not a major cause of high BMI in their offspring – indicating that childhood and teen obesity is more likely to be a result of lifestyle factors.

According to UK Government figures 9.9% of reception age children (age 4-5) are obese, with a further 13.1% overweight. At age 10-11 (year 6), 21.0% are obese and 14.1% overweight.

Research from the Centre for Longitudinal Studies (CLS) at the UCL Social Research Institute, published in December 2020, showed that one in five (21%) young people were obese at age 17, and a further one in seven (14%) were overweight.
 

Nature or nurture

Greater maternal BMI before or during pregnancy is known to be associated with higher BMI throughout childhood, but exactly how much a mother’s weight before or during pregnancy contributes to childhood obesity, or whether it is lifestyle and environmental factors that are responsible, remains unclear.

To investigate this question researchers from the University of Bristol (England) and Imperial College London used data from the “Children of the 90s” (also known as the Avon Longitudinal Study of Parents and Children), and data from the “Born in Bradford” longitudinal study.

For their study, published in BMC Medicine, researchers used Mendelian randomisation, measuring variation in genes to determine the effect of an exposure on an outcome, along with polygenic risk scores, to investigate if associations between before and during early pregnancy BMI, and a child’s BMI from birth to adolescence, are causal.

They looked at birth weight and BMI at age 1 and 4 years in both “Children of the 90s” and “Born in Bradford” participants, and then also BMI at age 10 and 15 years in just the Children of the 90s participants.

Since the effects being explored may differ by ethnicity the authors reported that they limited analyses to two ethnic groups – White European and South Asian.
 

Interventions targeting everyone needed

The researchers found that there was a moderate causal effect between maternal BMI and the birth weight of children, however they said they “found no strong evidence for a causal effect of maternal BMI on offspring adiposity beyond birth”.

Tom Bond, MSc, senior research associate at the University of Bristol, explained: “We found that if women are heavier at the start of pregnancy this isn’t a strong cause of their children being heavier as teenagers.”

The authors wrote that their results suggested that “higher maternal pre-/early-pregnancy BMI is not a key driver of higher adiposity in the next generation,” something that Mr. Bond said was “important to know”.

The authors concluded that their findings “support interventions that target the whole population for reducing overweight and obesity, rather than a specific focus on women of reproductive age”.

Mr. Bond pointed out that “it isn’t enough to just focus on women entering pregnancy.” However, “there is good evidence that maternal obesity causes other health problems for mothers and babies, so prospective mothers should still be encouraged and supported to maintain a healthy weight.”

A version of this article first appeared on Medscape UK.

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A test for cannabis-caused impairment

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You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

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You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

You have a 16-year-old patient who has been doing poorly in school. He has withdrawn from his social group and quit the sports in which he excelled. He admits to using marijuana “maybe once or twice a week.” But you and his parents suspect that it is much more often and contributing to the change in his behavior and school performance.

They would prefer he not use marijuana at all but could maybe be comfortable with some arrangement in which their son could demonstrate that his usage was indeed limited to once or twice on the weekends. They ask for your help with crafting a contract that might include “some urine or blood test” that would allow them to be sure their son was adhering to the contract.

Dr. William G. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years.
Dr. William G. Wilkoff

You explain to them that there are hazards associated with setting up contracts such as the one they are proposing. One revolving around the issue of trust. Another being that he may be addicted to the point that a compromise that includes scaling back his usage is unlikely to succeed. And, finally, you tell them that because of marijuana’s pharmacokinetics, their son’s urine tests will always be positive and not reflective of the how much he is using or whether he is intoxicated.

Scenarios similar to this are increasingly common for those of us living in states that have legalized recreational cannabis use. The absence of a laboratory test that can determine when a person is impaired by marijuana has made life difficult for law enforcement officers accustomed to relying on breath and blood tests for alcohol to confirm their suspicion that a driver is under the influence.

In addition, because marijuana is still detectable days after it is used, many well-paying jobs go unfilled when potential applicants are hesitant to submit to a required drug test. The quirky pharmacokinetics of cannabis are well-known to the recreational users and they see no reason to risk failing a urine test regardless of how good the job may be.

This lack of a reliable indicator of cannabis intoxication has not gone unnoticed, and in a recent study published in the journal Neuropharmacology, researchers at Massachusetts General Hospital in Boston report some hopeful results using fNIRS brain scanning. The investigators observed an increase in the level of oxygenated hemoglobin concentration (HbO), which is a type of neural activity signature, in the prefrontal cortex region of the volunteers who reported being impaired.

While a brain scan may sound like an unwieldy tool to use on roadside sobriety stops, the researchers report that portable scanners – some using skull cap sensors – could be easily adapted for use by law enforcement in the field. This technology also could be used by employers on the job site to test truck drivers and heavy machine operators at the beginning of each shift, thereby allaying the fears of responsible cannabis users.

This technology might be helpful to you in advising the parents of the 16-year-old you suspect of heavy usage. It would certainly help in confirming the suspicion that he is using more often than he claims. However, the contract the parents propose still may not work. If this young man demonstrates on multiple attempts that his word can’t be trusted, technology isn’t going to be the answer.

Dr. Wilkoff practiced primary care pediatrics in Brunswick, Maine, for nearly 40 years. He has authored several books on behavioral pediatrics, including “How to Say No to Your Toddler.” Other than a Littman stethoscope he accepted as a first-year medical student in 1966, Dr. Wilkoff reports having nothing to disclose. Email him at [email protected].

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EMA gives green light to new CAR T-cell therapy

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A new cell therapy will be available in Europe soon for the treatment of certain blood cancers.

At its late January meeting, the Committee for Medicinal Products for Human Use of the European Medicines Agency recommended for approval lisocabtagene maraleucel (Breyanzi, Bristol-Myers Squibb). This chimeric antigen receptor T-cell therapy is indicated for the treatment of relapsed or refractory diffuse large B-cell lymphoma (DLBCL), primary mediastinal large B-cell lymphoma (PMBCL), and follicular lymphoma grade 3B (FL3B). The indication is for use in patients who have received at least two lines of treatment.

The benefits of lisocabtagene maraleucel, noted the CHMP, are its ability to provide high and durable responses in patients with relapsed or refractory DLBCL, PMBCL, and FL3B. The most common side effects reported are neutropeniaanemia, cytokine release syndrome, fatigue, and thrombocytopenia.

The product is already approved in the United States for the same indication. The Food and Drug Administration’s approval came with a Risk Evaluation and Mitigation Strategy because of the risk for serious adverse events, including cytokine release syndrome.

During development, it was designated as an orphan medicine. The EMA will now review the information available to date to determine if the orphan designation can be maintained.
 

Biosimilar pegfilgrastim

At the same meeting, the committee recommended approval of a biosimilar product for pegfilgrastim (Stimufend, Fresenius Kabi Deutschland), which is used to reduce the duration of neutropenia and the incidence of febrile neutropenia after cytotoxic chemotherapy.

The committee noted that this product has been shown to be highly similar to the reference product Neulasta (pegfilgrastim), which has been available in the EU for 2 decades (authorized in 2002). Data have demonstrated that Stimufend has comparable quality, safety, and efficacy to Neulasta.

Its full indication is to reduce the duration of neutropenia and incidence of febrile neutropenia in adult patients treated with cytotoxic chemotherapy for malignancies, with the exception of chronic myeloid leukemia (CML) and myelodysplastic syndromes.
 

Generic versions of dasatinib

Also recommended for approval were for two generic formulations of dasatinib (Dasatinib Accord and Dasatinib Accordpharma, both from Accord Healthcare) for the treatment of various leukemias.

These are generic versions of dasatinib (Sprycel), which has been available in the European Union since 2006.

The CHMP noted that studies have demonstrated the satisfactory quality of Dasatinib Accord, as well as its bioequivalence to the reference product. This generic is indicated for the treatment of adult patients with Philadelphia chromosome–positive  acute lymphoblastic leukemia with resistance or intolerance to prior therapy and pediatric patients with newly diagnosed Ph+ ALL in combination with chemotherapy.

Dasatinib Accordpharma has a wider set of indications, which include the treatment of adult patients with newly diagnosed Ph+ CML in the chronic phase; chronic, accelerated, or blast phase CML with resistance or intolerance to prior therapy including imatinib; and Ph+ ALL and lymphoid blast CML with resistance or intolerance to prior therapy. In addition, this generic is indicated for the treatment of pediatric patients with newly diagnosed Ph+ CML in the chronic phase or Ph+ CML-CP resistant or intolerant to prior therapy including imatinib and newly diagnosed Ph+ ALL in combination with chemotherapy.

A version of this article first appeared on Medscape.com.

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A new cell therapy will be available in Europe soon for the treatment of certain blood cancers.

At its late January meeting, the Committee for Medicinal Products for Human Use of the European Medicines Agency recommended for approval lisocabtagene maraleucel (Breyanzi, Bristol-Myers Squibb). This chimeric antigen receptor T-cell therapy is indicated for the treatment of relapsed or refractory diffuse large B-cell lymphoma (DLBCL), primary mediastinal large B-cell lymphoma (PMBCL), and follicular lymphoma grade 3B (FL3B). The indication is for use in patients who have received at least two lines of treatment.

The benefits of lisocabtagene maraleucel, noted the CHMP, are its ability to provide high and durable responses in patients with relapsed or refractory DLBCL, PMBCL, and FL3B. The most common side effects reported are neutropeniaanemia, cytokine release syndrome, fatigue, and thrombocytopenia.

The product is already approved in the United States for the same indication. The Food and Drug Administration’s approval came with a Risk Evaluation and Mitigation Strategy because of the risk for serious adverse events, including cytokine release syndrome.

During development, it was designated as an orphan medicine. The EMA will now review the information available to date to determine if the orphan designation can be maintained.
 

Biosimilar pegfilgrastim

At the same meeting, the committee recommended approval of a biosimilar product for pegfilgrastim (Stimufend, Fresenius Kabi Deutschland), which is used to reduce the duration of neutropenia and the incidence of febrile neutropenia after cytotoxic chemotherapy.

The committee noted that this product has been shown to be highly similar to the reference product Neulasta (pegfilgrastim), which has been available in the EU for 2 decades (authorized in 2002). Data have demonstrated that Stimufend has comparable quality, safety, and efficacy to Neulasta.

Its full indication is to reduce the duration of neutropenia and incidence of febrile neutropenia in adult patients treated with cytotoxic chemotherapy for malignancies, with the exception of chronic myeloid leukemia (CML) and myelodysplastic syndromes.
 

Generic versions of dasatinib

Also recommended for approval were for two generic formulations of dasatinib (Dasatinib Accord and Dasatinib Accordpharma, both from Accord Healthcare) for the treatment of various leukemias.

These are generic versions of dasatinib (Sprycel), which has been available in the European Union since 2006.

The CHMP noted that studies have demonstrated the satisfactory quality of Dasatinib Accord, as well as its bioequivalence to the reference product. This generic is indicated for the treatment of adult patients with Philadelphia chromosome–positive  acute lymphoblastic leukemia with resistance or intolerance to prior therapy and pediatric patients with newly diagnosed Ph+ ALL in combination with chemotherapy.

Dasatinib Accordpharma has a wider set of indications, which include the treatment of adult patients with newly diagnosed Ph+ CML in the chronic phase; chronic, accelerated, or blast phase CML with resistance or intolerance to prior therapy including imatinib; and Ph+ ALL and lymphoid blast CML with resistance or intolerance to prior therapy. In addition, this generic is indicated for the treatment of pediatric patients with newly diagnosed Ph+ CML in the chronic phase or Ph+ CML-CP resistant or intolerant to prior therapy including imatinib and newly diagnosed Ph+ ALL in combination with chemotherapy.

A version of this article first appeared on Medscape.com.

A new cell therapy will be available in Europe soon for the treatment of certain blood cancers.

At its late January meeting, the Committee for Medicinal Products for Human Use of the European Medicines Agency recommended for approval lisocabtagene maraleucel (Breyanzi, Bristol-Myers Squibb). This chimeric antigen receptor T-cell therapy is indicated for the treatment of relapsed or refractory diffuse large B-cell lymphoma (DLBCL), primary mediastinal large B-cell lymphoma (PMBCL), and follicular lymphoma grade 3B (FL3B). The indication is for use in patients who have received at least two lines of treatment.

The benefits of lisocabtagene maraleucel, noted the CHMP, are its ability to provide high and durable responses in patients with relapsed or refractory DLBCL, PMBCL, and FL3B. The most common side effects reported are neutropeniaanemia, cytokine release syndrome, fatigue, and thrombocytopenia.

The product is already approved in the United States for the same indication. The Food and Drug Administration’s approval came with a Risk Evaluation and Mitigation Strategy because of the risk for serious adverse events, including cytokine release syndrome.

During development, it was designated as an orphan medicine. The EMA will now review the information available to date to determine if the orphan designation can be maintained.
 

Biosimilar pegfilgrastim

At the same meeting, the committee recommended approval of a biosimilar product for pegfilgrastim (Stimufend, Fresenius Kabi Deutschland), which is used to reduce the duration of neutropenia and the incidence of febrile neutropenia after cytotoxic chemotherapy.

The committee noted that this product has been shown to be highly similar to the reference product Neulasta (pegfilgrastim), which has been available in the EU for 2 decades (authorized in 2002). Data have demonstrated that Stimufend has comparable quality, safety, and efficacy to Neulasta.

Its full indication is to reduce the duration of neutropenia and incidence of febrile neutropenia in adult patients treated with cytotoxic chemotherapy for malignancies, with the exception of chronic myeloid leukemia (CML) and myelodysplastic syndromes.
 

Generic versions of dasatinib

Also recommended for approval were for two generic formulations of dasatinib (Dasatinib Accord and Dasatinib Accordpharma, both from Accord Healthcare) for the treatment of various leukemias.

These are generic versions of dasatinib (Sprycel), which has been available in the European Union since 2006.

The CHMP noted that studies have demonstrated the satisfactory quality of Dasatinib Accord, as well as its bioequivalence to the reference product. This generic is indicated for the treatment of adult patients with Philadelphia chromosome–positive  acute lymphoblastic leukemia with resistance or intolerance to prior therapy and pediatric patients with newly diagnosed Ph+ ALL in combination with chemotherapy.

Dasatinib Accordpharma has a wider set of indications, which include the treatment of adult patients with newly diagnosed Ph+ CML in the chronic phase; chronic, accelerated, or blast phase CML with resistance or intolerance to prior therapy including imatinib; and Ph+ ALL and lymphoid blast CML with resistance or intolerance to prior therapy. In addition, this generic is indicated for the treatment of pediatric patients with newly diagnosed Ph+ CML in the chronic phase or Ph+ CML-CP resistant or intolerant to prior therapy including imatinib and newly diagnosed Ph+ ALL in combination with chemotherapy.

A version of this article first appeared on Medscape.com.

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Screen time in first year may raise autism risk at age 3

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Thu, 02/03/2022 - 14:20

Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

 

 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

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Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

 

 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

Boys exposed to at least 2 hours a day of screen time by 1 year of age were significantly more likely to have an autism spectrum disorder (ASD) diagnosis at 3 years, based on data from more than 80,000 children.

The World Health Organization and the American Academy of Pediatrics recommend against any screen time for infants up to 1 year of age and 18 months of age, respectively, wrote Megumi Kushima, MA, of the University of Yamanashi (Japan), and colleagues on behalf of the Japan Environment and Children’s Study Group.

The extent to which screen time duration in infancy is associated with subsequent ASD diagnosis remains unclear, the researchers said. The ongoing COVID-19 pandemic has increased screen time among children worldwide, which makes an examination of the impact of screen time on children’s health an important public health issue.

In a study published in JAMA Pediatrics, the researchers recruited pregnant women between 2011 and 2014; data were analyzed in December 2020. The final study population included 84,030 mother-child pairs. The primary exposure of screen time at 1 year of age was assessed by questionnaire, in which mothers were asked to report their number of hours they let their child watch TV or DVDs daily. Responses were none (no screen time), less than 1 hour, 1 hour or more but less than 2 hours, 2 hours or more but less than 4 hours, and 4 hours or more.

The primary outcome was ASD diagnosis at 3 years of age, and mothers were asked via questionnaire whether their 3-year-old had been diagnosed with ASD from age 2.

The study was conducted by the Japan Environment and Children’s Study Group at 15 regional centers across Japan.

Overall, 330 children had received an ASD diagnosis at age 3 years, a prevalence of 0.4%. Of these, 251 (76%) were boys, and 79 (24%) were girls. Independent of ASD, the most common response for screen time was less than 1 hour, which was reported by 27,707 mothers. The proportion of children with ASD at age 3 increased as screen time at age 1 increased, the percentages were 5.8%, 22.3%, 30.2%, and 31.7% for children with no screen time, less than 1 hour, 1 to less than 2 hours, and 2 to less than 4 hours, respectively. The percentage of children with ASD diagnoses who had 4 hours or more of daily screen time was 10%.

Logistic regression analysis showed that longer screen time at age 1 year was significantly associated with higher odds of ASD at 3 years in boys, but not in girls. The researchers controlled for variables including maternal maltreatment and children’s predisposition to ASD. Among boys, the adjusted odds ratios for screen times of less than 1 hour, 1 hour to less than 2 hours, 2 hours to less than 4 hours, and more than 4 hours were 1.38, 2.16, 3.48, and 3.02, respectively.

Screen time at age 3 years was not associated with ASD diagnosis at age 3 years, potentially “because the association with environmental factors on brain development varies with age,” the researchers noted.

The study findings were limited by several factors including the reliance on parental reports of screen time and potential for reporting bias, the researchers noted. Other limitations included the possible missed diagnoses of mild ASD cases at 3 years, and the inability to consider variables such as childcare environment, living conditions, diseases, genetics, and disabilities.

However, the results were strengthened by the large study population and examination of screen time in early childhood, they said. More research is needed to examine other factors that contribute to the association between ASD and screen time, but given the rapid increase in device use in children, “it is necessary to review its health effects on infants and control excessive screen time.”
 

 

 

Strong study, but some gaps appear

The study is strong in many respects, Karalyn Kinsella, MD, a pediatrician in private practice in Cheshire, Conn., said in an interview.

However, “what I am not sure they addressed is that children on the spectrum are often not entertained by basic toys and may be hard to manage behaviorally,” Dr. Kinsella said. Consequently, parents may be more inclined to offer screen time as a way to pacify children with behavioral difficulties. “Parents also may see that their children are happier interacting with devices, so they may be more apt to let them continue with screen time.We know screen time is not good for the developing brain, however; I worry that the message from this study is that screen time causes autism in boys.

“What I would have liked to know from the parents who allowed more screen time was why they were offering it,” Dr. Kinsella said. “Was it because their child was difficult behaviorally or because that is the one place that they seemed to have satisfaction? To me, that would indicate the reverse hypothesis.” That said, the study findings “remind us to counsel families about screen time, especially in the age of COVID-19. Kids are home much longer than usual, which ultimately leads to more screen time.”

The study was funded by the Japanese Ministry of Environment. The researchers had no financial conflicts to disclose. Dr. Kinsella had no financial conflicts to disclose, but serves as a member of the Pediatric News editorial advisory board.

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FROM JAMA PEDIATRICS

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Alleviating chemo-related nausea is a huge unmet need

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Changed
Thu, 02/03/2022 - 16:41

 

This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

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This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

 

This transcript has been edited for clarity. The transcript and an accompanying video first appeared on Medscape.com.

This is Mark Kris from chilly New York and Memorial Sloan Kettering. Today I want to talk about a recent article in the Journal of Clinical Oncology that reported a study of a new neurokinin-1 antagonist called fosnetupitant. This was a well-conducted trial that demonstrates the noninferiority of IV fosnetupitant when compared with IV fosaprepitant. By their study criteria, fosnetupitant was not inferior.

But my reason for discussing this is that the paper and the trial miss the point for the field right now. Although the authors talk about the prevention of nausea and vomiting in the introduction, in the paper itself and in the abstract results section, there’s not a single mention about the medication’s ability to control nausea, which is the critical issue for our patients today. You have to go into the supplementary data to find it mentioned, and what you find is that the prevention of nausea is 50% for both the control and this new drug. We control nausea in only half of the patients who receive cisplatin in 2022. That is a huge issue.

When you ask patients what are the effects of cancer treatment that they fear most, that concerns them most, it’s nausea and emesis; indeed, nausea has replaced emesis as the biggest concern. And although this trial used emesis as the main endpoint, and it was useful in defining the drug, it was not useful in coming up with a new treatment that addresses a huge need. Further, the authors talk about an advantage to fosnetupitant based on infusion reactions, but it is a difference of 0.3% vs. 3%. They talk about that sort of thing in the abstract and in the discussion section but don’t include nausea as part of the key endpoint of this trial. Again, you had to dig deeply to find out that, frankly, fosnetupitant was no better than the drugs we already have.

The other concerning point is that we do have another drug that works well. If you go to the American Society of Clinical Oncology or National Comprehensive Cancer Network guidelines for patients receiving high dosages of cisplatin, you find a four-drug regimen, including olanzapine, and that was not used here. Why is olanzapine so critical? It’s an available drug, it’s an inexpensive drug, it’s a safe drug, and it improves nausea by 15%.

So they did this huge trial to show noninferiority, and they neglected to give a drug that could deal with the most serious side effect of cancer therapy – nausea – and improve things by 15%.

A challenge to people in this field: We have to do better. Nausea is a big problem. While noninferiority trials can be helpful for drug development, they’re not really helpful for the field. With a problem of this magnitude, we need better drugs to control nausea. In the meantime, I urge you all to follow the guidelines for high doses of cisplatin. Please use the four-drug regimen that is recommended in the guidelines and widely used in the United States. Going forward, make sure that when we expend huge amounts of energy to develop new agents and report them in our medical journals, that we look for ways to advance care where there are significant gaps in our ability to deliver what we want. Delivering better control of nausea is something we all need to be committed to. It’s a huge unmet need, and I hope future trials will address that need. Our patients will be better for it and we’ll be better in that we’re delivering what patients deserve, what they need, and what they ask for.

Mark G. Kris, MD, is chief of the thoracic oncology service and the William and Joy Ruane Chair in Thoracic Oncology at Memorial Sloan Kettering Cancer Center in New York City. He reported serving as a director, officer, partner, employee, adviser, consultant, or trustee for AstraZeneca, Roche/Genentech, and Ariad Pharmaceuticals, and has received research grants from Pfizer, PUMA, and Roche/Genentech.

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Global pediatric oncology workforce hit hard, but resilient amid pandemic

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Thu, 12/15/2022 - 14:34

The pediatric oncology workforce has faced a host of financial, physical, and psychological obstacles during the COVID-19 pandemic, according to a study that surveyed workers from more than 200 institutions in 79 countries.

A snapshot of the extensive findings reveals that half of participating institutions experienced staffing shortages that had a “major impact” on pediatric cancer care. On the financial front, many respondents pointed to instances of unpaid leave and diminished salary, and others highlighted the psychological toll of providing care, including high rates of burnout and stress. The challenges were evident across high- and low-income countries.

Despite these barriers, pediatric oncology clinicians demonstrated incredible perseverance.

Health care professionals “caring for children with cancer across the world were shown to be incredibly resilient, coming together to continue to provide care even in the direst circumstances,” Elizabeth R. Sniderman, MSN, APRN, of St. Jude Children’s Research Hospital, Memphis, and colleagues concluded.

The findings, published online Jan. 24, 2022, in Cancer, highlight the global impact of COVID-19 on pediatric oncology clinicians early in the pandemic.

The survey, conducted in summer 2020, included responses from 311 pediatric oncology clinicians who completed a 60-item questionnaire about their experiences of clinical care, resources, and support. The investigators also convened 19 multidisciplinary focus groups who answered questions related to teamwork, communication, and changes to care. Respondents practiced in low- to high-income countries, and included pediatric hematologists and oncologists, nurses, and infectious disease physicians.

Overall, the investigators found that just over half of institutions experienced “major” shortages of clinical staff (108 of 213), and two-thirds experienced reductions in staffing availability (141 of 213). Notably, national income was not associated with this reduction; rather, staffing shortages were more likely to occur in countries with greater COVID-19 incidence and mortality rates.

Respondents reported experiencing threats to their physical health, with half pointing to a lack of necessary personal protective equipment. The financial and psychological toll of the pandemic represented another major stressor, with the effects described across all income levels.

One respondent from Belarus commented on financial concerns, noting that “people don’t really want to admit that they don’t feel well ... they know, that if infected, unpaid self-isolation is waiting for them. Either you don’t go to work for 2 weeks, unpaid, or you go to work for 2 weeks, paid, and endanger all of your colleagues with your infection.”

A respondent from Mexico described the psychological stress: “Honestly, I think that sometimes we put aside the mental health of all of us involved, myself included. I think we were all on the verge of collapse ... practically all the residents who were rotating here told us that they had anxiety attacks, panic attacks, they could not sleep, [and] many of them needed psychiatric medicine.”

Others highlighted feelings of guilt about their ability to provide the highest level of care. An oncologist in the United States noted: “This was a major stress for many providers because [we are] feeling unable to provide the same level of care which we used to provide. And this is what eventually takes a toll.”

And despite these pandemic-related challenges, the study authors found that only 46% of institutions (99 of 213) made psychological support available to staff.


 

 

 

Rays of hope

But it was not all bad news.

Participants also described a greater sense of teamwork, communication, and collegiality throughout the pandemic – “stabilizing elements,” which helped mitigate the many physical, psychological, and financial stressors.

An infection-control physician in Belarus highlighted the importance of receiving “support and encouragement” from colleagues: “When a person gets tired and they have no more enthusiasm, it’s easy to give up and say: ‘I can’t do this anymore.’ But when you see a colleague who tries ... to share the work, and help each other, then you get extra strength.”

An oncologist in South Africa agreed, noting that “everyone has got their sleeves rolled up and are doing the work ... and that’s a testament to everyone that we work with. There was no one that shied away from work or used this as an excuse to do less work.”

An oncologist in Spain described practicing during the pandemic being “one of the best experiences I have had,” explaining that “I have been working in this hospital for ... 25 years, [and] I have never had the feeling of being so informed at all levels.”

Overall, the findings paint a picture of a resilient workforce, and offer lessons about preparedness for future crises, the investigators concluded.

“To protect pediatric oncology providers and their patients, organizations must pay attention to interventions that increase physical, psychological, and financial safety,” the authors stressed. For instance, providing adequate personal protective equipment and vaccines, allowing for time off and rest, and setting up professional psychology services as well as access to peer-support programs can help protect staff.

Although this survey took place relatively early in the pandemic, organizations should take heed of the findings, Lorena V. Baroni, MD, of Hospital J P Garrahan, Buenos Aires, and Eric Bouffet, MD, of The Hospital for Sick Children, Toronto, wrote in an accompanying editorial.

“The results presented in this study should not be taken lightly,” Dr. Baroni and Dr. Bouffet wrote. “The most concerning findings are the physical and psychological impact experienced by pediatric oncology providers.” And perhaps most surprisingly, “the survey did not identify any difference based on country income groups. Participants in both low- and high-income countries described similar oncologic care limitations.”

Overall, these findings “reflect a serious risk that can ultimately affect the care of children and compromise the success of their treatment,” Dr. Baroni and Dr. Bouffet wrote.

This study was supported by the American Lebanese Syrian Associated Charities. The study authors and editorialists have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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The pediatric oncology workforce has faced a host of financial, physical, and psychological obstacles during the COVID-19 pandemic, according to a study that surveyed workers from more than 200 institutions in 79 countries.

A snapshot of the extensive findings reveals that half of participating institutions experienced staffing shortages that had a “major impact” on pediatric cancer care. On the financial front, many respondents pointed to instances of unpaid leave and diminished salary, and others highlighted the psychological toll of providing care, including high rates of burnout and stress. The challenges were evident across high- and low-income countries.

Despite these barriers, pediatric oncology clinicians demonstrated incredible perseverance.

Health care professionals “caring for children with cancer across the world were shown to be incredibly resilient, coming together to continue to provide care even in the direst circumstances,” Elizabeth R. Sniderman, MSN, APRN, of St. Jude Children’s Research Hospital, Memphis, and colleagues concluded.

The findings, published online Jan. 24, 2022, in Cancer, highlight the global impact of COVID-19 on pediatric oncology clinicians early in the pandemic.

The survey, conducted in summer 2020, included responses from 311 pediatric oncology clinicians who completed a 60-item questionnaire about their experiences of clinical care, resources, and support. The investigators also convened 19 multidisciplinary focus groups who answered questions related to teamwork, communication, and changes to care. Respondents practiced in low- to high-income countries, and included pediatric hematologists and oncologists, nurses, and infectious disease physicians.

Overall, the investigators found that just over half of institutions experienced “major” shortages of clinical staff (108 of 213), and two-thirds experienced reductions in staffing availability (141 of 213). Notably, national income was not associated with this reduction; rather, staffing shortages were more likely to occur in countries with greater COVID-19 incidence and mortality rates.

Respondents reported experiencing threats to their physical health, with half pointing to a lack of necessary personal protective equipment. The financial and psychological toll of the pandemic represented another major stressor, with the effects described across all income levels.

One respondent from Belarus commented on financial concerns, noting that “people don’t really want to admit that they don’t feel well ... they know, that if infected, unpaid self-isolation is waiting for them. Either you don’t go to work for 2 weeks, unpaid, or you go to work for 2 weeks, paid, and endanger all of your colleagues with your infection.”

A respondent from Mexico described the psychological stress: “Honestly, I think that sometimes we put aside the mental health of all of us involved, myself included. I think we were all on the verge of collapse ... practically all the residents who were rotating here told us that they had anxiety attacks, panic attacks, they could not sleep, [and] many of them needed psychiatric medicine.”

Others highlighted feelings of guilt about their ability to provide the highest level of care. An oncologist in the United States noted: “This was a major stress for many providers because [we are] feeling unable to provide the same level of care which we used to provide. And this is what eventually takes a toll.”

And despite these pandemic-related challenges, the study authors found that only 46% of institutions (99 of 213) made psychological support available to staff.


 

 

 

Rays of hope

But it was not all bad news.

Participants also described a greater sense of teamwork, communication, and collegiality throughout the pandemic – “stabilizing elements,” which helped mitigate the many physical, psychological, and financial stressors.

An infection-control physician in Belarus highlighted the importance of receiving “support and encouragement” from colleagues: “When a person gets tired and they have no more enthusiasm, it’s easy to give up and say: ‘I can’t do this anymore.’ But when you see a colleague who tries ... to share the work, and help each other, then you get extra strength.”

An oncologist in South Africa agreed, noting that “everyone has got their sleeves rolled up and are doing the work ... and that’s a testament to everyone that we work with. There was no one that shied away from work or used this as an excuse to do less work.”

An oncologist in Spain described practicing during the pandemic being “one of the best experiences I have had,” explaining that “I have been working in this hospital for ... 25 years, [and] I have never had the feeling of being so informed at all levels.”

Overall, the findings paint a picture of a resilient workforce, and offer lessons about preparedness for future crises, the investigators concluded.

“To protect pediatric oncology providers and their patients, organizations must pay attention to interventions that increase physical, psychological, and financial safety,” the authors stressed. For instance, providing adequate personal protective equipment and vaccines, allowing for time off and rest, and setting up professional psychology services as well as access to peer-support programs can help protect staff.

Although this survey took place relatively early in the pandemic, organizations should take heed of the findings, Lorena V. Baroni, MD, of Hospital J P Garrahan, Buenos Aires, and Eric Bouffet, MD, of The Hospital for Sick Children, Toronto, wrote in an accompanying editorial.

“The results presented in this study should not be taken lightly,” Dr. Baroni and Dr. Bouffet wrote. “The most concerning findings are the physical and psychological impact experienced by pediatric oncology providers.” And perhaps most surprisingly, “the survey did not identify any difference based on country income groups. Participants in both low- and high-income countries described similar oncologic care limitations.”

Overall, these findings “reflect a serious risk that can ultimately affect the care of children and compromise the success of their treatment,” Dr. Baroni and Dr. Bouffet wrote.

This study was supported by the American Lebanese Syrian Associated Charities. The study authors and editorialists have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

The pediatric oncology workforce has faced a host of financial, physical, and psychological obstacles during the COVID-19 pandemic, according to a study that surveyed workers from more than 200 institutions in 79 countries.

A snapshot of the extensive findings reveals that half of participating institutions experienced staffing shortages that had a “major impact” on pediatric cancer care. On the financial front, many respondents pointed to instances of unpaid leave and diminished salary, and others highlighted the psychological toll of providing care, including high rates of burnout and stress. The challenges were evident across high- and low-income countries.

Despite these barriers, pediatric oncology clinicians demonstrated incredible perseverance.

Health care professionals “caring for children with cancer across the world were shown to be incredibly resilient, coming together to continue to provide care even in the direst circumstances,” Elizabeth R. Sniderman, MSN, APRN, of St. Jude Children’s Research Hospital, Memphis, and colleagues concluded.

The findings, published online Jan. 24, 2022, in Cancer, highlight the global impact of COVID-19 on pediatric oncology clinicians early in the pandemic.

The survey, conducted in summer 2020, included responses from 311 pediatric oncology clinicians who completed a 60-item questionnaire about their experiences of clinical care, resources, and support. The investigators also convened 19 multidisciplinary focus groups who answered questions related to teamwork, communication, and changes to care. Respondents practiced in low- to high-income countries, and included pediatric hematologists and oncologists, nurses, and infectious disease physicians.

Overall, the investigators found that just over half of institutions experienced “major” shortages of clinical staff (108 of 213), and two-thirds experienced reductions in staffing availability (141 of 213). Notably, national income was not associated with this reduction; rather, staffing shortages were more likely to occur in countries with greater COVID-19 incidence and mortality rates.

Respondents reported experiencing threats to their physical health, with half pointing to a lack of necessary personal protective equipment. The financial and psychological toll of the pandemic represented another major stressor, with the effects described across all income levels.

One respondent from Belarus commented on financial concerns, noting that “people don’t really want to admit that they don’t feel well ... they know, that if infected, unpaid self-isolation is waiting for them. Either you don’t go to work for 2 weeks, unpaid, or you go to work for 2 weeks, paid, and endanger all of your colleagues with your infection.”

A respondent from Mexico described the psychological stress: “Honestly, I think that sometimes we put aside the mental health of all of us involved, myself included. I think we were all on the verge of collapse ... practically all the residents who were rotating here told us that they had anxiety attacks, panic attacks, they could not sleep, [and] many of them needed psychiatric medicine.”

Others highlighted feelings of guilt about their ability to provide the highest level of care. An oncologist in the United States noted: “This was a major stress for many providers because [we are] feeling unable to provide the same level of care which we used to provide. And this is what eventually takes a toll.”

And despite these pandemic-related challenges, the study authors found that only 46% of institutions (99 of 213) made psychological support available to staff.


 

 

 

Rays of hope

But it was not all bad news.

Participants also described a greater sense of teamwork, communication, and collegiality throughout the pandemic – “stabilizing elements,” which helped mitigate the many physical, psychological, and financial stressors.

An infection-control physician in Belarus highlighted the importance of receiving “support and encouragement” from colleagues: “When a person gets tired and they have no more enthusiasm, it’s easy to give up and say: ‘I can’t do this anymore.’ But when you see a colleague who tries ... to share the work, and help each other, then you get extra strength.”

An oncologist in South Africa agreed, noting that “everyone has got their sleeves rolled up and are doing the work ... and that’s a testament to everyone that we work with. There was no one that shied away from work or used this as an excuse to do less work.”

An oncologist in Spain described practicing during the pandemic being “one of the best experiences I have had,” explaining that “I have been working in this hospital for ... 25 years, [and] I have never had the feeling of being so informed at all levels.”

Overall, the findings paint a picture of a resilient workforce, and offer lessons about preparedness for future crises, the investigators concluded.

“To protect pediatric oncology providers and their patients, organizations must pay attention to interventions that increase physical, psychological, and financial safety,” the authors stressed. For instance, providing adequate personal protective equipment and vaccines, allowing for time off and rest, and setting up professional psychology services as well as access to peer-support programs can help protect staff.

Although this survey took place relatively early in the pandemic, organizations should take heed of the findings, Lorena V. Baroni, MD, of Hospital J P Garrahan, Buenos Aires, and Eric Bouffet, MD, of The Hospital for Sick Children, Toronto, wrote in an accompanying editorial.

“The results presented in this study should not be taken lightly,” Dr. Baroni and Dr. Bouffet wrote. “The most concerning findings are the physical and psychological impact experienced by pediatric oncology providers.” And perhaps most surprisingly, “the survey did not identify any difference based on country income groups. Participants in both low- and high-income countries described similar oncologic care limitations.”

Overall, these findings “reflect a serious risk that can ultimately affect the care of children and compromise the success of their treatment,” Dr. Baroni and Dr. Bouffet wrote.

This study was supported by the American Lebanese Syrian Associated Charities. The study authors and editorialists have disclosed no relevant financial relationships.

A version of this article first appeared on Medscape.com.

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Hyperpigmented plaque on back

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Hyperpigmented plaque on back

Hyperpigmented plaque on back

Based on the thickness and size of this irregular lesion, a punch biopsy was performed and confirmed the diagnosis of dermatofibrosarcoma protuberans (DFSP).

DFSPs are usually found on the trunk and proximal extremities; they are most often located on the chest and shoulders. The lesion usually manifests as an asymptomatic, firm, and sometimes nodular plaque that may go undiagnosed for years. DFSP is an uncommon mesenchymal tumor with uncertain etiology. It is thought that prior injury to the affected skin may result in a translocation of chromosomes 17 and 22 in skin cells, as this molecular change characterizes the vast majority of DFSPs.

Black patients are more likely than other ethnic populations to develop DFSP and its variants; there is also a slight female predominance.1 Known variants of DFSP include violaceous plaques with telangiectatic atrophic skin, and plaques with dark brown pigmentation called Bednar tumors.1,2

DFSPs are rarely metastatic, but can be locally invasive, so primary treatment consists of wide local excision or Mohs micrographic surgery (MMS). There is a higher probability for cure when MMS is utilized to treat DFSPs with the added benefit of minimizing surgical margins and preserving healthy surrounding skin. In the rarer cases of advanced local, unresectable, or metastatic disease, inhibitor therapy with imatinib or radiation therapy may be considered.2 Due to the risk of local recurrence, patients with DFSP should have regular clinical follow-up every 6 months for 5 years, followed by annual lifelong surveillance.1

This patient was referred for MMS and has not yet returned for follow-up evaluation.

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Morgan Haynes, BS, University of New Mexico School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

1. Mendenhall WM, Scarborough MT, Flowers FP. Dermatofibrosarcoma protuberans: epidemiology, pathogenesis, clinical presentation, diagnosis, and staging. UpToDate. Updated March 31, 2021. Accessed February 2, 2022. www.uptodate.com/contents/dermatofibrosarcoma-protuberans-epidemiology-pathogenesis-clinical-presentation-diagnosis-and-staging

2. Brooks J, Ramsey ML. Dermatofibrosarcoma Protuberans. StatPearls. Updated November 14, 2021. Accessed January 27, 2022. www.ncbi.nlm.nih.gov/books/NBK513305

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Hyperpigmented plaque on back

Based on the thickness and size of this irregular lesion, a punch biopsy was performed and confirmed the diagnosis of dermatofibrosarcoma protuberans (DFSP).

DFSPs are usually found on the trunk and proximal extremities; they are most often located on the chest and shoulders. The lesion usually manifests as an asymptomatic, firm, and sometimes nodular plaque that may go undiagnosed for years. DFSP is an uncommon mesenchymal tumor with uncertain etiology. It is thought that prior injury to the affected skin may result in a translocation of chromosomes 17 and 22 in skin cells, as this molecular change characterizes the vast majority of DFSPs.

Black patients are more likely than other ethnic populations to develop DFSP and its variants; there is also a slight female predominance.1 Known variants of DFSP include violaceous plaques with telangiectatic atrophic skin, and plaques with dark brown pigmentation called Bednar tumors.1,2

DFSPs are rarely metastatic, but can be locally invasive, so primary treatment consists of wide local excision or Mohs micrographic surgery (MMS). There is a higher probability for cure when MMS is utilized to treat DFSPs with the added benefit of minimizing surgical margins and preserving healthy surrounding skin. In the rarer cases of advanced local, unresectable, or metastatic disease, inhibitor therapy with imatinib or radiation therapy may be considered.2 Due to the risk of local recurrence, patients with DFSP should have regular clinical follow-up every 6 months for 5 years, followed by annual lifelong surveillance.1

This patient was referred for MMS and has not yet returned for follow-up evaluation.

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Morgan Haynes, BS, University of New Mexico School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

Hyperpigmented plaque on back

Based on the thickness and size of this irregular lesion, a punch biopsy was performed and confirmed the diagnosis of dermatofibrosarcoma protuberans (DFSP).

DFSPs are usually found on the trunk and proximal extremities; they are most often located on the chest and shoulders. The lesion usually manifests as an asymptomatic, firm, and sometimes nodular plaque that may go undiagnosed for years. DFSP is an uncommon mesenchymal tumor with uncertain etiology. It is thought that prior injury to the affected skin may result in a translocation of chromosomes 17 and 22 in skin cells, as this molecular change characterizes the vast majority of DFSPs.

Black patients are more likely than other ethnic populations to develop DFSP and its variants; there is also a slight female predominance.1 Known variants of DFSP include violaceous plaques with telangiectatic atrophic skin, and plaques with dark brown pigmentation called Bednar tumors.1,2

DFSPs are rarely metastatic, but can be locally invasive, so primary treatment consists of wide local excision or Mohs micrographic surgery (MMS). There is a higher probability for cure when MMS is utilized to treat DFSPs with the added benefit of minimizing surgical margins and preserving healthy surrounding skin. In the rarer cases of advanced local, unresectable, or metastatic disease, inhibitor therapy with imatinib or radiation therapy may be considered.2 Due to the risk of local recurrence, patients with DFSP should have regular clinical follow-up every 6 months for 5 years, followed by annual lifelong surveillance.1

This patient was referred for MMS and has not yet returned for follow-up evaluation.

Photo courtesy of Daniel Stulberg, MD. Text courtesy of Morgan Haynes, BS, University of New Mexico School of Medicine and Daniel Stulberg, MD, FAAFP, Department of Family and Community Medicine, University of New Mexico School of Medicine, Albuquerque.

References

1. Mendenhall WM, Scarborough MT, Flowers FP. Dermatofibrosarcoma protuberans: epidemiology, pathogenesis, clinical presentation, diagnosis, and staging. UpToDate. Updated March 31, 2021. Accessed February 2, 2022. www.uptodate.com/contents/dermatofibrosarcoma-protuberans-epidemiology-pathogenesis-clinical-presentation-diagnosis-and-staging

2. Brooks J, Ramsey ML. Dermatofibrosarcoma Protuberans. StatPearls. Updated November 14, 2021. Accessed January 27, 2022. www.ncbi.nlm.nih.gov/books/NBK513305

References

1. Mendenhall WM, Scarborough MT, Flowers FP. Dermatofibrosarcoma protuberans: epidemiology, pathogenesis, clinical presentation, diagnosis, and staging. UpToDate. Updated March 31, 2021. Accessed February 2, 2022. www.uptodate.com/contents/dermatofibrosarcoma-protuberans-epidemiology-pathogenesis-clinical-presentation-diagnosis-and-staging

2. Brooks J, Ramsey ML. Dermatofibrosarcoma Protuberans. StatPearls. Updated November 14, 2021. Accessed January 27, 2022. www.ncbi.nlm.nih.gov/books/NBK513305

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