Alan Finkel, MD

Article Type
Changed
Mon, 01/07/2019 - 10:28

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Topics
Sections
Related Articles

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Lars Edvinsson, MD, PhD

Article Type
Changed
Mon, 01/07/2019 - 10:28

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Topics
Sections
Related Articles

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Parental reasons for HPV nonvaccination are shifting

Article Type
Changed
Fri, 01/18/2019 - 16:37

 

– Parents are now less concerned about whether their daughters are sexually active when weighing whether to vaccinate against human papillomavirus (HPV), compared with just a few years ago.

This shift in parental attitudes can inform physician guidance and shift the HPV vaccination discussion, Anna Beavis, MD, a clinical fellow in gynecologic oncology at Johns Hopkins Medicine, Baltimore, said at the annual meeting of the Society of Gynecologic Oncology.

About 90% of cervical cancer is preventable with the HPV vaccine, but “U.S. vaccination rates are still suboptimal,” putting the United States far behind many other developed countries, Dr. Beavis said.

It’s been shown that the physician recommendation is one of the strongest predictors of whether an adolescent will be immunized against HPV, yet many providers remain reluctant to raise the issue, she said. Discomfort about discussing adolescent sexuality with the teen and with parents has been cited by physicians as a primary barrier.

To evaluate why parents of adolescent girls would opt out of HPV vaccination and to identify whether the reasons had changed over time, Dr. Beavis and her colleagues formulated a study that compared parent responses to a nationwide survey about HPV vaccination given in 2014 to those in 2010.

The study drew from the National Immunization Survey–Teen, a random digit-dialing survey administered by the Centers for Disease Control and Prevention. Only data pertaining to girls aged 13-17 years was included in the analysis, and for the sake of accuracy, only provider-verified responses were used.

Of the 49,345 responses that could be provider verified during the period from 2010 to 2014, 54% had received at least one HPV vaccination. Of the remaining responses, 55% of the parents said they had no intention of vaccinating their daughters.

During this period, vaccination rates have climbed slowly, from a little less than half in 2010 to about 60% in 2014 (test of trend, P less than .001), according to Dr. Beavis.

However, the reasons parents gave for declining vaccination has shifted over time, she said. The primary reason given in 2010 was concern about safety or side effects, followed by the sense that the vaccine was not necessary. These remained the top two reasons in 2014, though they had swapped places.

In 2010, the third most common reason parents gave for declining the HPV vaccination was that their daughters were not sexually active. By 2014, this reason had slid to the bottom of the top five reasons, and now was given by fewer than 10% of parents (test of trend, P less than .01).

This is important information for physicians, Dr. Beavis said in a video interview. If a physician has been reluctant to start the HPV discussion for fear of stepping into awkward territory with parents of teen girls, they should know that it’s significantly less likely that issues of sexuality will be on the parental radar when talking about HPV vaccination.

Looking deeper into the data, the investigators found that white race, younger patient age, and living above the poverty level were risk factors for nonvaccination. This means, Dr. Beavis said, that physicians should consider “developing a targeted HPV message” for families at higher risk of nonvaccination.

“This vaccine message should focus on cancer prevention, necessity, and the safety of the HPV vaccine,” Dr. Beavis said.

She reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Topics
Sections

 

– Parents are now less concerned about whether their daughters are sexually active when weighing whether to vaccinate against human papillomavirus (HPV), compared with just a few years ago.

This shift in parental attitudes can inform physician guidance and shift the HPV vaccination discussion, Anna Beavis, MD, a clinical fellow in gynecologic oncology at Johns Hopkins Medicine, Baltimore, said at the annual meeting of the Society of Gynecologic Oncology.

About 90% of cervical cancer is preventable with the HPV vaccine, but “U.S. vaccination rates are still suboptimal,” putting the United States far behind many other developed countries, Dr. Beavis said.

It’s been shown that the physician recommendation is one of the strongest predictors of whether an adolescent will be immunized against HPV, yet many providers remain reluctant to raise the issue, she said. Discomfort about discussing adolescent sexuality with the teen and with parents has been cited by physicians as a primary barrier.

To evaluate why parents of adolescent girls would opt out of HPV vaccination and to identify whether the reasons had changed over time, Dr. Beavis and her colleagues formulated a study that compared parent responses to a nationwide survey about HPV vaccination given in 2014 to those in 2010.

The study drew from the National Immunization Survey–Teen, a random digit-dialing survey administered by the Centers for Disease Control and Prevention. Only data pertaining to girls aged 13-17 years was included in the analysis, and for the sake of accuracy, only provider-verified responses were used.

Of the 49,345 responses that could be provider verified during the period from 2010 to 2014, 54% had received at least one HPV vaccination. Of the remaining responses, 55% of the parents said they had no intention of vaccinating their daughters.

During this period, vaccination rates have climbed slowly, from a little less than half in 2010 to about 60% in 2014 (test of trend, P less than .001), according to Dr. Beavis.

However, the reasons parents gave for declining vaccination has shifted over time, she said. The primary reason given in 2010 was concern about safety or side effects, followed by the sense that the vaccine was not necessary. These remained the top two reasons in 2014, though they had swapped places.

In 2010, the third most common reason parents gave for declining the HPV vaccination was that their daughters were not sexually active. By 2014, this reason had slid to the bottom of the top five reasons, and now was given by fewer than 10% of parents (test of trend, P less than .01).

This is important information for physicians, Dr. Beavis said in a video interview. If a physician has been reluctant to start the HPV discussion for fear of stepping into awkward territory with parents of teen girls, they should know that it’s significantly less likely that issues of sexuality will be on the parental radar when talking about HPV vaccination.

Looking deeper into the data, the investigators found that white race, younger patient age, and living above the poverty level were risk factors for nonvaccination. This means, Dr. Beavis said, that physicians should consider “developing a targeted HPV message” for families at higher risk of nonvaccination.

“This vaccine message should focus on cancer prevention, necessity, and the safety of the HPV vaccine,” Dr. Beavis said.

She reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel

 

– Parents are now less concerned about whether their daughters are sexually active when weighing whether to vaccinate against human papillomavirus (HPV), compared with just a few years ago.

This shift in parental attitudes can inform physician guidance and shift the HPV vaccination discussion, Anna Beavis, MD, a clinical fellow in gynecologic oncology at Johns Hopkins Medicine, Baltimore, said at the annual meeting of the Society of Gynecologic Oncology.

About 90% of cervical cancer is preventable with the HPV vaccine, but “U.S. vaccination rates are still suboptimal,” putting the United States far behind many other developed countries, Dr. Beavis said.

It’s been shown that the physician recommendation is one of the strongest predictors of whether an adolescent will be immunized against HPV, yet many providers remain reluctant to raise the issue, she said. Discomfort about discussing adolescent sexuality with the teen and with parents has been cited by physicians as a primary barrier.

To evaluate why parents of adolescent girls would opt out of HPV vaccination and to identify whether the reasons had changed over time, Dr. Beavis and her colleagues formulated a study that compared parent responses to a nationwide survey about HPV vaccination given in 2014 to those in 2010.

The study drew from the National Immunization Survey–Teen, a random digit-dialing survey administered by the Centers for Disease Control and Prevention. Only data pertaining to girls aged 13-17 years was included in the analysis, and for the sake of accuracy, only provider-verified responses were used.

Of the 49,345 responses that could be provider verified during the period from 2010 to 2014, 54% had received at least one HPV vaccination. Of the remaining responses, 55% of the parents said they had no intention of vaccinating their daughters.

During this period, vaccination rates have climbed slowly, from a little less than half in 2010 to about 60% in 2014 (test of trend, P less than .001), according to Dr. Beavis.

However, the reasons parents gave for declining vaccination has shifted over time, she said. The primary reason given in 2010 was concern about safety or side effects, followed by the sense that the vaccine was not necessary. These remained the top two reasons in 2014, though they had swapped places.

In 2010, the third most common reason parents gave for declining the HPV vaccination was that their daughters were not sexually active. By 2014, this reason had slid to the bottom of the top five reasons, and now was given by fewer than 10% of parents (test of trend, P less than .01).

This is important information for physicians, Dr. Beavis said in a video interview. If a physician has been reluctant to start the HPV discussion for fear of stepping into awkward territory with parents of teen girls, they should know that it’s significantly less likely that issues of sexuality will be on the parental radar when talking about HPV vaccination.

Looking deeper into the data, the investigators found that white race, younger patient age, and living above the poverty level were risk factors for nonvaccination. This means, Dr. Beavis said, that physicians should consider “developing a targeted HPV message” for families at higher risk of nonvaccination.

“This vaccine message should focus on cancer prevention, necessity, and the safety of the HPV vaccine,” Dr. Beavis said.

She reported having no financial disclosures.

The video associated with this article is no longer available on this site. Please view all of our videos on the MDedge YouTube channel
Publications
Publications
Topics
Article Type
Sections
Article Source

AT THE ANNUAL MEETING ON WOMEN’S CANCER

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Postoperative Henoch-Schönlein Purpura

Article Type
Changed
Thu, 01/10/2019 - 13:39
Display Headline
Postoperative Henoch-Schönlein Purpura

To the Editor:

A 57-year-old man with a history of type 2 diabetes mellitus and hypertension was hospitalized for heart disease resulting in an aortic valve replacement and multiple-vessel bypass grafting. He experienced a stormy septic postoperative course during which he developed numerous palpable purplish plaques (Figure 1). The lesions were bilateral and more heavily involved the lower legs and buttocks. The head and neck remained free of skin lesions. Additionally, the patient reported a bilateral burning sensation from the knees to the feet.

Figure 1. Henoch-Schönlein purpura. Numerous palpable purplish plaques on the bilateral legs.

Punch biopsies of lesions from the right upper arm were obtained. Hematoxylin and eosin staining revealed neutrophilic-predominant small vessel vasculitis (Figure 2A) with the upper dermal location more heavily involved, as demonstrated by involvement of a superficial vascular plexus (Figures 2B and 2C) that was consistent with Henoch-Schönlein purpura (HSP). The diagnosis later was confirmed with immunofluorescence. Direct immunofluorescence revealed granular IgA deposition around the superficial vascular plexus (Figure 3). No IgG, IgM, C3, C5b-9 complement complex, or fibrinogen deposition was seen. Additionally, periodic acid-Schiff staining failed to show microorganisms, thrombi, or intravascular hyaline material.

Figure 2. Henoch-Schönlein purpura. Acute neutrophilrich perivascular and interstitial inflammation with vascular disruption of superficial vascular plexus and red blood cell extravasation (A)(H&E, original magnification ×50). Early leukocytoclastic vasculitis of a papillary dermal vessel (B)(H&E, original magnification ×200). High magnification of a superficial vascular plexus with leukocytoclastic vasculitis with fibrinoid necrosis of the vessel wall (C)(H&E, original magnification ×400).

Figure 3. Henoch-Schönlein purpura. Direct immunofluorescence of IgA deposition in a papillary dermal vessel (A)(original magnification ×400) and a superficial dermal vascular plexus with IgA deposition in vessel walls (B)(original magnification ×400).

At our initial consultation, we observed an ill-appearing afebrile man with purplish plaques. Our impression was that he had vasculitis and not warfarin necrosis, which had been suspected by the cardiovascular team. The burning sensation noted by the patient lent credence to our vasculitic diagnosis. Proteinuria and hematuria were present; however, the values for blood urea nitrogen, creatinine, and glomerular filtration rate all remained within reference range. His signs and symptoms responded dramatically to prednisone. He remains on 1 mg of prednisone daily and a nephrologist continues to monitor renal function as an outpatient.

 

 

Henoch-Schönlein purpura is a systemic leukocytoclastic vasculitis involving small vessels. The small vessel vasculitis is associated with IgA antigen-antibody complex deposition in areas throughout the body. Palpable purpura typically is seen on the skin, which characteristically involves dependent areas such as the legs and the buttocks. Lesions normally are present bilaterally in a symmetric distribution. Initially, the lesions develop as erythematous macules that progress to purple, nonblanching, palpable, and purpuric plaques.1 Henoch-Schönlein purpura most commonly involves the skin; however, other locations for the immune complexes include the gastrointestinal tract, joints, and kidneys.2 The cause for the body's immunogenic deposition response is unknown in a majority of cases.

Henoch-Schönlein purpura most commonly is seen in the pediatric population with a predilection for males.3 The incidence in the pediatric population is 13.5 to 20 per 100,000 children per year; HSP is more rare in adults.4-6 Henoch-Schönlein purpura most often is a self-limiting disease that requires only supportive treatment. The signs and symptoms last 4 to 6 weeks in most patients and resolve completely in 94% of children and 89% of adults.7 Renal involvement carries a worse prognosis. Adult patients have a higher incidence of renal involvement, renal insufficiency, and subsequent progression to end-stage renal disease.3,8-10 In a study by Hung et al8 of 65 children and 22 adult HSP patients, 12 adults presented with renal involvement in which hematuria or proteinuria were present. Of them, 6 progressed to renal insufficiency (defined as having a plasma creatinine concentration>1.2 mg/dL).8 Fogazzi et al11 reported similar findings; 8 of 16 patients affected with HSP progressed to renal insufficiency with creatinine clearances ranging from 31 to 60 mL/min, and 3 patients required chronic dialysis. Pillebout et al9 evaluated 250 adults with HSP and 32% reached renal insufficiency with creatinine clearances of less than 50 mL/min, with 11% of patients developing end-stage renal disease. The degree of hematuria and/or proteinuria has been shown to be an effective prognostic indicator.9,10 Coppo et al10 found a similar prognosis among children and adults with HSP-related nephritis.

Our patient described the burning sensation as occurring bilaterally from the knees down to the feet, which provided an additional clue that small vessel vasculitis was involved, as occluded blood vessels can cause ischemia to nerves and perivascular involvement can affect nearby neural structures. Sais et al12 demonstrated that paresthesia in the setting of HSP was a risk factor for systemic involvement. Of note,  our patient's paresthesia lasted only several days.

The cause of HSP is not always as evident in the adult population as in the pediatric population. Early diagnosis of HSP in adults may allow for the proper instatement of treatment to deter long-term renal complications. Follow-up with urinalysis is recommended because a small percentage of patients have a late progression to renal failure.13,14

Because the dermatologists involved in this case knew where and what types of biopsies to perform, a correct diagnosis was obtained quickly, allowing for the correct therapeutic intervention. After the diagnosis of HSP is made in an adult, nephrology should be consulted early in the treatment course.

References
  1. Rai A, Nast C, Adler S. Henoch-Schönlein purpura nephritis. J Am Soc Nephrol. 1999;10:2637-2644.
  2. Helander SD, De Castro FR, Gibson LE. Henoch-Schönlein purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis. Acta Derm Venereol. 1995;75:125-129.
  3. Garcia-Porrua C, Calvino MC, Llorca J, et al. Henoch-Schönlein purpura in children and adults: clinical differences in a defined population. Semin Arthritis Rheum. 2002;32:149-156.
  4. Stewart M, Savage JM, Bell B, et al. Long term renal prognosis of Henoch-Schönlein purpura in an unselected childhood population. Eur J Pediatr. 1988;147:113-115.
  5. Watts RA, Scott DG. Epidemiology of the vasculitides. Semin Respir Crit Care. 2004;25:455-464.
  6. Gardner-Medwin JM, Dolezalova P, Cummins C, et al. Incidence of Henoch-Schönlein purpura, Kawasaki disease, and rare vasculitides in children of different ethnic origins. Lancet. 2002;360:1197-1202.
  7. Blanco R, Martínez-Taboada VM, Rodríguez-Valverde V, et al. Henoch-Schönlein purpura in adulthood and childhood: two different expressions of the same syndrome. Arthritis Rheum. 1997;40:859-864.
  8. Hung SP, Yang YH, Lin YT, et al. Clinical manifestations and outcomes of Henoch-Schönlein purpura: comparison between adults and children. Pediatr Neonatol. 2009;50:162-168.
  9. Pillebout E, Thervet E, Hill G, et al. Henoch-Schönlein purpura in adults: outcomes and prognostic factors. J Am Soc Nephrol. 2002;13:1271-1278.
  10. Coppo R, Mazzucco G, Cagnoli L, et al. Long-term prognosis of Henoch-Schönlein nephritis in adults and children. Italian Group of Renal Immunopathology collaborative study on Henoch-Schönlein purpura. Nephrol Dial Transplant. 1997;12:2277-2283.
  11. Fogazzi GB, Pasquali S, Moriggi M, et al. Long-term outcome of Schönlein-Henoch nephritis in the adult. Clin Nephrol. 1989;31:60-66.
  12. Sais G, Vidaller A, Jucgla A. Prognostic factors in leukocytoclastic vasculitis. a clinicopathologic study of 160 patients. Arch Dermatol. 1998;134:309-315.
  13. Kraft DM, McKee D, Scott C. Henoch-Schönlein purpura: a review. Am Fam Physician. 1998;58:405-408.
  14. Narchi H. Risk of long-term renal impairment and duration of follow up recommended for Henoch-Schönlein purpura with normal or minimal urinary findings: a systematic review. Arch Dis Child. 2005;90:916-920.
Article PDF
Author and Disclosure Information

Dr. J.A. Gross is from St. George's University School of Medicine, Grenada, West Indies. Dr. Grady is from DeBusk College of Osteopathic Medicine, Lincoln Memorial University, Harrogate, Tennessee. Dr. Sanchez is from Dermpath Diagnostics, Pompano Beach, Florida. Dr. D.J. Gross is in private practice, St. Augustine, Florida.

The authors report no conflict of interest. 

Correspondence: David J. Gross, MD, 1100-3B, S Ponce De Leon Blvd, Saint Augustine, FL 32084 ([email protected]).

Issue
Cutis - 99(3)
Publications
Topics
Page Number
E10-E12
Sections
Author and Disclosure Information

Dr. J.A. Gross is from St. George's University School of Medicine, Grenada, West Indies. Dr. Grady is from DeBusk College of Osteopathic Medicine, Lincoln Memorial University, Harrogate, Tennessee. Dr. Sanchez is from Dermpath Diagnostics, Pompano Beach, Florida. Dr. D.J. Gross is in private practice, St. Augustine, Florida.

The authors report no conflict of interest. 

Correspondence: David J. Gross, MD, 1100-3B, S Ponce De Leon Blvd, Saint Augustine, FL 32084 ([email protected]).

Author and Disclosure Information

Dr. J.A. Gross is from St. George's University School of Medicine, Grenada, West Indies. Dr. Grady is from DeBusk College of Osteopathic Medicine, Lincoln Memorial University, Harrogate, Tennessee. Dr. Sanchez is from Dermpath Diagnostics, Pompano Beach, Florida. Dr. D.J. Gross is in private practice, St. Augustine, Florida.

The authors report no conflict of interest. 

Correspondence: David J. Gross, MD, 1100-3B, S Ponce De Leon Blvd, Saint Augustine, FL 32084 ([email protected]).

Article PDF
Article PDF

To the Editor:

A 57-year-old man with a history of type 2 diabetes mellitus and hypertension was hospitalized for heart disease resulting in an aortic valve replacement and multiple-vessel bypass grafting. He experienced a stormy septic postoperative course during which he developed numerous palpable purplish plaques (Figure 1). The lesions were bilateral and more heavily involved the lower legs and buttocks. The head and neck remained free of skin lesions. Additionally, the patient reported a bilateral burning sensation from the knees to the feet.

Figure 1. Henoch-Schönlein purpura. Numerous palpable purplish plaques on the bilateral legs.

Punch biopsies of lesions from the right upper arm were obtained. Hematoxylin and eosin staining revealed neutrophilic-predominant small vessel vasculitis (Figure 2A) with the upper dermal location more heavily involved, as demonstrated by involvement of a superficial vascular plexus (Figures 2B and 2C) that was consistent with Henoch-Schönlein purpura (HSP). The diagnosis later was confirmed with immunofluorescence. Direct immunofluorescence revealed granular IgA deposition around the superficial vascular plexus (Figure 3). No IgG, IgM, C3, C5b-9 complement complex, or fibrinogen deposition was seen. Additionally, periodic acid-Schiff staining failed to show microorganisms, thrombi, or intravascular hyaline material.

Figure 2. Henoch-Schönlein purpura. Acute neutrophilrich perivascular and interstitial inflammation with vascular disruption of superficial vascular plexus and red blood cell extravasation (A)(H&E, original magnification ×50). Early leukocytoclastic vasculitis of a papillary dermal vessel (B)(H&E, original magnification ×200). High magnification of a superficial vascular plexus with leukocytoclastic vasculitis with fibrinoid necrosis of the vessel wall (C)(H&E, original magnification ×400).

Figure 3. Henoch-Schönlein purpura. Direct immunofluorescence of IgA deposition in a papillary dermal vessel (A)(original magnification ×400) and a superficial dermal vascular plexus with IgA deposition in vessel walls (B)(original magnification ×400).

At our initial consultation, we observed an ill-appearing afebrile man with purplish plaques. Our impression was that he had vasculitis and not warfarin necrosis, which had been suspected by the cardiovascular team. The burning sensation noted by the patient lent credence to our vasculitic diagnosis. Proteinuria and hematuria were present; however, the values for blood urea nitrogen, creatinine, and glomerular filtration rate all remained within reference range. His signs and symptoms responded dramatically to prednisone. He remains on 1 mg of prednisone daily and a nephrologist continues to monitor renal function as an outpatient.

 

 

Henoch-Schönlein purpura is a systemic leukocytoclastic vasculitis involving small vessels. The small vessel vasculitis is associated with IgA antigen-antibody complex deposition in areas throughout the body. Palpable purpura typically is seen on the skin, which characteristically involves dependent areas such as the legs and the buttocks. Lesions normally are present bilaterally in a symmetric distribution. Initially, the lesions develop as erythematous macules that progress to purple, nonblanching, palpable, and purpuric plaques.1 Henoch-Schönlein purpura most commonly involves the skin; however, other locations for the immune complexes include the gastrointestinal tract, joints, and kidneys.2 The cause for the body's immunogenic deposition response is unknown in a majority of cases.

Henoch-Schönlein purpura most commonly is seen in the pediatric population with a predilection for males.3 The incidence in the pediatric population is 13.5 to 20 per 100,000 children per year; HSP is more rare in adults.4-6 Henoch-Schönlein purpura most often is a self-limiting disease that requires only supportive treatment. The signs and symptoms last 4 to 6 weeks in most patients and resolve completely in 94% of children and 89% of adults.7 Renal involvement carries a worse prognosis. Adult patients have a higher incidence of renal involvement, renal insufficiency, and subsequent progression to end-stage renal disease.3,8-10 In a study by Hung et al8 of 65 children and 22 adult HSP patients, 12 adults presented with renal involvement in which hematuria or proteinuria were present. Of them, 6 progressed to renal insufficiency (defined as having a plasma creatinine concentration>1.2 mg/dL).8 Fogazzi et al11 reported similar findings; 8 of 16 patients affected with HSP progressed to renal insufficiency with creatinine clearances ranging from 31 to 60 mL/min, and 3 patients required chronic dialysis. Pillebout et al9 evaluated 250 adults with HSP and 32% reached renal insufficiency with creatinine clearances of less than 50 mL/min, with 11% of patients developing end-stage renal disease. The degree of hematuria and/or proteinuria has been shown to be an effective prognostic indicator.9,10 Coppo et al10 found a similar prognosis among children and adults with HSP-related nephritis.

Our patient described the burning sensation as occurring bilaterally from the knees down to the feet, which provided an additional clue that small vessel vasculitis was involved, as occluded blood vessels can cause ischemia to nerves and perivascular involvement can affect nearby neural structures. Sais et al12 demonstrated that paresthesia in the setting of HSP was a risk factor for systemic involvement. Of note,  our patient's paresthesia lasted only several days.

The cause of HSP is not always as evident in the adult population as in the pediatric population. Early diagnosis of HSP in adults may allow for the proper instatement of treatment to deter long-term renal complications. Follow-up with urinalysis is recommended because a small percentage of patients have a late progression to renal failure.13,14

Because the dermatologists involved in this case knew where and what types of biopsies to perform, a correct diagnosis was obtained quickly, allowing for the correct therapeutic intervention. After the diagnosis of HSP is made in an adult, nephrology should be consulted early in the treatment course.

To the Editor:

A 57-year-old man with a history of type 2 diabetes mellitus and hypertension was hospitalized for heart disease resulting in an aortic valve replacement and multiple-vessel bypass grafting. He experienced a stormy septic postoperative course during which he developed numerous palpable purplish plaques (Figure 1). The lesions were bilateral and more heavily involved the lower legs and buttocks. The head and neck remained free of skin lesions. Additionally, the patient reported a bilateral burning sensation from the knees to the feet.

Figure 1. Henoch-Schönlein purpura. Numerous palpable purplish plaques on the bilateral legs.

Punch biopsies of lesions from the right upper arm were obtained. Hematoxylin and eosin staining revealed neutrophilic-predominant small vessel vasculitis (Figure 2A) with the upper dermal location more heavily involved, as demonstrated by involvement of a superficial vascular plexus (Figures 2B and 2C) that was consistent with Henoch-Schönlein purpura (HSP). The diagnosis later was confirmed with immunofluorescence. Direct immunofluorescence revealed granular IgA deposition around the superficial vascular plexus (Figure 3). No IgG, IgM, C3, C5b-9 complement complex, or fibrinogen deposition was seen. Additionally, periodic acid-Schiff staining failed to show microorganisms, thrombi, or intravascular hyaline material.

Figure 2. Henoch-Schönlein purpura. Acute neutrophilrich perivascular and interstitial inflammation with vascular disruption of superficial vascular plexus and red blood cell extravasation (A)(H&E, original magnification ×50). Early leukocytoclastic vasculitis of a papillary dermal vessel (B)(H&E, original magnification ×200). High magnification of a superficial vascular plexus with leukocytoclastic vasculitis with fibrinoid necrosis of the vessel wall (C)(H&E, original magnification ×400).

Figure 3. Henoch-Schönlein purpura. Direct immunofluorescence of IgA deposition in a papillary dermal vessel (A)(original magnification ×400) and a superficial dermal vascular plexus with IgA deposition in vessel walls (B)(original magnification ×400).

At our initial consultation, we observed an ill-appearing afebrile man with purplish plaques. Our impression was that he had vasculitis and not warfarin necrosis, which had been suspected by the cardiovascular team. The burning sensation noted by the patient lent credence to our vasculitic diagnosis. Proteinuria and hematuria were present; however, the values for blood urea nitrogen, creatinine, and glomerular filtration rate all remained within reference range. His signs and symptoms responded dramatically to prednisone. He remains on 1 mg of prednisone daily and a nephrologist continues to monitor renal function as an outpatient.

 

 

Henoch-Schönlein purpura is a systemic leukocytoclastic vasculitis involving small vessels. The small vessel vasculitis is associated with IgA antigen-antibody complex deposition in areas throughout the body. Palpable purpura typically is seen on the skin, which characteristically involves dependent areas such as the legs and the buttocks. Lesions normally are present bilaterally in a symmetric distribution. Initially, the lesions develop as erythematous macules that progress to purple, nonblanching, palpable, and purpuric plaques.1 Henoch-Schönlein purpura most commonly involves the skin; however, other locations for the immune complexes include the gastrointestinal tract, joints, and kidneys.2 The cause for the body's immunogenic deposition response is unknown in a majority of cases.

Henoch-Schönlein purpura most commonly is seen in the pediatric population with a predilection for males.3 The incidence in the pediatric population is 13.5 to 20 per 100,000 children per year; HSP is more rare in adults.4-6 Henoch-Schönlein purpura most often is a self-limiting disease that requires only supportive treatment. The signs and symptoms last 4 to 6 weeks in most patients and resolve completely in 94% of children and 89% of adults.7 Renal involvement carries a worse prognosis. Adult patients have a higher incidence of renal involvement, renal insufficiency, and subsequent progression to end-stage renal disease.3,8-10 In a study by Hung et al8 of 65 children and 22 adult HSP patients, 12 adults presented with renal involvement in which hematuria or proteinuria were present. Of them, 6 progressed to renal insufficiency (defined as having a plasma creatinine concentration>1.2 mg/dL).8 Fogazzi et al11 reported similar findings; 8 of 16 patients affected with HSP progressed to renal insufficiency with creatinine clearances ranging from 31 to 60 mL/min, and 3 patients required chronic dialysis. Pillebout et al9 evaluated 250 adults with HSP and 32% reached renal insufficiency with creatinine clearances of less than 50 mL/min, with 11% of patients developing end-stage renal disease. The degree of hematuria and/or proteinuria has been shown to be an effective prognostic indicator.9,10 Coppo et al10 found a similar prognosis among children and adults with HSP-related nephritis.

Our patient described the burning sensation as occurring bilaterally from the knees down to the feet, which provided an additional clue that small vessel vasculitis was involved, as occluded blood vessels can cause ischemia to nerves and perivascular involvement can affect nearby neural structures. Sais et al12 demonstrated that paresthesia in the setting of HSP was a risk factor for systemic involvement. Of note,  our patient's paresthesia lasted only several days.

The cause of HSP is not always as evident in the adult population as in the pediatric population. Early diagnosis of HSP in adults may allow for the proper instatement of treatment to deter long-term renal complications. Follow-up with urinalysis is recommended because a small percentage of patients have a late progression to renal failure.13,14

Because the dermatologists involved in this case knew where and what types of biopsies to perform, a correct diagnosis was obtained quickly, allowing for the correct therapeutic intervention. After the diagnosis of HSP is made in an adult, nephrology should be consulted early in the treatment course.

References
  1. Rai A, Nast C, Adler S. Henoch-Schönlein purpura nephritis. J Am Soc Nephrol. 1999;10:2637-2644.
  2. Helander SD, De Castro FR, Gibson LE. Henoch-Schönlein purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis. Acta Derm Venereol. 1995;75:125-129.
  3. Garcia-Porrua C, Calvino MC, Llorca J, et al. Henoch-Schönlein purpura in children and adults: clinical differences in a defined population. Semin Arthritis Rheum. 2002;32:149-156.
  4. Stewart M, Savage JM, Bell B, et al. Long term renal prognosis of Henoch-Schönlein purpura in an unselected childhood population. Eur J Pediatr. 1988;147:113-115.
  5. Watts RA, Scott DG. Epidemiology of the vasculitides. Semin Respir Crit Care. 2004;25:455-464.
  6. Gardner-Medwin JM, Dolezalova P, Cummins C, et al. Incidence of Henoch-Schönlein purpura, Kawasaki disease, and rare vasculitides in children of different ethnic origins. Lancet. 2002;360:1197-1202.
  7. Blanco R, Martínez-Taboada VM, Rodríguez-Valverde V, et al. Henoch-Schönlein purpura in adulthood and childhood: two different expressions of the same syndrome. Arthritis Rheum. 1997;40:859-864.
  8. Hung SP, Yang YH, Lin YT, et al. Clinical manifestations and outcomes of Henoch-Schönlein purpura: comparison between adults and children. Pediatr Neonatol. 2009;50:162-168.
  9. Pillebout E, Thervet E, Hill G, et al. Henoch-Schönlein purpura in adults: outcomes and prognostic factors. J Am Soc Nephrol. 2002;13:1271-1278.
  10. Coppo R, Mazzucco G, Cagnoli L, et al. Long-term prognosis of Henoch-Schönlein nephritis in adults and children. Italian Group of Renal Immunopathology collaborative study on Henoch-Schönlein purpura. Nephrol Dial Transplant. 1997;12:2277-2283.
  11. Fogazzi GB, Pasquali S, Moriggi M, et al. Long-term outcome of Schönlein-Henoch nephritis in the adult. Clin Nephrol. 1989;31:60-66.
  12. Sais G, Vidaller A, Jucgla A. Prognostic factors in leukocytoclastic vasculitis. a clinicopathologic study of 160 patients. Arch Dermatol. 1998;134:309-315.
  13. Kraft DM, McKee D, Scott C. Henoch-Schönlein purpura: a review. Am Fam Physician. 1998;58:405-408.
  14. Narchi H. Risk of long-term renal impairment and duration of follow up recommended for Henoch-Schönlein purpura with normal or minimal urinary findings: a systematic review. Arch Dis Child. 2005;90:916-920.
References
  1. Rai A, Nast C, Adler S. Henoch-Schönlein purpura nephritis. J Am Soc Nephrol. 1999;10:2637-2644.
  2. Helander SD, De Castro FR, Gibson LE. Henoch-Schönlein purpura: clinicopathologic correlation of cutaneous vascular IgA deposits and the relationship to leukocytoclastic vasculitis. Acta Derm Venereol. 1995;75:125-129.
  3. Garcia-Porrua C, Calvino MC, Llorca J, et al. Henoch-Schönlein purpura in children and adults: clinical differences in a defined population. Semin Arthritis Rheum. 2002;32:149-156.
  4. Stewart M, Savage JM, Bell B, et al. Long term renal prognosis of Henoch-Schönlein purpura in an unselected childhood population. Eur J Pediatr. 1988;147:113-115.
  5. Watts RA, Scott DG. Epidemiology of the vasculitides. Semin Respir Crit Care. 2004;25:455-464.
  6. Gardner-Medwin JM, Dolezalova P, Cummins C, et al. Incidence of Henoch-Schönlein purpura, Kawasaki disease, and rare vasculitides in children of different ethnic origins. Lancet. 2002;360:1197-1202.
  7. Blanco R, Martínez-Taboada VM, Rodríguez-Valverde V, et al. Henoch-Schönlein purpura in adulthood and childhood: two different expressions of the same syndrome. Arthritis Rheum. 1997;40:859-864.
  8. Hung SP, Yang YH, Lin YT, et al. Clinical manifestations and outcomes of Henoch-Schönlein purpura: comparison between adults and children. Pediatr Neonatol. 2009;50:162-168.
  9. Pillebout E, Thervet E, Hill G, et al. Henoch-Schönlein purpura in adults: outcomes and prognostic factors. J Am Soc Nephrol. 2002;13:1271-1278.
  10. Coppo R, Mazzucco G, Cagnoli L, et al. Long-term prognosis of Henoch-Schönlein nephritis in adults and children. Italian Group of Renal Immunopathology collaborative study on Henoch-Schönlein purpura. Nephrol Dial Transplant. 1997;12:2277-2283.
  11. Fogazzi GB, Pasquali S, Moriggi M, et al. Long-term outcome of Schönlein-Henoch nephritis in the adult. Clin Nephrol. 1989;31:60-66.
  12. Sais G, Vidaller A, Jucgla A. Prognostic factors in leukocytoclastic vasculitis. a clinicopathologic study of 160 patients. Arch Dermatol. 1998;134:309-315.
  13. Kraft DM, McKee D, Scott C. Henoch-Schönlein purpura: a review. Am Fam Physician. 1998;58:405-408.
  14. Narchi H. Risk of long-term renal impairment and duration of follow up recommended for Henoch-Schönlein purpura with normal or minimal urinary findings: a systematic review. Arch Dis Child. 2005;90:916-920.
Issue
Cutis - 99(3)
Issue
Cutis - 99(3)
Page Number
E10-E12
Page Number
E10-E12
Publications
Publications
Topics
Article Type
Display Headline
Postoperative Henoch-Schönlein Purpura
Display Headline
Postoperative Henoch-Schönlein Purpura
Sections
Inside the Article

Practice Points

  • Henoch-Schönlein purpura is a multidisciplinary problem.
  • Henoch-Schönlein purpura is an IgA-mediated disorder that is more common in children and has a more severe course in adults.
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Article PDF Media

Maintenance taxane therapy of no benefit in advanced ovarian cancer

Article Type
Changed
Fri, 01/04/2019 - 13:32

 

– Using either a polymerized formulation of paclitaxel or paclitaxel alone as maintenance therapy conferred no survival benefit for women with advanced ovarian, fallopian tube, or peritoneal cancer.

In a phase III randomized trial, patients survived a median 54.8 months with surveillance alone, 51.3 months with maintenance paclitaxel, and 60.0 months with maintenance paclitaxel poliglumex; these differences were not statistically significant.

In a presentation at the annual meeting of the Society of Gynecologic Oncology, Larry Copeland, MD, a professor of gynecologic oncology at Ohio State University, Columbus, said that treatment with surgery and chemotherapy yields a clinical complete response in many patients with these cancers. However, he said, recurrent progressive disease is still very common; the rationale behind maintenance chemotherapy is that it may “reduce the risk of recurrence and extend survival.”

There had been promising earlier data supporting this approach from a previous phase III comparison trial that evaluated the difference in clinical complete response between 3 or 12 cycles of paclitaxel, said Dr. Copeland. The results of a predefined interim analysis prompted the data monitoring committee to close that study (J Clin Oncol. 2003;21[13]:2460-5) since the 12-cycle, 7-month arm of the study had better progression-free survival. However, the 12-cycle protocol did not confer a benefit in overall survival, the investigators later reported (Gynecol Oncol 2009;114[2]:195-8).

The current stage III randomized trial enrolled women with stage III or IV ovarian, fallopian tube, or peritoneal cancer who had had five to eight cycles of chemotherapy and achieved clinical complete response. If patients had neuropathy, it could not exceed grade 1, and their cancer performance status scores could not exceed 2, Dr. Copeland said.

Patients were randomized 1:1:1 to a surveillance arm, to receive paclitaxel as a 3-hour infusion, or to receive paclitaxel poliglumex as a 10- to 20-minute infusion. Both study drugs were dosed at 35 mg/m2 every 28 days for 12 cycles.

The study ran from March 2005 to January 2014, enrolling 1,157 patients who were followed for a median of 71 months. Over 80% of patients in each study arm had ovarian cancer, and a similar number had stage III cancer and serous histology. Over 90% of patients in each arm had grade 2 or higher histology.

The study was designed as a superiority design, and patients were not to receive other cancer treatments until they had disease progression. Primary clinical endpoints for the study included overall survival, quality of life as measured by the Ovarian Specific Questionnaire Quality of Life–Cancer, and patient-reported neurotoxicity as reported on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group/Neurotoxicity questionnaire.

The third scheduled interim analysis, in May 2016, examined the primary endpoint of overall survival, triggered when at least 200 deaths occurred in the surveillance group. The overall final analysis had been scheduled for the point at which at least 301 deaths happened in the surveillance group. In the abstract accompanying the presentation, Dr. Copeland wrote that the data at the point of this interim analysis indicated that “the relative death hazards passed the futility boundaries for both taxane regimens.”

“The log-rank statistic for each taxane regimen was below the interval specific in the study design, making it unlikely either of the taxane regimens has superior overall survival compared to surveillance,” said Dr. Copeland.

The hazard ratio for overall survival of the paclitaxel group compared to surveillance was 1.104, with a 97.5% confidence interval (CI) of 0.884-1.38. For the paclitaxel poliglumex group, the hazard ratio compared to surveillance alone was 0.979 (97.5% CI, 0.781-1.23).

Dr. Copeland and his colleagues also looked at progression-free survival, not a primary endpoint of the study. For the paclitaxel patients compared to surveillance, the HR for progression-free survival was 0.783 (95% CI, 0.666-0.921). For paclitaxel poliglumex, the HR was 0.847 (95% CI, 0.666-0.921).

Not unexpectedly, more patients who received taxane treatment than those in the surveillance arm experienced adverse events, said Dr. Copeland. The most common adverse events were hypersensitivity or allergic reactions, fatigue, alopecia, nausea, constipation, and sensory neuropathies. Grade 2 alopecia was experienced by about a quarter of the paclitaxel poliglumex cohort, and by a little less than half of the paclitaxel cohort. Neurologic adverse events were very common, reported by three quarters of the paclitaxel poliglumex cohort, four in five of the paclitaxel group, and by a little over half of the surveillance cohort.

Overall quality of life scores did not differ significantly among the treatment arms.

In an exploratory analysis, Dr. Copeland and his colleagues determined that patients with no residual disease (R0 patients) after initial cytoreductive surgery fared better, with a median 70 months of survival compared to a median 43.6 months for individuals with gross residual disease. When those patients were sorted out by treatment arm, there was no significant difference in OS for R0 patients who received any intervention or surveillance.

“Overall survival was not improved with taxane maintenance, though progression-free survival is slightly delayed,” Dr. Copeland concluded.

In discussion after the presentation, he said that he is not sure that further investigations will be pursued for paclitaxel poliglumex in the treatment of ovarian cancers.

Paclitaxel poliglumex (CT-2103; Opaxio) is paclitaxel conjugated to a polyglutamate polymer, a formulation that may enhance tumor penetration and retention, and that allows shorter infusion at a peripheral site. Previous work had shown that CT-2103’s structure enhanced pharmacokinetics and potentially decreased toxicity (Expert Opin Investig Drugs. 2004 Nov;13[11]:1501-8).

Dr. Copeland reported receiving consulting or honoraria fees from Clovis, Advaxis, Janssen, and Tesaro, and is a stockholder or shareholder in Merck, Eli Lilly, and Cardinal Health. The study was sponsored by the Cancer Therapy Evaluation Program of the National Cancer Institute and by Cell Therapeutics, which plans to market paclitaxel poliglumex.
 

 

 

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– Using either a polymerized formulation of paclitaxel or paclitaxel alone as maintenance therapy conferred no survival benefit for women with advanced ovarian, fallopian tube, or peritoneal cancer.

In a phase III randomized trial, patients survived a median 54.8 months with surveillance alone, 51.3 months with maintenance paclitaxel, and 60.0 months with maintenance paclitaxel poliglumex; these differences were not statistically significant.

In a presentation at the annual meeting of the Society of Gynecologic Oncology, Larry Copeland, MD, a professor of gynecologic oncology at Ohio State University, Columbus, said that treatment with surgery and chemotherapy yields a clinical complete response in many patients with these cancers. However, he said, recurrent progressive disease is still very common; the rationale behind maintenance chemotherapy is that it may “reduce the risk of recurrence and extend survival.”

There had been promising earlier data supporting this approach from a previous phase III comparison trial that evaluated the difference in clinical complete response between 3 or 12 cycles of paclitaxel, said Dr. Copeland. The results of a predefined interim analysis prompted the data monitoring committee to close that study (J Clin Oncol. 2003;21[13]:2460-5) since the 12-cycle, 7-month arm of the study had better progression-free survival. However, the 12-cycle protocol did not confer a benefit in overall survival, the investigators later reported (Gynecol Oncol 2009;114[2]:195-8).

The current stage III randomized trial enrolled women with stage III or IV ovarian, fallopian tube, or peritoneal cancer who had had five to eight cycles of chemotherapy and achieved clinical complete response. If patients had neuropathy, it could not exceed grade 1, and their cancer performance status scores could not exceed 2, Dr. Copeland said.

Patients were randomized 1:1:1 to a surveillance arm, to receive paclitaxel as a 3-hour infusion, or to receive paclitaxel poliglumex as a 10- to 20-minute infusion. Both study drugs were dosed at 35 mg/m2 every 28 days for 12 cycles.

The study ran from March 2005 to January 2014, enrolling 1,157 patients who were followed for a median of 71 months. Over 80% of patients in each study arm had ovarian cancer, and a similar number had stage III cancer and serous histology. Over 90% of patients in each arm had grade 2 or higher histology.

The study was designed as a superiority design, and patients were not to receive other cancer treatments until they had disease progression. Primary clinical endpoints for the study included overall survival, quality of life as measured by the Ovarian Specific Questionnaire Quality of Life–Cancer, and patient-reported neurotoxicity as reported on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group/Neurotoxicity questionnaire.

The third scheduled interim analysis, in May 2016, examined the primary endpoint of overall survival, triggered when at least 200 deaths occurred in the surveillance group. The overall final analysis had been scheduled for the point at which at least 301 deaths happened in the surveillance group. In the abstract accompanying the presentation, Dr. Copeland wrote that the data at the point of this interim analysis indicated that “the relative death hazards passed the futility boundaries for both taxane regimens.”

“The log-rank statistic for each taxane regimen was below the interval specific in the study design, making it unlikely either of the taxane regimens has superior overall survival compared to surveillance,” said Dr. Copeland.

The hazard ratio for overall survival of the paclitaxel group compared to surveillance was 1.104, with a 97.5% confidence interval (CI) of 0.884-1.38. For the paclitaxel poliglumex group, the hazard ratio compared to surveillance alone was 0.979 (97.5% CI, 0.781-1.23).

Dr. Copeland and his colleagues also looked at progression-free survival, not a primary endpoint of the study. For the paclitaxel patients compared to surveillance, the HR for progression-free survival was 0.783 (95% CI, 0.666-0.921). For paclitaxel poliglumex, the HR was 0.847 (95% CI, 0.666-0.921).

Not unexpectedly, more patients who received taxane treatment than those in the surveillance arm experienced adverse events, said Dr. Copeland. The most common adverse events were hypersensitivity or allergic reactions, fatigue, alopecia, nausea, constipation, and sensory neuropathies. Grade 2 alopecia was experienced by about a quarter of the paclitaxel poliglumex cohort, and by a little less than half of the paclitaxel cohort. Neurologic adverse events were very common, reported by three quarters of the paclitaxel poliglumex cohort, four in five of the paclitaxel group, and by a little over half of the surveillance cohort.

Overall quality of life scores did not differ significantly among the treatment arms.

In an exploratory analysis, Dr. Copeland and his colleagues determined that patients with no residual disease (R0 patients) after initial cytoreductive surgery fared better, with a median 70 months of survival compared to a median 43.6 months for individuals with gross residual disease. When those patients were sorted out by treatment arm, there was no significant difference in OS for R0 patients who received any intervention or surveillance.

“Overall survival was not improved with taxane maintenance, though progression-free survival is slightly delayed,” Dr. Copeland concluded.

In discussion after the presentation, he said that he is not sure that further investigations will be pursued for paclitaxel poliglumex in the treatment of ovarian cancers.

Paclitaxel poliglumex (CT-2103; Opaxio) is paclitaxel conjugated to a polyglutamate polymer, a formulation that may enhance tumor penetration and retention, and that allows shorter infusion at a peripheral site. Previous work had shown that CT-2103’s structure enhanced pharmacokinetics and potentially decreased toxicity (Expert Opin Investig Drugs. 2004 Nov;13[11]:1501-8).

Dr. Copeland reported receiving consulting or honoraria fees from Clovis, Advaxis, Janssen, and Tesaro, and is a stockholder or shareholder in Merck, Eli Lilly, and Cardinal Health. The study was sponsored by the Cancer Therapy Evaluation Program of the National Cancer Institute and by Cell Therapeutics, which plans to market paclitaxel poliglumex.
 

 

 

 

– Using either a polymerized formulation of paclitaxel or paclitaxel alone as maintenance therapy conferred no survival benefit for women with advanced ovarian, fallopian tube, or peritoneal cancer.

In a phase III randomized trial, patients survived a median 54.8 months with surveillance alone, 51.3 months with maintenance paclitaxel, and 60.0 months with maintenance paclitaxel poliglumex; these differences were not statistically significant.

In a presentation at the annual meeting of the Society of Gynecologic Oncology, Larry Copeland, MD, a professor of gynecologic oncology at Ohio State University, Columbus, said that treatment with surgery and chemotherapy yields a clinical complete response in many patients with these cancers. However, he said, recurrent progressive disease is still very common; the rationale behind maintenance chemotherapy is that it may “reduce the risk of recurrence and extend survival.”

There had been promising earlier data supporting this approach from a previous phase III comparison trial that evaluated the difference in clinical complete response between 3 or 12 cycles of paclitaxel, said Dr. Copeland. The results of a predefined interim analysis prompted the data monitoring committee to close that study (J Clin Oncol. 2003;21[13]:2460-5) since the 12-cycle, 7-month arm of the study had better progression-free survival. However, the 12-cycle protocol did not confer a benefit in overall survival, the investigators later reported (Gynecol Oncol 2009;114[2]:195-8).

The current stage III randomized trial enrolled women with stage III or IV ovarian, fallopian tube, or peritoneal cancer who had had five to eight cycles of chemotherapy and achieved clinical complete response. If patients had neuropathy, it could not exceed grade 1, and their cancer performance status scores could not exceed 2, Dr. Copeland said.

Patients were randomized 1:1:1 to a surveillance arm, to receive paclitaxel as a 3-hour infusion, or to receive paclitaxel poliglumex as a 10- to 20-minute infusion. Both study drugs were dosed at 35 mg/m2 every 28 days for 12 cycles.

The study ran from March 2005 to January 2014, enrolling 1,157 patients who were followed for a median of 71 months. Over 80% of patients in each study arm had ovarian cancer, and a similar number had stage III cancer and serous histology. Over 90% of patients in each arm had grade 2 or higher histology.

The study was designed as a superiority design, and patients were not to receive other cancer treatments until they had disease progression. Primary clinical endpoints for the study included overall survival, quality of life as measured by the Ovarian Specific Questionnaire Quality of Life–Cancer, and patient-reported neurotoxicity as reported on the Functional Assessment of Cancer Therapy/Gynecologic Oncology Group/Neurotoxicity questionnaire.

The third scheduled interim analysis, in May 2016, examined the primary endpoint of overall survival, triggered when at least 200 deaths occurred in the surveillance group. The overall final analysis had been scheduled for the point at which at least 301 deaths happened in the surveillance group. In the abstract accompanying the presentation, Dr. Copeland wrote that the data at the point of this interim analysis indicated that “the relative death hazards passed the futility boundaries for both taxane regimens.”

“The log-rank statistic for each taxane regimen was below the interval specific in the study design, making it unlikely either of the taxane regimens has superior overall survival compared to surveillance,” said Dr. Copeland.

The hazard ratio for overall survival of the paclitaxel group compared to surveillance was 1.104, with a 97.5% confidence interval (CI) of 0.884-1.38. For the paclitaxel poliglumex group, the hazard ratio compared to surveillance alone was 0.979 (97.5% CI, 0.781-1.23).

Dr. Copeland and his colleagues also looked at progression-free survival, not a primary endpoint of the study. For the paclitaxel patients compared to surveillance, the HR for progression-free survival was 0.783 (95% CI, 0.666-0.921). For paclitaxel poliglumex, the HR was 0.847 (95% CI, 0.666-0.921).

Not unexpectedly, more patients who received taxane treatment than those in the surveillance arm experienced adverse events, said Dr. Copeland. The most common adverse events were hypersensitivity or allergic reactions, fatigue, alopecia, nausea, constipation, and sensory neuropathies. Grade 2 alopecia was experienced by about a quarter of the paclitaxel poliglumex cohort, and by a little less than half of the paclitaxel cohort. Neurologic adverse events were very common, reported by three quarters of the paclitaxel poliglumex cohort, four in five of the paclitaxel group, and by a little over half of the surveillance cohort.

Overall quality of life scores did not differ significantly among the treatment arms.

In an exploratory analysis, Dr. Copeland and his colleagues determined that patients with no residual disease (R0 patients) after initial cytoreductive surgery fared better, with a median 70 months of survival compared to a median 43.6 months for individuals with gross residual disease. When those patients were sorted out by treatment arm, there was no significant difference in OS for R0 patients who received any intervention or surveillance.

“Overall survival was not improved with taxane maintenance, though progression-free survival is slightly delayed,” Dr. Copeland concluded.

In discussion after the presentation, he said that he is not sure that further investigations will be pursued for paclitaxel poliglumex in the treatment of ovarian cancers.

Paclitaxel poliglumex (CT-2103; Opaxio) is paclitaxel conjugated to a polyglutamate polymer, a formulation that may enhance tumor penetration and retention, and that allows shorter infusion at a peripheral site. Previous work had shown that CT-2103’s structure enhanced pharmacokinetics and potentially decreased toxicity (Expert Opin Investig Drugs. 2004 Nov;13[11]:1501-8).

Dr. Copeland reported receiving consulting or honoraria fees from Clovis, Advaxis, Janssen, and Tesaro, and is a stockholder or shareholder in Merck, Eli Lilly, and Cardinal Health. The study was sponsored by the Cancer Therapy Evaluation Program of the National Cancer Institute and by Cell Therapeutics, which plans to market paclitaxel poliglumex.
 

 

 

Publications
Publications
Topics
Article Type
Click for Credit Status
Ready
Sections
Article Source

AT THE ANNUAL MEETING ON WOMEN’S CANCER

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: A phase III trial of a polymerized formulation of paclitaxel for advanced ovarian cancer showed no benefit in overall survival compared with surveillance.

Major finding: There was no statistically significant overall survival benefit of maintenance taxane therapy for advanced ovarian, fallopian tube, or peritoneal cancer, compared with surveillance.

Data source: Phase III randomized trial of 1,157 patients with advanced ovarian, fallopian tube, or peritoneal cancer.

Disclosures: Dr. Copeland reported receiving consulting or honoraria fees from Clovis, Advaxis, Janssen, and Tesaro, and is a stockholder or shareholder in Merck, Eli Lilly, and Cardinal Health. The study was sponsored by the Cancer Therapy Evaluation Program of the National Cancer Institute and by Cell Therapeutics, which plans to market paclitaxel poliglumex.

Are new medications on horizon for patients with depression, inflammation?

Article Type
Changed
Fri, 01/18/2019 - 16:37

 

– Inflammation is inextricably linked to depression in a subset of patients who differ from other depressed patients in their responses to certain interventions, according to Charles L. Raison, MD.

“The brains of people who are depressed and who have inflammation look very different from those of people who are depressed without inflammation,” Dr. Raison said in an interview at the annual meeting of the American College of Psychiatrists. “They have different connectivity patterns, different glutaminergic patterns, different signaling. It seems that inflammatory processes change the way different parts of the brain talk to each other and seem to do so in consistent ways.”

Dr. Raison, the Mary Sue and Mike Shannon Chair for Healthy Minds, Children & Families at the University of Wisconsin–Madison, told a plenary audience at the meeting: “We [psychiatrists] are so brain centric, it’s easy to forget how much the immune system drives us. It’s either like a second brain, or it is at least part of the brain.”

Dr. Charles Raison


Over the years, Dr. Raison and his colleagues have observed how inflammation can interfere with mood, leading to depression in people who previously did not report or describe depressive symptoms.

In the early 2000s, Dr. Raison and others such as Andrew H. Miller, MD, a psychiatric oncologist, investigated the inflammatory response and levels of depression in people treated with interferon-alpha for hepatitis C infection (J Clin Psychiatry. 2005 Jan;66[1]:41-8). They found that more than half of people who had not reported or described depressive symptoms at baseline subsequently reported depressive symptoms. “In a nutshell, we found that interferon-alpha induces every single brain-body function associated with regular old major depression,” said Dr. Raison, also a professor of psychiatry at the university.

In another study, this one led by neuropsychosomatic specialist Dominique L. Musselman, MD, a similar cohort of hepatitis C patients assessed for baseline depression was randomly assigned to either placebo or paroxetine during the course of interferon-alpha treatment. Patients treated with placebo had a 0.24 relative risk (95% confidence interval, 0.08-0.93) of developing depression, compared with the paroxetine group (N Eng J Med. 2001;344:961-6).

The real “breakthrough” in understanding the role of inflammation in depression, Dr. Raison said, came from studies that made the association between early-life adversity, depression, and inflammation. In one particular study, Dr. Raison and colleagues found that stress-induced spikes in interleukin-6 and NF-kappaB DNA-binding were greater in patients with higher baseline levels of depression and higher levels of early life stress (Am J Psychiatry. 2006 Sep;163[9]:1630-3).

Spikes in the inflammatory response independently correlated with depression severity but not with early life stress, which Dr. Raison said suggests that adversity likely can cause inflammation – and thus predisposes people to depression, and not necessarily vice versa.

“Something about early adversity in life programs the brain-body complex to run inflammatory systems hot, probably because it’s an effective way to be ready for [a stream of] unpredictable miseries,” Dr. Raison said during the session. “Chronic, elevated inflammation [early on] seems to predict increased depression later.”

Now that the link has been established between some depression and inflammation, the next step for science is to tease out who is most likely to respond to anti-inflammatory interventions for depression, Dr. Raison said.

“Something that is just starting to emerge is that maybe the relationship between inflammation and depression is not a straight line but a U-shaped curve, such that if you have too much inflammation, you’re in trouble, and if you have too little, you’re also in trouble,” he said in the interview, citing a study he and others conducted into blocking the inflammatory response. In that study, people with major depression who were otherwise medically healthy received either three infusions of the anti-inflammatory tumor necrosis factor–alpha antagonist infliximab (5 mg/kg), or of salt water. The investigators found that placebo worked just as well as infliximab. But patients with lower levels of inflammation at baseline had the greatest improvements in their Hamilton Rating Scale for Depression scores with placebo when compared with treatment (JAMA Psychiatry. 2013 Jan;70[1]:31-41).

Data are not yet conclusive, but Dr. Raison said the field soon could use biomarkers such as levels of C-reactive protein to determine whether patients will respond to anti-inflammatories such as omega-3 essential fatty acids. “Everyone in psychiatry is desperate to find clear, unambiguous answers. We’re right on the edge, but we’re not there yet.”

Until then, Dr. Raison cautioned against the “indiscriminate” use of anti-inflammatories, lest they exacerbate patients’ depressive symptoms. “For instance, omega-3 fatty acids might actually be counterproductive in a lot of depressed people,” he said. Still, he believes that “developing and studying anti-inflammatory strategies is probably going to lead to a novel way of treating depression in some people. What is beautiful is that if these studies continue, we might actually be able – for the first time – to target a subgroup of patients for a specific treatment.”

Dr. Raison is on the scientific advisory board of the Usona Institute, a nonprofit medical research firm.

 

 

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– Inflammation is inextricably linked to depression in a subset of patients who differ from other depressed patients in their responses to certain interventions, according to Charles L. Raison, MD.

“The brains of people who are depressed and who have inflammation look very different from those of people who are depressed without inflammation,” Dr. Raison said in an interview at the annual meeting of the American College of Psychiatrists. “They have different connectivity patterns, different glutaminergic patterns, different signaling. It seems that inflammatory processes change the way different parts of the brain talk to each other and seem to do so in consistent ways.”

Dr. Raison, the Mary Sue and Mike Shannon Chair for Healthy Minds, Children & Families at the University of Wisconsin–Madison, told a plenary audience at the meeting: “We [psychiatrists] are so brain centric, it’s easy to forget how much the immune system drives us. It’s either like a second brain, or it is at least part of the brain.”

Dr. Charles Raison


Over the years, Dr. Raison and his colleagues have observed how inflammation can interfere with mood, leading to depression in people who previously did not report or describe depressive symptoms.

In the early 2000s, Dr. Raison and others such as Andrew H. Miller, MD, a psychiatric oncologist, investigated the inflammatory response and levels of depression in people treated with interferon-alpha for hepatitis C infection (J Clin Psychiatry. 2005 Jan;66[1]:41-8). They found that more than half of people who had not reported or described depressive symptoms at baseline subsequently reported depressive symptoms. “In a nutshell, we found that interferon-alpha induces every single brain-body function associated with regular old major depression,” said Dr. Raison, also a professor of psychiatry at the university.

In another study, this one led by neuropsychosomatic specialist Dominique L. Musselman, MD, a similar cohort of hepatitis C patients assessed for baseline depression was randomly assigned to either placebo or paroxetine during the course of interferon-alpha treatment. Patients treated with placebo had a 0.24 relative risk (95% confidence interval, 0.08-0.93) of developing depression, compared with the paroxetine group (N Eng J Med. 2001;344:961-6).

The real “breakthrough” in understanding the role of inflammation in depression, Dr. Raison said, came from studies that made the association between early-life adversity, depression, and inflammation. In one particular study, Dr. Raison and colleagues found that stress-induced spikes in interleukin-6 and NF-kappaB DNA-binding were greater in patients with higher baseline levels of depression and higher levels of early life stress (Am J Psychiatry. 2006 Sep;163[9]:1630-3).

Spikes in the inflammatory response independently correlated with depression severity but not with early life stress, which Dr. Raison said suggests that adversity likely can cause inflammation – and thus predisposes people to depression, and not necessarily vice versa.

“Something about early adversity in life programs the brain-body complex to run inflammatory systems hot, probably because it’s an effective way to be ready for [a stream of] unpredictable miseries,” Dr. Raison said during the session. “Chronic, elevated inflammation [early on] seems to predict increased depression later.”

Now that the link has been established between some depression and inflammation, the next step for science is to tease out who is most likely to respond to anti-inflammatory interventions for depression, Dr. Raison said.

“Something that is just starting to emerge is that maybe the relationship between inflammation and depression is not a straight line but a U-shaped curve, such that if you have too much inflammation, you’re in trouble, and if you have too little, you’re also in trouble,” he said in the interview, citing a study he and others conducted into blocking the inflammatory response. In that study, people with major depression who were otherwise medically healthy received either three infusions of the anti-inflammatory tumor necrosis factor–alpha antagonist infliximab (5 mg/kg), or of salt water. The investigators found that placebo worked just as well as infliximab. But patients with lower levels of inflammation at baseline had the greatest improvements in their Hamilton Rating Scale for Depression scores with placebo when compared with treatment (JAMA Psychiatry. 2013 Jan;70[1]:31-41).

Data are not yet conclusive, but Dr. Raison said the field soon could use biomarkers such as levels of C-reactive protein to determine whether patients will respond to anti-inflammatories such as omega-3 essential fatty acids. “Everyone in psychiatry is desperate to find clear, unambiguous answers. We’re right on the edge, but we’re not there yet.”

Until then, Dr. Raison cautioned against the “indiscriminate” use of anti-inflammatories, lest they exacerbate patients’ depressive symptoms. “For instance, omega-3 fatty acids might actually be counterproductive in a lot of depressed people,” he said. Still, he believes that “developing and studying anti-inflammatory strategies is probably going to lead to a novel way of treating depression in some people. What is beautiful is that if these studies continue, we might actually be able – for the first time – to target a subgroup of patients for a specific treatment.”

Dr. Raison is on the scientific advisory board of the Usona Institute, a nonprofit medical research firm.

 

 

 

– Inflammation is inextricably linked to depression in a subset of patients who differ from other depressed patients in their responses to certain interventions, according to Charles L. Raison, MD.

“The brains of people who are depressed and who have inflammation look very different from those of people who are depressed without inflammation,” Dr. Raison said in an interview at the annual meeting of the American College of Psychiatrists. “They have different connectivity patterns, different glutaminergic patterns, different signaling. It seems that inflammatory processes change the way different parts of the brain talk to each other and seem to do so in consistent ways.”

Dr. Raison, the Mary Sue and Mike Shannon Chair for Healthy Minds, Children & Families at the University of Wisconsin–Madison, told a plenary audience at the meeting: “We [psychiatrists] are so brain centric, it’s easy to forget how much the immune system drives us. It’s either like a second brain, or it is at least part of the brain.”

Dr. Charles Raison


Over the years, Dr. Raison and his colleagues have observed how inflammation can interfere with mood, leading to depression in people who previously did not report or describe depressive symptoms.

In the early 2000s, Dr. Raison and others such as Andrew H. Miller, MD, a psychiatric oncologist, investigated the inflammatory response and levels of depression in people treated with interferon-alpha for hepatitis C infection (J Clin Psychiatry. 2005 Jan;66[1]:41-8). They found that more than half of people who had not reported or described depressive symptoms at baseline subsequently reported depressive symptoms. “In a nutshell, we found that interferon-alpha induces every single brain-body function associated with regular old major depression,” said Dr. Raison, also a professor of psychiatry at the university.

In another study, this one led by neuropsychosomatic specialist Dominique L. Musselman, MD, a similar cohort of hepatitis C patients assessed for baseline depression was randomly assigned to either placebo or paroxetine during the course of interferon-alpha treatment. Patients treated with placebo had a 0.24 relative risk (95% confidence interval, 0.08-0.93) of developing depression, compared with the paroxetine group (N Eng J Med. 2001;344:961-6).

The real “breakthrough” in understanding the role of inflammation in depression, Dr. Raison said, came from studies that made the association between early-life adversity, depression, and inflammation. In one particular study, Dr. Raison and colleagues found that stress-induced spikes in interleukin-6 and NF-kappaB DNA-binding were greater in patients with higher baseline levels of depression and higher levels of early life stress (Am J Psychiatry. 2006 Sep;163[9]:1630-3).

Spikes in the inflammatory response independently correlated with depression severity but not with early life stress, which Dr. Raison said suggests that adversity likely can cause inflammation – and thus predisposes people to depression, and not necessarily vice versa.

“Something about early adversity in life programs the brain-body complex to run inflammatory systems hot, probably because it’s an effective way to be ready for [a stream of] unpredictable miseries,” Dr. Raison said during the session. “Chronic, elevated inflammation [early on] seems to predict increased depression later.”

Now that the link has been established between some depression and inflammation, the next step for science is to tease out who is most likely to respond to anti-inflammatory interventions for depression, Dr. Raison said.

“Something that is just starting to emerge is that maybe the relationship between inflammation and depression is not a straight line but a U-shaped curve, such that if you have too much inflammation, you’re in trouble, and if you have too little, you’re also in trouble,” he said in the interview, citing a study he and others conducted into blocking the inflammatory response. In that study, people with major depression who were otherwise medically healthy received either three infusions of the anti-inflammatory tumor necrosis factor–alpha antagonist infliximab (5 mg/kg), or of salt water. The investigators found that placebo worked just as well as infliximab. But patients with lower levels of inflammation at baseline had the greatest improvements in their Hamilton Rating Scale for Depression scores with placebo when compared with treatment (JAMA Psychiatry. 2013 Jan;70[1]:31-41).

Data are not yet conclusive, but Dr. Raison said the field soon could use biomarkers such as levels of C-reactive protein to determine whether patients will respond to anti-inflammatories such as omega-3 essential fatty acids. “Everyone in psychiatry is desperate to find clear, unambiguous answers. We’re right on the edge, but we’re not there yet.”

Until then, Dr. Raison cautioned against the “indiscriminate” use of anti-inflammatories, lest they exacerbate patients’ depressive symptoms. “For instance, omega-3 fatty acids might actually be counterproductive in a lot of depressed people,” he said. Still, he believes that “developing and studying anti-inflammatory strategies is probably going to lead to a novel way of treating depression in some people. What is beautiful is that if these studies continue, we might actually be able – for the first time – to target a subgroup of patients for a specific treatment.”

Dr. Raison is on the scientific advisory board of the Usona Institute, a nonprofit medical research firm.

 

 

Publications
Publications
Topics
Article Type
Sections
Article Source

EXPERT OPINION FROM THE AMERICAN COLLEGE OF PSYCHIATRISTS MEETING

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Portfolio of physician-led measures nets better quality of care

Article Type
Changed
Fri, 01/04/2019 - 13:32

 

– A multifaceted portfolio of physician-led measures with feedback and financial incentives can dramatically improve the quality of care provided at cancer centers, suggests the experience of Stanford (Calif.) Health Care.

Physician leaders of 13 disease-specific cancer care programs (CCPs) identified measures of care that were meaningful to their team and patients, spanning the spectrum from new diagnosis through end of life and survivorship care. Quality and analytics teams developed 16 corresponding metrics and performance reports used for feedback. Programs were also given a financial incentive to meet jointly set targets.

After a year, the CCPs had improved on 12 of the metrics and maintained high baseline levels of performance on the other 4 metrics, investigators reported at a symposium on quality care sponsored by the American Society of Clinical Oncology. For example, they got better at entering staging information in a dedicated field in the electronic health record (+50% absolute increase), recording hand and foot pain (+34%), performing hepatitis B testing before rituximab use (+17%), and referring patients with ovarian cancer for genetic counseling (+43%).

Susan London/Frontline Medical News
Ms. Julie Bryar Porter
“This [initiative] was quite resource intensive for the modest number of patients’ lives covered in our measurements,” commented lead investigator Julie Bryar Porter, MSc, administrative director of the Blood and Marrow Transplant Program and the Cancer Quality Program at Stanford Health Care. “However, it was encouraging that all metrics maintained their strong results or improved performance over time to meet their target.”

“The main drivers, I would argue, besides the Hawthorne effect, were a high level of physician engagement in the selection, management, and improvement of the metrics, and these metrics excited the care teams, which also provided some motivation,” she said. “We provided real-time, high-quality feedback of performance. And last but probably not least was a financial incentive for the CCP as a team, not part of any individual compensation.”

The investigators plan to continue measuring the metrics, to expand them to other sites in their network, and to add new metrics that are common across the programs to minimize measurement burden, according to Ms. Porter. “We also plan to build cohorts for value-based care and unplanned care like ED visits and unplanned admissions. Finally, we want to keep momentum going and capitalize upon a provider engagement in value measurement and improvement,” she said.

“Based on this work and prior abstracts, … there are many validated metrics to be used. So, to choose those metrics and to choose them through local leadership support, most importantly, engaging frontline staff and having their buy-in of the measures that you are collecting are important,” commented invited discussant Jessica A. Zerillo, MD, MPH, of the Beth Israel Deaconess Medical Center in Boston. “And this can include using incentives that drive such stakeholders, whether they be financial or simply pride with public reporting.”

Susan London/Frontline Medical News
Dr. Jessica A. Zerillo
To take this effort forward, certain issues will need to be addressed, she maintained. First, “how do we sustain data collection and change with the fewer resources that continue to be available to us? How do we integrate quality measurement into overall system metrics so that we can demonstrate to our administrative colleagues that the work that we do in quality has an importance at the system level? And lastly, how do we implement patient-reported and long-term outcomes to enhance these measures?”

Study details

“In the summer of 2015, we were starting to feel a lot of pressure to prepare for evolving reimbursement models,” Ms. Porter said, explaining the initiative’s genesis. “Mainly, how do we define our value, and how can we measure and improve on that value of the care we deliver? One answer, of course, is to measure and reduce unnecessary variation. And we knew, to be successful, we had to increase our physician engagement and leadership in the selection and improvement of our metrics.”

 

 

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– A multifaceted portfolio of physician-led measures with feedback and financial incentives can dramatically improve the quality of care provided at cancer centers, suggests the experience of Stanford (Calif.) Health Care.

Physician leaders of 13 disease-specific cancer care programs (CCPs) identified measures of care that were meaningful to their team and patients, spanning the spectrum from new diagnosis through end of life and survivorship care. Quality and analytics teams developed 16 corresponding metrics and performance reports used for feedback. Programs were also given a financial incentive to meet jointly set targets.

After a year, the CCPs had improved on 12 of the metrics and maintained high baseline levels of performance on the other 4 metrics, investigators reported at a symposium on quality care sponsored by the American Society of Clinical Oncology. For example, they got better at entering staging information in a dedicated field in the electronic health record (+50% absolute increase), recording hand and foot pain (+34%), performing hepatitis B testing before rituximab use (+17%), and referring patients with ovarian cancer for genetic counseling (+43%).

Susan London/Frontline Medical News
Ms. Julie Bryar Porter
“This [initiative] was quite resource intensive for the modest number of patients’ lives covered in our measurements,” commented lead investigator Julie Bryar Porter, MSc, administrative director of the Blood and Marrow Transplant Program and the Cancer Quality Program at Stanford Health Care. “However, it was encouraging that all metrics maintained their strong results or improved performance over time to meet their target.”

“The main drivers, I would argue, besides the Hawthorne effect, were a high level of physician engagement in the selection, management, and improvement of the metrics, and these metrics excited the care teams, which also provided some motivation,” she said. “We provided real-time, high-quality feedback of performance. And last but probably not least was a financial incentive for the CCP as a team, not part of any individual compensation.”

The investigators plan to continue measuring the metrics, to expand them to other sites in their network, and to add new metrics that are common across the programs to minimize measurement burden, according to Ms. Porter. “We also plan to build cohorts for value-based care and unplanned care like ED visits and unplanned admissions. Finally, we want to keep momentum going and capitalize upon a provider engagement in value measurement and improvement,” she said.

“Based on this work and prior abstracts, … there are many validated metrics to be used. So, to choose those metrics and to choose them through local leadership support, most importantly, engaging frontline staff and having their buy-in of the measures that you are collecting are important,” commented invited discussant Jessica A. Zerillo, MD, MPH, of the Beth Israel Deaconess Medical Center in Boston. “And this can include using incentives that drive such stakeholders, whether they be financial or simply pride with public reporting.”

Susan London/Frontline Medical News
Dr. Jessica A. Zerillo
To take this effort forward, certain issues will need to be addressed, she maintained. First, “how do we sustain data collection and change with the fewer resources that continue to be available to us? How do we integrate quality measurement into overall system metrics so that we can demonstrate to our administrative colleagues that the work that we do in quality has an importance at the system level? And lastly, how do we implement patient-reported and long-term outcomes to enhance these measures?”

Study details

“In the summer of 2015, we were starting to feel a lot of pressure to prepare for evolving reimbursement models,” Ms. Porter said, explaining the initiative’s genesis. “Mainly, how do we define our value, and how can we measure and improve on that value of the care we deliver? One answer, of course, is to measure and reduce unnecessary variation. And we knew, to be successful, we had to increase our physician engagement and leadership in the selection and improvement of our metrics.”

 

 

 

– A multifaceted portfolio of physician-led measures with feedback and financial incentives can dramatically improve the quality of care provided at cancer centers, suggests the experience of Stanford (Calif.) Health Care.

Physician leaders of 13 disease-specific cancer care programs (CCPs) identified measures of care that were meaningful to their team and patients, spanning the spectrum from new diagnosis through end of life and survivorship care. Quality and analytics teams developed 16 corresponding metrics and performance reports used for feedback. Programs were also given a financial incentive to meet jointly set targets.

After a year, the CCPs had improved on 12 of the metrics and maintained high baseline levels of performance on the other 4 metrics, investigators reported at a symposium on quality care sponsored by the American Society of Clinical Oncology. For example, they got better at entering staging information in a dedicated field in the electronic health record (+50% absolute increase), recording hand and foot pain (+34%), performing hepatitis B testing before rituximab use (+17%), and referring patients with ovarian cancer for genetic counseling (+43%).

Susan London/Frontline Medical News
Ms. Julie Bryar Porter
“This [initiative] was quite resource intensive for the modest number of patients’ lives covered in our measurements,” commented lead investigator Julie Bryar Porter, MSc, administrative director of the Blood and Marrow Transplant Program and the Cancer Quality Program at Stanford Health Care. “However, it was encouraging that all metrics maintained their strong results or improved performance over time to meet their target.”

“The main drivers, I would argue, besides the Hawthorne effect, were a high level of physician engagement in the selection, management, and improvement of the metrics, and these metrics excited the care teams, which also provided some motivation,” she said. “We provided real-time, high-quality feedback of performance. And last but probably not least was a financial incentive for the CCP as a team, not part of any individual compensation.”

The investigators plan to continue measuring the metrics, to expand them to other sites in their network, and to add new metrics that are common across the programs to minimize measurement burden, according to Ms. Porter. “We also plan to build cohorts for value-based care and unplanned care like ED visits and unplanned admissions. Finally, we want to keep momentum going and capitalize upon a provider engagement in value measurement and improvement,” she said.

“Based on this work and prior abstracts, … there are many validated metrics to be used. So, to choose those metrics and to choose them through local leadership support, most importantly, engaging frontline staff and having their buy-in of the measures that you are collecting are important,” commented invited discussant Jessica A. Zerillo, MD, MPH, of the Beth Israel Deaconess Medical Center in Boston. “And this can include using incentives that drive such stakeholders, whether they be financial or simply pride with public reporting.”

Susan London/Frontline Medical News
Dr. Jessica A. Zerillo
To take this effort forward, certain issues will need to be addressed, she maintained. First, “how do we sustain data collection and change with the fewer resources that continue to be available to us? How do we integrate quality measurement into overall system metrics so that we can demonstrate to our administrative colleagues that the work that we do in quality has an importance at the system level? And lastly, how do we implement patient-reported and long-term outcomes to enhance these measures?”

Study details

“In the summer of 2015, we were starting to feel a lot of pressure to prepare for evolving reimbursement models,” Ms. Porter said, explaining the initiative’s genesis. “Mainly, how do we define our value, and how can we measure and improve on that value of the care we deliver? One answer, of course, is to measure and reduce unnecessary variation. And we knew, to be successful, we had to increase our physician engagement and leadership in the selection and improvement of our metrics.”

 

 

Publications
Publications
Topics
Article Type
Sections
Article Source

AT THE QUALITY CARE SYMPOSIUM

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: Implementation of the portfolio of measures selected by physician leaders improved metrics of quality care.

Major finding: Over a 1-year period, the center saw improvements in practices such as completion of staging modules (+50%), recording of hand and foot pain (+34%), hepatitis B testing before rituximab use (+17%), and referral of patients with ovarian cancer for genetic counseling (+43%).

Data source: An initiative targeting 16 quality metrics undertaken by 13 cancer care programs at Stanford Health Care.

Disclosures: Ms. Porter disclosed that she had no relevant conflicts of interest.

Machine learning melanoma

Article Type
Changed
Fri, 01/18/2019 - 16:37

 

What if an app could diagnose melanoma from a photo? That was my idea. In December 2009, Google introduced Google Goggles, an application that recognized images. At the time, I thought, “Wouldn’t it be neat if we could use this with telederm?” I even pitched it to a friend at the search giant. “Great idea!” he wrote back, placating me. For those uninitiated in innovation, “Great idea!” is a euphemism for “Yeah, we thought of that.”

Yes, it isn’t only mine; no doubt, many of you had this same idea: Let’s use amazing image interpretation capabilities from companies like Google or Apple to help us make diagnoses. Sounds simple. It isn’t. This is why most melanoma-finding apps are for entertainment purposes only – they don’t work.

Dr. Jeffrey Benabio
To reliably get this right takes immense experience and intuition, things we do better than computers. Or do we? Since 2009, processors have sped up and machine learning has become exponentially better. Now cars drive themselves and software can ID someone even in a grainy video. The two are related: Both require tremendous processing power and sophisticated algorithms to achieve artificial intelligence (AI). You’ve likely heard about AI or machine learning lately. If you’re unsure what all the fuss is about, read my previous column (Dermatology News, March 2017, p. 30).

So can melanoma be diagnosed from an app? A Stanford University team believes so. They trained a machine learning system to make dermatologic diagnoses from photos of skin lesions. To overcome previous barriers, they used open-sourced software from Google and awesome processors. For a start, they pretrained the program on over 1.28 million images. Then they fed it 128,450 images of known diagnoses.

Then, just as when Google’s AlphaGo algorithm challenged Lee Sedol, the world Go champion, the Stanford research team challenged 21 dermatologists. They had to choose if they would biopsy/treat or reassure patients based on photos of benign lesions, keratinocyte carcinomas, clinical melanomas, and dermoscopic melanomas. Guess who won?

In a stunning victory (or defeat, if you’re rooting for our team), the trained algorithm matched or outperformed all the dermatologists when scored on sensitivity-specificity curves. While we dermatologists, of course, use more than just a photo to diagnose skin cancer, many around the globe don’t have access to us. Based on these findings, they might need access only to a smartphone to get potentially life-saving advice.

But, what does this mean? Will we someday be outsourced to AI? Will a future POTUS promise to “bring back the doctor industry?” Not if we adapt. The future is bright – if we learn to apply machine learning in ways that can have an impact. (Brain + Computer > Brain.) Consider the following: An optimized ophthalmologist who reads retinal scans prediagnosed by a computer. A teledermatologist who uses AI to perform perfectly in diagnosing melanoma.

Patients have always wanted high quality and high touch care. In the history of medicine, we’ve never been better at both than we are today. Until tomorrow, when we’ll be better still.


 

Jeff Benabio, MD, MBA, is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]. He has no disclosures related to this column.

Publications
Topics
Sections
Related Articles

 

What if an app could diagnose melanoma from a photo? That was my idea. In December 2009, Google introduced Google Goggles, an application that recognized images. At the time, I thought, “Wouldn’t it be neat if we could use this with telederm?” I even pitched it to a friend at the search giant. “Great idea!” he wrote back, placating me. For those uninitiated in innovation, “Great idea!” is a euphemism for “Yeah, we thought of that.”

Yes, it isn’t only mine; no doubt, many of you had this same idea: Let’s use amazing image interpretation capabilities from companies like Google or Apple to help us make diagnoses. Sounds simple. It isn’t. This is why most melanoma-finding apps are for entertainment purposes only – they don’t work.

Dr. Jeffrey Benabio
To reliably get this right takes immense experience and intuition, things we do better than computers. Or do we? Since 2009, processors have sped up and machine learning has become exponentially better. Now cars drive themselves and software can ID someone even in a grainy video. The two are related: Both require tremendous processing power and sophisticated algorithms to achieve artificial intelligence (AI). You’ve likely heard about AI or machine learning lately. If you’re unsure what all the fuss is about, read my previous column (Dermatology News, March 2017, p. 30).

So can melanoma be diagnosed from an app? A Stanford University team believes so. They trained a machine learning system to make dermatologic diagnoses from photos of skin lesions. To overcome previous barriers, they used open-sourced software from Google and awesome processors. For a start, they pretrained the program on over 1.28 million images. Then they fed it 128,450 images of known diagnoses.

Then, just as when Google’s AlphaGo algorithm challenged Lee Sedol, the world Go champion, the Stanford research team challenged 21 dermatologists. They had to choose if they would biopsy/treat or reassure patients based on photos of benign lesions, keratinocyte carcinomas, clinical melanomas, and dermoscopic melanomas. Guess who won?

In a stunning victory (or defeat, if you’re rooting for our team), the trained algorithm matched or outperformed all the dermatologists when scored on sensitivity-specificity curves. While we dermatologists, of course, use more than just a photo to diagnose skin cancer, many around the globe don’t have access to us. Based on these findings, they might need access only to a smartphone to get potentially life-saving advice.

But, what does this mean? Will we someday be outsourced to AI? Will a future POTUS promise to “bring back the doctor industry?” Not if we adapt. The future is bright – if we learn to apply machine learning in ways that can have an impact. (Brain + Computer > Brain.) Consider the following: An optimized ophthalmologist who reads retinal scans prediagnosed by a computer. A teledermatologist who uses AI to perform perfectly in diagnosing melanoma.

Patients have always wanted high quality and high touch care. In the history of medicine, we’ve never been better at both than we are today. Until tomorrow, when we’ll be better still.


 

Jeff Benabio, MD, MBA, is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]. He has no disclosures related to this column.

 

What if an app could diagnose melanoma from a photo? That was my idea. In December 2009, Google introduced Google Goggles, an application that recognized images. At the time, I thought, “Wouldn’t it be neat if we could use this with telederm?” I even pitched it to a friend at the search giant. “Great idea!” he wrote back, placating me. For those uninitiated in innovation, “Great idea!” is a euphemism for “Yeah, we thought of that.”

Yes, it isn’t only mine; no doubt, many of you had this same idea: Let’s use amazing image interpretation capabilities from companies like Google or Apple to help us make diagnoses. Sounds simple. It isn’t. This is why most melanoma-finding apps are for entertainment purposes only – they don’t work.

Dr. Jeffrey Benabio
To reliably get this right takes immense experience and intuition, things we do better than computers. Or do we? Since 2009, processors have sped up and machine learning has become exponentially better. Now cars drive themselves and software can ID someone even in a grainy video. The two are related: Both require tremendous processing power and sophisticated algorithms to achieve artificial intelligence (AI). You’ve likely heard about AI or machine learning lately. If you’re unsure what all the fuss is about, read my previous column (Dermatology News, March 2017, p. 30).

So can melanoma be diagnosed from an app? A Stanford University team believes so. They trained a machine learning system to make dermatologic diagnoses from photos of skin lesions. To overcome previous barriers, they used open-sourced software from Google and awesome processors. For a start, they pretrained the program on over 1.28 million images. Then they fed it 128,450 images of known diagnoses.

Then, just as when Google’s AlphaGo algorithm challenged Lee Sedol, the world Go champion, the Stanford research team challenged 21 dermatologists. They had to choose if they would biopsy/treat or reassure patients based on photos of benign lesions, keratinocyte carcinomas, clinical melanomas, and dermoscopic melanomas. Guess who won?

In a stunning victory (or defeat, if you’re rooting for our team), the trained algorithm matched or outperformed all the dermatologists when scored on sensitivity-specificity curves. While we dermatologists, of course, use more than just a photo to diagnose skin cancer, many around the globe don’t have access to us. Based on these findings, they might need access only to a smartphone to get potentially life-saving advice.

But, what does this mean? Will we someday be outsourced to AI? Will a future POTUS promise to “bring back the doctor industry?” Not if we adapt. The future is bright – if we learn to apply machine learning in ways that can have an impact. (Brain + Computer > Brain.) Consider the following: An optimized ophthalmologist who reads retinal scans prediagnosed by a computer. A teledermatologist who uses AI to perform perfectly in diagnosing melanoma.

Patients have always wanted high quality and high touch care. In the history of medicine, we’ve never been better at both than we are today. Until tomorrow, when we’ll be better still.


 

Jeff Benabio, MD, MBA, is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. Dr. Benabio is @Dermdoc on Twitter. Write to him at [email protected]. He has no disclosures related to this column.

Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME

Auto-HCT patients run high risks for myeloid neoplasms

Article Type
Changed
Fri, 01/04/2019 - 10:01

 

– For post–autologous hematopoietic cell transplant (auto-HCT) patients, the 10-year risk of developing a myeloid neoplasm was as high as 6%, based on a recent review of two large cancer databases.

Older age at transplant, receiving total body irradiation, and receiving multiple lines of chemotherapy before transplant all upped the risk of later cancers, according to a study presented by Shahrukh Hashmi, MD, and his collaborators at the combined annual meetings of the Center for International Blood & Marrow Transplant Research (CIBMTR) and the American Society for Blood and Marrow Transplantation.

“The guidelines for autologous stem cell transplantation for surveillance for AML [acute myeloid leukemia] and MDS [myelodysplastic syndrome] need to be clearly formulated. We are doing 30,000 autologous transplants a year globally and these patients are at risk for the most feared cancer, which is leukemia and MDS, for which outcomes are very poor,” said Dr. Hashmi of the Mayo Clinic in Rochester, Minn.

The researchers examined data from auto-HCT patients with diagnoses of non-Hodgkin lymphoma (NHL), Hodgkin lymphoma, and multiple myeloma to determine the relative risks of developing AML and MDS. The study also explored which patient characteristics and aspects of the conditioning regimen might affect risk for later myeloid neoplasms.

In the dataset of 9,108 patients that Dr. Hashmi and his colleagues obtained from CIBMTR, 3,540 patients had NHL.

“As age progresses, the risk of acquiring myeloid neoplasms increases significantly,” he said, noting that the relative risk (RR) rose to 4.52 for patients aged 55 years and older at the time of transplant (95% confidence interval [CI], 2.63-7.77; P less than .0001).

Patients with NHL who received more than two lines of chemotherapy had approximately double the rate of myeloid cancers (RR, 1.93; 95% CI, 1.34-2.78; P = .0004).

The type of conditioning regimen made a difference for NHL patients as well. With total-body irradiation set as the reference at RR = 1, carmustine-etoposide-cytarabine-melphalan (BEAM) or similar therapies were relatively protective, with an RR of 0.59 (95% CI, 0.40-0.87; P = .0083). Also protective were cyclophosphamide-carmustine-etoposide (CBV) and similar therapies (RR, 0.57; 95% CI, 0.33-0.99; P = .0463).

Age at transplant was a factor among the 4,653 patients with multiple myeloma, with an RR of 2.47 for those transplanted at age 55 years or older (95% CI, 1.55-3.93; P = .0001). Multiple lines of chemotherapy also increased risk, with patients who received more than two lines having an RR of 1.77 for neoplasm (95% CI, 0.04-2.06; P = .0302). Women had less than half the risk of recurrence as men (RR, 0.44; 95% CI, 0.28-0.69; P = .0003).

Among the 915 study patients with Hodgkin lymphoma, patients aged 45 years and older at the time of transplant carried an RR of 5.59 for new myeloid neoplasms (95% CI, 2.98-11.70; P less than .0001).

Total-body irradiation was received by 14% of patients with non-Hodgkin lymphoma and by 5% of patients with multiple myeloma and Hodgkin lymphoma. Total-body irradiation was associated with a fourfold increase in neoplasm risk (RR, 4.02; 95% CI, 1.40-11.55; P = .0096).

Dr. Hashmi and his colleagues then examined the incidence rates for myelodysplastic syndrome and acute myelogenous leukemia in the Surveillance, Epidemiology, and End Results (SEER) database , finding that, even at baseline, the rates of myeloid neoplasms were higher for patients with NHL, Hodgkin lymphoma, or MM patients than for the general population of cancer survivors. “Post NHL, Hodgkin lymphoma, and myeloma, the risks are significantly higher to begin with. … We saw a high risk of AML and MDS compared to the SEER controls – risks as high as 100 times greater for auto-transplant patients,” said Dr. Hashmi. “A risk of one hundred times more for MDS was astounding, surprising, unexpected,” he said. The risk of AML, he said, was elevated about 10-50 times in the CIBMTR data.

The cumulative incidence of MDS or AML for NHL was 6% at 10 years post transplant, 4% for Hodgkin lymphoma, and 3% for multiple myeloma.

A limitation of the study, said Dr. Hashmi, was that the investigators did not assess for post-transplant maintenance chemotherapy.

“We have to prospectively assess our transplant patients in a fashion to detect changes early. Or maybe they were present at the time of transplant and we never did sophisticated methods [like] next-generation sequencing” to detect them, he said.

Dr. Hashmi reported no conflicts of interest.
 

Meeting/Event
Publications
Topics
Sections
Meeting/Event
Meeting/Event

 

– For post–autologous hematopoietic cell transplant (auto-HCT) patients, the 10-year risk of developing a myeloid neoplasm was as high as 6%, based on a recent review of two large cancer databases.

Older age at transplant, receiving total body irradiation, and receiving multiple lines of chemotherapy before transplant all upped the risk of later cancers, according to a study presented by Shahrukh Hashmi, MD, and his collaborators at the combined annual meetings of the Center for International Blood & Marrow Transplant Research (CIBMTR) and the American Society for Blood and Marrow Transplantation.

“The guidelines for autologous stem cell transplantation for surveillance for AML [acute myeloid leukemia] and MDS [myelodysplastic syndrome] need to be clearly formulated. We are doing 30,000 autologous transplants a year globally and these patients are at risk for the most feared cancer, which is leukemia and MDS, for which outcomes are very poor,” said Dr. Hashmi of the Mayo Clinic in Rochester, Minn.

The researchers examined data from auto-HCT patients with diagnoses of non-Hodgkin lymphoma (NHL), Hodgkin lymphoma, and multiple myeloma to determine the relative risks of developing AML and MDS. The study also explored which patient characteristics and aspects of the conditioning regimen might affect risk for later myeloid neoplasms.

In the dataset of 9,108 patients that Dr. Hashmi and his colleagues obtained from CIBMTR, 3,540 patients had NHL.

“As age progresses, the risk of acquiring myeloid neoplasms increases significantly,” he said, noting that the relative risk (RR) rose to 4.52 for patients aged 55 years and older at the time of transplant (95% confidence interval [CI], 2.63-7.77; P less than .0001).

Patients with NHL who received more than two lines of chemotherapy had approximately double the rate of myeloid cancers (RR, 1.93; 95% CI, 1.34-2.78; P = .0004).

The type of conditioning regimen made a difference for NHL patients as well. With total-body irradiation set as the reference at RR = 1, carmustine-etoposide-cytarabine-melphalan (BEAM) or similar therapies were relatively protective, with an RR of 0.59 (95% CI, 0.40-0.87; P = .0083). Also protective were cyclophosphamide-carmustine-etoposide (CBV) and similar therapies (RR, 0.57; 95% CI, 0.33-0.99; P = .0463).

Age at transplant was a factor among the 4,653 patients with multiple myeloma, with an RR of 2.47 for those transplanted at age 55 years or older (95% CI, 1.55-3.93; P = .0001). Multiple lines of chemotherapy also increased risk, with patients who received more than two lines having an RR of 1.77 for neoplasm (95% CI, 0.04-2.06; P = .0302). Women had less than half the risk of recurrence as men (RR, 0.44; 95% CI, 0.28-0.69; P = .0003).

Among the 915 study patients with Hodgkin lymphoma, patients aged 45 years and older at the time of transplant carried an RR of 5.59 for new myeloid neoplasms (95% CI, 2.98-11.70; P less than .0001).

Total-body irradiation was received by 14% of patients with non-Hodgkin lymphoma and by 5% of patients with multiple myeloma and Hodgkin lymphoma. Total-body irradiation was associated with a fourfold increase in neoplasm risk (RR, 4.02; 95% CI, 1.40-11.55; P = .0096).

Dr. Hashmi and his colleagues then examined the incidence rates for myelodysplastic syndrome and acute myelogenous leukemia in the Surveillance, Epidemiology, and End Results (SEER) database , finding that, even at baseline, the rates of myeloid neoplasms were higher for patients with NHL, Hodgkin lymphoma, or MM patients than for the general population of cancer survivors. “Post NHL, Hodgkin lymphoma, and myeloma, the risks are significantly higher to begin with. … We saw a high risk of AML and MDS compared to the SEER controls – risks as high as 100 times greater for auto-transplant patients,” said Dr. Hashmi. “A risk of one hundred times more for MDS was astounding, surprising, unexpected,” he said. The risk of AML, he said, was elevated about 10-50 times in the CIBMTR data.

The cumulative incidence of MDS or AML for NHL was 6% at 10 years post transplant, 4% for Hodgkin lymphoma, and 3% for multiple myeloma.

A limitation of the study, said Dr. Hashmi, was that the investigators did not assess for post-transplant maintenance chemotherapy.

“We have to prospectively assess our transplant patients in a fashion to detect changes early. Or maybe they were present at the time of transplant and we never did sophisticated methods [like] next-generation sequencing” to detect them, he said.

Dr. Hashmi reported no conflicts of interest.
 

 

– For post–autologous hematopoietic cell transplant (auto-HCT) patients, the 10-year risk of developing a myeloid neoplasm was as high as 6%, based on a recent review of two large cancer databases.

Older age at transplant, receiving total body irradiation, and receiving multiple lines of chemotherapy before transplant all upped the risk of later cancers, according to a study presented by Shahrukh Hashmi, MD, and his collaborators at the combined annual meetings of the Center for International Blood & Marrow Transplant Research (CIBMTR) and the American Society for Blood and Marrow Transplantation.

“The guidelines for autologous stem cell transplantation for surveillance for AML [acute myeloid leukemia] and MDS [myelodysplastic syndrome] need to be clearly formulated. We are doing 30,000 autologous transplants a year globally and these patients are at risk for the most feared cancer, which is leukemia and MDS, for which outcomes are very poor,” said Dr. Hashmi of the Mayo Clinic in Rochester, Minn.

The researchers examined data from auto-HCT patients with diagnoses of non-Hodgkin lymphoma (NHL), Hodgkin lymphoma, and multiple myeloma to determine the relative risks of developing AML and MDS. The study also explored which patient characteristics and aspects of the conditioning regimen might affect risk for later myeloid neoplasms.

In the dataset of 9,108 patients that Dr. Hashmi and his colleagues obtained from CIBMTR, 3,540 patients had NHL.

“As age progresses, the risk of acquiring myeloid neoplasms increases significantly,” he said, noting that the relative risk (RR) rose to 4.52 for patients aged 55 years and older at the time of transplant (95% confidence interval [CI], 2.63-7.77; P less than .0001).

Patients with NHL who received more than two lines of chemotherapy had approximately double the rate of myeloid cancers (RR, 1.93; 95% CI, 1.34-2.78; P = .0004).

The type of conditioning regimen made a difference for NHL patients as well. With total-body irradiation set as the reference at RR = 1, carmustine-etoposide-cytarabine-melphalan (BEAM) or similar therapies were relatively protective, with an RR of 0.59 (95% CI, 0.40-0.87; P = .0083). Also protective were cyclophosphamide-carmustine-etoposide (CBV) and similar therapies (RR, 0.57; 95% CI, 0.33-0.99; P = .0463).

Age at transplant was a factor among the 4,653 patients with multiple myeloma, with an RR of 2.47 for those transplanted at age 55 years or older (95% CI, 1.55-3.93; P = .0001). Multiple lines of chemotherapy also increased risk, with patients who received more than two lines having an RR of 1.77 for neoplasm (95% CI, 0.04-2.06; P = .0302). Women had less than half the risk of recurrence as men (RR, 0.44; 95% CI, 0.28-0.69; P = .0003).

Among the 915 study patients with Hodgkin lymphoma, patients aged 45 years and older at the time of transplant carried an RR of 5.59 for new myeloid neoplasms (95% CI, 2.98-11.70; P less than .0001).

Total-body irradiation was received by 14% of patients with non-Hodgkin lymphoma and by 5% of patients with multiple myeloma and Hodgkin lymphoma. Total-body irradiation was associated with a fourfold increase in neoplasm risk (RR, 4.02; 95% CI, 1.40-11.55; P = .0096).

Dr. Hashmi and his colleagues then examined the incidence rates for myelodysplastic syndrome and acute myelogenous leukemia in the Surveillance, Epidemiology, and End Results (SEER) database , finding that, even at baseline, the rates of myeloid neoplasms were higher for patients with NHL, Hodgkin lymphoma, or MM patients than for the general population of cancer survivors. “Post NHL, Hodgkin lymphoma, and myeloma, the risks are significantly higher to begin with. … We saw a high risk of AML and MDS compared to the SEER controls – risks as high as 100 times greater for auto-transplant patients,” said Dr. Hashmi. “A risk of one hundred times more for MDS was astounding, surprising, unexpected,” he said. The risk of AML, he said, was elevated about 10-50 times in the CIBMTR data.

The cumulative incidence of MDS or AML for NHL was 6% at 10 years post transplant, 4% for Hodgkin lymphoma, and 3% for multiple myeloma.

A limitation of the study, said Dr. Hashmi, was that the investigators did not assess for post-transplant maintenance chemotherapy.

“We have to prospectively assess our transplant patients in a fashion to detect changes early. Or maybe they were present at the time of transplant and we never did sophisticated methods [like] next-generation sequencing” to detect them, he said.

Dr. Hashmi reported no conflicts of interest.
 

Publications
Publications
Topics
Article Type
Sections
Article Source

AT THE BMT TANDEM MEETINGS

Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Vitals

 

Key clinical point: Autologous hematopoietic cell transplant (auto-HCT) patients were at increased risk for later myelodysplastic syndrome and acute myeloid leukemia.

Major finding: The 10-year cumulative risk for auto-HCT patients with Hodgkin or non-Hodgkin lymphoma or multiple myeloma was as high at 6%.

Data source: Review of 9,108 patients from an international transplant database.

Disclosures: Dr. Hashmi reported no conflicts of interest.

Local Data on Cancer Mortality Reveal Valuable ‘Patterns’ in Changes

Article Type
Changed
Thu, 12/15/2022 - 14:54
Researchers find that different factors contribute to the variation of mortality rates from state to county across the U.S. for certain cancer types.

Cancer death rates in the U.S. declined by 20% between 1980 and 2014, but not everywhere:  In 160 counties, mortality rose substantially during the same time, according to University of Washington researchers. And those weren’t the only striking variations they found.

The researchers analyzed data on deaths from 29 cancer types. Deaths dropped from about 240 per 100,000 people in 1980 to 192 per 100,000 in 2014. But the researchers say they found “stark” disparities. In 2014, the county with the highest overall cancer mortality had about 7 times as many cancer deaths per 100,000 residents as the county with the lowest overall cancer mortality. For many cancers there were distinct clusters of counties in different regions with especially high mortality, such as in Kentucky, West Virginia, and Alabama.

Related: Major Cancer Death Rates Are Down

The pattern of changes across counties also varied tremendously by type, the researchers say. For instance, breast, cervical, prostate, testicular, and other cancers, mortality rates declined in nearly all counties, whereas liver cancer and mesothelioma increased in nearly all counties.

Previous reports on geographic differences in cancer mortality have focused on variation by state, the researchers say. But the local patterns they found would have been masked by a national or state number. Their innovative approach to aggregating and analyzing the data at the county level has value, they note, because “public health programs and policies are mainly designed and implemented at the local level.”

Related: Demographic and Clinical Characteristics of Patients With Polycythemia Vera (PV) in the U.S. Veterans Population

The policy response from the public health and medical care communities, the researchers add, depends on “parsing these trends into component factors”: trends driven by known risk factors, unexplained trends in incidence, cancers for which screening and early detection can make a major difference, and cancers for which high-quality treatment can make a major difference. Local information, the researchers point out, can be useful for health care practitioners to understand community needs for care and aid in identifying “cancer hot spots” that need more investigation.

In an article for the National Cancer Institute’s newsletter, Eric Durbin, DPh, director of cancer informatics for the Kentucky Cancer Registry at the University of Kentucky Markey Cancer Center, cautioned against basing too many assumptions on local data, especially in rural, sparsely populated areas where small number changes can translate into giant percentages. “We really have no other way to guide cancer prevention and control activities other than using [that] data. Otherwise, you’re just throwing money or resources at a problem without any way to measure the impact,” added Durbin.

Sources:

  1. National Cancer Institute. U.S. cancer mortality rates falling, but some regions left behind, study finds. https://www.cancer.gov/news-events/cancer-currents-blog/2017/cancer-death-disparities. Published February 21, 2017. Accessed March 15, 2017. 
  2. Mokdad AH, Dwyer-Lindgren L, Fitzmaurice C, et al. JAMA. 2017;317(4):388-406.
    doi: 10.1001/jama.2016.20324.
Publications
Topics
Sections
Related Articles
Researchers find that different factors contribute to the variation of mortality rates from state to county across the U.S. for certain cancer types.
Researchers find that different factors contribute to the variation of mortality rates from state to county across the U.S. for certain cancer types.

Cancer death rates in the U.S. declined by 20% between 1980 and 2014, but not everywhere:  In 160 counties, mortality rose substantially during the same time, according to University of Washington researchers. And those weren’t the only striking variations they found.

The researchers analyzed data on deaths from 29 cancer types. Deaths dropped from about 240 per 100,000 people in 1980 to 192 per 100,000 in 2014. But the researchers say they found “stark” disparities. In 2014, the county with the highest overall cancer mortality had about 7 times as many cancer deaths per 100,000 residents as the county with the lowest overall cancer mortality. For many cancers there were distinct clusters of counties in different regions with especially high mortality, such as in Kentucky, West Virginia, and Alabama.

Related: Major Cancer Death Rates Are Down

The pattern of changes across counties also varied tremendously by type, the researchers say. For instance, breast, cervical, prostate, testicular, and other cancers, mortality rates declined in nearly all counties, whereas liver cancer and mesothelioma increased in nearly all counties.

Previous reports on geographic differences in cancer mortality have focused on variation by state, the researchers say. But the local patterns they found would have been masked by a national or state number. Their innovative approach to aggregating and analyzing the data at the county level has value, they note, because “public health programs and policies are mainly designed and implemented at the local level.”

Related: Demographic and Clinical Characteristics of Patients With Polycythemia Vera (PV) in the U.S. Veterans Population

The policy response from the public health and medical care communities, the researchers add, depends on “parsing these trends into component factors”: trends driven by known risk factors, unexplained trends in incidence, cancers for which screening and early detection can make a major difference, and cancers for which high-quality treatment can make a major difference. Local information, the researchers point out, can be useful for health care practitioners to understand community needs for care and aid in identifying “cancer hot spots” that need more investigation.

In an article for the National Cancer Institute’s newsletter, Eric Durbin, DPh, director of cancer informatics for the Kentucky Cancer Registry at the University of Kentucky Markey Cancer Center, cautioned against basing too many assumptions on local data, especially in rural, sparsely populated areas where small number changes can translate into giant percentages. “We really have no other way to guide cancer prevention and control activities other than using [that] data. Otherwise, you’re just throwing money or resources at a problem without any way to measure the impact,” added Durbin.

Sources:

  1. National Cancer Institute. U.S. cancer mortality rates falling, but some regions left behind, study finds. https://www.cancer.gov/news-events/cancer-currents-blog/2017/cancer-death-disparities. Published February 21, 2017. Accessed March 15, 2017. 
  2. Mokdad AH, Dwyer-Lindgren L, Fitzmaurice C, et al. JAMA. 2017;317(4):388-406.
    doi: 10.1001/jama.2016.20324.

Cancer death rates in the U.S. declined by 20% between 1980 and 2014, but not everywhere:  In 160 counties, mortality rose substantially during the same time, according to University of Washington researchers. And those weren’t the only striking variations they found.

The researchers analyzed data on deaths from 29 cancer types. Deaths dropped from about 240 per 100,000 people in 1980 to 192 per 100,000 in 2014. But the researchers say they found “stark” disparities. In 2014, the county with the highest overall cancer mortality had about 7 times as many cancer deaths per 100,000 residents as the county with the lowest overall cancer mortality. For many cancers there were distinct clusters of counties in different regions with especially high mortality, such as in Kentucky, West Virginia, and Alabama.

Related: Major Cancer Death Rates Are Down

The pattern of changes across counties also varied tremendously by type, the researchers say. For instance, breast, cervical, prostate, testicular, and other cancers, mortality rates declined in nearly all counties, whereas liver cancer and mesothelioma increased in nearly all counties.

Previous reports on geographic differences in cancer mortality have focused on variation by state, the researchers say. But the local patterns they found would have been masked by a national or state number. Their innovative approach to aggregating and analyzing the data at the county level has value, they note, because “public health programs and policies are mainly designed and implemented at the local level.”

Related: Demographic and Clinical Characteristics of Patients With Polycythemia Vera (PV) in the U.S. Veterans Population

The policy response from the public health and medical care communities, the researchers add, depends on “parsing these trends into component factors”: trends driven by known risk factors, unexplained trends in incidence, cancers for which screening and early detection can make a major difference, and cancers for which high-quality treatment can make a major difference. Local information, the researchers point out, can be useful for health care practitioners to understand community needs for care and aid in identifying “cancer hot spots” that need more investigation.

In an article for the National Cancer Institute’s newsletter, Eric Durbin, DPh, director of cancer informatics for the Kentucky Cancer Registry at the University of Kentucky Markey Cancer Center, cautioned against basing too many assumptions on local data, especially in rural, sparsely populated areas where small number changes can translate into giant percentages. “We really have no other way to guide cancer prevention and control activities other than using [that] data. Otherwise, you’re just throwing money or resources at a problem without any way to measure the impact,” added Durbin.

Sources:

  1. National Cancer Institute. U.S. cancer mortality rates falling, but some regions left behind, study finds. https://www.cancer.gov/news-events/cancer-currents-blog/2017/cancer-death-disparities. Published February 21, 2017. Accessed March 15, 2017. 
  2. Mokdad AH, Dwyer-Lindgren L, Fitzmaurice C, et al. JAMA. 2017;317(4):388-406.
    doi: 10.1001/jama.2016.20324.
Publications
Publications
Topics
Article Type
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)
Alternative CME