The use of laser epilation (LE) as a supplement to standard care significantly reduces recurrence of pilonidal disease, compared with standard care alone, according to the results of a randomized trial.

The study, recently published in JAMA Surgery, enrolled 302 patients ages 11-21 with pilonidal disease. Half of the participants were assigned to receive LE (laser hair removal) plus standard treatment (improved hygiene plus mechanical or chemical hair removal), and half were assigned to receive standard care alone.

At 1 year, 10.4% of the patients who had received LE plus standard treatment had experienced a recurrence of pilonidal disease, compared with 33.6% of patients in the standard treatment group (P < .001). Rates were based on the data available on 96 patients in the LE group and 134 patients in the standard care group.

“These results provide further evidence that laser epilation is safe, well-tolerated, and should be available as an initial treatment option or adjunct treatment modality for all eligible patients,” first author Peter C. Minneci, MD, chair of surgery at Nemours Children’s Health, Delaware Valley, Wilmington, Del, said in a press release reporting the results. “There have been few comparative studies that have investigated recurrence rates after LE versus other treatment modalities,” he and his coauthors wrote in the study, noting that the study “was the first, to our knowledge, to compare LE as an adjunct to standard care versus standard care alone and demonstrate a decrease in recurrence rates.”

Pilonidal disease, a common condition, results when cysts form between the buttocks and is most common in adolescents and young adults. It is thought to recur about 33% of the time, with most cases recurring within 1 year of treatment.

In practice, there are large variations in management strategies for pilonidal disease because evidence for an ideal treatment approach is lacking, Dr. Minneci and coauthors wrote. Although lifestyle modifications and nonepilation hair removal strategies have been linked to a reduced need for surgery, compliance with these strategies is low. Additionally, recurrence contributes to “a high degree of psychosocial stress in patients, who often miss school or sports and may avoid social activities,” Dr. Minneci said in the press release. Therefore, some practitioners have begun using LE – which uses selective thermolysis to remove the hair shaft, follicle, and bulb – as an adjunct to standard treatments in the hopes of avoiding surgery. 

A few studies have shown LE is effective in reducing pilonidal disease recurrence, but these studies had small sample sizes, according to the authors.

Study methods

The randomized, nonblinded clinical trial was conducted between 2017 and 2022 at Nationwide Children’s Hospital, Columbus, and enrolled patients aged 11-21 years with a history of pilonidal disease, who did not have active disease.

Those in the control group (151 patients) had an in-person clinic visit where they received education and training about hair removal in the gluteal cleft, and were provided with supplies for hair removal (chemical epilation or shaving) for 6 months (standard of care). Those in the LE group (151 patients) received standard of care therapy, and also received one LE treatment every 4-6 weeks for a total of five treatments. They were encouraged to perform hair removal using chemical or mechanical depilation between visits.

At the 1-year follow-up, data were available in 96 patients in the LE group and 134 patients in the standard care group. At that time, the proportion of those who had a recurrence within 1 year was significantly lower in the LE group than in the standard care group (mean difference, –23.2%; 95% CI, –33.2% to –13.1%; P < .001).

In addition, over the course of a year, those in the LE-treated group had significantly higher Child Attitude Toward Illness scores, indicating that they felt more positively about their illness at 6 months than participants in the standard care group. There were no differences between the groups in terms of patient or caregiver disability days, patient- or caregiver-reported health-related quality of life, health care satisfaction, or perceived stigma. In the LE group, no burns were reported, and no inability to tolerate treatment because of pain.

The study had several limitations, including the potential for participation bias, and because of a loss to follow-up, primary and secondary outcomes were missing data points, which was higher in the LE group. Loss to follow-up in the LE arm increased after 6 months, when laser treatments ended, with many of those patients not completing surveys at 9 and 12 months. The hospital’s pilonidal clinic shut down for 3 months during the COVID-19 pandemic, and when the clinic reopened, 15 patients in the LE arm withdrew from the study.

|In the press release, Dr. Minneci said that confirmation of the effectiveness of LE could help justify insurance coverage for pilonidal disease, noting that LE is usually not covered with insurance, and a course of treatment could cost $800-$1,500.

Dr. Minneci and four of the other six coauthors reported receiving grants from Patient-Centered Outcomes Research Institute during the conduct of the study. One author reported receiving grants from the National Institute on Minority Health and Health Disparities outside the submitted work. The research was funded by a grant from the Patient-Centered Outcomes Research Institute.

The use of laser epilation (LE) as a supplement to standard care significantly reduces recurrence of pilonidal disease, compared with standard care alone, according to the results of a randomized trial.

The study, recently published in JAMA Surgery, enrolled 302 patients ages 11-21 with pilonidal disease. Half of the participants were assigned to receive LE (laser hair removal) plus standard treatment (improved hygiene plus mechanical or chemical hair removal), and half were assigned to receive standard care alone.

At 1 year, 10.4% of the patients who had received LE plus standard treatment had experienced a recurrence of pilonidal disease, compared with 33.6% of patients in the standard treatment group (P < .001). Rates were based on the data available on 96 patients in the LE group and 134 patients in the standard care group.

“These results provide further evidence that laser epilation is safe, well-tolerated, and should be available as an initial treatment option or adjunct treatment modality for all eligible patients,” first author Peter C. Minneci, MD, chair of surgery at Nemours Children’s Health, Delaware Valley, Wilmington, Del, said in a press release reporting the results. “There have been few comparative studies that have investigated recurrence rates after LE versus other treatment modalities,” he and his coauthors wrote in the study, noting that the study “was the first, to our knowledge, to compare LE as an adjunct to standard care versus standard care alone and demonstrate a decrease in recurrence rates.”

Pilonidal disease, a common condition, results when cysts form between the buttocks and is most common in adolescents and young adults. It is thought to recur about 33% of the time, with most cases recurring within 1 year of treatment.

In practice, there are large variations in management strategies for pilonidal disease because evidence for an ideal treatment approach is lacking, Dr. Minneci and coauthors wrote. Although lifestyle modifications and nonepilation hair removal strategies have been linked to a reduced need for surgery, compliance with these strategies is low. Additionally, recurrence contributes to “a high degree of psychosocial stress in patients, who often miss school or sports and may avoid social activities,” Dr. Minneci said in the press release. Therefore, some practitioners have begun using LE – which uses selective thermolysis to remove the hair shaft, follicle, and bulb – as an adjunct to standard treatments in the hopes of avoiding surgery. 

A few studies have shown LE is effective in reducing pilonidal disease recurrence, but these studies had small sample sizes, according to the authors.

Study methods

The randomized, nonblinded clinical trial was conducted between 2017 and 2022 at Nationwide Children’s Hospital, Columbus, and enrolled patients aged 11-21 years with a history of pilonidal disease, who did not have active disease.

Those in the control group (151 patients) had an in-person clinic visit where they received education and training about hair removal in the gluteal cleft, and were provided with supplies for hair removal (chemical epilation or shaving) for 6 months (standard of care). Those in the LE group (151 patients) received standard of care therapy, and also received one LE treatment every 4-6 weeks for a total of five treatments. They were encouraged to perform hair removal using chemical or mechanical depilation between visits.

At the 1-year follow-up, data were available in 96 patients in the LE group and 134 patients in the standard care group. At that time, the proportion of those who had a recurrence within 1 year was significantly lower in the LE group than in the standard care group (mean difference, –23.2%; 95% CI, –33.2% to –13.1%; P < .001).

In addition, over the course of a year, those in the LE-treated group had significantly higher Child Attitude Toward Illness scores, indicating that they felt more positively about their illness at 6 months than participants in the standard care group. There were no differences between the groups in terms of patient or caregiver disability days, patient- or caregiver-reported health-related quality of life, health care satisfaction, or perceived stigma. In the LE group, no burns were reported, and no inability to tolerate treatment because of pain.

The study had several limitations, including the potential for participation bias, and because of a loss to follow-up, primary and secondary outcomes were missing data points, which was higher in the LE group. Loss to follow-up in the LE arm increased after 6 months, when laser treatments ended, with many of those patients not completing surveys at 9 and 12 months. The hospital’s pilonidal clinic shut down for 3 months during the COVID-19 pandemic, and when the clinic reopened, 15 patients in the LE arm withdrew from the study.

|In the press release, Dr. Minneci said that confirmation of the effectiveness of LE could help justify insurance coverage for pilonidal disease, noting that LE is usually not covered with insurance, and a course of treatment could cost $800-$1,500.

Dr. Minneci and four of the other six coauthors reported receiving grants from Patient-Centered Outcomes Research Institute during the conduct of the study. One author reported receiving grants from the National Institute on Minority Health and Health Disparities outside the submitted work. The research was funded by a grant from the Patient-Centered Outcomes Research Institute.

The use of laser epilation (LE) as a supplement to standard care significantly reduces recurrence of pilonidal disease, compared with standard care alone, according to the results of a randomized trial.

The study, recently published in JAMA Surgery, enrolled 302 patients ages 11-21 with pilonidal disease. Half of the participants were assigned to receive LE (laser hair removal) plus standard treatment (improved hygiene plus mechanical or chemical hair removal), and half were assigned to receive standard care alone.

At 1 year, 10.4% of the patients who had received LE plus standard treatment had experienced a recurrence of pilonidal disease, compared with 33.6% of patients in the standard treatment group (P < .001). Rates were based on the data available on 96 patients in the LE group and 134 patients in the standard care group.

“These results provide further evidence that laser epilation is safe, well-tolerated, and should be available as an initial treatment option or adjunct treatment modality for all eligible patients,” first author Peter C. Minneci, MD, chair of surgery at Nemours Children’s Health, Delaware Valley, Wilmington, Del, said in a press release reporting the results. “There have been few comparative studies that have investigated recurrence rates after LE versus other treatment modalities,” he and his coauthors wrote in the study, noting that the study “was the first, to our knowledge, to compare LE as an adjunct to standard care versus standard care alone and demonstrate a decrease in recurrence rates.”

Pilonidal disease, a common condition, results when cysts form between the buttocks and is most common in adolescents and young adults. It is thought to recur about 33% of the time, with most cases recurring within 1 year of treatment.

In practice, there are large variations in management strategies for pilonidal disease because evidence for an ideal treatment approach is lacking, Dr. Minneci and coauthors wrote. Although lifestyle modifications and nonepilation hair removal strategies have been linked to a reduced need for surgery, compliance with these strategies is low. Additionally, recurrence contributes to “a high degree of psychosocial stress in patients, who often miss school or sports and may avoid social activities,” Dr. Minneci said in the press release. Therefore, some practitioners have begun using LE – which uses selective thermolysis to remove the hair shaft, follicle, and bulb – as an adjunct to standard treatments in the hopes of avoiding surgery. 

A few studies have shown LE is effective in reducing pilonidal disease recurrence, but these studies had small sample sizes, according to the authors.

Study methods

The randomized, nonblinded clinical trial was conducted between 2017 and 2022 at Nationwide Children’s Hospital, Columbus, and enrolled patients aged 11-21 years with a history of pilonidal disease, who did not have active disease.

Those in the control group (151 patients) had an in-person clinic visit where they received education and training about hair removal in the gluteal cleft, and were provided with supplies for hair removal (chemical epilation or shaving) for 6 months (standard of care). Those in the LE group (151 patients) received standard of care therapy, and also received one LE treatment every 4-6 weeks for a total of five treatments. They were encouraged to perform hair removal using chemical or mechanical depilation between visits.

At the 1-year follow-up, data were available in 96 patients in the LE group and 134 patients in the standard care group. At that time, the proportion of those who had a recurrence within 1 year was significantly lower in the LE group than in the standard care group (mean difference, –23.2%; 95% CI, –33.2% to –13.1%; P < .001).

In addition, over the course of a year, those in the LE-treated group had significantly higher Child Attitude Toward Illness scores, indicating that they felt more positively about their illness at 6 months than participants in the standard care group. There were no differences between the groups in terms of patient or caregiver disability days, patient- or caregiver-reported health-related quality of life, health care satisfaction, or perceived stigma. In the LE group, no burns were reported, and no inability to tolerate treatment because of pain.

The study had several limitations, including the potential for participation bias, and because of a loss to follow-up, primary and secondary outcomes were missing data points, which was higher in the LE group. Loss to follow-up in the LE arm increased after 6 months, when laser treatments ended, with many of those patients not completing surveys at 9 and 12 months. The hospital’s pilonidal clinic shut down for 3 months during the COVID-19 pandemic, and when the clinic reopened, 15 patients in the LE arm withdrew from the study.

|In the press release, Dr. Minneci said that confirmation of the effectiveness of LE could help justify insurance coverage for pilonidal disease, noting that LE is usually not covered with insurance, and a course of treatment could cost $800-$1,500.

Dr. Minneci and four of the other six coauthors reported receiving grants from Patient-Centered Outcomes Research Institute during the conduct of the study. One author reported receiving grants from the National Institute on Minority Health and Health Disparities outside the submitted work. The research was funded by a grant from the Patient-Centered Outcomes Research Institute.

The Diagnosis: Lelis Syndrome

Histopathology revealed spongiotic dermatitis with marked acanthosis and hyperkeratosis (Figure, A) with fungal colonization of the stratum corneum (Figure, B). Our patient was diagnosed with Lelis syndrome (also referred to as ectodermal dysplasia with acanthosis nigricans syndrome), a rare condition with hypotrichosis and hypohidrosis resulting from ectodermal dysplasia.^1,2 The pruritic rash was diagnosed as chronic dermatitis due to fungal colonization in the setting of acanthosis nigricans. The fungal infection was treated with a 4-week course of oral fluconazole 200 mg/wk, ketoconazole cream 2% twice daily, and discontinuation of topical steroids, resulting in the thinning of the plaques on the neck and antecubital fossae as well as resolution of the pruritus. Following antifungal treatment, our patient was started on tazarotene cream 0.1% for acanthosis nigricans.

Ectodermal dysplasias are inherited disorders with abnormalities of the skin, hair, sweat glands, nails, teeth, and sometimes internal organs.³ Patients with Lelis syndrome may have other manifestations of ectodermal dysplasia in addition to hypohidrosis and hypotrichosis, including deafness and abnormal dentition,^1,3 as seen in our patient. Intellectual disability has been described in many types of ectodermal dysplasia, including Lelis syndrome, but the association may be obscured by neurologic damage after repeat episodes of hyperthermia in infancy due to anhidrosis or hypohidrosis.⁴

When evaluating the differential diagnoses, the presence of hypotrichosis and hypohidrosis indicating ectodermal dysplasia is key. Confluent and reticulated papillomatosis presents with hyperkeratosis, papillomatosis, and focal acanthosis on histopathology. It can present on the neck and antecubital fossae; however, it is not associated with hypohidrosis and hypotrichosis.⁵ Although activating fibroblast growth factor receptor, FGFR, mutations have been implicated in the development of acanthosis nigricans in a variety of syndromes, these diagnoses are associated with abnormalities in skeletal development such as craniosynostosis and short stature; hypotrichosis and hypohidrosis are not seen.^6,7 HAIR-AN (hyperandrogenism, insulin resistance, and acanthosis nigricans) syndrome typically presents in the prepubertal period with obesity and insulin resistance; acanthosis nigricans and alopecia can occur due to insulin resistance and hyperandrogenism, but concurrent clitoromegaly and hirsutism are common.⁶ Sudden onset of extensive acanthosis nigricans also is among the paraneoplastic dermatoses; it has been associated with multiple malignancies, but in these cases, hypotrichosis and hypohidrosis are not observed. Adenocarcinomas are the most common neoplasms associated with paraneoplastic acanthosis nigricans, which occurs through growth factor secretion by tumor cells stimulating hyperkeratosis and papillomatosis.⁶

Lelis syndrome is rare, and our case is unique because the patient had severe manifestations of acanthosis nigricans and hypotrichosis. Because the inheritance pattern and specific genetics of the condition have not been fully elucidated, the diagnosis primarily is clinical.^1,8 Diagnosis may be complicated by the variety of other signs that can accompany acanthosis nigricans, hypohidrosis, and hypotrichosis.^1,2 The condition also may alter or obscure presentation of other dermatologic conditions, as in our case.

Although there is no cure for Lelis syndrome, one case report described treatment with acitretin that resulted in marked improvement of the patient’s hyperkeratosis and acanthosis nigricans.⁹ Due to lack of health insurance coverage of acitretin, our patient was started on tazarotene cream 0.1% for acanthosis nigricans. General treatment of ectodermal dysplasia primarily consists of multidisciplinary symptom management, including careful monitoring of temperature and heat intolerance as well as provision of dental prosthetics.^4,10 For ectodermal dysplasias caused by identified genetic mutations, prenatal interventions targeting gene pathways offer potentially curative treatment.¹⁰ However, for Lelis syndrome, along with many other disorders of ectodermal dysplasia, mitigation of signs and symptoms remains the primary treatment objective. Despite its rarity, increased awareness of Lelis syndrome is important to increase knowledge of ectodermal dysplasia syndromes and allow for the investigation of potential treatment options.

The Diagnosis: Lelis Syndrome

Histopathology revealed spongiotic dermatitis with marked acanthosis and hyperkeratosis (Figure, A) with fungal colonization of the stratum corneum (Figure, B). Our patient was diagnosed with Lelis syndrome (also referred to as ectodermal dysplasia with acanthosis nigricans syndrome), a rare condition with hypotrichosis and hypohidrosis resulting from ectodermal dysplasia.^1,2 The pruritic rash was diagnosed as chronic dermatitis due to fungal colonization in the setting of acanthosis nigricans. The fungal infection was treated with a 4-week course of oral fluconazole 200 mg/wk, ketoconazole cream 2% twice daily, and discontinuation of topical steroids, resulting in the thinning of the plaques on the neck and antecubital fossae as well as resolution of the pruritus. Following antifungal treatment, our patient was started on tazarotene cream 0.1% for acanthosis nigricans.

Ectodermal dysplasias are inherited disorders with abnormalities of the skin, hair, sweat glands, nails, teeth, and sometimes internal organs.³ Patients with Lelis syndrome may have other manifestations of ectodermal dysplasia in addition to hypohidrosis and hypotrichosis, including deafness and abnormal dentition,^1,3 as seen in our patient. Intellectual disability has been described in many types of ectodermal dysplasia, including Lelis syndrome, but the association may be obscured by neurologic damage after repeat episodes of hyperthermia in infancy due to anhidrosis or hypohidrosis.⁴

When evaluating the differential diagnoses, the presence of hypotrichosis and hypohidrosis indicating ectodermal dysplasia is key. Confluent and reticulated papillomatosis presents with hyperkeratosis, papillomatosis, and focal acanthosis on histopathology. It can present on the neck and antecubital fossae; however, it is not associated with hypohidrosis and hypotrichosis.⁵ Although activating fibroblast growth factor receptor, FGFR, mutations have been implicated in the development of acanthosis nigricans in a variety of syndromes, these diagnoses are associated with abnormalities in skeletal development such as craniosynostosis and short stature; hypotrichosis and hypohidrosis are not seen.^6,7 HAIR-AN (hyperandrogenism, insulin resistance, and acanthosis nigricans) syndrome typically presents in the prepubertal period with obesity and insulin resistance; acanthosis nigricans and alopecia can occur due to insulin resistance and hyperandrogenism, but concurrent clitoromegaly and hirsutism are common.⁶ Sudden onset of extensive acanthosis nigricans also is among the paraneoplastic dermatoses; it has been associated with multiple malignancies, but in these cases, hypotrichosis and hypohidrosis are not observed. Adenocarcinomas are the most common neoplasms associated with paraneoplastic acanthosis nigricans, which occurs through growth factor secretion by tumor cells stimulating hyperkeratosis and papillomatosis.⁶

Lelis syndrome is rare, and our case is unique because the patient had severe manifestations of acanthosis nigricans and hypotrichosis. Because the inheritance pattern and specific genetics of the condition have not been fully elucidated, the diagnosis primarily is clinical.^1,8 Diagnosis may be complicated by the variety of other signs that can accompany acanthosis nigricans, hypohidrosis, and hypotrichosis.^1,2 The condition also may alter or obscure presentation of other dermatologic conditions, as in our case.

Although there is no cure for Lelis syndrome, one case report described treatment with acitretin that resulted in marked improvement of the patient’s hyperkeratosis and acanthosis nigricans.⁹ Due to lack of health insurance coverage of acitretin, our patient was started on tazarotene cream 0.1% for acanthosis nigricans. General treatment of ectodermal dysplasia primarily consists of multidisciplinary symptom management, including careful monitoring of temperature and heat intolerance as well as provision of dental prosthetics.^4,10 For ectodermal dysplasias caused by identified genetic mutations, prenatal interventions targeting gene pathways offer potentially curative treatment.¹⁰ However, for Lelis syndrome, along with many other disorders of ectodermal dysplasia, mitigation of signs and symptoms remains the primary treatment objective. Despite its rarity, increased awareness of Lelis syndrome is important to increase knowledge of ectodermal dysplasia syndromes and allow for the investigation of potential treatment options.

The Diagnosis: Lelis Syndrome

Histopathology revealed spongiotic dermatitis with marked acanthosis and hyperkeratosis (Figure, A) with fungal colonization of the stratum corneum (Figure, B). Our patient was diagnosed with Lelis syndrome (also referred to as ectodermal dysplasia with acanthosis nigricans syndrome), a rare condition with hypotrichosis and hypohidrosis resulting from ectodermal dysplasia.^1,2 The pruritic rash was diagnosed as chronic dermatitis due to fungal colonization in the setting of acanthosis nigricans. The fungal infection was treated with a 4-week course of oral fluconazole 200 mg/wk, ketoconazole cream 2% twice daily, and discontinuation of topical steroids, resulting in the thinning of the plaques on the neck and antecubital fossae as well as resolution of the pruritus. Following antifungal treatment, our patient was started on tazarotene cream 0.1% for acanthosis nigricans.

Ectodermal dysplasias are inherited disorders with abnormalities of the skin, hair, sweat glands, nails, teeth, and sometimes internal organs.³ Patients with Lelis syndrome may have other manifestations of ectodermal dysplasia in addition to hypohidrosis and hypotrichosis, including deafness and abnormal dentition,^1,3 as seen in our patient. Intellectual disability has been described in many types of ectodermal dysplasia, including Lelis syndrome, but the association may be obscured by neurologic damage after repeat episodes of hyperthermia in infancy due to anhidrosis or hypohidrosis.⁴

When evaluating the differential diagnoses, the presence of hypotrichosis and hypohidrosis indicating ectodermal dysplasia is key. Confluent and reticulated papillomatosis presents with hyperkeratosis, papillomatosis, and focal acanthosis on histopathology. It can present on the neck and antecubital fossae; however, it is not associated with hypohidrosis and hypotrichosis.⁵ Although activating fibroblast growth factor receptor, FGFR, mutations have been implicated in the development of acanthosis nigricans in a variety of syndromes, these diagnoses are associated with abnormalities in skeletal development such as craniosynostosis and short stature; hypotrichosis and hypohidrosis are not seen.^6,7 HAIR-AN (hyperandrogenism, insulin resistance, and acanthosis nigricans) syndrome typically presents in the prepubertal period with obesity and insulin resistance; acanthosis nigricans and alopecia can occur due to insulin resistance and hyperandrogenism, but concurrent clitoromegaly and hirsutism are common.⁶ Sudden onset of extensive acanthosis nigricans also is among the paraneoplastic dermatoses; it has been associated with multiple malignancies, but in these cases, hypotrichosis and hypohidrosis are not observed. Adenocarcinomas are the most common neoplasms associated with paraneoplastic acanthosis nigricans, which occurs through growth factor secretion by tumor cells stimulating hyperkeratosis and papillomatosis.⁶

Lelis syndrome is rare, and our case is unique because the patient had severe manifestations of acanthosis nigricans and hypotrichosis. Because the inheritance pattern and specific genetics of the condition have not been fully elucidated, the diagnosis primarily is clinical.^1,8 Diagnosis may be complicated by the variety of other signs that can accompany acanthosis nigricans, hypohidrosis, and hypotrichosis.^1,2 The condition also may alter or obscure presentation of other dermatologic conditions, as in our case.

Although there is no cure for Lelis syndrome, one case report described treatment with acitretin that resulted in marked improvement of the patient’s hyperkeratosis and acanthosis nigricans.⁹ Due to lack of health insurance coverage of acitretin, our patient was started on tazarotene cream 0.1% for acanthosis nigricans. General treatment of ectodermal dysplasia primarily consists of multidisciplinary symptom management, including careful monitoring of temperature and heat intolerance as well as provision of dental prosthetics.^4,10 For ectodermal dysplasias caused by identified genetic mutations, prenatal interventions targeting gene pathways offer potentially curative treatment.¹⁰ However, for Lelis syndrome, along with many other disorders of ectodermal dysplasia, mitigation of signs and symptoms remains the primary treatment objective. Despite its rarity, increased awareness of Lelis syndrome is important to increase knowledge of ectodermal dysplasia syndromes and allow for the investigation of potential treatment options.

Prior studies show inconsistent outcomes in patients with invasive lobular carcinoma (ILC) and data in premenopausal women is limited. The retrospective cohort study by Yoon and colleagues analyzed the data from three databases and included 225,938 premenopausal women with stage I-III ILC or invasive ductal carcinoma (IDC) in their study to evaluate survival trends in young women with ILC. In the Surveillance, Epidemiology, and End Results (SEER) database, patients with ILC vs IDC showed superior breast cancer severity score (BCSS) outcomes during the first 10 years after diagnosis (HR 0.73; P < .001); similar results were seen in the Asan Medical Center Research (AMCR) database (HR 0.50; 95% CI 0.29-0.86; P = .01). After 10 years, the trend reversed, and BCSS outcomes worsened by 80% in patients with ILC in the SEER database (HR 1.80; P < .001). This was also seen in both the Korean Breast Cancer Registry (HR 2.79; 95% CI 1.32-5.88; P = .007) and AMCR database (HR 2.23; 95% CI 1.04-4.79; P = .04). These findings remained consistent after adjusting for tumor characteristics including age, stage, tumor grade, hormone receptor status, and after controlling for treatment with chemotherapy and radiation. In addition, in the SEER database, the histologic type exerted a statistically significant time-dependent association with BCSS, with ILC showing decreasing BCSS over time (time interaction HR 1.93; 95% CI 1.78-2.10; P < .001). Furthermore, on annual hazard function analysis, the ILC annual peak event of BCSS occurred 5 years after diagnosis, whereas the IDC recurrence events peaked at 5 years before diagnosis, suggesting a higher late recurrence rate for ILC. These findings may have implications on the duration of endocrine therapy used in these patients given concern for worse long-term outcomes in premenopausal patients with ILC.

Oral selective estrogen receptor degraders (SERD) have recently emerged as a new therapeutic mechanism for patients with hormone receptor–positive breast cancer who have developed resistance to other endocrine therapies. Two of these agents, elacestrant and camizestrant, have demonstrated statistically significant progression-free survival benefit in these populations, particularly in tumors with ESR1 mutations. The efficacy of these agents in tumors with ESR1 wild-type subgroup remains uncertain. A meta-analysis by Wong and colleagues of individual patient data from four randomized clinical trials (ACELERA, AMEERA-3, EMERALD, and SERENA-2) included 1290 patients with hormone receptor–positive/human epidermal growth factor receptor 2–negative metastatic breast cancer who received oral SERD or endocrine therapies (ET) of the physician's choice. In the overall cohort, oral SERD showed improved progression-free survival (PFS) outcomes compared with ET of the physician's choice (HR 0.783; 95% CI 0.681-0.900; P < .001). This was also noted in the subgroup of patients with ESR1 mutations (HR 0.557; 95% CI 0.440-0.705; P < .001); although no significant PFS benefit was observed with oral SERD in the ESR1 wild-type subgroup (HR 0.944; 95% CI 0.783-1.138; P = .543). These results suggest that the PFS benefit observed with oral SERD is mainly seen in patients with ESR1-mutated tumors, and, therefore, these drugs should be prescribed accordingly.

Additional Reference

1. Cold S, Cold F, Jensen M-B, et al. Systemic or vaginal hormone therapy after early breast cancer: A Danish observational cohort study. J Natl Cancer Inst. 2022;114:1347–1354. doi: 10.1093/jnci/djac112

Prior studies show inconsistent outcomes in patients with invasive lobular carcinoma (ILC) and data in premenopausal women is limited. The retrospective cohort study by Yoon and colleagues analyzed the data from three databases and included 225,938 premenopausal women with stage I-III ILC or invasive ductal carcinoma (IDC) in their study to evaluate survival trends in young women with ILC. In the Surveillance, Epidemiology, and End Results (SEER) database, patients with ILC vs IDC showed superior breast cancer severity score (BCSS) outcomes during the first 10 years after diagnosis (HR 0.73; P < .001); similar results were seen in the Asan Medical Center Research (AMCR) database (HR 0.50; 95% CI 0.29-0.86; P = .01). After 10 years, the trend reversed, and BCSS outcomes worsened by 80% in patients with ILC in the SEER database (HR 1.80; P < .001). This was also seen in both the Korean Breast Cancer Registry (HR 2.79; 95% CI 1.32-5.88; P = .007) and AMCR database (HR 2.23; 95% CI 1.04-4.79; P = .04). These findings remained consistent after adjusting for tumor characteristics including age, stage, tumor grade, hormone receptor status, and after controlling for treatment with chemotherapy and radiation. In addition, in the SEER database, the histologic type exerted a statistically significant time-dependent association with BCSS, with ILC showing decreasing BCSS over time (time interaction HR 1.93; 95% CI 1.78-2.10; P < .001). Furthermore, on annual hazard function analysis, the ILC annual peak event of BCSS occurred 5 years after diagnosis, whereas the IDC recurrence events peaked at 5 years before diagnosis, suggesting a higher late recurrence rate for ILC. These findings may have implications on the duration of endocrine therapy used in these patients given concern for worse long-term outcomes in premenopausal patients with ILC.

Oral selective estrogen receptor degraders (SERD) have recently emerged as a new therapeutic mechanism for patients with hormone receptor–positive breast cancer who have developed resistance to other endocrine therapies. Two of these agents, elacestrant and camizestrant, have demonstrated statistically significant progression-free survival benefit in these populations, particularly in tumors with ESR1 mutations. The efficacy of these agents in tumors with ESR1 wild-type subgroup remains uncertain. A meta-analysis by Wong and colleagues of individual patient data from four randomized clinical trials (ACELERA, AMEERA-3, EMERALD, and SERENA-2) included 1290 patients with hormone receptor–positive/human epidermal growth factor receptor 2–negative metastatic breast cancer who received oral SERD or endocrine therapies (ET) of the physician's choice. In the overall cohort, oral SERD showed improved progression-free survival (PFS) outcomes compared with ET of the physician's choice (HR 0.783; 95% CI 0.681-0.900; P < .001). This was also noted in the subgroup of patients with ESR1 mutations (HR 0.557; 95% CI 0.440-0.705; P < .001); although no significant PFS benefit was observed with oral SERD in the ESR1 wild-type subgroup (HR 0.944; 95% CI 0.783-1.138; P = .543). These results suggest that the PFS benefit observed with oral SERD is mainly seen in patients with ESR1-mutated tumors, and, therefore, these drugs should be prescribed accordingly.

Additional Reference

1. Cold S, Cold F, Jensen M-B, et al. Systemic or vaginal hormone therapy after early breast cancer: A Danish observational cohort study. J Natl Cancer Inst. 2022;114:1347–1354. doi: 10.1093/jnci/djac112

Prior studies show inconsistent outcomes in patients with invasive lobular carcinoma (ILC) and data in premenopausal women is limited. The retrospective cohort study by Yoon and colleagues analyzed the data from three databases and included 225,938 premenopausal women with stage I-III ILC or invasive ductal carcinoma (IDC) in their study to evaluate survival trends in young women with ILC. In the Surveillance, Epidemiology, and End Results (SEER) database, patients with ILC vs IDC showed superior breast cancer severity score (BCSS) outcomes during the first 10 years after diagnosis (HR 0.73; P < .001); similar results were seen in the Asan Medical Center Research (AMCR) database (HR 0.50; 95% CI 0.29-0.86; P = .01). After 10 years, the trend reversed, and BCSS outcomes worsened by 80% in patients with ILC in the SEER database (HR 1.80; P < .001). This was also seen in both the Korean Breast Cancer Registry (HR 2.79; 95% CI 1.32-5.88; P = .007) and AMCR database (HR 2.23; 95% CI 1.04-4.79; P = .04). These findings remained consistent after adjusting for tumor characteristics including age, stage, tumor grade, hormone receptor status, and after controlling for treatment with chemotherapy and radiation. In addition, in the SEER database, the histologic type exerted a statistically significant time-dependent association with BCSS, with ILC showing decreasing BCSS over time (time interaction HR 1.93; 95% CI 1.78-2.10; P < .001). Furthermore, on annual hazard function analysis, the ILC annual peak event of BCSS occurred 5 years after diagnosis, whereas the IDC recurrence events peaked at 5 years before diagnosis, suggesting a higher late recurrence rate for ILC. These findings may have implications on the duration of endocrine therapy used in these patients given concern for worse long-term outcomes in premenopausal patients with ILC.

Oral selective estrogen receptor degraders (SERD) have recently emerged as a new therapeutic mechanism for patients with hormone receptor–positive breast cancer who have developed resistance to other endocrine therapies. Two of these agents, elacestrant and camizestrant, have demonstrated statistically significant progression-free survival benefit in these populations, particularly in tumors with ESR1 mutations. The efficacy of these agents in tumors with ESR1 wild-type subgroup remains uncertain. A meta-analysis by Wong and colleagues of individual patient data from four randomized clinical trials (ACELERA, AMEERA-3, EMERALD, and SERENA-2) included 1290 patients with hormone receptor–positive/human epidermal growth factor receptor 2–negative metastatic breast cancer who received oral SERD or endocrine therapies (ET) of the physician's choice. In the overall cohort, oral SERD showed improved progression-free survival (PFS) outcomes compared with ET of the physician's choice (HR 0.783; 95% CI 0.681-0.900; P < .001). This was also noted in the subgroup of patients with ESR1 mutations (HR 0.557; 95% CI 0.440-0.705; P < .001); although no significant PFS benefit was observed with oral SERD in the ESR1 wild-type subgroup (HR 0.944; 95% CI 0.783-1.138; P = .543). These results suggest that the PFS benefit observed with oral SERD is mainly seen in patients with ESR1-mutated tumors, and, therefore, these drugs should be prescribed accordingly.

Additional Reference

1. Cold S, Cold F, Jensen M-B, et al. Systemic or vaginal hormone therapy after early breast cancer: A Danish observational cohort study. J Natl Cancer Inst. 2022;114:1347–1354. doi: 10.1093/jnci/djac112

I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.

In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.

This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?

Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.

The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.

While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.

Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.

Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.

When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.

Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.

So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).

So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.

Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.

In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.

This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?

Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.

The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.

While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.

Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.

Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.

When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.

Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.

So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).

So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.

Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

I’m a general neurologist. I consider myself a jack of all (or at least most) trades in my field, and a master of none.

In the April 2023 issue of JAMA Neurology there was an editorial about neurology training, with general neurology being renamed “comprehensive neurology” and a fellowship offered in practicing general neurology.

This seems rather silly to me. If 4 years of residency (1 of internship and 3 of neurology) don’t prepare you to practice general neurology, then what’s the point of residency at all? For that matter, what difference will renaming it do?

Imagine completing a 3-year internal medicine residency, then being told you need to do a fellowship in “comprehensive medicine” in order to practice. Or at least so you can add the word “comprehensive” to your shingle.

The authors bemoan the increasing number of neurology residents wanting to do fellowships and subspecialize, a situation that mirrors the general trend of people away from general medicine toward specialties.

While I agree we do need subspecialists in neurology (and currently there are at least 31 recognized, which is way more than I would have guessed), the fact is that patients, and sometimes their internists, aren’t going to be the best judge of who does or doesn’t need to see one, compared with a general neurologist.

Most of us general people can handle straightforward Parkinson’s disease, epilepsy, migraines, etc. Certainly, there are times where the condition is refractory to our care, or there’s something unusual about the case, that leads us to refer them to someone with more expertise. But isn’t that how it’s supposed to work? Like medicine in general, we need more general people than subspecialists.

Honestly, I can’t claim to be any different. Twenty-six years ago, when I finished residency, I did a clinical neurophysiology fellowship. From a practical view it was an epilepsy fellowship at my program. Some of this was an interest at the time in subspecializing, some of it was me putting off joining the “real world” of having to find a job for a year.

When I hung up my own shingle, my business card listed a subspecialty in epilepsy. Looking back years later, this wasn’t the best move. In solo practice I had no access to an epilepsy monitoring unit, vagus nerve stimulation capabilities, or epilepsy surgery at the hospital I rounded at. Not only that, I discovered it put me at a disadvantage, as internists were referring only epilepsy patients to me, and all the other stuff (which is the majority of patients) to the general (or comprehensive) neurologists around me. Which, financially, wasn’t a good thing when you’re young and starting out.

Not only that, but I discovered that I didn’t like only seeing one thing. I found it boring, and not for me.

So after a year or so, I took the word “epilepsy” off my card, left it at “general neurology,” and sent out letters reminding my referral base that I was willing to see the majority of things in my field (rare diseases, even today, I won’t attempt to handle).

So now my days are a mix of things, which I like. Neurology is enough of a specialty for me without going further up the pyramid. Having sub (and even sub-sub) specialists is important to maintain medical excellence, but we still need people willing to do general neurology, and I’m happy there.

Changing my title to “comprehensive” is unnecessary. I’m happy with what I am.

Dr. Block has a solo neurology practice in Scottsdale, Ariz.

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

Women, particularly those who are postmenopausal, who sleep less than the recommended 7 hours per night may have impaired insulin sensitivity regardless of their degree of adiposity, a randomized crossover trial reveals.

The research was published recently in Diabetes Care.

Nearly 40 women were randomly assigned to either restricted sleep or adequate sleep for 6 weeks, then crossed over to the other sleep condition. During sleep restriction, women slept an average of 6.2 hours per night versus 7-9 hours per night.

Both fasting insulin levels and insulin resistance were significantly increased during sleep restriction, with the effect on insulin resistance particularly notable in postmenopausal women. This was independent of adiposity and changes in adiposity.

“What we’re seeing is that more insulin is needed to normalize glucose levels in the women under conditions of sleep restriction,” said senior author Marie-Pierre St-Onge, PhD, director of the Center of Excellence for Sleep and Circadian Research at Columbia University Vagelos College of Physicians and Surgeons, New York, in a release.

“Even then, the insulin may not have been doing enough to counteract rising blood glucose levels of postmenopausal women,” she stated.
 

Prolonged lack of sleep may accelerate diabetes progression

Dr. St-Onge added, “If that’s sustained over time, it is possible that prolonged insufficient sleep among individuals with prediabetes could accelerate the progression to type 2 diabetes.”

Dr. St-Onge said in an interview that it was crucial to show the impact of sleep restriction in a randomized study, because “observational studies don’t provide information on causality.”

The study did not rely on people “living in our clinical research facility,” but instead enrolled individuals who were “living their lives,” and the reduction in sleep achieved was “similar to what is seen in the general population with sleep,” she said.

Dr. St-Onge therefore believes the findings indicate that sleep has been overlooked as a contributory factor in insulin sensitivity.

Robert Gabbay, MD, PhD, chief scientific and medical officer at the American Diabetes Association, said in an interview that this is an “important study [that] builds on what we have seen on the importance of sleep for metabolic outcomes and diabetes.”

Joslin Diabetes Center

A version of this article appeared on Medscape.com.

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

TOPLINE:

The Strong African American Families (SAAF) prevention program reduces depressive symptoms related to racial discrimination in Black adolescents, results of a post hoc analysis of a randomized controlled trial show.

METHODOLOGY:

• SAAF is a 7-week family skills training program delivered at local community centers that targets effective parenting behavior, adolescent self-regulation, and Black pride.
• In the original trial, 472 Black children aged 11-12 years were randomly allocated to SAAF or no treatment control.
• The post hoc analysis investigated changes in adolescent-reported depressive symptoms from age 13 to 14 years using the 20-item Center for Epidemiologic Studies Depression Scale for Children.

TAKEAWAY:

• Exposure to racial discrimination at age 13 years correlated with increased depressive symptoms at age 14 years (P < .001).
• Participation in the SAAF program significantly attenuated the association of racial discrimination at age 13 with increases in depressive symptoms at age 14 (P = .01).
• Racial discrimination was significantly associated with increases in depressive symptoms in the control group (P < .001) but not in the SAAF group.
• This moderating effect was observed using intent-to-treat design; the investigators accounted for family socioeconomic disadvantage and youth gender.

IN PRACTICE:

The findings add to other evidence suggesting that “prevention programs targeting aspects of racial identity, racial socialization processes, and parenting behavior may, to some extent, mitigate the mental health effects associated with racial discrimination. These processes appear to increase positive coping in the aftermath of discrimination, and prevent adolescents internalization of toxic messages regarding racial inferiority,” the authors wrote.

SOURCE:

The study, with first author Steven M. Kogan, PhD, University of Georgia in Athens, was published online in JAMA Network Open with a commentary by Kevin M. Simon, MD, MPH, with Boston Children’s Hospital.

LIMITATIONS:

This was a post hoc analysis of trial data. The sample consisted of Black adolescents from rural areas of Georgia, and the results may not be generalizable to Black adolescents from urban areas or adolescents from other racial groups. Because of the study’s focus on individual-level racial discrimination, the potential for SAAF to buffer the effects of structural and institutional forms of racism is unknown.

DISCLOSURES:

The study had no specific funding. The authors have disclosed no relevant conflicts of interest.

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

The Food and Drug Administration approved a new colony-stimulating factor, efbemalenograstim alfa (Ryzneuta, Evive Biotech), to decrease the incidence of infection, as manifested by febrile neutropenia, in adults with nonmyeloid malignancies receiving myelosuppressive anticancer drugs.

Efbemalenograstim joins other agents already on the U.S. market, including pegfilgrastim (Neulasta), that aim to reduce the incidence of chemotherapy-induced febrile neutropenia.

The approval of efbemalenograstim was based on two randomized trials. The first included 122 women with either metastatic or nonmetastatic breast cancer who were receiving doxorubicin and docetaxel. These patients were randomly assigned to receive either one subcutaneous injection of efbemalenograstim or placebo on the second day of their first chemotherapy cycle. All patients received efbemalenograstim on the second day of cycles two through four.

The mean duration of grade 4 neutropenia in the first cycle was 1.4 days with efbemalenograstim versus 4.3 days with placebo. Only 4.8% of patients who received efbemalenograstim experienced chemotherapy-induced febrile neutropenia, compared with 25.6% who received the placebo.

The new agent went up against pegfilgrastim in the second trial, which included 393 women who received docetaxel and cyclophosphamide as treatment for nonmetastatic breast cancer. These patients were randomly assigned to receive either a single subcutaneous injection of efbemalenograstim or pegfilgrastim on the second day of each cycle.

During the first cycle, patients in both arms of the trial experienced a mean of 0.2 days of grade 4 neutropenia.

The most common side effects associated with efbemalenograstim were nausea, anemia, and thrombocytopenia. Similar to pegfilgrastim’s label, efbemalenograstim’s label warns of possible splenic rupture, respiratory distress syndrome, sickle cell crisis, and other serious adverse events.

The FDA recommends a dose of 20 mg subcutaneous once per chemotherapy cycle.

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

The Food and Drug Administration approved a new colony-stimulating factor, efbemalenograstim alfa (Ryzneuta, Evive Biotech), to decrease the incidence of infection, as manifested by febrile neutropenia, in adults with nonmyeloid malignancies receiving myelosuppressive anticancer drugs.

Efbemalenograstim joins other agents already on the U.S. market, including pegfilgrastim (Neulasta), that aim to reduce the incidence of chemotherapy-induced febrile neutropenia.

The approval of efbemalenograstim was based on two randomized trials. The first included 122 women with either metastatic or nonmetastatic breast cancer who were receiving doxorubicin and docetaxel. These patients were randomly assigned to receive either one subcutaneous injection of efbemalenograstim or placebo on the second day of their first chemotherapy cycle. All patients received efbemalenograstim on the second day of cycles two through four.

The mean duration of grade 4 neutropenia in the first cycle was 1.4 days with efbemalenograstim versus 4.3 days with placebo. Only 4.8% of patients who received efbemalenograstim experienced chemotherapy-induced febrile neutropenia, compared with 25.6% who received the placebo.

The new agent went up against pegfilgrastim in the second trial, which included 393 women who received docetaxel and cyclophosphamide as treatment for nonmetastatic breast cancer. These patients were randomly assigned to receive either a single subcutaneous injection of efbemalenograstim or pegfilgrastim on the second day of each cycle.

During the first cycle, patients in both arms of the trial experienced a mean of 0.2 days of grade 4 neutropenia.

The most common side effects associated with efbemalenograstim were nausea, anemia, and thrombocytopenia. Similar to pegfilgrastim’s label, efbemalenograstim’s label warns of possible splenic rupture, respiratory distress syndrome, sickle cell crisis, and other serious adverse events.

The FDA recommends a dose of 20 mg subcutaneous once per chemotherapy cycle.

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

The Food and Drug Administration approved a new colony-stimulating factor, efbemalenograstim alfa (Ryzneuta, Evive Biotech), to decrease the incidence of infection, as manifested by febrile neutropenia, in adults with nonmyeloid malignancies receiving myelosuppressive anticancer drugs.

Efbemalenograstim joins other agents already on the U.S. market, including pegfilgrastim (Neulasta), that aim to reduce the incidence of chemotherapy-induced febrile neutropenia.

The approval of efbemalenograstim was based on two randomized trials. The first included 122 women with either metastatic or nonmetastatic breast cancer who were receiving doxorubicin and docetaxel. These patients were randomly assigned to receive either one subcutaneous injection of efbemalenograstim or placebo on the second day of their first chemotherapy cycle. All patients received efbemalenograstim on the second day of cycles two through four.

The mean duration of grade 4 neutropenia in the first cycle was 1.4 days with efbemalenograstim versus 4.3 days with placebo. Only 4.8% of patients who received efbemalenograstim experienced chemotherapy-induced febrile neutropenia, compared with 25.6% who received the placebo.

The new agent went up against pegfilgrastim in the second trial, which included 393 women who received docetaxel and cyclophosphamide as treatment for nonmetastatic breast cancer. These patients were randomly assigned to receive either a single subcutaneous injection of efbemalenograstim or pegfilgrastim on the second day of each cycle.

During the first cycle, patients in both arms of the trial experienced a mean of 0.2 days of grade 4 neutropenia.

The most common side effects associated with efbemalenograstim were nausea, anemia, and thrombocytopenia. Similar to pegfilgrastim’s label, efbemalenograstim’s label warns of possible splenic rupture, respiratory distress syndrome, sickle cell crisis, and other serious adverse events.

The FDA recommends a dose of 20 mg subcutaneous once per chemotherapy cycle.

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

The Food and Drug Administration is investigating whether chimeric antigen receptor (CAR) T-cell immunotherapies can cause secondary blood cancers.

Secondary cancers are a known risk for this class of immunotherapies, known as B-cell maturation antigen (BCMA)–directed or CD19-directed autologous CAR T-cell therapies, and are included in the prescribing information for these drugs. However, the FDA has received 19 reports of secondary cancers, including CAR-positive lymphoma, since 2017, when the first CAR T-cell treatments were approved, according to Endpoints News.

Most of these reports came from the FDA’s postmarketing adverse event system and others from clinical trial data.

Although the overall benefits of these products continue to outweigh their potential risks, “FDA is investigating the identified risk of T-cell malignancy with serious outcomes, including hospitalization and death, and is evaluating the need for regulatory action,” the agency said in a press release.

Currently approved products in this class include idecabtagene vicleucel (Abecma), lisocabtagene maraleucel (Breyanzi), ciltacabtagene autoleucel (Carvykti), tisagenlecleucel (Kymriah), brexucabtagene autoleucel (Tecartus), and axicabtagene ciloleucel (Yescarta).

“Patients and clinical trial participants receiving treatment with these products should be monitored life-long for new malignancies,” the FDA added.

Suspected adverse events, including T-cell cancers, should be reported by contacting the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

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

The Food and Drug Administration is investigating whether chimeric antigen receptor (CAR) T-cell immunotherapies can cause secondary blood cancers.

Secondary cancers are a known risk for this class of immunotherapies, known as B-cell maturation antigen (BCMA)–directed or CD19-directed autologous CAR T-cell therapies, and are included in the prescribing information for these drugs. However, the FDA has received 19 reports of secondary cancers, including CAR-positive lymphoma, since 2017, when the first CAR T-cell treatments were approved, according to Endpoints News.

Most of these reports came from the FDA’s postmarketing adverse event system and others from clinical trial data.

Although the overall benefits of these products continue to outweigh their potential risks, “FDA is investigating the identified risk of T-cell malignancy with serious outcomes, including hospitalization and death, and is evaluating the need for regulatory action,” the agency said in a press release.

Currently approved products in this class include idecabtagene vicleucel (Abecma), lisocabtagene maraleucel (Breyanzi), ciltacabtagene autoleucel (Carvykti), tisagenlecleucel (Kymriah), brexucabtagene autoleucel (Tecartus), and axicabtagene ciloleucel (Yescarta).

“Patients and clinical trial participants receiving treatment with these products should be monitored life-long for new malignancies,” the FDA added.

Suspected adverse events, including T-cell cancers, should be reported by contacting the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

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

The Food and Drug Administration is investigating whether chimeric antigen receptor (CAR) T-cell immunotherapies can cause secondary blood cancers.

Secondary cancers are a known risk for this class of immunotherapies, known as B-cell maturation antigen (BCMA)–directed or CD19-directed autologous CAR T-cell therapies, and are included in the prescribing information for these drugs. However, the FDA has received 19 reports of secondary cancers, including CAR-positive lymphoma, since 2017, when the first CAR T-cell treatments were approved, according to Endpoints News.

Most of these reports came from the FDA’s postmarketing adverse event system and others from clinical trial data.

Although the overall benefits of these products continue to outweigh their potential risks, “FDA is investigating the identified risk of T-cell malignancy with serious outcomes, including hospitalization and death, and is evaluating the need for regulatory action,” the agency said in a press release.

Currently approved products in this class include idecabtagene vicleucel (Abecma), lisocabtagene maraleucel (Breyanzi), ciltacabtagene autoleucel (Carvykti), tisagenlecleucel (Kymriah), brexucabtagene autoleucel (Tecartus), and axicabtagene ciloleucel (Yescarta).

“Patients and clinical trial participants receiving treatment with these products should be monitored life-long for new malignancies,” the FDA added.

Suspected adverse events, including T-cell cancers, should be reported by contacting the FDA at 1-800-FDA-1088 or www.fda.gov/medwatch.

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

High-impact presentations on chronic kidney disease from the American Society of Nephrology (ASN) 2023 meeting are discussed by Dr Matthew Weir from the University of Maryland School of Medicine in Baltimore.

He starts with the results of the PROTECT and DUPLEX trials, in which sparsentan was compared with irbesartan in immunoglobulin A nephropathy and focal segmental glomerulosclerosis, respectively. In both studies, sparsentan resulted in greater reduction in albuminuria compared with irbesartan but with no significant differences in estimated glomerular filtration rate (GFR).

He also talks about the AYAME study of bardoxolone methyl in diabetic kidney disease, which was intended to examine the percentage of patients reaching a 30% reduction in GFR or end-stage renal disease. Bardoxolone slowed the reduction in the GFR but showed no benefit in reducing end-stage renal disease.

Next, Dr Weir reports the results from the ALCHEMIST trial on spironolactone in patients with chronic hemodialysis, which showed a reduction in hospitalization rates for heart failure in the spironolactone group but no improvement in mortality.

Finally, he discusses two studies looking at combining newer therapies on a background of traditional ones that suggest a potential for reducing albuminuria.

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Matthew R. Weir, MD, Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Lutherville-Timonium, Maryland; Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland Medical Center, Baltimore, Maryland

Matthew R. Weir, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AstraZeneca; Bayer; NovoNordisk; Boehringer-Ingelheim; Johnson & Johnson; CSL Vifor

High-impact presentations on chronic kidney disease from the American Society of Nephrology (ASN) 2023 meeting are discussed by Dr Matthew Weir from the University of Maryland School of Medicine in Baltimore.

He starts with the results of the PROTECT and DUPLEX trials, in which sparsentan was compared with irbesartan in immunoglobulin A nephropathy and focal segmental glomerulosclerosis, respectively. In both studies, sparsentan resulted in greater reduction in albuminuria compared with irbesartan but with no significant differences in estimated glomerular filtration rate (GFR).

He also talks about the AYAME study of bardoxolone methyl in diabetic kidney disease, which was intended to examine the percentage of patients reaching a 30% reduction in GFR or end-stage renal disease. Bardoxolone slowed the reduction in the GFR but showed no benefit in reducing end-stage renal disease.

Next, Dr Weir reports the results from the ALCHEMIST trial on spironolactone in patients with chronic hemodialysis, which showed a reduction in hospitalization rates for heart failure in the spironolactone group but no improvement in mortality.

Finally, he discusses two studies looking at combining newer therapies on a background of traditional ones that suggest a potential for reducing albuminuria.

--

Matthew R. Weir, MD, Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Lutherville-Timonium, Maryland; Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland Medical Center, Baltimore, Maryland

Matthew R. Weir, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AstraZeneca; Bayer; NovoNordisk; Boehringer-Ingelheim; Johnson & Johnson; CSL Vifor

High-impact presentations on chronic kidney disease from the American Society of Nephrology (ASN) 2023 meeting are discussed by Dr Matthew Weir from the University of Maryland School of Medicine in Baltimore.

He starts with the results of the PROTECT and DUPLEX trials, in which sparsentan was compared with irbesartan in immunoglobulin A nephropathy and focal segmental glomerulosclerosis, respectively. In both studies, sparsentan resulted in greater reduction in albuminuria compared with irbesartan but with no significant differences in estimated glomerular filtration rate (GFR).

He also talks about the AYAME study of bardoxolone methyl in diabetic kidney disease, which was intended to examine the percentage of patients reaching a 30% reduction in GFR or end-stage renal disease. Bardoxolone slowed the reduction in the GFR but showed no benefit in reducing end-stage renal disease.

Next, Dr Weir reports the results from the ALCHEMIST trial on spironolactone in patients with chronic hemodialysis, which showed a reduction in hospitalization rates for heart failure in the spironolactone group but no improvement in mortality.

Finally, he discusses two studies looking at combining newer therapies on a background of traditional ones that suggest a potential for reducing albuminuria.

--

Matthew R. Weir, MD, Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland School of Medicine, Lutherville-Timonium, Maryland; Professor and Chief, Division of Nephrology, Department of Medicine, University of Maryland Medical Center, Baltimore, Maryland

Matthew R. Weir, MD, has disclosed the following relevant financial relationships:

Serve(d) as a director, officer, partner, employee, advisor, consultant, or trustee for: AstraZeneca; Bayer; NovoNordisk; Boehringer-Ingelheim; Johnson & Johnson; CSL Vifor

Key clinical point: Findings from this real-world study identified the protective and risk factors associated with SARS-CoV-2 breakthrough infections (BI) in patients with rheumatoid arthritis (RA) who had no COVID-19 infection and received the booster dose of anti-SARS-CoV-2 vaccine.

Major finding: Older patients who were age > 50 years (adjusted hazard ratio [aHR] 0.38; P = .004) and patients receiving conventional synthetic disease-modifying antirheumatic drugs (aHR 0.52; P = .021) had a significantly lower risk for BI, whereas patients receiving anti-interleukin 6 receptor (aHR 2.01; P = 0.039) and anti-CD20 (aHR 2.88; P = .011) treatments had ~2 and ~3 times higher risks for BI, respectively.

Study details: This prospective study included participants who had never been diagnosed with SARS-CoV-2 and had received three doses of the anti-SARS-CoV-2 vaccine, of whom 194 had RA and 1002 were control individuals.

Disclosures: This study was supported by the Italian Ministry of Health and other sources. The authors declared no conflicts of interest.

Source: Picchianti-Diamanti A et al. Older age, a high titre of neutralising antibodies and therapy with conventional DMARDs are associated with protection from breakthrough infection in rheumatoid arthritis patients after the booster dose of anti-SARS-CoV-2 vaccine. Vaccines. 2023;11(11):1684 (Nov 2). doi: 10.3390/vaccines11111684

Key clinical point: Findings from this real-world study identified the protective and risk factors associated with SARS-CoV-2 breakthrough infections (BI) in patients with rheumatoid arthritis (RA) who had no COVID-19 infection and received the booster dose of anti-SARS-CoV-2 vaccine.

Major finding: Older patients who were age > 50 years (adjusted hazard ratio [aHR] 0.38; P = .004) and patients receiving conventional synthetic disease-modifying antirheumatic drugs (aHR 0.52; P = .021) had a significantly lower risk for BI, whereas patients receiving anti-interleukin 6 receptor (aHR 2.01; P = 0.039) and anti-CD20 (aHR 2.88; P = .011) treatments had ~2 and ~3 times higher risks for BI, respectively.

Study details: This prospective study included participants who had never been diagnosed with SARS-CoV-2 and had received three doses of the anti-SARS-CoV-2 vaccine, of whom 194 had RA and 1002 were control individuals.

Disclosures: This study was supported by the Italian Ministry of Health and other sources. The authors declared no conflicts of interest.

Source: Picchianti-Diamanti A et al. Older age, a high titre of neutralising antibodies and therapy with conventional DMARDs are associated with protection from breakthrough infection in rheumatoid arthritis patients after the booster dose of anti-SARS-CoV-2 vaccine. Vaccines. 2023;11(11):1684 (Nov 2). doi: 10.3390/vaccines11111684

Key clinical point: Findings from this real-world study identified the protective and risk factors associated with SARS-CoV-2 breakthrough infections (BI) in patients with rheumatoid arthritis (RA) who had no COVID-19 infection and received the booster dose of anti-SARS-CoV-2 vaccine.

Major finding: Older patients who were age > 50 years (adjusted hazard ratio [aHR] 0.38; P = .004) and patients receiving conventional synthetic disease-modifying antirheumatic drugs (aHR 0.52; P = .021) had a significantly lower risk for BI, whereas patients receiving anti-interleukin 6 receptor (aHR 2.01; P = 0.039) and anti-CD20 (aHR 2.88; P = .011) treatments had ~2 and ~3 times higher risks for BI, respectively.

Study details: This prospective study included participants who had never been diagnosed with SARS-CoV-2 and had received three doses of the anti-SARS-CoV-2 vaccine, of whom 194 had RA and 1002 were control individuals.

Disclosures: This study was supported by the Italian Ministry of Health and other sources. The authors declared no conflicts of interest.

Source: Picchianti-Diamanti A et al. Older age, a high titre of neutralising antibodies and therapy with conventional DMARDs are associated with protection from breakthrough infection in rheumatoid arthritis patients after the booster dose of anti-SARS-CoV-2 vaccine. Vaccines. 2023;11(11):1684 (Nov 2). doi: 10.3390/vaccines11111684