Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Long-term eptinezumab treatment showed benefits in patients with chronic migraine (CM) who had concomitant medication-overuse headache (MOH).

Major findings: After eptinezumab treatment, the average number of headache days per 3 months reduced from 15.8 days (mean 47.5 headache days/month) at baseline to 3.8 days (mean 11.3 headache days/month) at 104 weeks, along with reductions observed in the Migraine Disability Assessment (mean change −51.9 points) and 6-item Headache Impact Test (mean change −9.7 points) scores. More than half (57.1%) the patients showed an improvement in their patient-identified most bothersome symptom at as early as 4 weeks.

Study details: This post hoc analysis of the PREVAIL study included 49 patients with CM and concomitant MOH.

Disclosures: This publication was supported by H. Lundbeck A/S, Copenhagen, Denmark. Two authors declared being employees of H. Lundbeck A/S. The other authors declared having ties with various sources, including H. Lundbeck A/S.

Source: Blumenfeld A, Kudrow D, McAllister P, et al. Long-term effectiveness of eptinezumab in the treatment of patients with chronic migraine and medication-overuse headache. Headache. 2024;64:738-749 (Jun 24). Doi: 10.1111/head.14767 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: Calcitonin gene-related peptide (CGRP)–induced migraine attacks did not affect therapeutic response to erenumab in patients with migraine.

Major finding: Overall, a similar proportion of patients who experienced vs did not experience CGRP-induced migraine attacks had a ≥50% reduction in monthly migraine days during weeks 13-24 following erenumab treatment (61% vs 52%; odds ratio [OR] 1.42; P = .498). No significant differences were seen between the two patient groups that achieved a ≥50% reduction in monthly migraine or headache days of moderate to severe intensity (OR 1.25; P = .625).

Study details: This interim analysis of the REFORM study included 124 patients with migraine who received CGRP infusion on a single experimental day and subsequently a 24-week treatment with erenumab.

Disclosures: This study was funded by Novartis Pharma and the Lundbeck Foundation. Two authors declared being employees of or holding shares in Novartis Pharma AG. Several authors declared receiving personal fees from various sources, including Novartis, outside of the submitted work. One author is an associate editor for Cephalalgia.

Source: Al-Khazali HM, Ashina H, Christensen RH, et al. Hypersensitivity to CGRP as a predictive biomarker of migraine prevention with erenumab. Cephalalgia. 2024;44(6):3331024241258734 (Jun 11). Doi: 10.1177/03331024241258734 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source

Key clinical point: In patients with episodic migraine (EM) or chronic migraine (CM), erenumab treatment interruption was associated with increased monthly migraine days (MMD) and worsening of migraine disability; these effects ameliorated on treatment restart.

Major finding: After erenumab treatment interruption for 3 months, the number of monthly migraine days (MMD) increased from 6.1 to 10.9 days for patients with EM and from 11.4 to 16.8 days for patients with CM; the modified Migraine Disability Assessment scores (mMIDAS) also worsened during this period. Both MMD and mMIDAS scores improved upon restarting treatment.

Study details: This interim analysis of the 24-month, multicentric, non-interventional observational study included 172 patients with CM or EM who received erenumab and underwent treatment interruptions on average 11.2 months after initiation, with interruptions lasting for a mean duration of 4 months.

Disclosures: This study was funded by Novartis Pharma Schweiz AG. Four authors declared being full-time employees of Novartis Pharma Schweiz AG, and others declared having ties with various sources, including Novartis.

Source: Gantenbein AR, Bonvin C, Kamm CP, et al. Implications of therapy interruption on monthly migraine days and modified migraine disability assessment in patients treated with erenumab for chronic and episodic migraine: SQUARE study interim results. J Neurol. 2024 (Jun 13). Doi: 10.1007/s00415-024-12470-6 Source

Key clinical point: Patients with migraine, migraine with aura (MA), or migraine without aura (MO) faced a significantly higher risk for retinal vascular occlusion.

Major findings: Compared with control individuals without migraine, those with migraine (adjusted hazard ratio [aHR] 1.69; 95% CI 1.57-1.83), MA (aHR 1.77; 95% CI 1.58-1.98), or MO (aHR 1.92; 95% CI 1.64-2.25; P < .001 for all) had a significantly higher risk for retinal vascular occlusion. The risk was, however, reduced in the migraine population that received nonsteroidal anti-inflammatory drugs (aHR 0.19; 95% CI 0.16-0.22), propranolol (aHR 0.73; 95% CI 0.62-0.86), or flunarizine (aHR 0.84; 95% CI 0.76-0.93; P < .001 for all).

Study details: This population-based retrospective cohort study included 628,760 patients with migraine and 628,760 control individuals without migraine.

Disclosures: This study was supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial Center, China Medical University Hospital, and National Science and Technology Council. The authors declared no conflicts of interest.

Source: Ho K-Y, Lin C-D, Hsu T-J, et al. Increased risks of retinal vascular occlusion in patients with migraine and the protective effects of migraine treatment: A population-based retrospective cohort study. Sci Rep. 2024;14:15429 (Jul 4). Doi: 10.1038/s41598-024-66363-9 Source

Key clinical point: Patients with migraine, migraine with aura (MA), or migraine without aura (MO) faced a significantly higher risk for retinal vascular occlusion.

Major findings: Compared with control individuals without migraine, those with migraine (adjusted hazard ratio [aHR] 1.69; 95% CI 1.57-1.83), MA (aHR 1.77; 95% CI 1.58-1.98), or MO (aHR 1.92; 95% CI 1.64-2.25; P < .001 for all) had a significantly higher risk for retinal vascular occlusion. The risk was, however, reduced in the migraine population that received nonsteroidal anti-inflammatory drugs (aHR 0.19; 95% CI 0.16-0.22), propranolol (aHR 0.73; 95% CI 0.62-0.86), or flunarizine (aHR 0.84; 95% CI 0.76-0.93; P < .001 for all).

Study details: This population-based retrospective cohort study included 628,760 patients with migraine and 628,760 control individuals without migraine.

Disclosures: This study was supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial Center, China Medical University Hospital, and National Science and Technology Council. The authors declared no conflicts of interest.

Source: Ho K-Y, Lin C-D, Hsu T-J, et al. Increased risks of retinal vascular occlusion in patients with migraine and the protective effects of migraine treatment: A population-based retrospective cohort study. Sci Rep. 2024;14:15429 (Jul 4). Doi: 10.1038/s41598-024-66363-9 Source

Key clinical point: Patients with migraine, migraine with aura (MA), or migraine without aura (MO) faced a significantly higher risk for retinal vascular occlusion.

Major findings: Compared with control individuals without migraine, those with migraine (adjusted hazard ratio [aHR] 1.69; 95% CI 1.57-1.83), MA (aHR 1.77; 95% CI 1.58-1.98), or MO (aHR 1.92; 95% CI 1.64-2.25; P < .001 for all) had a significantly higher risk for retinal vascular occlusion. The risk was, however, reduced in the migraine population that received nonsteroidal anti-inflammatory drugs (aHR 0.19; 95% CI 0.16-0.22), propranolol (aHR 0.73; 95% CI 0.62-0.86), or flunarizine (aHR 0.84; 95% CI 0.76-0.93; P < .001 for all).

Study details: This population-based retrospective cohort study included 628,760 patients with migraine and 628,760 control individuals without migraine.

Disclosures: This study was supported in part by the Taiwan Ministry of Health and Welfare Clinical Trial Center, China Medical University Hospital, and National Science and Technology Council. The authors declared no conflicts of interest.

Source: Ho K-Y, Lin C-D, Hsu T-J, et al. Increased risks of retinal vascular occlusion in patients with migraine and the protective effects of migraine treatment: A population-based retrospective cohort study. Sci Rep. 2024;14:15429 (Jul 4). Doi: 10.1038/s41598-024-66363-9 Source

Key clinical point: Atogepant was effective in reducing monthly migraine days (MMD), monthly headache days (MHD), and acute medication use days in patients with chronic migraine (CM), irrespective of acute medication overuse.

Major findings: Patients with acute medication overuse receiving 30 mg or 60 mg atogepant vs placebo had a significantly greater reduction in MMD (least squares mean difference [LSMD] −2.7 and −1.9, respectively), MHD (LSMD −2.8 and −2.1, respectively), and monthly acute medication use days (LSMD −2.8 and −2.6, respectively). Similar reductions were observed in patients without acute medication overuse.

Study details: This subgroup analysis of the PROGRESS trial included 755 patients with CM with or without acute medication overuse who were randomly assigned to receive atogepant (30 mg or 60 mg) or placebo.

Disclosures: This study was funded by AbbVie. Six authors declared being employees or stockholders of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Goadsby PJ, Friedman DI, Holle-Lee D, et al. Efficacy of atogepant in chronic migraine with and without acute medication overuse in the randomized, double-blind, phase 3 PROGRESS trial. Neurology. 2024;103(2):e209584 (July 23). Doi: 10.1212/WNL.0000000000209584 Source

Key clinical point: Atogepant was effective in reducing monthly migraine days (MMD), monthly headache days (MHD), and acute medication use days in patients with chronic migraine (CM), irrespective of acute medication overuse.

Major findings: Patients with acute medication overuse receiving 30 mg or 60 mg atogepant vs placebo had a significantly greater reduction in MMD (least squares mean difference [LSMD] −2.7 and −1.9, respectively), MHD (LSMD −2.8 and −2.1, respectively), and monthly acute medication use days (LSMD −2.8 and −2.6, respectively). Similar reductions were observed in patients without acute medication overuse.

Study details: This subgroup analysis of the PROGRESS trial included 755 patients with CM with or without acute medication overuse who were randomly assigned to receive atogepant (30 mg or 60 mg) or placebo.

Disclosures: This study was funded by AbbVie. Six authors declared being employees or stockholders of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Goadsby PJ, Friedman DI, Holle-Lee D, et al. Efficacy of atogepant in chronic migraine with and without acute medication overuse in the randomized, double-blind, phase 3 PROGRESS trial. Neurology. 2024;103(2):e209584 (July 23). Doi: 10.1212/WNL.0000000000209584 Source

Key clinical point: Atogepant was effective in reducing monthly migraine days (MMD), monthly headache days (MHD), and acute medication use days in patients with chronic migraine (CM), irrespective of acute medication overuse.

Major findings: Patients with acute medication overuse receiving 30 mg or 60 mg atogepant vs placebo had a significantly greater reduction in MMD (least squares mean difference [LSMD] −2.7 and −1.9, respectively), MHD (LSMD −2.8 and −2.1, respectively), and monthly acute medication use days (LSMD −2.8 and −2.6, respectively). Similar reductions were observed in patients without acute medication overuse.

Study details: This subgroup analysis of the PROGRESS trial included 755 patients with CM with or without acute medication overuse who were randomly assigned to receive atogepant (30 mg or 60 mg) or placebo.

Disclosures: This study was funded by AbbVie. Six authors declared being employees or stockholders of AbbVie. Several authors declared having ties with various sources, including AbbVie.

Source: Goadsby PJ, Friedman DI, Holle-Lee D, et al. Efficacy of atogepant in chronic migraine with and without acute medication overuse in the randomized, double-blind, phase 3 PROGRESS trial. Neurology. 2024;103(2):e209584 (July 23). Doi: 10.1212/WNL.0000000000209584 Source

To the Editor:

Immune checkpoint inhibitors have revolutionized the treatment of advanced-stage melanoma, with remarkably improved progression-free survival.¹ Anti–programmed death receptor 1 (anti–PD-1) therapies, such as nivolumab and pembrolizumab, are a class of checkpoint inhibitors that have been approved by the US Food and Drug Administration for unresectable metastatic melanoma. Anti–PD-1 agents block the interaction of programmed death-ligand 1 (PD-L1) found on tumor cells with the PD-1 receptor on T cells, facilitating a positive immune response.²

Although these therapies have demonstrated notable antitumor efficacy, they also give rise to numerous immune-related adverse events (irAEs). As many as 70% of patients treated with PD-1/PD-L1 inhibitors experience some type of organ system irAE, of which 30% to 40% are cutaneous.^3-6 Dermatologic adverse events are the most common irAEs, specifically spongiotic dermatitis, lichenoid dermatitis, pruritus, and vitiligo.⁷ Bullous pemphigoid (BP), an autoimmune bullous skin disorder caused by autoantibodies to basement membrane zone antigens, is a rare but potentially serious cutaneous irAE.⁸ Systemic corticosteroids commonly are used to treat immune checkpoint inhibitor–induced BP; other options include tetracyclines for maintenance therapy and rituximab for corticosteroid-refractory BP associated with anti-PD-1.⁹ We present a case of recalcitrant BP secondary to nivolumab therapy in a patient with metastatic melanoma who had near-complete resolution of BP following 2 months of cyclosporine.

A 41-year-old man presented with a generalized papular skin eruption of 1 month’s duration. He had a history of stage IIIC malignant melanoma of the lower right leg with positive sentinel lymph node biopsy. The largest lymph node deposit was 0.03 mm without extracapsular extension. Whole-body positron emission tomography–computed tomography showed no evidence of distant disease. The patient was treated with wide local excision with clear surgical margins plus 12 cycles of nivolumab, which was discontinued due to colitis. Four months after the final cycle of nivolumab, the patient developed widespread erythematous papules with hemorrhagic yellow crusting and no mucosal involvement. He was referred to dermatology by his primary oncologist for further evaluation.

A punch biopsy from the abdomen showed para­keratosis with leukocytoclasis and a superficial dermal infiltrate of neutrophils and eosinophils (Figure 1). Direct immunofluorescence revealed linear basement membrane deposits of IgG and C3, consistent with subepidermal blistering disease. Indirect immunofluorescence demonstrated trace IgG and IgG4 antibodies localized to the epidermal roof of salt-split skin and was negative for IgA antibodies. An enzyme-linked immunoassay was positive for BP antigen 2 (BP180) antibodies (98.4 U/mL [positive, ≥9 U/mL]) and negative for BP antigen 1 (BP230) antibodies (4.3 U/mL [positive, ≥9 U/mL]). Overall, these findings were consistent with a diagnosis of BP.

The patient was treated with prednisone 60 mg daily with initial response; however, there was disease recurrence with tapering. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily were added as steroid-sparing agents, as prednisone was discontinued due to mood changes. Three months after the prednisone taper, the patient continued to develop new blisters. He completed treatment with doxycycline and nicotinamide. Rituximab 375 mg weekly was then initiated for 4 weeks.

At 2-week follow-up after completing the rituximab course, the patient reported worsening symptoms and presented with new bullae on the abdomen and upper extremities (Figure 2). Because of the recent history of mood changes while taking prednisone, a trial of cyclosporine 100 mg twice daily (1.37 mg/kg/d) was initiated, with notable improvement within 2 weeks of treatment. After 2 months of cyclosporine, approximately 90% of the rash had resolved with a few tense bullae remaining on the left frontal scalp but no new flares (Figure 3). One month after treatment ended, the patient remained clear of lesions without relapse.

Programmed death receptor 1 inhibitors have shown dramatic efficacy for a growing number of solid and hematologic malignancies, especially malignant melanoma. However, their use is accompanied by nonspecific activation of the immune system, resulting in a variety of adverse events, many manifesting on the skin. Several cases of BP in patients treated with PD-1/PD-L1 inhibitors have been reported.⁹ Cutaneous irAEs usually manifest within 3 weeks of initiation of PD-1 inhibitor therapy; however, the onset of BP typically occurs later at approximately 21 weeks.^4,9 Our patient developed cutaneous manifestations 4 months after cessation of nivolumab.

To the Editor:

Immune checkpoint inhibitors have revolutionized the treatment of advanced-stage melanoma, with remarkably improved progression-free survival.¹ Anti–programmed death receptor 1 (anti–PD-1) therapies, such as nivolumab and pembrolizumab, are a class of checkpoint inhibitors that have been approved by the US Food and Drug Administration for unresectable metastatic melanoma. Anti–PD-1 agents block the interaction of programmed death-ligand 1 (PD-L1) found on tumor cells with the PD-1 receptor on T cells, facilitating a positive immune response.²

Although these therapies have demonstrated notable antitumor efficacy, they also give rise to numerous immune-related adverse events (irAEs). As many as 70% of patients treated with PD-1/PD-L1 inhibitors experience some type of organ system irAE, of which 30% to 40% are cutaneous.^3-6 Dermatologic adverse events are the most common irAEs, specifically spongiotic dermatitis, lichenoid dermatitis, pruritus, and vitiligo.⁷ Bullous pemphigoid (BP), an autoimmune bullous skin disorder caused by autoantibodies to basement membrane zone antigens, is a rare but potentially serious cutaneous irAE.⁸ Systemic corticosteroids commonly are used to treat immune checkpoint inhibitor–induced BP; other options include tetracyclines for maintenance therapy and rituximab for corticosteroid-refractory BP associated with anti-PD-1.⁹ We present a case of recalcitrant BP secondary to nivolumab therapy in a patient with metastatic melanoma who had near-complete resolution of BP following 2 months of cyclosporine.

A 41-year-old man presented with a generalized papular skin eruption of 1 month’s duration. He had a history of stage IIIC malignant melanoma of the lower right leg with positive sentinel lymph node biopsy. The largest lymph node deposit was 0.03 mm without extracapsular extension. Whole-body positron emission tomography–computed tomography showed no evidence of distant disease. The patient was treated with wide local excision with clear surgical margins plus 12 cycles of nivolumab, which was discontinued due to colitis. Four months after the final cycle of nivolumab, the patient developed widespread erythematous papules with hemorrhagic yellow crusting and no mucosal involvement. He was referred to dermatology by his primary oncologist for further evaluation.

A punch biopsy from the abdomen showed para­keratosis with leukocytoclasis and a superficial dermal infiltrate of neutrophils and eosinophils (Figure 1). Direct immunofluorescence revealed linear basement membrane deposits of IgG and C3, consistent with subepidermal blistering disease. Indirect immunofluorescence demonstrated trace IgG and IgG4 antibodies localized to the epidermal roof of salt-split skin and was negative for IgA antibodies. An enzyme-linked immunoassay was positive for BP antigen 2 (BP180) antibodies (98.4 U/mL [positive, ≥9 U/mL]) and negative for BP antigen 1 (BP230) antibodies (4.3 U/mL [positive, ≥9 U/mL]). Overall, these findings were consistent with a diagnosis of BP.

The patient was treated with prednisone 60 mg daily with initial response; however, there was disease recurrence with tapering. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily were added as steroid-sparing agents, as prednisone was discontinued due to mood changes. Three months after the prednisone taper, the patient continued to develop new blisters. He completed treatment with doxycycline and nicotinamide. Rituximab 375 mg weekly was then initiated for 4 weeks.

At 2-week follow-up after completing the rituximab course, the patient reported worsening symptoms and presented with new bullae on the abdomen and upper extremities (Figure 2). Because of the recent history of mood changes while taking prednisone, a trial of cyclosporine 100 mg twice daily (1.37 mg/kg/d) was initiated, with notable improvement within 2 weeks of treatment. After 2 months of cyclosporine, approximately 90% of the rash had resolved with a few tense bullae remaining on the left frontal scalp but no new flares (Figure 3). One month after treatment ended, the patient remained clear of lesions without relapse.

Programmed death receptor 1 inhibitors have shown dramatic efficacy for a growing number of solid and hematologic malignancies, especially malignant melanoma. However, their use is accompanied by nonspecific activation of the immune system, resulting in a variety of adverse events, many manifesting on the skin. Several cases of BP in patients treated with PD-1/PD-L1 inhibitors have been reported.⁹ Cutaneous irAEs usually manifest within 3 weeks of initiation of PD-1 inhibitor therapy; however, the onset of BP typically occurs later at approximately 21 weeks.^4,9 Our patient developed cutaneous manifestations 4 months after cessation of nivolumab.

To the Editor:

Immune checkpoint inhibitors have revolutionized the treatment of advanced-stage melanoma, with remarkably improved progression-free survival.¹ Anti–programmed death receptor 1 (anti–PD-1) therapies, such as nivolumab and pembrolizumab, are a class of checkpoint inhibitors that have been approved by the US Food and Drug Administration for unresectable metastatic melanoma. Anti–PD-1 agents block the interaction of programmed death-ligand 1 (PD-L1) found on tumor cells with the PD-1 receptor on T cells, facilitating a positive immune response.²

Although these therapies have demonstrated notable antitumor efficacy, they also give rise to numerous immune-related adverse events (irAEs). As many as 70% of patients treated with PD-1/PD-L1 inhibitors experience some type of organ system irAE, of which 30% to 40% are cutaneous.^3-6 Dermatologic adverse events are the most common irAEs, specifically spongiotic dermatitis, lichenoid dermatitis, pruritus, and vitiligo.⁷ Bullous pemphigoid (BP), an autoimmune bullous skin disorder caused by autoantibodies to basement membrane zone antigens, is a rare but potentially serious cutaneous irAE.⁸ Systemic corticosteroids commonly are used to treat immune checkpoint inhibitor–induced BP; other options include tetracyclines for maintenance therapy and rituximab for corticosteroid-refractory BP associated with anti-PD-1.⁹ We present a case of recalcitrant BP secondary to nivolumab therapy in a patient with metastatic melanoma who had near-complete resolution of BP following 2 months of cyclosporine.

A 41-year-old man presented with a generalized papular skin eruption of 1 month’s duration. He had a history of stage IIIC malignant melanoma of the lower right leg with positive sentinel lymph node biopsy. The largest lymph node deposit was 0.03 mm without extracapsular extension. Whole-body positron emission tomography–computed tomography showed no evidence of distant disease. The patient was treated with wide local excision with clear surgical margins plus 12 cycles of nivolumab, which was discontinued due to colitis. Four months after the final cycle of nivolumab, the patient developed widespread erythematous papules with hemorrhagic yellow crusting and no mucosal involvement. He was referred to dermatology by his primary oncologist for further evaluation.

A punch biopsy from the abdomen showed para­keratosis with leukocytoclasis and a superficial dermal infiltrate of neutrophils and eosinophils (Figure 1). Direct immunofluorescence revealed linear basement membrane deposits of IgG and C3, consistent with subepidermal blistering disease. Indirect immunofluorescence demonstrated trace IgG and IgG4 antibodies localized to the epidermal roof of salt-split skin and was negative for IgA antibodies. An enzyme-linked immunoassay was positive for BP antigen 2 (BP180) antibodies (98.4 U/mL [positive, ≥9 U/mL]) and negative for BP antigen 1 (BP230) antibodies (4.3 U/mL [positive, ≥9 U/mL]). Overall, these findings were consistent with a diagnosis of BP.

The patient was treated with prednisone 60 mg daily with initial response; however, there was disease recurrence with tapering. Doxycycline 100 mg twice daily and nicotinamide 500 mg twice daily were added as steroid-sparing agents, as prednisone was discontinued due to mood changes. Three months after the prednisone taper, the patient continued to develop new blisters. He completed treatment with doxycycline and nicotinamide. Rituximab 375 mg weekly was then initiated for 4 weeks.

At 2-week follow-up after completing the rituximab course, the patient reported worsening symptoms and presented with new bullae on the abdomen and upper extremities (Figure 2). Because of the recent history of mood changes while taking prednisone, a trial of cyclosporine 100 mg twice daily (1.37 mg/kg/d) was initiated, with notable improvement within 2 weeks of treatment. After 2 months of cyclosporine, approximately 90% of the rash had resolved with a few tense bullae remaining on the left frontal scalp but no new flares (Figure 3). One month after treatment ended, the patient remained clear of lesions without relapse.

Programmed death receptor 1 inhibitors have shown dramatic efficacy for a growing number of solid and hematologic malignancies, especially malignant melanoma. However, their use is accompanied by nonspecific activation of the immune system, resulting in a variety of adverse events, many manifesting on the skin. Several cases of BP in patients treated with PD-1/PD-L1 inhibitors have been reported.⁹ Cutaneous irAEs usually manifest within 3 weeks of initiation of PD-1 inhibitor therapy; however, the onset of BP typically occurs later at approximately 21 weeks.^4,9 Our patient developed cutaneous manifestations 4 months after cessation of nivolumab.

CHICAGO — Circulating tumor DNA (ctDNA) can predict relapse risk in some cases of early, high-risk breast cancer, but it’s too soon to use it to guide adjuvant therapy decisions, according to a study presented at the American Society of Clinical Oncology annual meeting.

Detectable ctDNA is “highly prognostic of worse outcomes, particularly in patients who [remain] persistently positive,” but the correlation isn’t perfect, said lead investigator Sherene Loi, MMBS, PhD, a breast cancer specialist at the Peter MacCallum Cancer Centre in Melbourne, Australia.

Although less likely, relapses also occurred in the study among women without ctDNA elevation. Conversely, there were women with elevated ctDNA who did not relapse, she said. The study was a subanalysis of the monarchE trial of adjuvant abemaciclib, a CDK 4/6 inhibitor.

Eventually, “we would like to use” ctDNA to guide adjuvant treatment decisions, but the research isn’t there yet, Dr. Loi said. It’s possible, for instance, that persistently detectable ctDNA indicates early treatment failure and the need for treatment intensification. Future research should tackle the issue.

Study discussant Francois-Clement Bidard, MD, PhD, a breast cancer specialist at Institut Curie, Paris, agreed that ctDNA isn’t ready for primetime in adjuvant early, high-risk breast cancer.

“There is no clinical evidence to suggest that there is clinical utility in this setting. There are several trials that are ongoing,” he said, but for now “you shouldn’t,” for example, “use ctDNA to de-escalate adjuvant CDK4/6 [inhibitors]. It could be in the future that we could have data on this, but at the moment, [the] clear clinical message [is] no way.”

At 5-year follow-up, the monarchE trial found a 7.6% invasive disease-free survival (IDFS) improvement when abemaciclib was added to the first 2 years of endocrine therapy in women with HR+, HER2-, node positive, high-risk early breast cancer. The combination is now a standard adjuvant option for the disease.

The ctDNA study focused on a subset of 910 subjects with adequate ctDNA testing to run the analysis. The study population was also selected to be enriched for overall IDFS events (27% versus 18% across the trial’s 5,637 subjects). An IDFS event was defined as a local, regional, contralateral or distant invasive recurrence; a new primary tumor; or death from any cause.

Testing was performed using the Signatera ctDNA assay. Baseline samples were taken after completion of adjuvant chemotherapy, then again at 3, 6, or 24 months.

Overall, ctDNA detection was infrequent. Just 8% of patients were positive at baseline and 17% were positive at any point during the trial. Even so, ctDNA detection at any point was adversely prognostic.

Patients who were ctDNA positive at baseline were more likely to experience an IDFS event, compared with those who were ctDNA negative at baseline (80% at 4 years follow-up versus 23%).

Similarly, those who remained positive or became positive during testing were more likely to experience an IDFS event compared with those who became negative or remained negative throughout testing.

For instance, all 34 patients who were positive at baseline and remained positive had an IDFS event by year 4, versus just 40% who started positive but then cleared their ctDNA.

Among women who were negative at baseline and remained negative, 13% had an IDFS event versus 89% who started negative but then turned positive. Subjects who turned positive also had the shortest time to an IDFS event, a median of 7 months.

Among women who recurred, those who were ctDNA negative tended to have local, regional, or contralateral recurrences, while ctDNA positive patients tended to have distant recurrences.

The finding “really highlights that ctDNA antedates the metastatic clinical relapse. What the ctDNA is telling you is that the metastatic process has been completed, and metastases are about to grow,” Dr. Bidard said.

The work was funded by Eli Lilly, maker of abemaciclib, with collaboration from Natera, maker of the Signatera assay. Dr. Loi is an adviser and researcher for Lilly, among other industry ties. Dr. Bidard is a speaker and consultant for Lilly, among other ties.

CHICAGO — Circulating tumor DNA (ctDNA) can predict relapse risk in some cases of early, high-risk breast cancer, but it’s too soon to use it to guide adjuvant therapy decisions, according to a study presented at the American Society of Clinical Oncology annual meeting.

Detectable ctDNA is “highly prognostic of worse outcomes, particularly in patients who [remain] persistently positive,” but the correlation isn’t perfect, said lead investigator Sherene Loi, MMBS, PhD, a breast cancer specialist at the Peter MacCallum Cancer Centre in Melbourne, Australia.

Although less likely, relapses also occurred in the study among women without ctDNA elevation. Conversely, there were women with elevated ctDNA who did not relapse, she said. The study was a subanalysis of the monarchE trial of adjuvant abemaciclib, a CDK 4/6 inhibitor.

Eventually, “we would like to use” ctDNA to guide adjuvant treatment decisions, but the research isn’t there yet, Dr. Loi said. It’s possible, for instance, that persistently detectable ctDNA indicates early treatment failure and the need for treatment intensification. Future research should tackle the issue.

Study discussant Francois-Clement Bidard, MD, PhD, a breast cancer specialist at Institut Curie, Paris, agreed that ctDNA isn’t ready for primetime in adjuvant early, high-risk breast cancer.

“There is no clinical evidence to suggest that there is clinical utility in this setting. There are several trials that are ongoing,” he said, but for now “you shouldn’t,” for example, “use ctDNA to de-escalate adjuvant CDK4/6 [inhibitors]. It could be in the future that we could have data on this, but at the moment, [the] clear clinical message [is] no way.”

At 5-year follow-up, the monarchE trial found a 7.6% invasive disease-free survival (IDFS) improvement when abemaciclib was added to the first 2 years of endocrine therapy in women with HR+, HER2-, node positive, high-risk early breast cancer. The combination is now a standard adjuvant option for the disease.

The ctDNA study focused on a subset of 910 subjects with adequate ctDNA testing to run the analysis. The study population was also selected to be enriched for overall IDFS events (27% versus 18% across the trial’s 5,637 subjects). An IDFS event was defined as a local, regional, contralateral or distant invasive recurrence; a new primary tumor; or death from any cause.

Testing was performed using the Signatera ctDNA assay. Baseline samples were taken after completion of adjuvant chemotherapy, then again at 3, 6, or 24 months.

Overall, ctDNA detection was infrequent. Just 8% of patients were positive at baseline and 17% were positive at any point during the trial. Even so, ctDNA detection at any point was adversely prognostic.

Patients who were ctDNA positive at baseline were more likely to experience an IDFS event, compared with those who were ctDNA negative at baseline (80% at 4 years follow-up versus 23%).

Similarly, those who remained positive or became positive during testing were more likely to experience an IDFS event compared with those who became negative or remained negative throughout testing.

For instance, all 34 patients who were positive at baseline and remained positive had an IDFS event by year 4, versus just 40% who started positive but then cleared their ctDNA.

Among women who were negative at baseline and remained negative, 13% had an IDFS event versus 89% who started negative but then turned positive. Subjects who turned positive also had the shortest time to an IDFS event, a median of 7 months.

Among women who recurred, those who were ctDNA negative tended to have local, regional, or contralateral recurrences, while ctDNA positive patients tended to have distant recurrences.

The finding “really highlights that ctDNA antedates the metastatic clinical relapse. What the ctDNA is telling you is that the metastatic process has been completed, and metastases are about to grow,” Dr. Bidard said.

The work was funded by Eli Lilly, maker of abemaciclib, with collaboration from Natera, maker of the Signatera assay. Dr. Loi is an adviser and researcher for Lilly, among other industry ties. Dr. Bidard is a speaker and consultant for Lilly, among other ties.

CHICAGO — Circulating tumor DNA (ctDNA) can predict relapse risk in some cases of early, high-risk breast cancer, but it’s too soon to use it to guide adjuvant therapy decisions, according to a study presented at the American Society of Clinical Oncology annual meeting.

Detectable ctDNA is “highly prognostic of worse outcomes, particularly in patients who [remain] persistently positive,” but the correlation isn’t perfect, said lead investigator Sherene Loi, MMBS, PhD, a breast cancer specialist at the Peter MacCallum Cancer Centre in Melbourne, Australia.

Although less likely, relapses also occurred in the study among women without ctDNA elevation. Conversely, there were women with elevated ctDNA who did not relapse, she said. The study was a subanalysis of the monarchE trial of adjuvant abemaciclib, a CDK 4/6 inhibitor.

Eventually, “we would like to use” ctDNA to guide adjuvant treatment decisions, but the research isn’t there yet, Dr. Loi said. It’s possible, for instance, that persistently detectable ctDNA indicates early treatment failure and the need for treatment intensification. Future research should tackle the issue.

Study discussant Francois-Clement Bidard, MD, PhD, a breast cancer specialist at Institut Curie, Paris, agreed that ctDNA isn’t ready for primetime in adjuvant early, high-risk breast cancer.

“There is no clinical evidence to suggest that there is clinical utility in this setting. There are several trials that are ongoing,” he said, but for now “you shouldn’t,” for example, “use ctDNA to de-escalate adjuvant CDK4/6 [inhibitors]. It could be in the future that we could have data on this, but at the moment, [the] clear clinical message [is] no way.”

At 5-year follow-up, the monarchE trial found a 7.6% invasive disease-free survival (IDFS) improvement when abemaciclib was added to the first 2 years of endocrine therapy in women with HR+, HER2-, node positive, high-risk early breast cancer. The combination is now a standard adjuvant option for the disease.

The ctDNA study focused on a subset of 910 subjects with adequate ctDNA testing to run the analysis. The study population was also selected to be enriched for overall IDFS events (27% versus 18% across the trial’s 5,637 subjects). An IDFS event was defined as a local, regional, contralateral or distant invasive recurrence; a new primary tumor; or death from any cause.

Testing was performed using the Signatera ctDNA assay. Baseline samples were taken after completion of adjuvant chemotherapy, then again at 3, 6, or 24 months.

Overall, ctDNA detection was infrequent. Just 8% of patients were positive at baseline and 17% were positive at any point during the trial. Even so, ctDNA detection at any point was adversely prognostic.

Patients who were ctDNA positive at baseline were more likely to experience an IDFS event, compared with those who were ctDNA negative at baseline (80% at 4 years follow-up versus 23%).

Similarly, those who remained positive or became positive during testing were more likely to experience an IDFS event compared with those who became negative or remained negative throughout testing.

For instance, all 34 patients who were positive at baseline and remained positive had an IDFS event by year 4, versus just 40% who started positive but then cleared their ctDNA.

Among women who were negative at baseline and remained negative, 13% had an IDFS event versus 89% who started negative but then turned positive. Subjects who turned positive also had the shortest time to an IDFS event, a median of 7 months.

Among women who recurred, those who were ctDNA negative tended to have local, regional, or contralateral recurrences, while ctDNA positive patients tended to have distant recurrences.

The finding “really highlights that ctDNA antedates the metastatic clinical relapse. What the ctDNA is telling you is that the metastatic process has been completed, and metastases are about to grow,” Dr. Bidard said.

The work was funded by Eli Lilly, maker of abemaciclib, with collaboration from Natera, maker of the Signatera assay. Dr. Loi is an adviser and researcher for Lilly, among other industry ties. Dr. Bidard is a speaker and consultant for Lilly, among other ties.

Lifetime skin cancer prevalence in sexual minority (SM) Americans varied by race, ethnicity, and individual sexual identity, compared with that in heterosexual peers, according to a large cross-sectional study. Addressing dynamics of each SM subgroup will require increasingly tailored prevention, screening, and research efforts, the study authors said.

“We identified specific subgroups within the sexual minority community who are at higher risk for skin cancer, specifically White gay males and Hispanic and non-Hispanic Black SM men and women — particularly individuals who identify as bisexual,” senior author Matthew Mansh, MD, said in an interview. He is an assistant professor of dermatology at the University of California, San Francisco. The study was published online in JAMA Dermatology.

Using data of adults in the US general population from the Behavioral Risk Factor Surveillance System from January 2014 to December 2021, investigators included more than 1.5 million respondents. The proportions of SM women and men (who self-identified as bisexual, lesbian, gay, “something else,” or other) were 2.6% and 2.0%, respectively.

Lifetime skin cancer prevalence was higher among SM men than among heterosexual men (7.4% vs 6.8%; adjusted odds ratio [aOR], 1.16). In analyses stratified by racial and ethnic group, AORs for non-Hispanic Black and Hispanic SM men vs their heterosexual counterparts were 2.18 and 3.81, respectively. The corresponding figures for non-Hispanic Black and Hispanic SM women were 2.33 and 2.46, respectively.

When investigators combined all minority respondents along gender lines, lifetime skin cancer prevalence was higher in bisexual men (aOR, 3.94), bisexual women (aOR, 1.51), and women identifying as something else or other (aOR, 2.70) than in their heterosexual peers.

“I wasn’t expecting that Hispanic or non-Hispanic Black SMs would be at higher risk for skin cancer,” Dr. Mansh said. Even if these groups have more behavioral risk factors for UV radiation (UVR) exposure, he explained, UVR exposure is less strongly linked with skin cancer in darker skin than in lighter skin. Reasons for the counterintuitive finding could include different screening habits among SM people of different racial and ethnic groups, he said, and analyzing such factors will require further research.

Although some effect sizes were modest, the authors wrote, their findings may have important implications for population-based research and public health efforts aimed at early skin cancer detection and prevention. Presently, the United States lacks established guidelines for skin cancer screening. In a 2023 statement published in JAMA, the US Preventive Services Task Force said that there is insufficient evidence to determine the benefit-harm balance of skin cancer screening in asymptomatic people.

“So there has been a lot of recent talk and a need to identify which subset groups of patients might be higher risk for skin cancer and might benefit from more screening,” Dr. Mansh said in an interview. “Understanding more about the high-risk demographic and clinical features that predispose someone to skin cancer helps identify these high-risk populations that could be used to develop better screening guidelines.”

Identifying groups at a higher risk for skin cancer also allows experts to design more targeted counseling or public health interventions focused on these groups, Dr. Mansh added. Absent screening guidelines, experts emphasize changing modifiable risk factors such as UVR exposure, smoking, and alcohol use. “And we know that the message that might change behaviors in a cisgender heterosexual man might be different than in a gay White male or a Hispanic bisexual male.”

A 2017 review showed that interventions to reduce behaviors involving UVR exposure, such as indoor tanning, among young cisgender women focused largely on aging and appearance-based concerns. A 2019 study showed that messages focused on avoiding skin cancer may help motivate SM men to reduce tanning behaviors.

Furthermore, said Dr. Mansh, all electronic health record products available in the United States must provide data fields for sexual orientation. “I don’t believe many dermatologists, depending on the setting, collect that information routinely. Integrating sexual orientation and/or gender identity data into patient intake forms so that it can be integrated into the electronic health record is probably very helpful, not only for your clinical practice but also for future research studies.”

Asked to comment on the results, Rebecca I. Hartman, MD, MPH, who was not involved with the study, said that its impact on clinical practice will be challenging to ascertain. She is chief of dermatology with the VA Boston Healthcare System, assistant professor of dermatology at Harvard Medical School, and director of melanoma epidemiology at Brigham and Women’s Hospital, all in Boston, Massachusetts.

“The study found significant adjusted odds ratios,” Dr. Hartman explained, “but for some of the different populations, the overall lifetime rate of skin cancer is still quite low.” For example, 1.0% for SM non-Hispanic Black men or a difference of 2.1% vs 1.8% in SM Hispanic women. “Thus, I am not sure specific screening recommendations are warranted, although some populations, such as Hispanic sexual minority males, seemed to have a much higher risk (3.8-fold on adjusted analysis) that warrants further investigation.”

For now, she advised assessing patients’ risks for skin cancer based on well-established risk factors such as sun exposure/indoor tanning, skin phototype, immunosuppression, and age.

Dr. Mansh reported no relevant conflicts or funding sources for the study. Dr. Hartman reported no relevant conflicts.

A version of this article appeared on Medscape.com.

Lifetime skin cancer prevalence in sexual minority (SM) Americans varied by race, ethnicity, and individual sexual identity, compared with that in heterosexual peers, according to a large cross-sectional study. Addressing dynamics of each SM subgroup will require increasingly tailored prevention, screening, and research efforts, the study authors said.

“We identified specific subgroups within the sexual minority community who are at higher risk for skin cancer, specifically White gay males and Hispanic and non-Hispanic Black SM men and women — particularly individuals who identify as bisexual,” senior author Matthew Mansh, MD, said in an interview. He is an assistant professor of dermatology at the University of California, San Francisco. The study was published online in JAMA Dermatology.

Using data of adults in the US general population from the Behavioral Risk Factor Surveillance System from January 2014 to December 2021, investigators included more than 1.5 million respondents. The proportions of SM women and men (who self-identified as bisexual, lesbian, gay, “something else,” or other) were 2.6% and 2.0%, respectively.

Lifetime skin cancer prevalence was higher among SM men than among heterosexual men (7.4% vs 6.8%; adjusted odds ratio [aOR], 1.16). In analyses stratified by racial and ethnic group, AORs for non-Hispanic Black and Hispanic SM men vs their heterosexual counterparts were 2.18 and 3.81, respectively. The corresponding figures for non-Hispanic Black and Hispanic SM women were 2.33 and 2.46, respectively.

When investigators combined all minority respondents along gender lines, lifetime skin cancer prevalence was higher in bisexual men (aOR, 3.94), bisexual women (aOR, 1.51), and women identifying as something else or other (aOR, 2.70) than in their heterosexual peers.

“I wasn’t expecting that Hispanic or non-Hispanic Black SMs would be at higher risk for skin cancer,” Dr. Mansh said. Even if these groups have more behavioral risk factors for UV radiation (UVR) exposure, he explained, UVR exposure is less strongly linked with skin cancer in darker skin than in lighter skin. Reasons for the counterintuitive finding could include different screening habits among SM people of different racial and ethnic groups, he said, and analyzing such factors will require further research.

Although some effect sizes were modest, the authors wrote, their findings may have important implications for population-based research and public health efforts aimed at early skin cancer detection and prevention. Presently, the United States lacks established guidelines for skin cancer screening. In a 2023 statement published in JAMA, the US Preventive Services Task Force said that there is insufficient evidence to determine the benefit-harm balance of skin cancer screening in asymptomatic people.

“So there has been a lot of recent talk and a need to identify which subset groups of patients might be higher risk for skin cancer and might benefit from more screening,” Dr. Mansh said in an interview. “Understanding more about the high-risk demographic and clinical features that predispose someone to skin cancer helps identify these high-risk populations that could be used to develop better screening guidelines.”

Identifying groups at a higher risk for skin cancer also allows experts to design more targeted counseling or public health interventions focused on these groups, Dr. Mansh added. Absent screening guidelines, experts emphasize changing modifiable risk factors such as UVR exposure, smoking, and alcohol use. “And we know that the message that might change behaviors in a cisgender heterosexual man might be different than in a gay White male or a Hispanic bisexual male.”

A 2017 review showed that interventions to reduce behaviors involving UVR exposure, such as indoor tanning, among young cisgender women focused largely on aging and appearance-based concerns. A 2019 study showed that messages focused on avoiding skin cancer may help motivate SM men to reduce tanning behaviors.

Furthermore, said Dr. Mansh, all electronic health record products available in the United States must provide data fields for sexual orientation. “I don’t believe many dermatologists, depending on the setting, collect that information routinely. Integrating sexual orientation and/or gender identity data into patient intake forms so that it can be integrated into the electronic health record is probably very helpful, not only for your clinical practice but also for future research studies.”

Asked to comment on the results, Rebecca I. Hartman, MD, MPH, who was not involved with the study, said that its impact on clinical practice will be challenging to ascertain. She is chief of dermatology with the VA Boston Healthcare System, assistant professor of dermatology at Harvard Medical School, and director of melanoma epidemiology at Brigham and Women’s Hospital, all in Boston, Massachusetts.

“The study found significant adjusted odds ratios,” Dr. Hartman explained, “but for some of the different populations, the overall lifetime rate of skin cancer is still quite low.” For example, 1.0% for SM non-Hispanic Black men or a difference of 2.1% vs 1.8% in SM Hispanic women. “Thus, I am not sure specific screening recommendations are warranted, although some populations, such as Hispanic sexual minority males, seemed to have a much higher risk (3.8-fold on adjusted analysis) that warrants further investigation.”

For now, she advised assessing patients’ risks for skin cancer based on well-established risk factors such as sun exposure/indoor tanning, skin phototype, immunosuppression, and age.

Dr. Mansh reported no relevant conflicts or funding sources for the study. Dr. Hartman reported no relevant conflicts.

A version of this article appeared on Medscape.com.

Lifetime skin cancer prevalence in sexual minority (SM) Americans varied by race, ethnicity, and individual sexual identity, compared with that in heterosexual peers, according to a large cross-sectional study. Addressing dynamics of each SM subgroup will require increasingly tailored prevention, screening, and research efforts, the study authors said.

“We identified specific subgroups within the sexual minority community who are at higher risk for skin cancer, specifically White gay males and Hispanic and non-Hispanic Black SM men and women — particularly individuals who identify as bisexual,” senior author Matthew Mansh, MD, said in an interview. He is an assistant professor of dermatology at the University of California, San Francisco. The study was published online in JAMA Dermatology.

Using data of adults in the US general population from the Behavioral Risk Factor Surveillance System from January 2014 to December 2021, investigators included more than 1.5 million respondents. The proportions of SM women and men (who self-identified as bisexual, lesbian, gay, “something else,” or other) were 2.6% and 2.0%, respectively.

Lifetime skin cancer prevalence was higher among SM men than among heterosexual men (7.4% vs 6.8%; adjusted odds ratio [aOR], 1.16). In analyses stratified by racial and ethnic group, AORs for non-Hispanic Black and Hispanic SM men vs their heterosexual counterparts were 2.18 and 3.81, respectively. The corresponding figures for non-Hispanic Black and Hispanic SM women were 2.33 and 2.46, respectively.

When investigators combined all minority respondents along gender lines, lifetime skin cancer prevalence was higher in bisexual men (aOR, 3.94), bisexual women (aOR, 1.51), and women identifying as something else or other (aOR, 2.70) than in their heterosexual peers.

“I wasn’t expecting that Hispanic or non-Hispanic Black SMs would be at higher risk for skin cancer,” Dr. Mansh said. Even if these groups have more behavioral risk factors for UV radiation (UVR) exposure, he explained, UVR exposure is less strongly linked with skin cancer in darker skin than in lighter skin. Reasons for the counterintuitive finding could include different screening habits among SM people of different racial and ethnic groups, he said, and analyzing such factors will require further research.

Although some effect sizes were modest, the authors wrote, their findings may have important implications for population-based research and public health efforts aimed at early skin cancer detection and prevention. Presently, the United States lacks established guidelines for skin cancer screening. In a 2023 statement published in JAMA, the US Preventive Services Task Force said that there is insufficient evidence to determine the benefit-harm balance of skin cancer screening in asymptomatic people.

“So there has been a lot of recent talk and a need to identify which subset groups of patients might be higher risk for skin cancer and might benefit from more screening,” Dr. Mansh said in an interview. “Understanding more about the high-risk demographic and clinical features that predispose someone to skin cancer helps identify these high-risk populations that could be used to develop better screening guidelines.”

Identifying groups at a higher risk for skin cancer also allows experts to design more targeted counseling or public health interventions focused on these groups, Dr. Mansh added. Absent screening guidelines, experts emphasize changing modifiable risk factors such as UVR exposure, smoking, and alcohol use. “And we know that the message that might change behaviors in a cisgender heterosexual man might be different than in a gay White male or a Hispanic bisexual male.”

A 2017 review showed that interventions to reduce behaviors involving UVR exposure, such as indoor tanning, among young cisgender women focused largely on aging and appearance-based concerns. A 2019 study showed that messages focused on avoiding skin cancer may help motivate SM men to reduce tanning behaviors.

Furthermore, said Dr. Mansh, all electronic health record products available in the United States must provide data fields for sexual orientation. “I don’t believe many dermatologists, depending on the setting, collect that information routinely. Integrating sexual orientation and/or gender identity data into patient intake forms so that it can be integrated into the electronic health record is probably very helpful, not only for your clinical practice but also for future research studies.”

Asked to comment on the results, Rebecca I. Hartman, MD, MPH, who was not involved with the study, said that its impact on clinical practice will be challenging to ascertain. She is chief of dermatology with the VA Boston Healthcare System, assistant professor of dermatology at Harvard Medical School, and director of melanoma epidemiology at Brigham and Women’s Hospital, all in Boston, Massachusetts.

“The study found significant adjusted odds ratios,” Dr. Hartman explained, “but for some of the different populations, the overall lifetime rate of skin cancer is still quite low.” For example, 1.0% for SM non-Hispanic Black men or a difference of 2.1% vs 1.8% in SM Hispanic women. “Thus, I am not sure specific screening recommendations are warranted, although some populations, such as Hispanic sexual minority males, seemed to have a much higher risk (3.8-fold on adjusted analysis) that warrants further investigation.”

For now, she advised assessing patients’ risks for skin cancer based on well-established risk factors such as sun exposure/indoor tanning, skin phototype, immunosuppression, and age.

Dr. Mansh reported no relevant conflicts or funding sources for the study. Dr. Hartman reported no relevant conflicts.

A version of this article appeared on Medscape.com.

This transcript has been edited for clarity. 

Rachel S. Rubin, MD: I have an interesting topic for you — kind of shocking, actually. Some of you may have read a story earlier this year in The New York Times about the alarming rise among young people of choking or strangulation during sex. I spoke recently with Dr. Debby Herbenick about this concerning and violent trend. Dr. Herbenick is a well-known sexuality researcher and professor at the Indiana University School of Public Health. Welcome, Dr. Herbenick. Can you tell us about your research into this new trend?

Debby Herbenick, PhD: This is some of the most important research that I’ve done. I’ve been studying sexual behaviors and trends for about 14 years in terms of nationally representative studies that we do. Over time, we noticed a trend of increasing prevalence of rough sex practices. 

Now, there’s always been a lot of sexual diversity in the world throughout history. But the main trend that we have focused on in recent years that is important for everyone in medicine to know about is this rapid increase — actually, a really big increase — in what people call “sexual choking,” even though it’s a form of strangulation. The increase is mostly seen in teenagers and young adults. 

We’ve done US nationally representative surveys as well as college campus representative surveys. We find that consistently across four campus representative surveys that 64% of women report having ever been choked during sex, and around 1 in 3 women (aged 18-24 years) throughout the whole country report having been choked during their most recent sexual activity with another person. They call it choking, but because it involves usually one hand — sometimes two hands or a forearm or an object, like a belt or a cord to tie around the neck — it is technically strangulation, because it’s external pressure to the neck to reduce or stop airflow or blood flow. 

Dr. Rubin: These numbers are staggering, right? Everyone listening now is taking care of someone who has been strangled as a form of sexual pleasure. What does this mean from a safety perspective? And as doctors who are working these patients up for migraines and other health problems, what is the research showing? 

Dr. Herbenick: We certainly are seeing people report recurrent headaches and ringing in the ears. There are things we’ve just barely scratched the surface on. Those of us working in this space believe that for anybody coming in for an unexplained stroke (for example, under age 50), you might consider some imaging to see if they have a dissection. We are hearing about people who, when you really probe to find out whether they’ve had pressure on the neck, they report that indeed that they have. So, we have to be thinking about neurologic symptoms. We know that they’re experiencing these at a pretty high rate. 

For people who are engaging in these practices, they should know about the health risks, but we find that most don’t. They may have heard that if it’s really intense high pressure, that in rare cases people can die, but most have never heard of anything in between. So, they’re not necessarily connecting their voice hoarseness, or the recurrent headaches or the sensitivity to light they are having, to an experience of being choked. We need to be paying attention to neurologic symptoms. 

Most physicians I speak with at conferences say that where they feel like they can step into this conversation is through anticipatory guidance and letting their patients know that they may have heard about this trend, and a lot of people are talking about the health consequences, and I want to share some information with you — not coming at it from a place of shame or judgment, but providing some information so that [patients] actually get some medical facts about this that could be lifesaving. 

Dr. Rubin: I see such a big gap in my medical training. I was taught to say, “Hey, do you smoke, do you drink, do you do drugs? Do you have sex? Men, women, or both?”And that’s it. And then maybe use birth control, and don’t get an STD, thinking about herpes, syphilis, gonorrhea, and chlamydia. We weren’t really trained to talk to patients about what kind of sex they are having, or how to talk to patients in a way that is open-minded but also safety-conscious and how the concept of safe sex is more than wear a condom and use birth control.

This idea of rough sex practices and how to talk to teenagers — maybe our pediatricians should be talking about this. Where do we start in terms of how to bring up these conversations and with what level of detail? 

Dr. Herbenick: We find that some young people are already being asked about some of the effects that might be showing on their bodies. It might be that their provider notices some bruising, or marks on their bodies from other types of rough sex practices like hitting and spanking. So that could be an entry point there. Choking is far more prevalent than slapping, so if you’re seeing some marks on the body, then it’s also a good time to ask about other practices they might be engaging in, especially higher risk ones like choking or strangulation. It’s offering some information and even saying, “Look, I’m not here to shame or judge you. I just want you to have some information about this” and giving them an opportunity to ask questions, too. 

We have found that almost nobody talks with their nurse or doctor, even if they have symptoms after being choked or strangled during sex. Just 1% of women with choking-related symptoms, 7% of men, and far fewer trans and nonbinary young people report talking with a nurse or doctor, mostly because they say it doesn’t seem like a big deal. The symptoms got better quickly. Sometimes they’re afraid of being shamed for their sexual behavior, and that’s why they say they don’t talk with somebody. 

They need some type of open-door anticipatory guidance as a way forward. Not everyone is comfortable directly asking whether a patient is engaging in this, but at least letting people know that you’ve heard of this behavior and providing some medical facts can give us a step forward with creating these conversations. 

Dr. Rubin: Can you tell us where is this research going in terms of next steps? Other things that you’re looking at? And what are you excited about? 

Dr. Herbenick: I’m excited about some work I did with a collaborator and colleague of mine, Dr. Keisuke Kawata, that he led a couple of years ago. He’s a neuroscientist. We were looking at potential cumulative effects on the brain. Now we’re taking some of that research into its next steps. We’re also doing more focused studies on other health consequences and hopefully finding out how we can test different educational messages and get people to learn more fact-based information about this, and then see if that is effective in prevention. 

Dr. Rubin: It sounds like a public health campaign is really needed about how to get the word out there about the health consequences of these activities. We’re asking people often enough. In my clinic, I try to keep it open-ended — tell me what sex looks like. What does it look like, and what do you want it to look like? Because I see a lot of people with problems, but if they don’t bring it to me, I don’t necessarily bring it up to them. Until I heard your lecture, and I thought, oh my gosh, I’m not even asking the right questions. Are you hopeful that there will be more public health messaging out there? 

Dr. Herbenick: I am. Years ago, when the child and adolescent choking game became a thing, the Centers for Disease Control and Prevention (CDC) issued reports about it and warnings to parents. And this is a far, far higher prevalence than that ever was. So, I would love to see organizations like the CDC and medical groups getting involved and educating their members and making statements. This is really impacting a huge generation of girls and women, because when it happens during sex between women and men, the choking is mostly happening to the girls and women. It’s also prevalent among sexual minority individuals. But we are talking about this whole generation of young women and what’s happening to their bodies and their brain health. We really need to step into this conversation. 

Dr. Rubin: Very few of us are sexual medicine–trained physicians, and very few of us feel confident and comfortable talking about sexual health issues. But people are getting hurt. People are having real consequences of these behaviors because of our lack of education, knowledge, and even discussion around it. So thank you for doing this research, because had you not done this research, we wouldn’t have found out that 64% of people are engaging in these types of activities. That is not rare.

Dr. Rubin is an assistant clinical professor, Department of Urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.

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

This transcript has been edited for clarity. 

Rachel S. Rubin, MD: I have an interesting topic for you — kind of shocking, actually. Some of you may have read a story earlier this year in The New York Times about the alarming rise among young people of choking or strangulation during sex. I spoke recently with Dr. Debby Herbenick about this concerning and violent trend. Dr. Herbenick is a well-known sexuality researcher and professor at the Indiana University School of Public Health. Welcome, Dr. Herbenick. Can you tell us about your research into this new trend?

Debby Herbenick, PhD: This is some of the most important research that I’ve done. I’ve been studying sexual behaviors and trends for about 14 years in terms of nationally representative studies that we do. Over time, we noticed a trend of increasing prevalence of rough sex practices. 

Now, there’s always been a lot of sexual diversity in the world throughout history. But the main trend that we have focused on in recent years that is important for everyone in medicine to know about is this rapid increase — actually, a really big increase — in what people call “sexual choking,” even though it’s a form of strangulation. The increase is mostly seen in teenagers and young adults. 

We’ve done US nationally representative surveys as well as college campus representative surveys. We find that consistently across four campus representative surveys that 64% of women report having ever been choked during sex, and around 1 in 3 women (aged 18-24 years) throughout the whole country report having been choked during their most recent sexual activity with another person. They call it choking, but because it involves usually one hand — sometimes two hands or a forearm or an object, like a belt or a cord to tie around the neck — it is technically strangulation, because it’s external pressure to the neck to reduce or stop airflow or blood flow. 

Dr. Rubin: These numbers are staggering, right? Everyone listening now is taking care of someone who has been strangled as a form of sexual pleasure. What does this mean from a safety perspective? And as doctors who are working these patients up for migraines and other health problems, what is the research showing? 

Dr. Herbenick: We certainly are seeing people report recurrent headaches and ringing in the ears. There are things we’ve just barely scratched the surface on. Those of us working in this space believe that for anybody coming in for an unexplained stroke (for example, under age 50), you might consider some imaging to see if they have a dissection. We are hearing about people who, when you really probe to find out whether they’ve had pressure on the neck, they report that indeed that they have. So, we have to be thinking about neurologic symptoms. We know that they’re experiencing these at a pretty high rate. 

For people who are engaging in these practices, they should know about the health risks, but we find that most don’t. They may have heard that if it’s really intense high pressure, that in rare cases people can die, but most have never heard of anything in between. So, they’re not necessarily connecting their voice hoarseness, or the recurrent headaches or the sensitivity to light they are having, to an experience of being choked. We need to be paying attention to neurologic symptoms. 

Most physicians I speak with at conferences say that where they feel like they can step into this conversation is through anticipatory guidance and letting their patients know that they may have heard about this trend, and a lot of people are talking about the health consequences, and I want to share some information with you — not coming at it from a place of shame or judgment, but providing some information so that [patients] actually get some medical facts about this that could be lifesaving. 

Dr. Rubin: I see such a big gap in my medical training. I was taught to say, “Hey, do you smoke, do you drink, do you do drugs? Do you have sex? Men, women, or both?”And that’s it. And then maybe use birth control, and don’t get an STD, thinking about herpes, syphilis, gonorrhea, and chlamydia. We weren’t really trained to talk to patients about what kind of sex they are having, or how to talk to patients in a way that is open-minded but also safety-conscious and how the concept of safe sex is more than wear a condom and use birth control.

This idea of rough sex practices and how to talk to teenagers — maybe our pediatricians should be talking about this. Where do we start in terms of how to bring up these conversations and with what level of detail? 

Dr. Herbenick: We find that some young people are already being asked about some of the effects that might be showing on their bodies. It might be that their provider notices some bruising, or marks on their bodies from other types of rough sex practices like hitting and spanking. So that could be an entry point there. Choking is far more prevalent than slapping, so if you’re seeing some marks on the body, then it’s also a good time to ask about other practices they might be engaging in, especially higher risk ones like choking or strangulation. It’s offering some information and even saying, “Look, I’m not here to shame or judge you. I just want you to have some information about this” and giving them an opportunity to ask questions, too. 

We have found that almost nobody talks with their nurse or doctor, even if they have symptoms after being choked or strangled during sex. Just 1% of women with choking-related symptoms, 7% of men, and far fewer trans and nonbinary young people report talking with a nurse or doctor, mostly because they say it doesn’t seem like a big deal. The symptoms got better quickly. Sometimes they’re afraid of being shamed for their sexual behavior, and that’s why they say they don’t talk with somebody. 

They need some type of open-door anticipatory guidance as a way forward. Not everyone is comfortable directly asking whether a patient is engaging in this, but at least letting people know that you’ve heard of this behavior and providing some medical facts can give us a step forward with creating these conversations. 

Dr. Rubin: Can you tell us where is this research going in terms of next steps? Other things that you’re looking at? And what are you excited about? 

Dr. Herbenick: I’m excited about some work I did with a collaborator and colleague of mine, Dr. Keisuke Kawata, that he led a couple of years ago. He’s a neuroscientist. We were looking at potential cumulative effects on the brain. Now we’re taking some of that research into its next steps. We’re also doing more focused studies on other health consequences and hopefully finding out how we can test different educational messages and get people to learn more fact-based information about this, and then see if that is effective in prevention. 

Dr. Rubin: It sounds like a public health campaign is really needed about how to get the word out there about the health consequences of these activities. We’re asking people often enough. In my clinic, I try to keep it open-ended — tell me what sex looks like. What does it look like, and what do you want it to look like? Because I see a lot of people with problems, but if they don’t bring it to me, I don’t necessarily bring it up to them. Until I heard your lecture, and I thought, oh my gosh, I’m not even asking the right questions. Are you hopeful that there will be more public health messaging out there? 

Dr. Herbenick: I am. Years ago, when the child and adolescent choking game became a thing, the Centers for Disease Control and Prevention (CDC) issued reports about it and warnings to parents. And this is a far, far higher prevalence than that ever was. So, I would love to see organizations like the CDC and medical groups getting involved and educating their members and making statements. This is really impacting a huge generation of girls and women, because when it happens during sex between women and men, the choking is mostly happening to the girls and women. It’s also prevalent among sexual minority individuals. But we are talking about this whole generation of young women and what’s happening to their bodies and their brain health. We really need to step into this conversation. 

Dr. Rubin: Very few of us are sexual medicine–trained physicians, and very few of us feel confident and comfortable talking about sexual health issues. But people are getting hurt. People are having real consequences of these behaviors because of our lack of education, knowledge, and even discussion around it. So thank you for doing this research, because had you not done this research, we wouldn’t have found out that 64% of people are engaging in these types of activities. That is not rare.

Dr. Rubin is an assistant clinical professor, Department of Urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.

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

This transcript has been edited for clarity. 

Rachel S. Rubin, MD: I have an interesting topic for you — kind of shocking, actually. Some of you may have read a story earlier this year in The New York Times about the alarming rise among young people of choking or strangulation during sex. I spoke recently with Dr. Debby Herbenick about this concerning and violent trend. Dr. Herbenick is a well-known sexuality researcher and professor at the Indiana University School of Public Health. Welcome, Dr. Herbenick. Can you tell us about your research into this new trend?

Debby Herbenick, PhD: This is some of the most important research that I’ve done. I’ve been studying sexual behaviors and trends for about 14 years in terms of nationally representative studies that we do. Over time, we noticed a trend of increasing prevalence of rough sex practices. 

Now, there’s always been a lot of sexual diversity in the world throughout history. But the main trend that we have focused on in recent years that is important for everyone in medicine to know about is this rapid increase — actually, a really big increase — in what people call “sexual choking,” even though it’s a form of strangulation. The increase is mostly seen in teenagers and young adults. 

We’ve done US nationally representative surveys as well as college campus representative surveys. We find that consistently across four campus representative surveys that 64% of women report having ever been choked during sex, and around 1 in 3 women (aged 18-24 years) throughout the whole country report having been choked during their most recent sexual activity with another person. They call it choking, but because it involves usually one hand — sometimes two hands or a forearm or an object, like a belt or a cord to tie around the neck — it is technically strangulation, because it’s external pressure to the neck to reduce or stop airflow or blood flow. 

Dr. Rubin: These numbers are staggering, right? Everyone listening now is taking care of someone who has been strangled as a form of sexual pleasure. What does this mean from a safety perspective? And as doctors who are working these patients up for migraines and other health problems, what is the research showing? 

Dr. Herbenick: We certainly are seeing people report recurrent headaches and ringing in the ears. There are things we’ve just barely scratched the surface on. Those of us working in this space believe that for anybody coming in for an unexplained stroke (for example, under age 50), you might consider some imaging to see if they have a dissection. We are hearing about people who, when you really probe to find out whether they’ve had pressure on the neck, they report that indeed that they have. So, we have to be thinking about neurologic symptoms. We know that they’re experiencing these at a pretty high rate. 

For people who are engaging in these practices, they should know about the health risks, but we find that most don’t. They may have heard that if it’s really intense high pressure, that in rare cases people can die, but most have never heard of anything in between. So, they’re not necessarily connecting their voice hoarseness, or the recurrent headaches or the sensitivity to light they are having, to an experience of being choked. We need to be paying attention to neurologic symptoms. 

Most physicians I speak with at conferences say that where they feel like they can step into this conversation is through anticipatory guidance and letting their patients know that they may have heard about this trend, and a lot of people are talking about the health consequences, and I want to share some information with you — not coming at it from a place of shame or judgment, but providing some information so that [patients] actually get some medical facts about this that could be lifesaving. 

Dr. Rubin: I see such a big gap in my medical training. I was taught to say, “Hey, do you smoke, do you drink, do you do drugs? Do you have sex? Men, women, or both?”And that’s it. And then maybe use birth control, and don’t get an STD, thinking about herpes, syphilis, gonorrhea, and chlamydia. We weren’t really trained to talk to patients about what kind of sex they are having, or how to talk to patients in a way that is open-minded but also safety-conscious and how the concept of safe sex is more than wear a condom and use birth control.

This idea of rough sex practices and how to talk to teenagers — maybe our pediatricians should be talking about this. Where do we start in terms of how to bring up these conversations and with what level of detail? 

Dr. Herbenick: We find that some young people are already being asked about some of the effects that might be showing on their bodies. It might be that their provider notices some bruising, or marks on their bodies from other types of rough sex practices like hitting and spanking. So that could be an entry point there. Choking is far more prevalent than slapping, so if you’re seeing some marks on the body, then it’s also a good time to ask about other practices they might be engaging in, especially higher risk ones like choking or strangulation. It’s offering some information and even saying, “Look, I’m not here to shame or judge you. I just want you to have some information about this” and giving them an opportunity to ask questions, too. 

We have found that almost nobody talks with their nurse or doctor, even if they have symptoms after being choked or strangled during sex. Just 1% of women with choking-related symptoms, 7% of men, and far fewer trans and nonbinary young people report talking with a nurse or doctor, mostly because they say it doesn’t seem like a big deal. The symptoms got better quickly. Sometimes they’re afraid of being shamed for their sexual behavior, and that’s why they say they don’t talk with somebody. 

They need some type of open-door anticipatory guidance as a way forward. Not everyone is comfortable directly asking whether a patient is engaging in this, but at least letting people know that you’ve heard of this behavior and providing some medical facts can give us a step forward with creating these conversations. 

Dr. Rubin: Can you tell us where is this research going in terms of next steps? Other things that you’re looking at? And what are you excited about? 

Dr. Herbenick: I’m excited about some work I did with a collaborator and colleague of mine, Dr. Keisuke Kawata, that he led a couple of years ago. He’s a neuroscientist. We were looking at potential cumulative effects on the brain. Now we’re taking some of that research into its next steps. We’re also doing more focused studies on other health consequences and hopefully finding out how we can test different educational messages and get people to learn more fact-based information about this, and then see if that is effective in prevention. 

Dr. Rubin: It sounds like a public health campaign is really needed about how to get the word out there about the health consequences of these activities. We’re asking people often enough. In my clinic, I try to keep it open-ended — tell me what sex looks like. What does it look like, and what do you want it to look like? Because I see a lot of people with problems, but if they don’t bring it to me, I don’t necessarily bring it up to them. Until I heard your lecture, and I thought, oh my gosh, I’m not even asking the right questions. Are you hopeful that there will be more public health messaging out there? 

Dr. Herbenick: I am. Years ago, when the child and adolescent choking game became a thing, the Centers for Disease Control and Prevention (CDC) issued reports about it and warnings to parents. And this is a far, far higher prevalence than that ever was. So, I would love to see organizations like the CDC and medical groups getting involved and educating their members and making statements. This is really impacting a huge generation of girls and women, because when it happens during sex between women and men, the choking is mostly happening to the girls and women. It’s also prevalent among sexual minority individuals. But we are talking about this whole generation of young women and what’s happening to their bodies and their brain health. We really need to step into this conversation. 

Dr. Rubin: Very few of us are sexual medicine–trained physicians, and very few of us feel confident and comfortable talking about sexual health issues. But people are getting hurt. People are having real consequences of these behaviors because of our lack of education, knowledge, and even discussion around it. So thank you for doing this research, because had you not done this research, we wouldn’t have found out that 64% of people are engaging in these types of activities. That is not rare.

Dr. Rubin is an assistant clinical professor, Department of Urology, at Georgetown University, Washington. She reported conflicts of interest with Sprout, Maternal Medical, Absorption Pharmaceuticals, GSK, and Endo.

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

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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

This transcript has been edited for clarity.

On today’s edition of Beyond BMI, I’ll be discussing weight plateaus. This is something that our patients are very familiar with. Sometimes, they’re happy with their weight when they plateau; sometimes, they’re not. A weight plateau is simply a state of equilibrium.

There’s a common adage that the last 5 pounds are the hardest. When people decrease their calorie intake and increase their activity — as we instruct our patients to do to lose weight — the body starts to fight back because it believes this is a famine state. Our bodies feel that we are running around the jungle looking for food to help us survive a perceived famine state.

The body does a few things to help us keep weight on, and this is what leads to the frustration of not being able to lose those last 5 pounds. The first thing that happens in this process, which is called metabolic adaptation, is that when someone loses weight, the body naturally increases appetite signals from the brain, so the person becomes hungrier. Satiety signals from the stomach also decrease, so they feel more hungry and less full. And finally, stable fat cells form to allow the person to seek out more food without losing weight. This eventually leads the patient to regain weight, or they may plateau at a weight they’re not happy with.

I’m sure you’ve seen many studies looking at weight plateaus and the amount of weight loss people are able to achieve with diet, exercise, and behavior change alone vs the same lifestyle modifications plus medication. Studies show that patients who are taking anti-obesity medications achieve far more weight loss than do those who are not taking medications. The reason is related to the different mechanisms of action of the anti-obesity medications. Patients taking these medications are able to tolerate a lower caloric intake for a longer period of time, thus they’re able to burn more fat cells and lose more weight. Some medications perform this by decreasing appetite signals, so patients can continue to eat a small number of calories. Some medications affect the stability of fat cells. Some medications also increase satiety signals, so patients can move beyond that degree of metabolic adaptation and get beyond their previous plateau.

What can we do for patients who are frustrated with their weight plateau? I recommend taking a dive into their daily routine. Find out how many calories they are eating. Find out how much exercise they are doing and see whether there’s any room to reorganize the day or change their meals to create a caloric deficit. Are they eating things that are not filling enough, so they can’t get to the next meal without having a snack in between? We are looking at the quality of the meals as well and making sure there’s an adequate amount of protein and fiber in their meals to help with those increased appetite signals. We should also make sure these patients are getting adequate fluid intake.

These are all strategies that can help our patients try to get beyond their weight plateaus.

If the patient meets criteria for anti-obesity medication, which means a body mass index (BMI) of 27-29 with a weight-related comorbidity or BMI ≥ 30 with or without a comorbidity, you may want to consider anti-obesity medication to help that patient get beyond the plateau.

Plateaus will occur as a natural process because of the appetite signaling and hormonal changes that occur when patients lose weight from any modality. It’s important that we work with our patients to determine whether their weight plateau is due to metabolic adaptation. If they aren’t meeting their goals and they have weight-related comorbidities, we can use other available modalities to help those patients continue to lose weight. Of course, whenever we are prescribing a medication, we need to make sure that it is safe for the patient and the patient is on board with the potential side effects and risks. And we should always make sure our patients know we are their advocates in their weight journey.

Holly Lofton, clinical associate professor of surgery and medicine, NYU Langone Health, New York, NY, has disclosed no relevant financial relationships.

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