Article

Key clinical point: Dupilumab demonstrated sustained clinical benefits and an acceptable long-term safety profile in children age 6 months to 5 years with uncontrolled moderate to severe atopic dermatitis (AD).

Major finding: At week 52, 36.2% of patients achieved an Investigator’s Global Assessment score of 0 or 1, and 96.6%, 79.3%, and 58.6% of patients achieved at least a 50%, 75%, and 90% improvement in the Eczema Area and Severity Index score, respectively. Overall, 78.2% of patients reported one or more treatment-emergent adverse events, most of mild or moderate severity.

Study details: Findings are from the phase 3 LIBERTY AD PED-OLE study that included 142 children with moderate to severe AD who had previously participated in the LIBERTY AD PRESCHOOL part B study and received a weight-tiered dose of 200 mg or 300 mg of subcutaneous dupilumab every 4 weeks.

Disclosures: The study was funded by Sanofi and Regeneron Pharmaceuticals Inc. Five authors declared being employees of or holding stocks or stock options in Sanofi or Regeneron. The other authors declared having ties with various sources, including Sanofi and Regeneron.

Source: Paller AS, Siegfried EC, Simpson EL, et al. Dupilumab safety and efficacy up to 1 year in children aged 6 months to 5 years with atopic dermatitis: Results from a phase 3 open-label extension study. Am J Clin Dermatol. 2024 (May 14). doi: 10.1007/s40257-024-00859-y Source

Key clinical point: Dupilumab demonstrated sustained clinical benefits and an acceptable long-term safety profile in children age 6 months to 5 years with uncontrolled moderate to severe atopic dermatitis (AD).

Major finding: At week 52, 36.2% of patients achieved an Investigator’s Global Assessment score of 0 or 1, and 96.6%, 79.3%, and 58.6% of patients achieved at least a 50%, 75%, and 90% improvement in the Eczema Area and Severity Index score, respectively. Overall, 78.2% of patients reported one or more treatment-emergent adverse events, most of mild or moderate severity.

Study details: Findings are from the phase 3 LIBERTY AD PED-OLE study that included 142 children with moderate to severe AD who had previously participated in the LIBERTY AD PRESCHOOL part B study and received a weight-tiered dose of 200 mg or 300 mg of subcutaneous dupilumab every 4 weeks.

Disclosures: The study was funded by Sanofi and Regeneron Pharmaceuticals Inc. Five authors declared being employees of or holding stocks or stock options in Sanofi or Regeneron. The other authors declared having ties with various sources, including Sanofi and Regeneron.

Source: Paller AS, Siegfried EC, Simpson EL, et al. Dupilumab safety and efficacy up to 1 year in children aged 6 months to 5 years with atopic dermatitis: Results from a phase 3 open-label extension study. Am J Clin Dermatol. 2024 (May 14). doi: 10.1007/s40257-024-00859-y Source

Key clinical point: Dupilumab demonstrated sustained clinical benefits and an acceptable long-term safety profile in children age 6 months to 5 years with uncontrolled moderate to severe atopic dermatitis (AD).

Major finding: At week 52, 36.2% of patients achieved an Investigator’s Global Assessment score of 0 or 1, and 96.6%, 79.3%, and 58.6% of patients achieved at least a 50%, 75%, and 90% improvement in the Eczema Area and Severity Index score, respectively. Overall, 78.2% of patients reported one or more treatment-emergent adverse events, most of mild or moderate severity.

Study details: Findings are from the phase 3 LIBERTY AD PED-OLE study that included 142 children with moderate to severe AD who had previously participated in the LIBERTY AD PRESCHOOL part B study and received a weight-tiered dose of 200 mg or 300 mg of subcutaneous dupilumab every 4 weeks.

Disclosures: The study was funded by Sanofi and Regeneron Pharmaceuticals Inc. Five authors declared being employees of or holding stocks or stock options in Sanofi or Regeneron. The other authors declared having ties with various sources, including Sanofi and Regeneron.

Source: Paller AS, Siegfried EC, Simpson EL, et al. Dupilumab safety and efficacy up to 1 year in children aged 6 months to 5 years with atopic dermatitis: Results from a phase 3 open-label extension study. Am J Clin Dermatol. 2024 (May 14). doi: 10.1007/s40257-024-00859-y Source

Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.

Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).

Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.

Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.

Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source

Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.

Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).

Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.

Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.

Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source

Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.

Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).

Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.

Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.

Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source

Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.

Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).

Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.

Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.

Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source

Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.

Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).

Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.

Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.

Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source

Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.

Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).

Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.

Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.

Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

A hot topic of PsA research is whether treating psoriasis patients with biologics reduces the risk of developing PsA. Floris and colleagues analyzed data from 1023 patients with psoriasis aged 18 years or older, of whom 29.6% received biologics at least once and 21.0% had PsA. They observed that patients treated at least once vs never treated with biologics had a significantly lower risk for PsA. The "protective" effect of biologics against PsA persisted irrespective of the class of biologic used. However, the study has many built-in biases; it was not a prospective study of psoriasis patients without PsA, but rather a retrospective analysis of data collected at enrollment. Nevertheless, effective psoriasis therapies may indeed reduce the risk for PsA; prospective interventional studies are required and are currently underway.

Development of radiographic damage indicates severe PsA and affects quality of life and physical function. Identifying patients at risk for joint damage may help treatment stratification. Using data from a real-world cohort of 476 patients with early PsA, of whom 14% demonstrated progressive radiographic damage, Koc and colleagues found that female sex was a protective factor whereas old age and initial radiographic damage were risk factors for radiographic progression. These results are consistent with previous studies. Male sex, older age, and presence of radiographic damage at first visit should prompt more aggressive management to prevent further joint damage.

Regarding newer treatments, Gossec and colleagues demonstrated that bimekizumab, a monoclonal antibody targeting both interleukin (IL)-17A and IL-17F, improved disease effects in a rapid and sustained manner in patients with PsA who had not used biologic disease-modifying antirheumatic drugs or had prior inadequate response to tumor necrosis factor inhibitors. Bimekizumab is a welcome addition to the drugs available to manage PsA. Its comparative efficacy against other targeted therapies, especially other IL-17 inhibitors, is yet to be determined.

Finally, a study from the Greek multicenter PsA registry by Vassilakis and colleagues showed that, of 467 patients with PsA, 16.5% had D2T PsA. Compared with non–D2T patients, those with D2T disease were more likely to have extensive psoriasis at diagnosis, higher body mass index, and a history of inflammatory bowel disease (IBD). Treatment-resistant disease is increasingly prevalent in PsA. Certain diseases and comorbidities, such as IBD and obesity, are associated with D2T PsA. A uniform definition of D2T PsA and prospective studies to identify risk factors, as well as new strategies to manage D2T PsA, are required.

Not too long ago, prostate-cancer genetics didn’t mean much to patient care. But in recent years, the landscape of therapy has transformed as researchers have discovered links between multiple genes and aggressive tumors. 

Now, as a hematologist-oncologist explained to attendees at an Association of VA Hematology/Oncology regional meeting in Detroit, genetic tests can guide treatment for some—but not all—men with prostate cancer.

For patients with mutations, appropriate supplemental medications “can improve overall outcomes and have a long-standing impact on patients” said Scott J. Dawsey, MD, of the John D. Dingell Veterans Affairs Medical Center in Detroit in an interview following the AVAHO meeting, which focused on the management of prostate cancer.

As Dawsey explained, about 10% of patients with prostate cancer appear to have genetic mutations, although the exact percentage is unclear. The mutations are especially common in metastatic forms of prostate cancer. They’re estimated to be present in 11.8%-16.2% of those cases.

While these proportions are relatively small, the number of overall prostate-cancer cases with mutations is large due to the high burden of the disease, Dawsey said. Prostate cancer is by far the most common cancer in men, and estimated 299,010 cases will be diagnosed in the United States this year.

According to Dawsey, genetic mutations seem to boost the risk of more aggressive disease—and the risk of other malignancies—by disrupting DNA repair. This process can lead to even more mutations that may “make the cancer behave and grow more aggressively.”

But not all prostate cancer patients need to undergo genetic testing. Dawsey urged colleagues to figure out which patients should be tested by consulting National Comprehensive Cancer Network (NCCN) guidelines and the newly updated US Department of Veterans Affairs (VA) prostate cancer clinical pathway.

The two sets of recommendations agree on germline testing in patients with cases that are metastatic, very high risk, and high risk. Lower-risk cases should only be tested if patients meet family history criteria. The sets of guidelines also recommend somatic testing in patients with metastatic cancer.

In addition to providing guidance about treatment, genetic test results can have implications regarding other potential malignancies that may affect patients, Dawsey said. The results may also have implications for cancer risk in family members.

Several drugs are now available for patients with genetic mutations, including checkpoint inhibitors and PARP inhibitors. The drugs, which have unique mechanisms of action, are given in addition to standard prostate cancer treatments, he said.

“If a patient doesn’t have one of these genetic changes,” he said, “these drugs aren’t an option.”

A long list of drugs or combinations of drugs are in clinical trials, including the poly(adenosine diphosphate–ribose) polymerase (PARP) inhibitors olaparib, abiraterone, and niraparib and the checkpoint inhibitors nivolumab and cemiplimab.

The drugs generally improve response rates and progression-free survival, Dawsey said, and patients are generally able to tolerate them. In regard to which drugs to choose, he suggested consulting the and NCCN guidelines and the VA oncology clinical pathway for prostate cancer.

Not too long ago, prostate-cancer genetics didn’t mean much to patient care. But in recent years, the landscape of therapy has transformed as researchers have discovered links between multiple genes and aggressive tumors. 

Now, as a hematologist-oncologist explained to attendees at an Association of VA Hematology/Oncology regional meeting in Detroit, genetic tests can guide treatment for some—but not all—men with prostate cancer.

For patients with mutations, appropriate supplemental medications “can improve overall outcomes and have a long-standing impact on patients” said Scott J. Dawsey, MD, of the John D. Dingell Veterans Affairs Medical Center in Detroit in an interview following the AVAHO meeting, which focused on the management of prostate cancer.

As Dawsey explained, about 10% of patients with prostate cancer appear to have genetic mutations, although the exact percentage is unclear. The mutations are especially common in metastatic forms of prostate cancer. They’re estimated to be present in 11.8%-16.2% of those cases.

While these proportions are relatively small, the number of overall prostate-cancer cases with mutations is large due to the high burden of the disease, Dawsey said. Prostate cancer is by far the most common cancer in men, and estimated 299,010 cases will be diagnosed in the United States this year.

According to Dawsey, genetic mutations seem to boost the risk of more aggressive disease—and the risk of other malignancies—by disrupting DNA repair. This process can lead to even more mutations that may “make the cancer behave and grow more aggressively.”

But not all prostate cancer patients need to undergo genetic testing. Dawsey urged colleagues to figure out which patients should be tested by consulting National Comprehensive Cancer Network (NCCN) guidelines and the newly updated US Department of Veterans Affairs (VA) prostate cancer clinical pathway.

The two sets of recommendations agree on germline testing in patients with cases that are metastatic, very high risk, and high risk. Lower-risk cases should only be tested if patients meet family history criteria. The sets of guidelines also recommend somatic testing in patients with metastatic cancer.

In addition to providing guidance about treatment, genetic test results can have implications regarding other potential malignancies that may affect patients, Dawsey said. The results may also have implications for cancer risk in family members.

Several drugs are now available for patients with genetic mutations, including checkpoint inhibitors and PARP inhibitors. The drugs, which have unique mechanisms of action, are given in addition to standard prostate cancer treatments, he said.

“If a patient doesn’t have one of these genetic changes,” he said, “these drugs aren’t an option.”

A long list of drugs or combinations of drugs are in clinical trials, including the poly(adenosine diphosphate–ribose) polymerase (PARP) inhibitors olaparib, abiraterone, and niraparib and the checkpoint inhibitors nivolumab and cemiplimab.

The drugs generally improve response rates and progression-free survival, Dawsey said, and patients are generally able to tolerate them. In regard to which drugs to choose, he suggested consulting the and NCCN guidelines and the VA oncology clinical pathway for prostate cancer.

Not too long ago, prostate-cancer genetics didn’t mean much to patient care. But in recent years, the landscape of therapy has transformed as researchers have discovered links between multiple genes and aggressive tumors. 

Now, as a hematologist-oncologist explained to attendees at an Association of VA Hematology/Oncology regional meeting in Detroit, genetic tests can guide treatment for some—but not all—men with prostate cancer.

For patients with mutations, appropriate supplemental medications “can improve overall outcomes and have a long-standing impact on patients” said Scott J. Dawsey, MD, of the John D. Dingell Veterans Affairs Medical Center in Detroit in an interview following the AVAHO meeting, which focused on the management of prostate cancer.

As Dawsey explained, about 10% of patients with prostate cancer appear to have genetic mutations, although the exact percentage is unclear. The mutations are especially common in metastatic forms of prostate cancer. They’re estimated to be present in 11.8%-16.2% of those cases.

While these proportions are relatively small, the number of overall prostate-cancer cases with mutations is large due to the high burden of the disease, Dawsey said. Prostate cancer is by far the most common cancer in men, and estimated 299,010 cases will be diagnosed in the United States this year.

According to Dawsey, genetic mutations seem to boost the risk of more aggressive disease—and the risk of other malignancies—by disrupting DNA repair. This process can lead to even more mutations that may “make the cancer behave and grow more aggressively.”

But not all prostate cancer patients need to undergo genetic testing. Dawsey urged colleagues to figure out which patients should be tested by consulting National Comprehensive Cancer Network (NCCN) guidelines and the newly updated US Department of Veterans Affairs (VA) prostate cancer clinical pathway.

The two sets of recommendations agree on germline testing in patients with cases that are metastatic, very high risk, and high risk. Lower-risk cases should only be tested if patients meet family history criteria. The sets of guidelines also recommend somatic testing in patients with metastatic cancer.

In addition to providing guidance about treatment, genetic test results can have implications regarding other potential malignancies that may affect patients, Dawsey said. The results may also have implications for cancer risk in family members.

Several drugs are now available for patients with genetic mutations, including checkpoint inhibitors and PARP inhibitors. The drugs, which have unique mechanisms of action, are given in addition to standard prostate cancer treatments, he said.

“If a patient doesn’t have one of these genetic changes,” he said, “these drugs aren’t an option.”

A long list of drugs or combinations of drugs are in clinical trials, including the poly(adenosine diphosphate–ribose) polymerase (PARP) inhibitors olaparib, abiraterone, and niraparib and the checkpoint inhibitors nivolumab and cemiplimab.

The drugs generally improve response rates and progression-free survival, Dawsey said, and patients are generally able to tolerate them. In regard to which drugs to choose, he suggested consulting the and NCCN guidelines and the VA oncology clinical pathway for prostate cancer.

To the Editor:

Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.^1-5

Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York^3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.⁷ Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.⁸ We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.

An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A_1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.

Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.

To the Editor:

Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.^1-5

Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York^3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.⁷ Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.⁸ We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.

An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A_1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.

Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.

To the Editor:

Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.^1-5

Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York^3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.⁷ Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.⁸ We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.

An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A_1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.

Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.

Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. ^1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.

Creating Effective Teaching and Learning Experiences

Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.³ By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning ­objectives depending on the cognitive process being tested (Table 2).⁴

Creating a Safe Educational Environment

Psychological safety is the belief that a learning environment is a safe place in which to take risks.⁵ A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.⁶ The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—­display discomfort and debrief—are responses that may be ­utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.

Teaching in the Clinic and Hospital

There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.^3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.³

Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.^3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.³

Modeling involves describing a thought process out loud for a learner^3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.

Effectively Integrating Visual Media and Presentations

Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.^3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.³

Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.³

Final Thoughts

There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.

Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. ^1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.

Creating Effective Teaching and Learning Experiences

Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.³ By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning ­objectives depending on the cognitive process being tested (Table 2).⁴

Creating a Safe Educational Environment

Psychological safety is the belief that a learning environment is a safe place in which to take risks.⁵ A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.⁶ The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—­display discomfort and debrief—are responses that may be ­utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.

Teaching in the Clinic and Hospital

There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.^3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.³

Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.^3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.³

Modeling involves describing a thought process out loud for a learner^3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.

Effectively Integrating Visual Media and Presentations

Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.^3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.³

Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.³

Final Thoughts

There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.

Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. ^1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.

Creating Effective Teaching and Learning Experiences

Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.³ By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning ­objectives depending on the cognitive process being tested (Table 2).⁴

Creating a Safe Educational Environment

Psychological safety is the belief that a learning environment is a safe place in which to take risks.⁵ A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.⁶ The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—­display discomfort and debrief—are responses that may be ­utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.

Teaching in the Clinic and Hospital

There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.^3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.³

Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.^3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.³

Modeling involves describing a thought process out loud for a learner^3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.

Effectively Integrating Visual Media and Presentations

Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.^3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.³

Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.³

Final Thoughts

There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.

Data have shown that CD20-expressing B cells are crucial to the pathogenesis of multiple sclerosis (MS). First approved by the US Food and Drug Administration for MS in 2017, anti-CD20 monoclonal antibody therapies including ocrelizumab, ofatumumab, and ublituximab have proven effective at controlling the symptoms of relapsing-remitting MS (RRMS).

In this ReCAP, Dr Fred D. Lublin, of the Mount Sinai School of Medicine, discusses recent data on anti-CD20 agents for RRMS, including results presented at the 2024 meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

He discusses a protocol examining the effect on RRMS of extending dosage intervals or stopping anti-CD20 therapy after 1 or 2 years of treatment based on results suggesting that the B cells that return post depletion are predominantly regulatory rather than pathogenic.

Next, Dr Lublin discusses a paper presented at CMSC on risks for serious infections in individuals taking ocrelizumab or ofatumumab. Major predictors were found to be progressive disease, prior use of a disease-modifying therapy, and longer duration of therapy.

Finally, he considers recent studies comparing rituximab, an anti-CD20 therapy not approved for MS in the United States but commonly used off-label internationally, with more recent therapies such as ocrelizumab. Data currently indicate that an increased risk for infections are associated with rituximab vs ocrelizumab, but further research is under way.

--

Fred D. Lublin, MD, Director, The Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY

Fred D. Lublin, MD, has disclosed the following relevant financial relationships:

Sources of Funding for Research: Novartis; Biogen; Sanofi; NMSS; NIH; Brainstorm Cell Therapeutics

Consulting Agreements/Advisory Boards/DSMB: Biogen; EMD Serono; Novartis; Actelion/Janssen; Sanofi/Genzyme; Roche/Genentech; Horizon Therapeutics/Amgen; Bristol Myers Squibb; Mapi Pharma; Brainstorm Cell Therapeutics; Mylan/Viatris; Immunic; Avotres; Neurogene; LabCorp; Entelexo Biotherapeutics; Neuralight; SetPoint Medical; Hexal/Sandoz; Baim Institute; Sudo Biosciences; Lapix Therapeutics; Biohaven Pharmaceuticals; Abata Therapeutics; Cognito Therapeutics; ImmPACT Bio

Speaker: Sanofi

Stock Options: Avotres; Neuralight; Lapix Therapeutics; Entelexo

I may discuss unapproved agents that are in the MS developmental pipeline without any recommendation on their use.

Data have shown that CD20-expressing B cells are crucial to the pathogenesis of multiple sclerosis (MS). First approved by the US Food and Drug Administration for MS in 2017, anti-CD20 monoclonal antibody therapies including ocrelizumab, ofatumumab, and ublituximab have proven effective at controlling the symptoms of relapsing-remitting MS (RRMS).

In this ReCAP, Dr Fred D. Lublin, of the Mount Sinai School of Medicine, discusses recent data on anti-CD20 agents for RRMS, including results presented at the 2024 meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

He discusses a protocol examining the effect on RRMS of extending dosage intervals or stopping anti-CD20 therapy after 1 or 2 years of treatment based on results suggesting that the B cells that return post depletion are predominantly regulatory rather than pathogenic.

Next, Dr Lublin discusses a paper presented at CMSC on risks for serious infections in individuals taking ocrelizumab or ofatumumab. Major predictors were found to be progressive disease, prior use of a disease-modifying therapy, and longer duration of therapy.

Finally, he considers recent studies comparing rituximab, an anti-CD20 therapy not approved for MS in the United States but commonly used off-label internationally, with more recent therapies such as ocrelizumab. Data currently indicate that an increased risk for infections are associated with rituximab vs ocrelizumab, but further research is under way.

--

Fred D. Lublin, MD, Director, The Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY

Fred D. Lublin, MD, has disclosed the following relevant financial relationships:

Sources of Funding for Research: Novartis; Biogen; Sanofi; NMSS; NIH; Brainstorm Cell Therapeutics

Consulting Agreements/Advisory Boards/DSMB: Biogen; EMD Serono; Novartis; Actelion/Janssen; Sanofi/Genzyme; Roche/Genentech; Horizon Therapeutics/Amgen; Bristol Myers Squibb; Mapi Pharma; Brainstorm Cell Therapeutics; Mylan/Viatris; Immunic; Avotres; Neurogene; LabCorp; Entelexo Biotherapeutics; Neuralight; SetPoint Medical; Hexal/Sandoz; Baim Institute; Sudo Biosciences; Lapix Therapeutics; Biohaven Pharmaceuticals; Abata Therapeutics; Cognito Therapeutics; ImmPACT Bio

Speaker: Sanofi

Stock Options: Avotres; Neuralight; Lapix Therapeutics; Entelexo

I may discuss unapproved agents that are in the MS developmental pipeline without any recommendation on their use.

Data have shown that CD20-expressing B cells are crucial to the pathogenesis of multiple sclerosis (MS). First approved by the US Food and Drug Administration for MS in 2017, anti-CD20 monoclonal antibody therapies including ocrelizumab, ofatumumab, and ublituximab have proven effective at controlling the symptoms of relapsing-remitting MS (RRMS).

In this ReCAP, Dr Fred D. Lublin, of the Mount Sinai School of Medicine, discusses recent data on anti-CD20 agents for RRMS, including results presented at the 2024 meeting of the Consortium of Multiple Sclerosis Centers (CMSC).

He discusses a protocol examining the effect on RRMS of extending dosage intervals or stopping anti-CD20 therapy after 1 or 2 years of treatment based on results suggesting that the B cells that return post depletion are predominantly regulatory rather than pathogenic.

Next, Dr Lublin discusses a paper presented at CMSC on risks for serious infections in individuals taking ocrelizumab or ofatumumab. Major predictors were found to be progressive disease, prior use of a disease-modifying therapy, and longer duration of therapy.

Finally, he considers recent studies comparing rituximab, an anti-CD20 therapy not approved for MS in the United States but commonly used off-label internationally, with more recent therapies such as ocrelizumab. Data currently indicate that an increased risk for infections are associated with rituximab vs ocrelizumab, but further research is under way.

--

Fred D. Lublin, MD, Director, The Corinne Goldsmith Dickinson Center for Multiple Sclerosis, Icahn School of Medicine at Mount Sinai, New York, NY

Fred D. Lublin, MD, has disclosed the following relevant financial relationships:

Sources of Funding for Research: Novartis; Biogen; Sanofi; NMSS; NIH; Brainstorm Cell Therapeutics

Consulting Agreements/Advisory Boards/DSMB: Biogen; EMD Serono; Novartis; Actelion/Janssen; Sanofi/Genzyme; Roche/Genentech; Horizon Therapeutics/Amgen; Bristol Myers Squibb; Mapi Pharma; Brainstorm Cell Therapeutics; Mylan/Viatris; Immunic; Avotres; Neurogene; LabCorp; Entelexo Biotherapeutics; Neuralight; SetPoint Medical; Hexal/Sandoz; Baim Institute; Sudo Biosciences; Lapix Therapeutics; Biohaven Pharmaceuticals; Abata Therapeutics; Cognito Therapeutics; ImmPACT Bio

Speaker: Sanofi

Stock Options: Avotres; Neuralight; Lapix Therapeutics; Entelexo

I may discuss unapproved agents that are in the MS developmental pipeline without any recommendation on their use.

To the Editor:

Cardiac rhabdomyomas are benign hamartomas that are common in patients with tuberous sclerosis complex (TSC).¹ We describe a patient who presented with large infantile hemangiomas (IHs) and hypopigmented macules, which prompted further testing that eventually showed concomitant multiple cardiac rhabdomyomas in the context of TSC.

A 5-week-old girl—who was born at 38 weeks and 3 days’ gestation via uncomplicated vaginal delivery—was referred to our pediatric dermatology clinic for evaluation of multiple erythematous lesions on the scalp and left buttock that were first noticed 2 weeks prior to presentation. There was a family history of seizures in the patient’s mother. The patient’s older brother did not have similar symptoms.

Physical examination revealed 2 nonulcerating erythematous nodules on the middle and posterior left vertex scalp that measured 2.5×2 cm (Figure 1A) as well as 1 bright red plaque on the left buttock (Figure 1B). Five hypopigmented macules, ranging from 5 mm to 1.5 cm in diameter, also were detected on the left thorax (Figure 2A) as well as the middle and lower back (Figure 2B). These findings, along with the history of seizures in the patient’s mother, prompted further evaluation of the family history, which uncovered TSC in the patient’s mother, maternal aunt, and maternal grandmother.

The large IHs on the scalp did not pose concerns for potential functional impairment but were still considered high risk for permanent alopecia based on clinical practice guidelines for the management of IH.² Treatment with oral propranolol was recommended; however, because of a strong suspicion of TSC due to the presence of 5 hypopigmented macules measuring more than 5 mm in diameter (≥3 hypopigmented macules of ≥5 mm is one of the major criterion for TSC), the patient was referred to cardiology prior to initiation of propranolol.

Echocardiography revealed 3 intracardiac masses measuring 4 to 5 mm in diameter in the left ventricle (LV), along the interventricular septum and the LV posterior wall. These masses were consistent with rhabdomyomas (Figure 3)—a major criterion for TSC—which had not been detected by prenatal ultrasonography. No obstruction to LV inflow or outflow was observed. Additionally, no arrhythmias were detected on electrocardiography.

The patient was cleared for propranolol, which was slowly uptitrated to 2 mg/kg/d. She completed the course without adverse effects. The treatment of IH was successful with substantial reduction in size over the following months until clearance. She also was referred to neurology for magnetic resonance imaging of the brain, which showed a 3-mm subependymal nodule in the lateral right ventricle, another major feature of TSC.

Cardiac rhabdomyomas are benign hamartomas that affect as many as 80% of patients with TSC¹ and are primarily localized in the ventricles. Although cardiac rhabdomyomas usually regress over time, they can compromise ventricular function or valvular function, or both, and result in outflow obstruction, arrhythmias, and Wolff- Parkinson-White syndrome.³ Surgical resection may be needed in patients whose condition is refractory to medical management for heart failure.

The pathophysiologic mechanism behind the natural involution of cardiac rhabdomyomas has not been fully elucidated. It has been hypothesized that these masses stem from the inability of rhabdomyoma cells to divide after birth due to their embryonic myocyte derivation.⁴

According to the TSC diagnostic criteria from the Tuberous Sclerosis Complex International Consensus Group, at least 2 major features or 1 major and 2 minor features are required to make a definitive diagnosis of TSC. Cutaneous signs represent more than one-third of major features of TSC; almost all patients with TSC have skin findings.⁵

Identification of pathogenic mutations in either TSC¹ (on chromosome 9q34.3, encoding for hamartin) or TSC² (on chromosome 16p13.3, encoding for tuberin), resulting in constitutive activation of mammalian target of rapamycin and subsequent increased cell growth, is sufficient for a definitive diagnosis of TSC. However, mutations cannot be identified by conventional genetic testing in as many as one-quarter of patients with TSC; therefore, a negative result does not exclude TSC if the patient meets clinical diagnostic criteria.

Although a cardiology workup is indicated prior to initiating propranolol in the presence of possible cardiac rhabdomyomas, most of those lesions are hemodynamically stable and do not require treatment. There also is no contraindication for β-blocker therapy. In fact, propranolol has been reported as a successful treatment in rhabdomyoma-associated arrhythmias in children.⁶ Notably, obstructive cardiac rhabdomyomas have been successfully treated with mammalian target of rapamycin inhibitors, such as sirolimus⁷ and everolimus.⁸

Baseline cardiology screening with echocardiography prior to initiating propranolol for treatment of IH is not routinely indicated in babies with uncomplicated IH. However, in a patient with TSC, cardiology screening is necessary to rule out rhabdomyomas with associated arrhythmias or obstructed blood flow, or both, prior to initiating treatment.

We presented a case of concomitant IH and TSC in a patient with cardiac rhabdomyomas. The manifestation of large IHs in our patient prompted further testing that revealed multiple cardiac rhabdomyomas in the context of TSC. It is imperative for cardiologists, cardiac surgeons, and dermatologists to be familiar with the TSC diagnostic criteria so that they can reach a prompt diagnosis and make appropriate referrals for further evaluation of cardiac, neurologic, and ophthalmologic signs.

To the Editor:

Cardiac rhabdomyomas are benign hamartomas that are common in patients with tuberous sclerosis complex (TSC).¹ We describe a patient who presented with large infantile hemangiomas (IHs) and hypopigmented macules, which prompted further testing that eventually showed concomitant multiple cardiac rhabdomyomas in the context of TSC.

A 5-week-old girl—who was born at 38 weeks and 3 days’ gestation via uncomplicated vaginal delivery—was referred to our pediatric dermatology clinic for evaluation of multiple erythematous lesions on the scalp and left buttock that were first noticed 2 weeks prior to presentation. There was a family history of seizures in the patient’s mother. The patient’s older brother did not have similar symptoms.

Physical examination revealed 2 nonulcerating erythematous nodules on the middle and posterior left vertex scalp that measured 2.5×2 cm (Figure 1A) as well as 1 bright red plaque on the left buttock (Figure 1B). Five hypopigmented macules, ranging from 5 mm to 1.5 cm in diameter, also were detected on the left thorax (Figure 2A) as well as the middle and lower back (Figure 2B). These findings, along with the history of seizures in the patient’s mother, prompted further evaluation of the family history, which uncovered TSC in the patient’s mother, maternal aunt, and maternal grandmother.

The large IHs on the scalp did not pose concerns for potential functional impairment but were still considered high risk for permanent alopecia based on clinical practice guidelines for the management of IH.² Treatment with oral propranolol was recommended; however, because of a strong suspicion of TSC due to the presence of 5 hypopigmented macules measuring more than 5 mm in diameter (≥3 hypopigmented macules of ≥5 mm is one of the major criterion for TSC), the patient was referred to cardiology prior to initiation of propranolol.

Echocardiography revealed 3 intracardiac masses measuring 4 to 5 mm in diameter in the left ventricle (LV), along the interventricular septum and the LV posterior wall. These masses were consistent with rhabdomyomas (Figure 3)—a major criterion for TSC—which had not been detected by prenatal ultrasonography. No obstruction to LV inflow or outflow was observed. Additionally, no arrhythmias were detected on electrocardiography.

The patient was cleared for propranolol, which was slowly uptitrated to 2 mg/kg/d. She completed the course without adverse effects. The treatment of IH was successful with substantial reduction in size over the following months until clearance. She also was referred to neurology for magnetic resonance imaging of the brain, which showed a 3-mm subependymal nodule in the lateral right ventricle, another major feature of TSC.

Cardiac rhabdomyomas are benign hamartomas that affect as many as 80% of patients with TSC¹ and are primarily localized in the ventricles. Although cardiac rhabdomyomas usually regress over time, they can compromise ventricular function or valvular function, or both, and result in outflow obstruction, arrhythmias, and Wolff- Parkinson-White syndrome.³ Surgical resection may be needed in patients whose condition is refractory to medical management for heart failure.

The pathophysiologic mechanism behind the natural involution of cardiac rhabdomyomas has not been fully elucidated. It has been hypothesized that these masses stem from the inability of rhabdomyoma cells to divide after birth due to their embryonic myocyte derivation.⁴

According to the TSC diagnostic criteria from the Tuberous Sclerosis Complex International Consensus Group, at least 2 major features or 1 major and 2 minor features are required to make a definitive diagnosis of TSC. Cutaneous signs represent more than one-third of major features of TSC; almost all patients with TSC have skin findings.⁵

Identification of pathogenic mutations in either TSC¹ (on chromosome 9q34.3, encoding for hamartin) or TSC² (on chromosome 16p13.3, encoding for tuberin), resulting in constitutive activation of mammalian target of rapamycin and subsequent increased cell growth, is sufficient for a definitive diagnosis of TSC. However, mutations cannot be identified by conventional genetic testing in as many as one-quarter of patients with TSC; therefore, a negative result does not exclude TSC if the patient meets clinical diagnostic criteria.

Although a cardiology workup is indicated prior to initiating propranolol in the presence of possible cardiac rhabdomyomas, most of those lesions are hemodynamically stable and do not require treatment. There also is no contraindication for β-blocker therapy. In fact, propranolol has been reported as a successful treatment in rhabdomyoma-associated arrhythmias in children.⁶ Notably, obstructive cardiac rhabdomyomas have been successfully treated with mammalian target of rapamycin inhibitors, such as sirolimus⁷ and everolimus.⁸

Baseline cardiology screening with echocardiography prior to initiating propranolol for treatment of IH is not routinely indicated in babies with uncomplicated IH. However, in a patient with TSC, cardiology screening is necessary to rule out rhabdomyomas with associated arrhythmias or obstructed blood flow, or both, prior to initiating treatment.

We presented a case of concomitant IH and TSC in a patient with cardiac rhabdomyomas. The manifestation of large IHs in our patient prompted further testing that revealed multiple cardiac rhabdomyomas in the context of TSC. It is imperative for cardiologists, cardiac surgeons, and dermatologists to be familiar with the TSC diagnostic criteria so that they can reach a prompt diagnosis and make appropriate referrals for further evaluation of cardiac, neurologic, and ophthalmologic signs.

To the Editor:

Cardiac rhabdomyomas are benign hamartomas that are common in patients with tuberous sclerosis complex (TSC).¹ We describe a patient who presented with large infantile hemangiomas (IHs) and hypopigmented macules, which prompted further testing that eventually showed concomitant multiple cardiac rhabdomyomas in the context of TSC.

A 5-week-old girl—who was born at 38 weeks and 3 days’ gestation via uncomplicated vaginal delivery—was referred to our pediatric dermatology clinic for evaluation of multiple erythematous lesions on the scalp and left buttock that were first noticed 2 weeks prior to presentation. There was a family history of seizures in the patient’s mother. The patient’s older brother did not have similar symptoms.

Physical examination revealed 2 nonulcerating erythematous nodules on the middle and posterior left vertex scalp that measured 2.5×2 cm (Figure 1A) as well as 1 bright red plaque on the left buttock (Figure 1B). Five hypopigmented macules, ranging from 5 mm to 1.5 cm in diameter, also were detected on the left thorax (Figure 2A) as well as the middle and lower back (Figure 2B). These findings, along with the history of seizures in the patient’s mother, prompted further evaluation of the family history, which uncovered TSC in the patient’s mother, maternal aunt, and maternal grandmother.

The large IHs on the scalp did not pose concerns for potential functional impairment but were still considered high risk for permanent alopecia based on clinical practice guidelines for the management of IH.² Treatment with oral propranolol was recommended; however, because of a strong suspicion of TSC due to the presence of 5 hypopigmented macules measuring more than 5 mm in diameter (≥3 hypopigmented macules of ≥5 mm is one of the major criterion for TSC), the patient was referred to cardiology prior to initiation of propranolol.

Echocardiography revealed 3 intracardiac masses measuring 4 to 5 mm in diameter in the left ventricle (LV), along the interventricular septum and the LV posterior wall. These masses were consistent with rhabdomyomas (Figure 3)—a major criterion for TSC—which had not been detected by prenatal ultrasonography. No obstruction to LV inflow or outflow was observed. Additionally, no arrhythmias were detected on electrocardiography.

The patient was cleared for propranolol, which was slowly uptitrated to 2 mg/kg/d. She completed the course without adverse effects. The treatment of IH was successful with substantial reduction in size over the following months until clearance. She also was referred to neurology for magnetic resonance imaging of the brain, which showed a 3-mm subependymal nodule in the lateral right ventricle, another major feature of TSC.

Cardiac rhabdomyomas are benign hamartomas that affect as many as 80% of patients with TSC¹ and are primarily localized in the ventricles. Although cardiac rhabdomyomas usually regress over time, they can compromise ventricular function or valvular function, or both, and result in outflow obstruction, arrhythmias, and Wolff- Parkinson-White syndrome.³ Surgical resection may be needed in patients whose condition is refractory to medical management for heart failure.

The pathophysiologic mechanism behind the natural involution of cardiac rhabdomyomas has not been fully elucidated. It has been hypothesized that these masses stem from the inability of rhabdomyoma cells to divide after birth due to their embryonic myocyte derivation.⁴

According to the TSC diagnostic criteria from the Tuberous Sclerosis Complex International Consensus Group, at least 2 major features or 1 major and 2 minor features are required to make a definitive diagnosis of TSC. Cutaneous signs represent more than one-third of major features of TSC; almost all patients with TSC have skin findings.⁵

Identification of pathogenic mutations in either TSC¹ (on chromosome 9q34.3, encoding for hamartin) or TSC² (on chromosome 16p13.3, encoding for tuberin), resulting in constitutive activation of mammalian target of rapamycin and subsequent increased cell growth, is sufficient for a definitive diagnosis of TSC. However, mutations cannot be identified by conventional genetic testing in as many as one-quarter of patients with TSC; therefore, a negative result does not exclude TSC if the patient meets clinical diagnostic criteria.

Although a cardiology workup is indicated prior to initiating propranolol in the presence of possible cardiac rhabdomyomas, most of those lesions are hemodynamically stable and do not require treatment. There also is no contraindication for β-blocker therapy. In fact, propranolol has been reported as a successful treatment in rhabdomyoma-associated arrhythmias in children.⁶ Notably, obstructive cardiac rhabdomyomas have been successfully treated with mammalian target of rapamycin inhibitors, such as sirolimus⁷ and everolimus.⁸

Baseline cardiology screening with echocardiography prior to initiating propranolol for treatment of IH is not routinely indicated in babies with uncomplicated IH. However, in a patient with TSC, cardiology screening is necessary to rule out rhabdomyomas with associated arrhythmias or obstructed blood flow, or both, prior to initiating treatment.

We presented a case of concomitant IH and TSC in a patient with cardiac rhabdomyomas. The manifestation of large IHs in our patient prompted further testing that revealed multiple cardiac rhabdomyomas in the context of TSC. It is imperative for cardiologists, cardiac surgeons, and dermatologists to be familiar with the TSC diagnostic criteria so that they can reach a prompt diagnosis and make appropriate referrals for further evaluation of cardiac, neurologic, and ophthalmologic signs.