SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

SCOTTSDALE, ARIZ. –Among patients with atopic dermatitis, persistently active disease was significantly more common among females of nonwhite race with a history of atopy than among patients without these characteristics, in an analysis of survey data from the Pediatric Elective Eczema Registry.

Annual household income under $50,000 also was a significant predictor of persistently active eczema, according to Katrina Abuabara, MD, of the department of dermatology, University of California, San Francisco, and her associates, who reported their results in a poster at the annual meeting of the Society for Investigative Dermatology.

Atopic dermatitis often persists into adulthood, but few studies have explored contributors to poor disease control. To help fill that gap, the investigators analyzed 65,237 surveys from the Pediatric Eczema Elective Registry (PEER), which tracks children and young adults aged 2-26 years with physician-diagnosed atopic dermatitis. The average age of the 6,237 patients was 7 years at enrollment (standard deviation, 4 years). They were followed at 6-month intervals for up to 10 years, with an average of about 10 surveys per respondent (standard deviation, 6.3 surveys).

In all, 4,607 patients (74% of the cohort) returned surveys spanning early childhood through their mid-20s. Only 15% of patients had “resolving” disease, meaning that as they aged, they increasingly reported complete disease control for periods of 6 months and longer.

The remaining 85% of patients had persistently active disease. In this group, 54% were female, 77% had a household income under $50,000 per year, 71% were nonwhite, and 75% had a history of atopy. Each of these characteristics significantly increased the odds of persistently active atopic dermatitis in the multivariable model (P less than .05 for each association).

Nonwhite race and history of atopy were the strongest predictors of persistently active disease – each lowered the odds of complete disease control by almost 50% (odds ratio, 0.53). Furthermore, females had 37% lower odds of complete disease control compared with males (OR, 0.63), and individuals with household income under $50,000 had 16% lower odds of complete disease control compared with those with higher annual incomes (OR, 0.84).

The link between lower socioeconomic status and persistently active eczema belies previous findings, the researchers noted. Those studies found that individuals of higher socioeconomic status were at greater risk for developing atopic dermatitis, but “failed to account for the chronic nature of the disease. In contrast, our results suggest that atopic dermatitis persistence may be associated with lower income and nonwhite race, and highlight the importance of longitudinal studies that permit analysis of mechanisms of disease control over time.”

Dr. Abuabara received a grant from the Clinical & Translational Science Institute of UCSF. She had no disclosures.

To determine the unique characteristics of cluster seizures, investigators looked at 92 subjects, 83% of whom had at least one seizure cluster. They found that seizures occurring within a cluster were significantly shorter than the last seizure that occurred in the cluster. They also discovered that the terminal seizure in a cluster is similar to duration in isolated seizures that are not part of a cluster. Finally, the researchers found that cluster seizures are more likely to occur in the frontal and temporal lobes.

Ferastraoaru V, Schulze-Bonhage A, Lipton RB, Dumpelmann M, Legatt AD, Hunt SR. Termination of seizure clusters is related to duration of focal seizures. Epilepsia. 2016;57(6):889-895.

To determine the unique characteristics of cluster seizures, investigators looked at 92 subjects, 83% of whom had at least one seizure cluster. They found that seizures occurring within a cluster were significantly shorter than the last seizure that occurred in the cluster. They also discovered that the terminal seizure in a cluster is similar to duration in isolated seizures that are not part of a cluster. Finally, the researchers found that cluster seizures are more likely to occur in the frontal and temporal lobes.

Ferastraoaru V, Schulze-Bonhage A, Lipton RB, Dumpelmann M, Legatt AD, Hunt SR. Termination of seizure clusters is related to duration of focal seizures. Epilepsia. 2016;57(6):889-895.

To determine the unique characteristics of cluster seizures, investigators looked at 92 subjects, 83% of whom had at least one seizure cluster. They found that seizures occurring within a cluster were significantly shorter than the last seizure that occurred in the cluster. They also discovered that the terminal seizure in a cluster is similar to duration in isolated seizures that are not part of a cluster. Finally, the researchers found that cluster seizures are more likely to occur in the frontal and temporal lobes.

Ferastraoaru V, Schulze-Bonhage A, Lipton RB, Dumpelmann M, Legatt AD, Hunt SR. Termination of seizure clusters is related to duration of focal seizures. Epilepsia. 2016;57(6):889-895.

To determine if genetic variation influences the susceptibility to traumatic brain injury and the subsequent posttraumatic seizures, Anne Ritter and her associates from the University of Pittsburgh analyzed the relationship between posttraumatic seizures and single nucleotide polymorphisms (SNPs). Thirty two SNPs were evaluated within SLC1A1 and SLC1A6, which are protein coding genes for glutamate transporters. (Glutamate transporters control glutamate levels and excitatory neurotransmission and have been associated with traumatic brain injury.) The analysis found that among 253 individuals, 49 had experienced posttraumatic seizures. Within this smaller group, they found genotypes at SNP rs10974620 (SLC1A1) linked to the time to the first seizure during a three year follow-up. And after factoring in several confounding variables, rs10974620 remained statistically significant (P = .017).

Rittner AC, Kammerer CM, Brooks MM, Conley YP, Wagner AM. Genetic variation in neuronal glutamate transport genes and associations with posttraumatic seizure. Epilepsia. 2016;57(6):984-993. 

To determine if genetic variation influences the susceptibility to traumatic brain injury and the subsequent posttraumatic seizures, Anne Ritter and her associates from the University of Pittsburgh analyzed the relationship between posttraumatic seizures and single nucleotide polymorphisms (SNPs). Thirty two SNPs were evaluated within SLC1A1 and SLC1A6, which are protein coding genes for glutamate transporters. (Glutamate transporters control glutamate levels and excitatory neurotransmission and have been associated with traumatic brain injury.) The analysis found that among 253 individuals, 49 had experienced posttraumatic seizures. Within this smaller group, they found genotypes at SNP rs10974620 (SLC1A1) linked to the time to the first seizure during a three year follow-up. And after factoring in several confounding variables, rs10974620 remained statistically significant (P = .017).

Rittner AC, Kammerer CM, Brooks MM, Conley YP, Wagner AM. Genetic variation in neuronal glutamate transport genes and associations with posttraumatic seizure. Epilepsia. 2016;57(6):984-993. 

To determine if genetic variation influences the susceptibility to traumatic brain injury and the subsequent posttraumatic seizures, Anne Ritter and her associates from the University of Pittsburgh analyzed the relationship between posttraumatic seizures and single nucleotide polymorphisms (SNPs). Thirty two SNPs were evaluated within SLC1A1 and SLC1A6, which are protein coding genes for glutamate transporters. (Glutamate transporters control glutamate levels and excitatory neurotransmission and have been associated with traumatic brain injury.) The analysis found that among 253 individuals, 49 had experienced posttraumatic seizures. Within this smaller group, they found genotypes at SNP rs10974620 (SLC1A1) linked to the time to the first seizure during a three year follow-up. And after factoring in several confounding variables, rs10974620 remained statistically significant (P = .017).

Rittner AC, Kammerer CM, Brooks MM, Conley YP, Wagner AM. Genetic variation in neuronal glutamate transport genes and associations with posttraumatic seizure. Epilepsia. 2016;57(6):984-993. 

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 20-year-old female with a history of primary generalized epilepsy presents for establishment of care, as the patient’s insurance had changed. She is currently taking levetiracetam (Keppra) 1500 mg twice daily and divalproex (Depakote) 500 mg once daily by mouth at bedtime. The patient’s last breakthrough seizure was 10 months ago, at which time divalproex was added. The patient has a history of anxiety and depression, for which she is taking escitalopram (Lexapro) 10 mg once daily. The patient also has a history of “sporadic” headaches. The patient used to be on oral contraceptives, but about 3 months ago an intrauterine device was placed.

Questions:

Given the patient’s gender and age, is this the ideal antiepileptic drug (AED) regimen for this patient?

Items to consider: The patient is a young female of child-bearing age. Divalproex has been shown to be among the least safe AEDs during pregnancy due to a higher risk for birth defects and cognitive side effects on the child.

Ideally, an AED other than divalproex should be chosen. Divalproex also has numerous other side effects.

Polytherapy and higher doses of AEDs can increase the risk of teratogenic side effects.

Levetiracetam is considered to be a relatively safe AED for pregnancy.

The goal should be to simplify the patient’s AED regimen to monotherapy and minimize the dose.

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 20-year-old female with a history of primary generalized epilepsy presents for establishment of care, as the patient’s insurance had changed. She is currently taking levetiracetam (Keppra) 1500 mg twice daily and divalproex (Depakote) 500 mg once daily by mouth at bedtime. The patient’s last breakthrough seizure was 10 months ago, at which time divalproex was added. The patient has a history of anxiety and depression, for which she is taking escitalopram (Lexapro) 10 mg once daily. The patient also has a history of “sporadic” headaches. The patient used to be on oral contraceptives, but about 3 months ago an intrauterine device was placed.

Questions:

Given the patient’s gender and age, is this the ideal antiepileptic drug (AED) regimen for this patient?

Items to consider: The patient is a young female of child-bearing age. Divalproex has been shown to be among the least safe AEDs during pregnancy due to a higher risk for birth defects and cognitive side effects on the child.

Ideally, an AED other than divalproex should be chosen. Divalproex also has numerous other side effects.

Polytherapy and higher doses of AEDs can increase the risk of teratogenic side effects.

Levetiracetam is considered to be a relatively safe AED for pregnancy.

The goal should be to simplify the patient’s AED regimen to monotherapy and minimize the dose.

Nikesh Ardeshna, MD

Dr. Ardeshna is the Medical Director of Adult Epilepsy Services at Royal Oak Hospital, Beaumont Health System, in Royal Oak, Michigan.

A 20-year-old female with a history of primary generalized epilepsy presents for establishment of care, as the patient’s insurance had changed. She is currently taking levetiracetam (Keppra) 1500 mg twice daily and divalproex (Depakote) 500 mg once daily by mouth at bedtime. The patient’s last breakthrough seizure was 10 months ago, at which time divalproex was added. The patient has a history of anxiety and depression, for which she is taking escitalopram (Lexapro) 10 mg once daily. The patient also has a history of “sporadic” headaches. The patient used to be on oral contraceptives, but about 3 months ago an intrauterine device was placed.

Questions:

Given the patient’s gender and age, is this the ideal antiepileptic drug (AED) regimen for this patient?

Items to consider: The patient is a young female of child-bearing age. Divalproex has been shown to be among the least safe AEDs during pregnancy due to a higher risk for birth defects and cognitive side effects on the child.

Ideally, an AED other than divalproex should be chosen. Divalproex also has numerous other side effects.

Polytherapy and higher doses of AEDs can increase the risk of teratogenic side effects.

Levetiracetam is considered to be a relatively safe AED for pregnancy.

The goal should be to simplify the patient’s AED regimen to monotherapy and minimize the dose.

LONDON – Biosimilar etanercept (CHS-0214) is as effective and well tolerated as etanercept (Enbrel) for the treatment of rheumatoid arthritis according to the results of a randomized, double-blind, phase III trial conducted in 13 countries.

The primary endpoint of an American College of Rheumatology (ACR) 20 at 24 weeks was achieved by 91% of patients given CHS-0214 and 90.6% of those given etanercept, giving a treatment difference of just 0.4%. The percentages of patients achieving ACR 50 (67.6% and 63.7%) and ACR 70 (38.3% and 37.9%) were also comparable.

These are the first clinical data to be presented on this biosimilar, which is a fusion protein comprising the soluble human p75 tumor necrosis factor (TNF) receptor and the Fc region of human immunoglobulin G1.

“Like all biosimilars CHD-0214 has undergone extensive analytical characterization, which had demonstrated highly similar structure and function to etanercept,” study investigator James O’Dell, MD, of the University of Nebraska Medical Center, Omaha, said at the European Congress of Rheumatology. “Studies have demonstrated that CHS-0214 is similar to etanercept with regard to in vitro pharmacology, in vivo pharmacokinetics, and toxicology,” he observed.

A total of 644 patients with moderate to severe rheumatoid arthritis who had an inadequate response to methotrexate were enrolled in the phase III trial and randomized to receive CHS-0214 or etanercept at a subcutaneous dose of 50 mg once a week for 24 weeks. After the double-blind period had ended, patients could continue on open-label CHS-0214 for another 24 weeks. Assessment of efficacy was performed on 512 patients as an issue with the production of the biosimilar resulted in a dosing interruption for 132 patients.

Remission, defined as a DAS28-CRP (Disease Activity Score 28–C-reactive protein) score of less than 2.6, was achieved in a similar percentage of subjects in the CHS-0214 and etanercept groups, at 40.6% and 42.4%, respectively.

There was a similar percentage of any adverse event (60.8% vs. 65%) occurring among patients receiving the biosimilar and those getting etanercept. Treatment-related adverse events (16.4% vs. 21.9%), and treatment-related serious adverse events (0.9% vs. 0.3%) were also comparable. Drug-drug antibodies occurred in numerically fewer patients treated with the biosimilar than with etanercept (1.3% vs. 4.7%).

Asked after his presentation about why he thought the ACR responses seen in the study were so high, Dr. O’Dell said: “We were surprised by that.” There are a number of potential explanations, he suggested. “We had a remarkable completion rate in the trial, 95%, so we lost very few patients, and we are in the process of analyzing other trials to see if that is a major factor.” In addition, patients were on relatively lower doses of methotrexate than in some other trials “because a quarter of them came from Japan,” he said. Patients were also all biologic naive and many were recruited from countries where they don’t have the opportunity to be exposed to a lot of therapies.

“The studies on all biosimilars so far suggest that they are indeed biosimilar,” Dr. O’Dell said in an interview. So how might clinicians begin to choose between the various biosimilars? “Well, there is very, very little data to compare any biologic to another biologic,” he answered.

“You haven’t seen studies comparing one TNF inhibitor to another TNF inhibitor. So it’s not surprising that we don’t have data that compare this biosimilar to that biosimilar,” he added. Such studies are probably also unlikely to ever be conducted so the choice of biosimilar, like anti-TNF therapy is probably going to be dictated by national and local guidelines, and medical insurance policies.

“Today, the biosimilars look biosimilar, so I have no problems if somebody tells me I have to start a biosimilar as opposed to the innovator product. I do have a problem if they tell me I have to switch, because that’s interchangeability and that’s a whole different story,” he noted.

Dr. O’Dell observed, however, that data from the DANBIO registry presented during the same session had shown that an enforced national switch from infliximab (Remicade) to biosimilar infliximab had shown that this did not appear to pose a problem in routine care in Denmark. Indeed 3 months’ clinical outcomes in patients with RA, psoriatic arthritis, or axial spondyloarthritis who were switched appeared to be comparable. Whether this is true across all the biosimilars needs to be established.

Coherus Biosciences funded the study. Dr. O’Dell has been a study investigator for, received research grants from, or acted as a speaker or consultant to Coherus Biosciences, Medac, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, Antares, and Crescendo.

LONDON – Biosimilar etanercept (CHS-0214) is as effective and well tolerated as etanercept (Enbrel) for the treatment of rheumatoid arthritis according to the results of a randomized, double-blind, phase III trial conducted in 13 countries.

The primary endpoint of an American College of Rheumatology (ACR) 20 at 24 weeks was achieved by 91% of patients given CHS-0214 and 90.6% of those given etanercept, giving a treatment difference of just 0.4%. The percentages of patients achieving ACR 50 (67.6% and 63.7%) and ACR 70 (38.3% and 37.9%) were also comparable.

These are the first clinical data to be presented on this biosimilar, which is a fusion protein comprising the soluble human p75 tumor necrosis factor (TNF) receptor and the Fc region of human immunoglobulin G1.

“Like all biosimilars CHD-0214 has undergone extensive analytical characterization, which had demonstrated highly similar structure and function to etanercept,” study investigator James O’Dell, MD, of the University of Nebraska Medical Center, Omaha, said at the European Congress of Rheumatology. “Studies have demonstrated that CHS-0214 is similar to etanercept with regard to in vitro pharmacology, in vivo pharmacokinetics, and toxicology,” he observed.

A total of 644 patients with moderate to severe rheumatoid arthritis who had an inadequate response to methotrexate were enrolled in the phase III trial and randomized to receive CHS-0214 or etanercept at a subcutaneous dose of 50 mg once a week for 24 weeks. After the double-blind period had ended, patients could continue on open-label CHS-0214 for another 24 weeks. Assessment of efficacy was performed on 512 patients as an issue with the production of the biosimilar resulted in a dosing interruption for 132 patients.

Remission, defined as a DAS28-CRP (Disease Activity Score 28–C-reactive protein) score of less than 2.6, was achieved in a similar percentage of subjects in the CHS-0214 and etanercept groups, at 40.6% and 42.4%, respectively.

There was a similar percentage of any adverse event (60.8% vs. 65%) occurring among patients receiving the biosimilar and those getting etanercept. Treatment-related adverse events (16.4% vs. 21.9%), and treatment-related serious adverse events (0.9% vs. 0.3%) were also comparable. Drug-drug antibodies occurred in numerically fewer patients treated with the biosimilar than with etanercept (1.3% vs. 4.7%).

Asked after his presentation about why he thought the ACR responses seen in the study were so high, Dr. O’Dell said: “We were surprised by that.” There are a number of potential explanations, he suggested. “We had a remarkable completion rate in the trial, 95%, so we lost very few patients, and we are in the process of analyzing other trials to see if that is a major factor.” In addition, patients were on relatively lower doses of methotrexate than in some other trials “because a quarter of them came from Japan,” he said. Patients were also all biologic naive and many were recruited from countries where they don’t have the opportunity to be exposed to a lot of therapies.

“The studies on all biosimilars so far suggest that they are indeed biosimilar,” Dr. O’Dell said in an interview. So how might clinicians begin to choose between the various biosimilars? “Well, there is very, very little data to compare any biologic to another biologic,” he answered.

“You haven’t seen studies comparing one TNF inhibitor to another TNF inhibitor. So it’s not surprising that we don’t have data that compare this biosimilar to that biosimilar,” he added. Such studies are probably also unlikely to ever be conducted so the choice of biosimilar, like anti-TNF therapy is probably going to be dictated by national and local guidelines, and medical insurance policies.

“Today, the biosimilars look biosimilar, so I have no problems if somebody tells me I have to start a biosimilar as opposed to the innovator product. I do have a problem if they tell me I have to switch, because that’s interchangeability and that’s a whole different story,” he noted.

Dr. O’Dell observed, however, that data from the DANBIO registry presented during the same session had shown that an enforced national switch from infliximab (Remicade) to biosimilar infliximab had shown that this did not appear to pose a problem in routine care in Denmark. Indeed 3 months’ clinical outcomes in patients with RA, psoriatic arthritis, or axial spondyloarthritis who were switched appeared to be comparable. Whether this is true across all the biosimilars needs to be established.

Coherus Biosciences funded the study. Dr. O’Dell has been a study investigator for, received research grants from, or acted as a speaker or consultant to Coherus Biosciences, Medac, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, Antares, and Crescendo.

LONDON – Biosimilar etanercept (CHS-0214) is as effective and well tolerated as etanercept (Enbrel) for the treatment of rheumatoid arthritis according to the results of a randomized, double-blind, phase III trial conducted in 13 countries.

The primary endpoint of an American College of Rheumatology (ACR) 20 at 24 weeks was achieved by 91% of patients given CHS-0214 and 90.6% of those given etanercept, giving a treatment difference of just 0.4%. The percentages of patients achieving ACR 50 (67.6% and 63.7%) and ACR 70 (38.3% and 37.9%) were also comparable.

These are the first clinical data to be presented on this biosimilar, which is a fusion protein comprising the soluble human p75 tumor necrosis factor (TNF) receptor and the Fc region of human immunoglobulin G1.

“Like all biosimilars CHD-0214 has undergone extensive analytical characterization, which had demonstrated highly similar structure and function to etanercept,” study investigator James O’Dell, MD, of the University of Nebraska Medical Center, Omaha, said at the European Congress of Rheumatology. “Studies have demonstrated that CHS-0214 is similar to etanercept with regard to in vitro pharmacology, in vivo pharmacokinetics, and toxicology,” he observed.

A total of 644 patients with moderate to severe rheumatoid arthritis who had an inadequate response to methotrexate were enrolled in the phase III trial and randomized to receive CHS-0214 or etanercept at a subcutaneous dose of 50 mg once a week for 24 weeks. After the double-blind period had ended, patients could continue on open-label CHS-0214 for another 24 weeks. Assessment of efficacy was performed on 512 patients as an issue with the production of the biosimilar resulted in a dosing interruption for 132 patients.

Remission, defined as a DAS28-CRP (Disease Activity Score 28–C-reactive protein) score of less than 2.6, was achieved in a similar percentage of subjects in the CHS-0214 and etanercept groups, at 40.6% and 42.4%, respectively.

There was a similar percentage of any adverse event (60.8% vs. 65%) occurring among patients receiving the biosimilar and those getting etanercept. Treatment-related adverse events (16.4% vs. 21.9%), and treatment-related serious adverse events (0.9% vs. 0.3%) were also comparable. Drug-drug antibodies occurred in numerically fewer patients treated with the biosimilar than with etanercept (1.3% vs. 4.7%).

Asked after his presentation about why he thought the ACR responses seen in the study were so high, Dr. O’Dell said: “We were surprised by that.” There are a number of potential explanations, he suggested. “We had a remarkable completion rate in the trial, 95%, so we lost very few patients, and we are in the process of analyzing other trials to see if that is a major factor.” In addition, patients were on relatively lower doses of methotrexate than in some other trials “because a quarter of them came from Japan,” he said. Patients were also all biologic naive and many were recruited from countries where they don’t have the opportunity to be exposed to a lot of therapies.

“The studies on all biosimilars so far suggest that they are indeed biosimilar,” Dr. O’Dell said in an interview. So how might clinicians begin to choose between the various biosimilars? “Well, there is very, very little data to compare any biologic to another biologic,” he answered.

“You haven’t seen studies comparing one TNF inhibitor to another TNF inhibitor. So it’s not surprising that we don’t have data that compare this biosimilar to that biosimilar,” he added. Such studies are probably also unlikely to ever be conducted so the choice of biosimilar, like anti-TNF therapy is probably going to be dictated by national and local guidelines, and medical insurance policies.

“Today, the biosimilars look biosimilar, so I have no problems if somebody tells me I have to start a biosimilar as opposed to the innovator product. I do have a problem if they tell me I have to switch, because that’s interchangeability and that’s a whole different story,” he noted.

Dr. O’Dell observed, however, that data from the DANBIO registry presented during the same session had shown that an enforced national switch from infliximab (Remicade) to biosimilar infliximab had shown that this did not appear to pose a problem in routine care in Denmark. Indeed 3 months’ clinical outcomes in patients with RA, psoriatic arthritis, or axial spondyloarthritis who were switched appeared to be comparable. Whether this is true across all the biosimilars needs to be established.

Coherus Biosciences funded the study. Dr. O’Dell has been a study investigator for, received research grants from, or acted as a speaker or consultant to Coherus Biosciences, Medac, Eli Lilly, Bristol-Myers Squibb, GlaxoSmithKline, Antares, and Crescendo.

On June 30, New Mexico became the latest state to throw out a challenge to a law banning physician-assisted suicide. In Morris v. Brandenburg, proponents of the right-to-die movement contended that medical aid in dying was a fundamental right, meaning that any law that restricted the right should be presumed to be invalid unless the state had a compelling reason for the restriction.

In a unanimous decision, the New Mexico Supreme Court held that there was no such right under that state’s constitution, and that even if the right had existed, the state had several compelling reasons to restrict it: to protect “the integrity and ethics of the medical profession”; to protect “vulnerable groups – including the poor, the elderly, and disabled persons – from the risk of subtle coercion and undue influence in end-of-life situations, including pressures associated with the substantial financial burden of end-of-life health care costs”; and to protect “against voluntary or involuntary euthanasia because if physician aid in dying is a constitutional right, it must be made available to everyone, even when a duly appointed surrogate makes the decision, and even when the patient is unable to self-administer the life-ending medication.”¹

Let me repeat that last point:

If aid in dying is a constitutional right, then medical euthanasia is inevitable. In other words, if a patient is too disabled to commit suicide on his or her own, a physician would be obligated to kill the patient.

Proponents will dismiss this last statement as alarmist and unfounded. They will point to a 20-year history of legalized aid in dying in Oregon, and insist there has never been a problem and no attempt to expand the practice to include euthanasia.

What they don’t mention is that such an attempt would be politically disastrous for the right-to-die movement. In 2015, 25 states and the District of Columbia considered legalization bills.² After careful consideration and debate, these bills failed in every state except California, and in that state it passed only because of an extraordinary and unusual legislative maneuver. The bill initially failed in regular session, but passed in special session when the California Medical Association (CMA) shifted to a neutral stance. That shift would never have happened had CMA members been aware of the legal inevitability of euthanasia. At this stage of the political process, the goal of the right-to-die movement is to get laws on the books in as many states as possible before pushing for more.

The New Mexico opinion echoes a similar decision issued this past May by a New York appellate court. The plaintiffs in that case were three terminally ill New Yorkers and five doctors, as well as two euthanasia advocacy groups. The arguments were virtually identical to those made in New Mexico, asserting a fundamental right to medical aid in dying based upon personal autonomy. They additionally sought an exception to New York criminal law, which defined assisted suicide as second-degree manslaughter. In Myers v. Schneiderman, the court observed that no appellate court had ever found medical aid in dying to be a fundamental right and that no new developments justified a change in this interpretation.³ While the court acknowledged some change in public opinion as reflected in telephone surveys, it correctly gave little weight to this argument: “Plaintiffs fail to allege whether those public polls reflect the opinion of people who are fully informed of the arguments espoused by those who caution against permitting aid-in-dying, such as those articulated in the New York State Task Force on Life and the Law.”

This task force issued the following recommendation in its 1994 report,⁴ “When Death is Sought: Assisted Suicide and Euthanasia in the Medical Context”: “The Task Force members unanimously recommend that existing law should not be changed to permit assisted suicide or euthanasia. Legalizing assisted suicide and euthanasia would pose profound risks to many individuals who are ill and vulnerable. The Task Force members concluded that the potential dangers of this dramatic change in public policy would outweigh any benefit that might be achieved” (Chapter 6, p. 120).

The New York aid-in-dying bill did not progress out of committee by the time the session ended in June.

Lastly, both of these cases concluded that medical aid in dying was suicide. In Myers, Judge Angela M. Mazzarelli stated: “The word ‘suicide’ has a straightforward meaning, and a dictionary is hardly necessary … It is traditionally defined as ‘the act or instance of taking one’s own life voluntarily and intentionally.’ ... Whatever label one puts on the act that plaintiffs are asking us to permit, it unquestionably fits that literal description.”

Regardless of the label used – aid in dying, assisted suicide, or self-deliverance – it is not a civil right.

Resources

1. http://www.nmcompcomm.us/nmcases/nmsc/slips/SC35,478.pdf

2. https://www.deathwithdignity.org/assisted-dying-chronology/

3. http://www.nycourts.gov/reporter/3dseries/2016/2016_03457.htm

4. https://www.health.ny.gov/regulations/task_force/reports_publications/when_death_is_sought/

Dr. Hanson is a forensic psychiatrist and coauthor of “Shrink Rap: Three Psychiatrists Explain Their Work.” The opinions expressed are those of the author only, and do not represent those of any of Dr. Hanson’s employers or consultees, including the Maryland Department of Health and Mental Hygiene or the Maryland Division of Correction.

On June 30, New Mexico became the latest state to throw out a challenge to a law banning physician-assisted suicide. In Morris v. Brandenburg, proponents of the right-to-die movement contended that medical aid in dying was a fundamental right, meaning that any law that restricted the right should be presumed to be invalid unless the state had a compelling reason for the restriction.

In a unanimous decision, the New Mexico Supreme Court held that there was no such right under that state’s constitution, and that even if the right had existed, the state had several compelling reasons to restrict it: to protect “the integrity and ethics of the medical profession”; to protect “vulnerable groups – including the poor, the elderly, and disabled persons – from the risk of subtle coercion and undue influence in end-of-life situations, including pressures associated with the substantial financial burden of end-of-life health care costs”; and to protect “against voluntary or involuntary euthanasia because if physician aid in dying is a constitutional right, it must be made available to everyone, even when a duly appointed surrogate makes the decision, and even when the patient is unable to self-administer the life-ending medication.”¹

Let me repeat that last point:

If aid in dying is a constitutional right, then medical euthanasia is inevitable. In other words, if a patient is too disabled to commit suicide on his or her own, a physician would be obligated to kill the patient.

Proponents will dismiss this last statement as alarmist and unfounded. They will point to a 20-year history of legalized aid in dying in Oregon, and insist there has never been a problem and no attempt to expand the practice to include euthanasia.

What they don’t mention is that such an attempt would be politically disastrous for the right-to-die movement. In 2015, 25 states and the District of Columbia considered legalization bills.² After careful consideration and debate, these bills failed in every state except California, and in that state it passed only because of an extraordinary and unusual legislative maneuver. The bill initially failed in regular session, but passed in special session when the California Medical Association (CMA) shifted to a neutral stance. That shift would never have happened had CMA members been aware of the legal inevitability of euthanasia. At this stage of the political process, the goal of the right-to-die movement is to get laws on the books in as many states as possible before pushing for more.

The New Mexico opinion echoes a similar decision issued this past May by a New York appellate court. The plaintiffs in that case were three terminally ill New Yorkers and five doctors, as well as two euthanasia advocacy groups. The arguments were virtually identical to those made in New Mexico, asserting a fundamental right to medical aid in dying based upon personal autonomy. They additionally sought an exception to New York criminal law, which defined assisted suicide as second-degree manslaughter. In Myers v. Schneiderman, the court observed that no appellate court had ever found medical aid in dying to be a fundamental right and that no new developments justified a change in this interpretation.³ While the court acknowledged some change in public opinion as reflected in telephone surveys, it correctly gave little weight to this argument: “Plaintiffs fail to allege whether those public polls reflect the opinion of people who are fully informed of the arguments espoused by those who caution against permitting aid-in-dying, such as those articulated in the New York State Task Force on Life and the Law.”

This task force issued the following recommendation in its 1994 report,⁴ “When Death is Sought: Assisted Suicide and Euthanasia in the Medical Context”: “The Task Force members unanimously recommend that existing law should not be changed to permit assisted suicide or euthanasia. Legalizing assisted suicide and euthanasia would pose profound risks to many individuals who are ill and vulnerable. The Task Force members concluded that the potential dangers of this dramatic change in public policy would outweigh any benefit that might be achieved” (Chapter 6, p. 120).

The New York aid-in-dying bill did not progress out of committee by the time the session ended in June.

Lastly, both of these cases concluded that medical aid in dying was suicide. In Myers, Judge Angela M. Mazzarelli stated: “The word ‘suicide’ has a straightforward meaning, and a dictionary is hardly necessary … It is traditionally defined as ‘the act or instance of taking one’s own life voluntarily and intentionally.’ ... Whatever label one puts on the act that plaintiffs are asking us to permit, it unquestionably fits that literal description.”

Regardless of the label used – aid in dying, assisted suicide, or self-deliverance – it is not a civil right.

Resources

1. http://www.nmcompcomm.us/nmcases/nmsc/slips/SC35,478.pdf

2. https://www.deathwithdignity.org/assisted-dying-chronology/

3. http://www.nycourts.gov/reporter/3dseries/2016/2016_03457.htm

4. https://www.health.ny.gov/regulations/task_force/reports_publications/when_death_is_sought/

Dr. Hanson is a forensic psychiatrist and coauthor of “Shrink Rap: Three Psychiatrists Explain Their Work.” The opinions expressed are those of the author only, and do not represent those of any of Dr. Hanson’s employers or consultees, including the Maryland Department of Health and Mental Hygiene or the Maryland Division of Correction.

On June 30, New Mexico became the latest state to throw out a challenge to a law banning physician-assisted suicide. In Morris v. Brandenburg, proponents of the right-to-die movement contended that medical aid in dying was a fundamental right, meaning that any law that restricted the right should be presumed to be invalid unless the state had a compelling reason for the restriction.

In a unanimous decision, the New Mexico Supreme Court held that there was no such right under that state’s constitution, and that even if the right had existed, the state had several compelling reasons to restrict it: to protect “the integrity and ethics of the medical profession”; to protect “vulnerable groups – including the poor, the elderly, and disabled persons – from the risk of subtle coercion and undue influence in end-of-life situations, including pressures associated with the substantial financial burden of end-of-life health care costs”; and to protect “against voluntary or involuntary euthanasia because if physician aid in dying is a constitutional right, it must be made available to everyone, even when a duly appointed surrogate makes the decision, and even when the patient is unable to self-administer the life-ending medication.”¹

Let me repeat that last point:

If aid in dying is a constitutional right, then medical euthanasia is inevitable. In other words, if a patient is too disabled to commit suicide on his or her own, a physician would be obligated to kill the patient.

Proponents will dismiss this last statement as alarmist and unfounded. They will point to a 20-year history of legalized aid in dying in Oregon, and insist there has never been a problem and no attempt to expand the practice to include euthanasia.

What they don’t mention is that such an attempt would be politically disastrous for the right-to-die movement. In 2015, 25 states and the District of Columbia considered legalization bills.² After careful consideration and debate, these bills failed in every state except California, and in that state it passed only because of an extraordinary and unusual legislative maneuver. The bill initially failed in regular session, but passed in special session when the California Medical Association (CMA) shifted to a neutral stance. That shift would never have happened had CMA members been aware of the legal inevitability of euthanasia. At this stage of the political process, the goal of the right-to-die movement is to get laws on the books in as many states as possible before pushing for more.

The New Mexico opinion echoes a similar decision issued this past May by a New York appellate court. The plaintiffs in that case were three terminally ill New Yorkers and five doctors, as well as two euthanasia advocacy groups. The arguments were virtually identical to those made in New Mexico, asserting a fundamental right to medical aid in dying based upon personal autonomy. They additionally sought an exception to New York criminal law, which defined assisted suicide as second-degree manslaughter. In Myers v. Schneiderman, the court observed that no appellate court had ever found medical aid in dying to be a fundamental right and that no new developments justified a change in this interpretation.³ While the court acknowledged some change in public opinion as reflected in telephone surveys, it correctly gave little weight to this argument: “Plaintiffs fail to allege whether those public polls reflect the opinion of people who are fully informed of the arguments espoused by those who caution against permitting aid-in-dying, such as those articulated in the New York State Task Force on Life and the Law.”

This task force issued the following recommendation in its 1994 report,⁴ “When Death is Sought: Assisted Suicide and Euthanasia in the Medical Context”: “The Task Force members unanimously recommend that existing law should not be changed to permit assisted suicide or euthanasia. Legalizing assisted suicide and euthanasia would pose profound risks to many individuals who are ill and vulnerable. The Task Force members concluded that the potential dangers of this dramatic change in public policy would outweigh any benefit that might be achieved” (Chapter 6, p. 120).

The New York aid-in-dying bill did not progress out of committee by the time the session ended in June.

Lastly, both of these cases concluded that medical aid in dying was suicide. In Myers, Judge Angela M. Mazzarelli stated: “The word ‘suicide’ has a straightforward meaning, and a dictionary is hardly necessary … It is traditionally defined as ‘the act or instance of taking one’s own life voluntarily and intentionally.’ ... Whatever label one puts on the act that plaintiffs are asking us to permit, it unquestionably fits that literal description.”

Regardless of the label used – aid in dying, assisted suicide, or self-deliverance – it is not a civil right.

Resources

1. http://www.nmcompcomm.us/nmcases/nmsc/slips/SC35,478.pdf

2. https://www.deathwithdignity.org/assisted-dying-chronology/

3. http://www.nycourts.gov/reporter/3dseries/2016/2016_03457.htm

4. https://www.health.ny.gov/regulations/task_force/reports_publications/when_death_is_sought/

Dr. Hanson is a forensic psychiatrist and coauthor of “Shrink Rap: Three Psychiatrists Explain Their Work.” The opinions expressed are those of the author only, and do not represent those of any of Dr. Hanson’s employers or consultees, including the Maryland Department of Health and Mental Hygiene or the Maryland Division of Correction.

To the Editor:

Azathioprine (AZA) hypersensitivity is an immunologically mediated reaction that presents within 1 to 4 weeks of drug initiation.¹ Its cutaneous manifestations include Sweet syndrome, erythema nodosum (EN), and acute generalized exanthematous pustulosis, with 88% of cases presenting as neutrophilic dermatoses.² Confirmation with cutaneous biopsy and cessation of medication is essential to prevent life-threatening anaphylactoid reactions.

A 58-year-old man with a history of Crohn disease was admitted with high fevers (>38.9°C); abdominal pain; diarrhea; and a nonpruritic “pimplelike” rash on the face, chest, and back with a tender nodule on the right leg of 5 days’ duration. Eight days prior to admission, he had started AZA for treatment of Crohn disease. In the hospital he received intravenous metronidazole for a presumed bowel infection; however, the lesions and symptoms did not resolve. Other medical history included psoriatic arthritis for which he was taking oral prednisone 50 mg daily; prednisone was continued during hospitalization.

Physical examination showed that the patient was alert and well appearing. On the face, upper chest and back (Figure 1), shoulders, and knees were fewer than 20 sparsely distributed, nontender, 3- to 4-mm pustules. The patient’s scalp, lower back, abdomen, arms, and feet were spared. There also was a solitary 3.5-cm, tender, erythematous nodule on the right lower leg (Figure 2). Blood tests revealed leukocytosis (15,000/mm³ [reference range, 4300–10,300/mm³]) with neutrophilia (90%) and an elevated C-reactive protein level of 173 mg/L (reference range, <10 mg/L). Liver function tests were normal. Thiopurine methyltransferase (TPMT) was on the low end of the reference range. Tissue culture of a shoulder pustule grew only Staphylococcus non-aureus. Blood cultures were negative. A 4-mm punch biopsy specimen from the right leg nodule revealed septal panniculitis with neutrophilic and granulomatous infiltrate consistent with EN.

A clinical diagnosis of AZA hypersensitivity was made. Antibiotics and AZA were discontinued and the patient’s lesions resolved within 6 days. Medication rechallenge was not attempted and the patient is now managed with infliximab.

Azathioprine is a well-known and commonly used drug for inflammatory bowel diseases, rheumatoid arthritis, and prevention of transplant rejection. Hypersensitivity is a lesser-known complication of AZA therapy, with most reactions occurring within 4 weeks of treatment initiation. A PubMed search of articles indexed for MEDLINE using the search terms azathioprine and hypersensitivity found only 67 documented cases of AZA hypersensitivity between 1986 and 2009.² Common findings include fever, malaise, arthralgia, nausea, vomiting, diarrhea, headache, and neutrophilic dermatoses.

Previously reported cases of AZA hypersensitivity with cutaneous manifestations include Sweet syndrome (17.9%), small vessel vasculitis (10.4%), EN (4.4%), acute generalized exanthematous pustulosis (4.4%), and nonspecific cutaneous findings (11.9%).² One other case reported AZA hypersensitivity presenting as EN with a neutrophilic pustular dermatosis.³ Although Sweet syndrome–like lesions, EN, and acute generalized exanthematous pustulosis have been reported in the context of inflammatory bowel disease, in this case the appearance of these symptoms within 1 week of AZA initiation and resolution after AZA discontinuation is highly suggestive of AZA hypersensitivity. Also, several reports have documented rapid (within a few hours) recurrence of symptoms on rechallenge with AZA.^4-6 Moreover, cases of cutaneous AZA hypersensitivity reactions in patients with no history of inflammatory bowel diseases have been reported.^6-8

As in this case, cutaneous AZA hypersensitivity can occur even in the setting of normal TPMT levels, suggesting that this phenomenon is a dose-independent reaction.² Abnormal metabolism of AZA does not appear to be related to previously reported neutrophilic pustular dermatosis^3,4 or EN.⁴ Although the mechanism of hypersensitivity is unclear, there is a report of a patient who developed AZA hypersensitivity but was able to tolerate 6-mercaptopurine, a metabolite of AZA. The authors suggested that the imidazole component of AZA might be responsible for hypersensitivity reactions.⁹

The differential diagnosis of a patient with these findings includes infectious, rheumatologic, neurologic, or autoimmune diseases, as well as septic shock. Hence, negative cultures and a failure to respond to antibiotics make infection less likely. An appropriate time course of AZA initiation, the development of rash, and a cutaneous biopsy can lead to prompt diagnosis and cessation of AZA.

Once AZA hypersensitivity is suspected, the drug should be discontinued and the reaction should resolve within 2 to 3 days² and the skin lesions within 5 to 6 days.^2,10 Medication rechallenge is contraindicated because AZA rarely has been associated with shock syndrome and hypotension.^11-19

Azathioprine hypersensitivity is a serious yet still underrecognized condition in the dermatologic community. In our case, symptoms appeared rapidly and resolved quickly after AZA was discontinued. Azathioprine-induced neutrophilic dermatosis presenting with EN should be recognized as a potential dermatologic manifestation of AZA hypersensitivity, which is a dose-dependent reaction even with normal TPMT levels. Rechallenge with AZA is not recommended due to the risk of a life-threatening anaphylactoid reaction.

To the Editor:

Azathioprine (AZA) hypersensitivity is an immunologically mediated reaction that presents within 1 to 4 weeks of drug initiation.¹ Its cutaneous manifestations include Sweet syndrome, erythema nodosum (EN), and acute generalized exanthematous pustulosis, with 88% of cases presenting as neutrophilic dermatoses.² Confirmation with cutaneous biopsy and cessation of medication is essential to prevent life-threatening anaphylactoid reactions.

A 58-year-old man with a history of Crohn disease was admitted with high fevers (>38.9°C); abdominal pain; diarrhea; and a nonpruritic “pimplelike” rash on the face, chest, and back with a tender nodule on the right leg of 5 days’ duration. Eight days prior to admission, he had started AZA for treatment of Crohn disease. In the hospital he received intravenous metronidazole for a presumed bowel infection; however, the lesions and symptoms did not resolve. Other medical history included psoriatic arthritis for which he was taking oral prednisone 50 mg daily; prednisone was continued during hospitalization.

Physical examination showed that the patient was alert and well appearing. On the face, upper chest and back (Figure 1), shoulders, and knees were fewer than 20 sparsely distributed, nontender, 3- to 4-mm pustules. The patient’s scalp, lower back, abdomen, arms, and feet were spared. There also was a solitary 3.5-cm, tender, erythematous nodule on the right lower leg (Figure 2). Blood tests revealed leukocytosis (15,000/mm³ [reference range, 4300–10,300/mm³]) with neutrophilia (90%) and an elevated C-reactive protein level of 173 mg/L (reference range, <10 mg/L). Liver function tests were normal. Thiopurine methyltransferase (TPMT) was on the low end of the reference range. Tissue culture of a shoulder pustule grew only Staphylococcus non-aureus. Blood cultures were negative. A 4-mm punch biopsy specimen from the right leg nodule revealed septal panniculitis with neutrophilic and granulomatous infiltrate consistent with EN.

A clinical diagnosis of AZA hypersensitivity was made. Antibiotics and AZA were discontinued and the patient’s lesions resolved within 6 days. Medication rechallenge was not attempted and the patient is now managed with infliximab.

Azathioprine is a well-known and commonly used drug for inflammatory bowel diseases, rheumatoid arthritis, and prevention of transplant rejection. Hypersensitivity is a lesser-known complication of AZA therapy, with most reactions occurring within 4 weeks of treatment initiation. A PubMed search of articles indexed for MEDLINE using the search terms azathioprine and hypersensitivity found only 67 documented cases of AZA hypersensitivity between 1986 and 2009.² Common findings include fever, malaise, arthralgia, nausea, vomiting, diarrhea, headache, and neutrophilic dermatoses.

Previously reported cases of AZA hypersensitivity with cutaneous manifestations include Sweet syndrome (17.9%), small vessel vasculitis (10.4%), EN (4.4%), acute generalized exanthematous pustulosis (4.4%), and nonspecific cutaneous findings (11.9%).² One other case reported AZA hypersensitivity presenting as EN with a neutrophilic pustular dermatosis.³ Although Sweet syndrome–like lesions, EN, and acute generalized exanthematous pustulosis have been reported in the context of inflammatory bowel disease, in this case the appearance of these symptoms within 1 week of AZA initiation and resolution after AZA discontinuation is highly suggestive of AZA hypersensitivity. Also, several reports have documented rapid (within a few hours) recurrence of symptoms on rechallenge with AZA.^4-6 Moreover, cases of cutaneous AZA hypersensitivity reactions in patients with no history of inflammatory bowel diseases have been reported.^6-8

As in this case, cutaneous AZA hypersensitivity can occur even in the setting of normal TPMT levels, suggesting that this phenomenon is a dose-independent reaction.² Abnormal metabolism of AZA does not appear to be related to previously reported neutrophilic pustular dermatosis^3,4 or EN.⁴ Although the mechanism of hypersensitivity is unclear, there is a report of a patient who developed AZA hypersensitivity but was able to tolerate 6-mercaptopurine, a metabolite of AZA. The authors suggested that the imidazole component of AZA might be responsible for hypersensitivity reactions.⁹

The differential diagnosis of a patient with these findings includes infectious, rheumatologic, neurologic, or autoimmune diseases, as well as septic shock. Hence, negative cultures and a failure to respond to antibiotics make infection less likely. An appropriate time course of AZA initiation, the development of rash, and a cutaneous biopsy can lead to prompt diagnosis and cessation of AZA.

Once AZA hypersensitivity is suspected, the drug should be discontinued and the reaction should resolve within 2 to 3 days² and the skin lesions within 5 to 6 days.^2,10 Medication rechallenge is contraindicated because AZA rarely has been associated with shock syndrome and hypotension.^11-19

Azathioprine hypersensitivity is a serious yet still underrecognized condition in the dermatologic community. In our case, symptoms appeared rapidly and resolved quickly after AZA was discontinued. Azathioprine-induced neutrophilic dermatosis presenting with EN should be recognized as a potential dermatologic manifestation of AZA hypersensitivity, which is a dose-dependent reaction even with normal TPMT levels. Rechallenge with AZA is not recommended due to the risk of a life-threatening anaphylactoid reaction.

To the Editor:

Azathioprine (AZA) hypersensitivity is an immunologically mediated reaction that presents within 1 to 4 weeks of drug initiation.¹ Its cutaneous manifestations include Sweet syndrome, erythema nodosum (EN), and acute generalized exanthematous pustulosis, with 88% of cases presenting as neutrophilic dermatoses.² Confirmation with cutaneous biopsy and cessation of medication is essential to prevent life-threatening anaphylactoid reactions.

A 58-year-old man with a history of Crohn disease was admitted with high fevers (>38.9°C); abdominal pain; diarrhea; and a nonpruritic “pimplelike” rash on the face, chest, and back with a tender nodule on the right leg of 5 days’ duration. Eight days prior to admission, he had started AZA for treatment of Crohn disease. In the hospital he received intravenous metronidazole for a presumed bowel infection; however, the lesions and symptoms did not resolve. Other medical history included psoriatic arthritis for which he was taking oral prednisone 50 mg daily; prednisone was continued during hospitalization.

Physical examination showed that the patient was alert and well appearing. On the face, upper chest and back (Figure 1), shoulders, and knees were fewer than 20 sparsely distributed, nontender, 3- to 4-mm pustules. The patient’s scalp, lower back, abdomen, arms, and feet were spared. There also was a solitary 3.5-cm, tender, erythematous nodule on the right lower leg (Figure 2). Blood tests revealed leukocytosis (15,000/mm³ [reference range, 4300–10,300/mm³]) with neutrophilia (90%) and an elevated C-reactive protein level of 173 mg/L (reference range, <10 mg/L). Liver function tests were normal. Thiopurine methyltransferase (TPMT) was on the low end of the reference range. Tissue culture of a shoulder pustule grew only Staphylococcus non-aureus. Blood cultures were negative. A 4-mm punch biopsy specimen from the right leg nodule revealed septal panniculitis with neutrophilic and granulomatous infiltrate consistent with EN.

A clinical diagnosis of AZA hypersensitivity was made. Antibiotics and AZA were discontinued and the patient’s lesions resolved within 6 days. Medication rechallenge was not attempted and the patient is now managed with infliximab.

Azathioprine is a well-known and commonly used drug for inflammatory bowel diseases, rheumatoid arthritis, and prevention of transplant rejection. Hypersensitivity is a lesser-known complication of AZA therapy, with most reactions occurring within 4 weeks of treatment initiation. A PubMed search of articles indexed for MEDLINE using the search terms azathioprine and hypersensitivity found only 67 documented cases of AZA hypersensitivity between 1986 and 2009.² Common findings include fever, malaise, arthralgia, nausea, vomiting, diarrhea, headache, and neutrophilic dermatoses.

Previously reported cases of AZA hypersensitivity with cutaneous manifestations include Sweet syndrome (17.9%), small vessel vasculitis (10.4%), EN (4.4%), acute generalized exanthematous pustulosis (4.4%), and nonspecific cutaneous findings (11.9%).² One other case reported AZA hypersensitivity presenting as EN with a neutrophilic pustular dermatosis.³ Although Sweet syndrome–like lesions, EN, and acute generalized exanthematous pustulosis have been reported in the context of inflammatory bowel disease, in this case the appearance of these symptoms within 1 week of AZA initiation and resolution after AZA discontinuation is highly suggestive of AZA hypersensitivity. Also, several reports have documented rapid (within a few hours) recurrence of symptoms on rechallenge with AZA.^4-6 Moreover, cases of cutaneous AZA hypersensitivity reactions in patients with no history of inflammatory bowel diseases have been reported.^6-8

As in this case, cutaneous AZA hypersensitivity can occur even in the setting of normal TPMT levels, suggesting that this phenomenon is a dose-independent reaction.² Abnormal metabolism of AZA does not appear to be related to previously reported neutrophilic pustular dermatosis^3,4 or EN.⁴ Although the mechanism of hypersensitivity is unclear, there is a report of a patient who developed AZA hypersensitivity but was able to tolerate 6-mercaptopurine, a metabolite of AZA. The authors suggested that the imidazole component of AZA might be responsible for hypersensitivity reactions.⁹

The differential diagnosis of a patient with these findings includes infectious, rheumatologic, neurologic, or autoimmune diseases, as well as septic shock. Hence, negative cultures and a failure to respond to antibiotics make infection less likely. An appropriate time course of AZA initiation, the development of rash, and a cutaneous biopsy can lead to prompt diagnosis and cessation of AZA.

Once AZA hypersensitivity is suspected, the drug should be discontinued and the reaction should resolve within 2 to 3 days² and the skin lesions within 5 to 6 days.^2,10 Medication rechallenge is contraindicated because AZA rarely has been associated with shock syndrome and hypotension.^11-19

Azathioprine hypersensitivity is a serious yet still underrecognized condition in the dermatologic community. In our case, symptoms appeared rapidly and resolved quickly after AZA was discontinued. Azathioprine-induced neutrophilic dermatosis presenting with EN should be recognized as a potential dermatologic manifestation of AZA hypersensitivity, which is a dose-dependent reaction even with normal TPMT levels. Rechallenge with AZA is not recommended due to the risk of a life-threatening anaphylactoid reaction.

To the Editor:

Disseminated granuloma annulare is a noninfectious granulomatous disease of unknown etiology. Reported precipitating factors include trauma, sun exposure, viral infection, vaccination, and malignancy.¹ In contrast to a localized variant, disseminated granuloma annulare is associated with a later age of onset, longer duration, and recalcitrance to therapy.² Although a variety of therapeutic approaches exist, there are limited efficacy data, which is complicated by the spontaneous, self-limited nature of the disease.^3,4

A 47-year-old man presented with an eruption of a thick red plaque on the dorsal aspect of the left hand (Figure). The eruption began 6 weeks following fixation of a Galeazzi fracture of the right radius with a stainless steel volar plate. Subsequent to the initial eruption, similar indurated plaques developed on the left thenar area, bilateral axillae, and bilateral legs. A punch biopsy was conducted to rule out necrobiosis lipoidica diabeticorum and sarcoidosis as well as to histopathologically confirm the clinical diagnosis of disseminated granuloma annulare. Following diagnosis, the patient received topical clobetasol for application to the advancing borders of the plaques. At 4-month follow-up, additional plaques continued to develop. The patient was not interested in pursuing alternative courses of therapy and felt that the implantation of surgical hardware was the cause. To the best of our knowledge, there have been no reports of precipitation of disseminated granuloma annulare in response to surgical hardware. Given the time course of onset of the eruption it was plausible that the hardware was the inciting event. The orthopedist thought that the fracture had healed sufficiently to remove the volar plate. The patient elected to have the hardware removed to potentially resolve or arrest the progression of the plaques. Resolution of the plaques was observed by the patient 2 weeks following surgical removal of the volar plate. At 4 months following hardware removal, the patient only had 2 slightly pink, hyperpigmented lesions on the left hand in the areas most severely affected, with complete resolution of all other plaques. The patient was given topical clobetasol for the residual lesions.

Precipitation and spontaneous resolution of disseminated granuloma annulare following the implantation and removal of surgical hardware is rare. Resolution following hardware removal is consistent with the theory that pathogenesis is due to a delayed-type hypersensitivity reaction to an inciting factor.⁵ Our case suggests that disseminated granuloma annulare may occur as a delayed-type hypersensitivity reaction to implanted surgical hardware, which should be considered in the etiology and potential therapeutic options for this disorder.

To the Editor:

Disseminated granuloma annulare is a noninfectious granulomatous disease of unknown etiology. Reported precipitating factors include trauma, sun exposure, viral infection, vaccination, and malignancy.¹ In contrast to a localized variant, disseminated granuloma annulare is associated with a later age of onset, longer duration, and recalcitrance to therapy.² Although a variety of therapeutic approaches exist, there are limited efficacy data, which is complicated by the spontaneous, self-limited nature of the disease.^3,4

A 47-year-old man presented with an eruption of a thick red plaque on the dorsal aspect of the left hand (Figure). The eruption began 6 weeks following fixation of a Galeazzi fracture of the right radius with a stainless steel volar plate. Subsequent to the initial eruption, similar indurated plaques developed on the left thenar area, bilateral axillae, and bilateral legs. A punch biopsy was conducted to rule out necrobiosis lipoidica diabeticorum and sarcoidosis as well as to histopathologically confirm the clinical diagnosis of disseminated granuloma annulare. Following diagnosis, the patient received topical clobetasol for application to the advancing borders of the plaques. At 4-month follow-up, additional plaques continued to develop. The patient was not interested in pursuing alternative courses of therapy and felt that the implantation of surgical hardware was the cause. To the best of our knowledge, there have been no reports of precipitation of disseminated granuloma annulare in response to surgical hardware. Given the time course of onset of the eruption it was plausible that the hardware was the inciting event. The orthopedist thought that the fracture had healed sufficiently to remove the volar plate. The patient elected to have the hardware removed to potentially resolve or arrest the progression of the plaques. Resolution of the plaques was observed by the patient 2 weeks following surgical removal of the volar plate. At 4 months following hardware removal, the patient only had 2 slightly pink, hyperpigmented lesions on the left hand in the areas most severely affected, with complete resolution of all other plaques. The patient was given topical clobetasol for the residual lesions.

Precipitation and spontaneous resolution of disseminated granuloma annulare following the implantation and removal of surgical hardware is rare. Resolution following hardware removal is consistent with the theory that pathogenesis is due to a delayed-type hypersensitivity reaction to an inciting factor.⁵ Our case suggests that disseminated granuloma annulare may occur as a delayed-type hypersensitivity reaction to implanted surgical hardware, which should be considered in the etiology and potential therapeutic options for this disorder.

To the Editor:

Disseminated granuloma annulare is a noninfectious granulomatous disease of unknown etiology. Reported precipitating factors include trauma, sun exposure, viral infection, vaccination, and malignancy.¹ In contrast to a localized variant, disseminated granuloma annulare is associated with a later age of onset, longer duration, and recalcitrance to therapy.² Although a variety of therapeutic approaches exist, there are limited efficacy data, which is complicated by the spontaneous, self-limited nature of the disease.^3,4

A 47-year-old man presented with an eruption of a thick red plaque on the dorsal aspect of the left hand (Figure). The eruption began 6 weeks following fixation of a Galeazzi fracture of the right radius with a stainless steel volar plate. Subsequent to the initial eruption, similar indurated plaques developed on the left thenar area, bilateral axillae, and bilateral legs. A punch biopsy was conducted to rule out necrobiosis lipoidica diabeticorum and sarcoidosis as well as to histopathologically confirm the clinical diagnosis of disseminated granuloma annulare. Following diagnosis, the patient received topical clobetasol for application to the advancing borders of the plaques. At 4-month follow-up, additional plaques continued to develop. The patient was not interested in pursuing alternative courses of therapy and felt that the implantation of surgical hardware was the cause. To the best of our knowledge, there have been no reports of precipitation of disseminated granuloma annulare in response to surgical hardware. Given the time course of onset of the eruption it was plausible that the hardware was the inciting event. The orthopedist thought that the fracture had healed sufficiently to remove the volar plate. The patient elected to have the hardware removed to potentially resolve or arrest the progression of the plaques. Resolution of the plaques was observed by the patient 2 weeks following surgical removal of the volar plate. At 4 months following hardware removal, the patient only had 2 slightly pink, hyperpigmented lesions on the left hand in the areas most severely affected, with complete resolution of all other plaques. The patient was given topical clobetasol for the residual lesions.

Precipitation and spontaneous resolution of disseminated granuloma annulare following the implantation and removal of surgical hardware is rare. Resolution following hardware removal is consistent with the theory that pathogenesis is due to a delayed-type hypersensitivity reaction to an inciting factor.⁵ Our case suggests that disseminated granuloma annulare may occur as a delayed-type hypersensitivity reaction to implanted surgical hardware, which should be considered in the etiology and potential therapeutic options for this disorder.