Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are T-cell-mediated skin eruptions that are part of a broader category known as severe cutaneous adverse drug reactions (SCAR). SJS involves less than 10%of the body surface area, whereas skin detachment in TEN is more severe and involves 30% of the body surface area. Skin detachment that falls between 10% and 30% is described as SJS-TEN overlap.1 SJS and TEN are rare syndromes, with an estimated incidence at 1 to 2 cases per 1 million inhabitants per year in European countries.2 However, these conditions may lead to mortality or severe disability of previously healthy people and have prompted the withdrawal of newly released drugs3. Drugs highly suspected to cause SJS/TEN include allopurinol, aromatic anticonvulsants (carbamazepine, phenobarbital, phenytoin, and lamotrigine), nevirapine, sulfonamides, and oxicam-NSAIDs. Weaker associations have been additionally found for paracetamol, aminopenicillins, cephalosporins, and quinolones.2,4 Although hypersensitivity reactions have been considered as “type B” or dose-independent reactions, accumulating evidence suggests that the risk may be greater with high doses and rapid dose escalation, at least for allopurinol and lamotrigine.5–7 The propensity to develop SJS and TEN varies across populations of different ethnicities. The most prominent example is the strong association between carbamazepine-induced SJS/TEN and the presence of the human leukocyte antigen (HLA) allele B*15:02 in individuals of Han Chinese and other Southeast Asian origin8 but not in Northern Europeans.9 In the latter population10 and in patients of Japanese origin,11 carbamazepine-induced cutaneous adverse reactions have been linked to another HLA allele, A*31:01. This information has been translated into an FDA boxed warning that requires screening for HLA-B*15:02 in patients of high-risk ethnic origin and a warning for HLA-A*31:01.12 Likewise, the association between HLA-B*58:01 and allopurinol-induced SCAR is strong in patients of Asian origin13 but is weaker in white populations in Europe, in which HLA-B*58:01 is also much less prevalent than in Han Chinese.14–16 The variability among ethnic groups may also apply to Israeli populations. For instance, we have recently shown that

Causative Drugs of Stevens-Johnson Syndrome and Toxic Epidermal Necrolysis in Israel.

Severe cutaneous adverse reaction associated with antiseizure medications: Diagnosis, management, and prevention.

Drug rash with eosinophilia and systemic symptoms (DRESS) is a rare but potentially life-threatening condition with high mortality. Diagnosis is challenging due to variable clinical presentation and a protracted latency period following initiation of the offending drug. DRESS is a complex interplay that starts by introduction of the offending drug, reactivation of viruses and activation of the immune system. Herpes virus reactivation is considered a diagnostic marker and indicator of illness severity. Prompt recognition and the removal of offending agent remain the key to successful treatment. In cases of severe organ involvement, corticosteroids, immunoglobulins, antiviral and specialist consultation may be helpful. Here we present a case of a 36-year-old African-American male who presented with symptoms mimicking sepsis with an associated skin eruption that was diagnosed as DRESS.

/pdf/drug-rash-with-eosinophilia-and-systemic-symptoms-dress-tidctza3od.pdf

Drug rash with eosinophilia and systemic symptoms (DRESS) caused by phenytoin.

Similar antiseizure medication refill characteristics in Hispanic and White pediatric patients

Ethnic Differences in Clinical Presentations and Esophageal High-Resolution Manometry Findings in Patients with Achalasia

The human leukocyte antigen (HLA) alleles B*15:02 and A*31:01 have been identified as predictive markers of adverse cutaneous effects of carbamazepine and phenytoin in Asian and North European populations, respectively. Our aim was to estimate the distribution of these alleles in Jewish and Arab populations in Israel. The HLA-B*15:02 and HLA-A*31:01 carrier rate was estimated based on data from the Hadassah Bone Marrow Registry. Data on Stevens-Johnson syndrome (SJS)- and toxic epidermal necrolysis (TEN)-related hospitalizations were obtained from the Israeli Ministry of Health (MOH) registries and from four Israeli medical centers. Of 83,705 Jewish and Arab-Muslim donors, 81 individuals of known origin carried the HLA-B*15:02. Among them, 66 were Jews of India-Cochin descent. Of the Cochin Jewish donors, 12.7% were B*15:02 carriers. HLA-A*31:01 carrier incidence among Arab and Jewish Israeli populations (3.5% and 2.2%, respectively) was within the range reported in other countries. We did not identify SJS- or TEN-related hospitalizations of Jews of Indian descent. Yet, this population should be considered at greater risk for antiepileptic drug-induced SJS and TEN. Until further data on actual risk are available, such patients should be typed for HLA-B before treatment with carbamazepine or phenytoin.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1111/epi.13498

Genetic risk factors for antiepileptic drug-induced hypersensitivity reactions in Israeli populations.

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Genetic risk factors for antiepileptic drug-induced hypersensitivity reactions in Israeli populations.