Drug Allergy: A 2022 Practice Parameter Update.

Drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome is a severe multiorgan hypersensitivity reaction mostly caused by a limited number of eliciting drugs in patients with a genetic predisposition. Patients with DRESS syndrome present with characteristic but variable clinical and pathological features. Reactivation of human herpesviruses (HHV), especially HHV-6, is the hallmark of the disease. Anti-viral immune responses intertwined with drug hypersensitivity make the disease more complicated and protracted. In recent years, emerging studies have outlined the disease more clearly, though several important questions remain unresolved. In this review, we provide an overview of DRESS syndrome, including clinical presentations, histopathological features, pathomechanisms, and treatments.

https://www.mdpi.com/1422-0067/18/6/1243/pdf

Drug Reaction with Eosinophilia and Systemic Symptoms (DRESS): An Interplay among Drugs, Viruses, and Immune System.

BACKGROUND Cytotoxic T lymphocyte–mediated (CTL-mediated) severe cutaneous adverse reactions (SCARs), including Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN), are rare but life-threatening adverse reactions commonly induced by drugs Although high levels of CTL-associated cytokines, chemokines, or cytotoxic proteins, including TNF-α and granulysin, were observed in SJS-TEN patients in recent studies, the optimal treatment for these diseases remains controversial We aimed to evaluate the efficacy, safety, and therapeutic mechanism of a TNF-α antagonist in CTL-mediated SCARs

METHODS We enrolled 96 patients with SJS-TEN in a randomized trial to compare the effects of the TNF-α antagonist etanercept versus traditional corticosteroids 

RESULTS Etanercept improved clinical outcomes in patients with SJS-TEN Etanercept decreased the SCORTEN-based predicted mortality rate (predicted and observed rates, 177% and 83%, respectively) Compared with corticosteroids, etanercept further reduced the skin-healing time in moderate-to-severe SJS-TEN patients (median time for skin healing was 14 and 19 days for etanercept and corticosteroids, respectively; P = 0010), with a lower incidence of gastrointestinal hemorrhage in all SJS-TEN patients (26% for etanercept and 182% for corticosteroids; P = 003) In the therapeutic mechanism study, etanercept decreased the TNF-α and granulysin secretions in blister fluids and plasma (457%–625% decrease after treatment; all P < 005) and increased the Treg population (2-fold percentage increase after treatment; P = 0002), which was related to mortality in severe SJS-TEN

CONCLUSIONS The anti–TNF-α biologic agent etanercept serves as an effective alternative for the treatment of CTL-mediated SCARs

TRIAL REGISTRATION ClinicalTrialsgov {"type":"clinical-trial","attrs":{"text":"NCT01276314","term_id":"NCT01276314"}}NCT01276314

FUNDING Ministry of Science and Technology of Taiwan

/pdf/randomized-controlled-trial-of-tnf-a-antagonist-in-ctl-503mngndmw.pdf

Randomized, controlled trial of TNF-α antagonist in CTL-mediated severe cutaneous adverse reactions

Drug hypersensitivity reactions (DHR) are based on distinct mechanisms and are clinically heterogeneous. Taking into account that also off-target activities of drugs may lead to stimulations of immune or inflammatory cells, three forms of DHR were discriminated: the allergic-immune mechanism relies on the covalent binding of drugs/chemicals to proteins, which thereby form new antigens, to which a humoural and/or cellular immune response can develop. In IgE-mediated drug allergies, a possible tolerance mechanism to the drug during sensitization and the need of a covalent hapten-carrier link for initiation, but not for elicitation of IgE-mediated reactions is discussed. The p-i ("pharmacological interaction with immune receptor") concept represents an off-target activity of drugs with immune receptors (HLA or TCR), which can result in unorthodox, alloimmune-like stimulations of T cells. Some of these p-i stimulations occur only in carriers of certain HLA alleles and can result in clinically severe reactions. The third form of DHR ("pseudo-allergy") is represented by drug interactions with receptors or enzymes of inflammatory cells, which may lead to their direct activation or enhanced levels of inflammatory products. Specific IgE or T cells are not involved. This classification is based on the action of drugs and is clinically useful, as it can explain differences in sensitizations, unusual clinical symptoms, dependence on drug concentrations, predictability and immunological and pharmacological cross-reactivities in DHR.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/all.13765

Immune pathomechanism and classification of drug hypersensitivity.

/pdf/sjs-ten-2017-building-multidisciplinary-networks-to-drive-1i5mx17l2l.pdf

SJS/TEN 2017: Building Multidisciplinary Networks to Drive Science and Translation

Background Dapsone is used in the treatment of infections and inflammatory diseases. The dapsone hypersensitivity syndrome, which is associated with a reported mortality of 9.9%, develops in about 0.5 to 3.6% of persons treated with the drug. Currently, no tests are available to predict the risk of the dapsone hypersensitivity syndrome. Methods We performed a genomewide association study involving 872 participants who had received dapsone as part of multidrug therapy for leprosy (39 participants with the dapsone hypersensitivity syndrome and 833 controls), using log-additive tests of single-nucleotide polymorphisms (SNPs) and imputed HLA molecules. For a replication analysis, we genotyped 24 SNPs in an additional 31 participants with the dapsone hypersensitivity syndrome and 1089 controls and performed next-generation sequencing for HLA-B and HLA-C typing at four-digit resolution in an independent series of 37 participants with the dapsone hypersensitivity syndrome and 201 controls. Results Genomewide ass...

https://www.nejm.org/doi/pdf/10.1056/NEJMoa1213096

HLA-B*13:01 and the Dapsone Hypersensitivity Syndrome

The role of LRP1 in Aβ efflux transport across the blood-brain barrier and cognitive dysfunction in diabetes mellitus

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HLA-B*13:01 and the Dapsone Hypersensitivity Syndrome

The role of LRP1 in Aβ efflux transport across the blood-brain barrier and cognitive dysfunction in diabetes mellitus