Recognition and timely adequate treatment of erythema multiforme remain a major challenge. In this review, current diagnostic guidelines, potential pitfalls, and modern/novel treatment options are summarized with the aim to help clinicians with diagnostic and therapeutic decision-making. The diagnosis of erythema multiforme, that has an acute, self-limiting course, is based on its typical clinical picture of targetoid erythematous lesions with predominant acral localization as well as histological findings.
View Article and Find Full Text PDFClin Rev Allergy Immunol
February 2018
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN) are considered a delayed-type hypersensitivity reaction to drugs. They represent true medical emergencies and an early recognition and appropriate management is decisive for the survival. SJS/TEN manifest with an "influenza-like" prodromal phase (malaise, fever), followed by painful cutaneous and mucous membrane (ocular, oral, and genital) lesions, and other systemic symptoms.
View Article and Find Full Text PDFAngioedema (AE) is the end result of deep dermal, subcutaneous and/or submucosal swelling, and represents a major criterion in the definition of anaphylaxis. Drug-induced AE, like other cutaneous drug reactions, is most frequently elicited by betalactam antibiotics and nonsteroidal antiinflammatory drugs. However, differences exist in their underlying pathophysiology (IgE mediated vs.
View Article and Find Full Text PDFJ Allergy Clin Immunol
June 2007
Background: Approximately 3% of patients exposed to iodinated contrast media develop delayed hypersensitivity reactions.
Objective: We wanted to better understand the molecular basis of contrast media cross-reactivity.
Methods: Cross-reactivity was assessed by skin testing and measurement of T-cell activation (CD69 upregulation) and proliferation ((3)H-thymidine uptake, 5,6-carboxyfluorescein diacetate succinimidyl ester staining) of PBMCs, T-cell lines, and T-cell clones of 2 patients with delayed hypersensitivity reactions to iohexol and iomeprol, respectively.
Drug-induced hypersensitivity reactions have been explained by the hapten concept, according to which a small chemical compound is too small to be recognized by the immune system. Only after covalently binding to an endogenous protein the immune system reacts to this so called hapten-carrier complex, as the larger molecule (protein) is modified, and thus immunogenic for B and T cells. Consequently, a B and T cell immune response might develop to the drug with very heterogeneous clinical manifestations.
View Article and Find Full Text PDFCurr Opin Allergy Clin Immunol
October 2004
Purpose Of Review: Drug-induced exanthems are the most common manifestations of drug hypersensitivity and are observed in as much as 2-3% of hospitalized patients. Here we summarize new concepts of the immune mechanisms underlying various forms of drug-induced exanthems.
Recent Findings: Alpha-betaTCR+, CD4 and CD8+ T cells are involved in different drug hypersensitivity reactions.
Cutaneous reactions to mercury can manifest themselves in different forms. Apart from contact dermatitis, flare-up reactions, disseminated exanthem as well as skin symptoms in previously unaffected skin are known. Regarding systemic allergen application, 2 separate clinical patterns, namely acute generalized exanthematous pustulosis (AGEP) and symmetric flexural exanthem 'baboon syndrome' have been described.
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