PubMed · 13108176
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E LANDES, R HERGER. 1953. [Iododerma tuberosum].. https://pubmed.ncbi.nlm.nih.gov/13108176/
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We report the case of a 58-year-old man who suffered from a generalized and intolerable itching one month after starting treatment with colchicine, amiodarone, perindopril, allopurinol and spironolactone. From the start of treatment he had progressively developed erythroderma, fever, anorexia and prostration, oedema of both hands and face, hypereosinophilia (42%; 5810 eosinophils/mm3), hepatic failure (including cholestatic jaundice, cytolysis, coagulation abnormalities and hypoproteinaemia), exocrine pancreatic failure (with severe steatorrhoea), renal failure, metabolic acidosis, aggravation of pre-existing cardiac insufficiency and oedema of the lower extremities. All medications were stopped and the condition improved slowly until complete remission was reached 4 months later. Patch-testing was performed, including the various drugs. All the tests (including components of the vehicles) were negative, except for spironolactone, which gave a strong positive reaction. Ten controls in healthy volunteers were negative. The diagnosis of drug rash with eosinophilia and systemic symptoms (DRESS) induced by spironolactone was made. This is the first report of DRESS due to spironolactone.
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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. Their function determines the clinical picture. In maculopapular, bullous and pustular exanthems cytotoxic T cells are involved, while a high IL-5 and eotaxin production by tissue cells is frequently found in maculopapular and occasionally in bullous and in pustular exanthems. High IL-8 (CXCL-8) and granulocyte-macrophage colony stimulating factor production by T cells is a hallmark of pustular drug exanthems. In the most severe and potentially life-threatening forms of exanthems (Stevens-Johnson syndrome/toxic epidermal necrolysis) cytotoxic CD8+ T cells with natural killer cell markers can be found in the blister fluid. SUMMARY: These findings are the basis for a new subclassification of delayed, type IV hypersensitivity reactions into type IVa (T helper type 1 cells, e.g. tuberculin reaction and contact dermatitis), IVb (T helper type 2 cells, maculopapular exanthem with eosinophilia), IVc (cytotoxic T cells, contact dermatitis, maculopapular and bullous exanthem), and IVd reactions (CXCL-8/granulocyte-macrophage colony stimulating factor-producing T cells and neutrophil attraction, pustular exanthems), by which, in most reactions, various mechanisms occur together but one reaction dominates the clinical picture.