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Allopurinol has been linked to severe cutaneous adverse reactions (SCAR), toxic epidermal necrolysis, Stevens-Johnson syndrome, and drug reaction with eosinophilia and systemic symptoms (DRESS). Clinically, these syndromes are similar in that they both involve fever, eosinophilia, rash, and dysfunction of the liver and kidneys. [1]
The symptoms of DRESS syndrome usually begin 2 to 6 weeks but uncommonly up to 8–16 weeks after exposure to an offending drug. Symptoms generally include fever, an often itchy rash which may be morbilliform or consist mainly of macules or plaques, facial edema (i.e. swelling, which is a hallmark of the disease), enlarged and sometimes painful lymph nodes, and other symptoms due to ...
Allopurinol has been marketed in the United States since 19 August 1966, when it was first approved by FDA under the trade name Zyloprim. [40] Allopurinol was marketed at the time by Burroughs Wellcome. Allopurinol is a generic drug sold under a variety of brand names, including Allohexal, Allosig, Milurit, Alloril, Progout, Ürikoliz, Zyloprim ...
[6] [7] The drugs most commonly triggering the SJS, TEN, and SJS/TEN spectrum of disorders are anti-infective sulfonamides, anticonvulsants (e.g. carbamazepine and lamotrigine), non-steroidal anti-inflammatory drugs, allopurinol, nevirapine, and chlormezanone. Allopurinol appears in some studies to be the most common instigator of these disorders.
Agents that have been implicated in serum sickness–like reactions include cefaclor, amoxicillin, sulfonamides, tetracyclines, ciprofloxacin, nonsteroidal anti-inflammatory drugs, barbiturates, carbamazepine, propranolol, thiouracil, and allopurinol. Metabolites of these drugs might bind with tissue proteins inappropriately, eliciting an acute ...
This is a list of drugs and substances that are known or suspected to cause Stevens–Johnson syndrome This is a dynamic list and may never be able to satisfy particular standards for completeness. You can help by adding missing items with reliable sources .
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The p-i concept refers to the pharmacological interaction of drugs with immune receptors. It explains a form of drug hypersensitivity, namely T cell stimulation, which can lead to various acute inflammatory manifestations such as exanthems, eosinophilia and systemic symptoms, Stevens–Johnson syndrome, toxic epidermal nercrolysis, and complications upon withdrawing the drug.