Current causes of fixed drug eruption in the U.K.

Savin, J.A.

doi:10.1046/j.1365-2133.2001.04422.x

Cited by 48 publications

(35 citation statements)

References 2 publications

(2 reference statements)

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“…Dans les pays occidentaux, les principaux médicaments identifiés comme pourvoyeurs d'EPF sont le paracétamol, les AINS (en particulier les oxicams), les antibiotiques (bêta-lactamines, quinolones, sulfamides, cyclines, macrolides), la carbocystéine. Mais de nombreuses autres familles sont concernées comme les antiépileptiques, les benzodiazépines, les inhibiteurs de la pompe à protons, les antihistaminiques, certains antifongiques (terbinafine, fluconazole) [69,75,76]. Longtemps considéré comme pathognomonique d'une étiologie médicamenteuse, d'autres causes d'EPF ont été identifiées, en particulier alimentaires [67].…”

Section: éRythème Pigmenté Fixeunclassified

Toxidermies

Lebrun‐Vignes

Valeyrie‐Allanore

2015

La Revue de Médecine Interne

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Cutaneous adverse drug reactions (CADR) represent a heterogeneous field including various clinical patterns without specific features suggesting drug causality. Exanthematous eruptions, urticaria and vasculitis are the most common forms of CADR. Fixed eruption is uncommon in western countries. Serious reactions (fatal outcome, sequelae) represent 2% of CADR: bullous reactions (Stevens-Johnson syndrome, toxic epidermal necrolysis), DRESS (drug reaction with eosinophilia and systemic symptoms or drug-induced hypersensitivity syndrome) and acute generalized exanthematous pustulosis (AGEP). These forms must be quickly diagnosed to guide their management. The main risk factors are immunosuppression, autoimmunity and some HLA alleles in bullous reactions and DRESS. Most systemic drugs may induce cutaneous adverse reactions, especially antibiotics, anticonvulsivants, antineoplastic drugs, non-steroidal anti-inflammatory drugs, allopurinol and contrast media. Pathogenesis includes immediate or delayed immunologic mechanism, usually not related to dose, and pharmacologic/toxic mechanism, commonly dose-dependent or time-dependent. In case of immunologic mechanism, allergologic exploration is possible to clarify drug causality, with a variable sensitivity according to the drug and to the CADR type. It includes epicutaneous patch testing, prick test and intradermal test. However, no in vivo or in vitro test can confirm the drug causality. To determine the cause of the eruption, a logical approach based on clinical characteristics, chronologic factors and elimination of differential diagnosis is required, completed with a literature search. A reporting to pharmacovigilance network is essential in case of a serious CADR whatever the suspected drug and in any case if the involved drug is a newly marketed one or unusually related to cutaneous reactions.

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Section: éRythème Pigmenté Fixeunclassified

Toxidermies

Lebrun‐Vignes

Valeyrie‐Allanore

2015

La Revue de Médecine Interne

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“…Fixed drug eruptions (FDE) constitute about 10% of all drug reactions, and NSAIDs are among the most common causes of FDE (79). Pyrazolones, piroxicam, phenylbutazone, paracetamol, aspirin, mefenamic acid, diclofenac, indomethacin, ibuprofen, diflunisal, naproxen and nimesulide have been associated with FDE.…”

Section: Fixed Drug Eruptionsmentioning

confidence: 99%

“…Several NSAIDs including sulindac, ibuprofen and naproxen have been suspected to induce hypersensitivity pneumonitis (79,86). Differential diagnosis should be carefully considered.…”

Section: Pneumonitismentioning

confidence: 99%

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

Kowalski

Makowska

Blanca³

et al. 2011

Allergy

391

366

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Following the first description of hypersensitivity reaction to aspirin (ASA) by Hirschberg in 1902, several types of hypersensitivity reactions to nonsteroidal anti-inflammatory drugs (NSAIDs) have been described. The NSAIDs-induced hypersensitivity reactions involve different mechanisms and present a wide range of clinical manifestations from anaphylaxis AbstractNonsteroidal anti-inflammatory drugs (NSAIDs) are responsible for 21-25% of reported adverse drug events which include immunological and nonimmunological hypersensitivity reactions. This study presents up-to-date information on pathomechanisms, clinical spectrum, diagnostic tools and management of hypersensitivity reactions to NSAIDs. Clinically, NSAID hypersensitivity is particularly manifested by bronchial asthma, rhinosinusitis, anaphylaxis or urticaria and variety of late cutaneous and organ-specific reactions. Diagnosis of hypersensitivity to a NSAID includes understanding of the underlying mechanism and is necessary for prevention and management. A stepwise approach to the diagnosis of hypersensitivity to NSAIDs is proposed, including clinical history, in vitro testing and/ or provocation test with a culprit or alternative drug depending on the type of the reaction. The diagnostic process should result in providing the patient with written information both on forbidden and on alternative drugs.

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“…Cutaneous reactions present as angioedema, urticaria, anaphylaxis, maculopapular rashes, hyperpigmentation, erythema multiforme and erythroderma, exfoliative dermatitis, and bullous eruption [4]. As per literature, only a few cases of fixed drug eruptions have been reported with proton-pump inhibitors mainly omeprazole [6][7][8][9]. In our patient, rabeprazole was given and other drugs causing it was ruled out.…”

Section: Discussionmentioning

confidence: 98%