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

Abstract

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.

Adverse drug reactions in a tertiary care teaching hospital in India: analysis of spontaneously reported cases

“…They affect 0.3% of the general population. 28 However, not a single case of gastrointestinal system disorder was reported with diclofenac. This may be because of spontaneous reporting nature of this study and physicians may have felt that gastrointestinal symptoms are not worth to report.…”

Review of Medical Disease Symptoms Prediction Using Data Mining Technique

“…De Weck, A. Szczeklik and K. Brockow Et al. [2] as indicated by specialists, Nonsteroidal hostile to inflammatory drugs (NSAIDs) are in charge of 21-25% of detailed unfriendly medication occasions which incorporate immunological and nonimmunological excessive touchiness responses. This review displays state-of-the-art data on patho-systems, clinical range, symptomatic devices and administration of excessive touchiness responses to NSAIDs.…”

Food-dependent drug-induced angioedema: a case report

“…In short, the cyclooxygenases pathway generate pro-inflammatory autacoids such as the prostaglandins and thromboxanes; while the lipoxygenases pathway generates the leukotrienes, a group of autacoids with a strong effect on postcapillary venules and smooth musculature, resulting in increased extravascular exudation and muscle constriction respectively [5,7]. When the activity of the phospholipases is increased for whatsoever reason, the inhibition of the cyclooxygenases promoted by NSAIDs provides to the lipoxygenase pathway an additional amount of arachidonic acid resulting in an increased production of leukotrienes, what explain the collateral effects such as the angioedema [8,9].…”