Analgesic intolerance syndrome (ais)T88.7

Author:Prof. Dr. med. Peter Altmeyer

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Last updated on: 29.10.2020

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Synonym(s)

Analgesic hypersensitivity; Analgesic Intolerance; ASS Intolerance Syndrome; NSAID hypersensitivity; NSR hypersensitivity

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DefinitionThis section has been translated automatically.

Intolerance reaction to non-steroidal anti-inflammatory drugs (NSAIDs), probably caused by a dysbalance in the arachidonic acid metabolism. S.a.o. Urticaria, intolerance urticaria.

EtiopathogenesisThis section has been translated automatically.

Dysbalance in arachidonic acid metabolism. Arachidonic acid is provided by phosopholipases from the phospholipids of the cell membranes of eosinophils, mast cells and leucocytes. Via lipoxygenases and cyclooxygenases (COX) two metabolic pathways are optionally taken, some of whose products have an antagonistic effect. Prostaglandins (e.g. prostaglandin E2) are produced via the leukotriene C4 (LTC4) cyclooxygenase metabolic pathway. Peptide leukotrienes (PLT) are formed via the lipoxygenase metabolic pathway. In contrast to prostaglandins, PLT have a bronchospastic and mucous-forming effect. Patients with AIS tend to produce PLT in excess, probably due to an increased activity of LTC4 synthetase (cause: possible polymorphism of the gene sequence of LTC4 synthetase on chromosome 5q). In patients with AIS, a "shifting" (unchecked change) to the lipoxygenase metabolic pathway was described after administration of NSAIDs.

Clinical featuresThis section has been translated automatically.

Acutely intermittent or chronically recurrent urticaria, polyposis nasi and bronchial asthma (ASA asthma, analgesic asthma).

LaboratoryThis section has been translated automatically.

Urine: leukotriene 4 increased.

DiagnosisThis section has been translated automatically.

Medical history: therapy-resistant urticaria, polyposis nasi (usually multiple operations of the paranasal sinuses in the medical history), bronchial asthma).

Provocation tests by nasal, oral (see below urticaria, chronic) or bronchial provocation.

Measurement of the cysteinylleukotriene release provoked by NSAIDs in vitro using commercially available tests ( CAST). In addition, a method still undergoing clinical trials, the Analgesic Intolerance Test (AIT), can be used to assess the balance between PGE2 and leukotriene release after provocation.

TherapyThis section has been translated automatically.

Analgesic leave. Test with montelukast (e.g. Singulair film-coated tablets) 10 mg/day before bed rest. Adaptive deactivation (development of tolerance to analgesics, especially COX-1 inhibitors).

LiteratureThis section has been translated automatically.

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Last updated on: 29.10.2020