A variety of allergic or allergic-like NSAID hypersensitivity reactions

Allergy and allergy-like hypersensitivity reactions A variety of allergic or allergic-like NSAID hypersensitivity reactions following the ingestion of NSAIDs.

These hypersensitivity reactions differ from the other adverse reactions listed here: toxicity reactions, i.e. unwanted reactions that result from a drug's pharmacological action, are dose-related, and can occur in any treated individual; hypersensitivity reactions are idiosyncratic reactions to a drug. Some NSAID hypersensitivity reactions are genuinely allergic in origin:

1) repetitive IgE-mediated urticarial skin eruptions, angioedema, and anaphylaxis following immediately to hours after ingesting one structural type of NSAID but not after ingesting structurally unrelated NSAIDs; and

2) Comparatively mild to moderately severe T cell-mediated delayed onset (usually more than 24 hours), skin reactions such as maculopapular rash, fixed drug eruptions, photosensitivity reactions, delayed urticaria, and contact dermatitis; or

3) far more severe and potentially life-threatening t-cell-mediated delayed systemic reactions such as the DRES's syndrome, acute generalized exanthematous pustulosis, the Stevens-Johnson syndrome, and toxic epidermal necrolysis.

Other NSAID hypersensitivity reactions are allergy-like symptoms but do not involve true allergic mechanisms; rather, they appear due to the ability of NSAIDs to alter the metabolism of arachidonic acid in favour of forming metabolites that promote allergic symptoms.

Afflicted individuals may be abnormally sensitive to these provocative metabolites or overproduce them and typically are susceptible to a wide range of structurally dissimilar NSAIDs, particularly those that inhibit COX1.

Symptoms, which develop immediately to hours after ingesting any of various NSAIDs that inhibit COX-1, are:

1) exacerbations of asthmatic and rhinitis (see aspirin-induced asthma) symptoms in individuals with a history of asthma or rhinitis and

2) exacerbation or first-time development of wheals or angioedema in individuals with or without a history of chronic urticarial lesions or angioedema.

Possible effects on bone and soft tissue healing :

It has been hypothesised that NSAIDs may delay healing from bone and soft-tissue injuries by inhibiting inflammation. On the other hand, it has also been hypothesized that NSAIDs might speed recovery from soft tissue injuries by preventing inflammatory processes from damaging adjacent, non-injured muscles. There is moderate evidence that they delay bone healing. Their overall effect on soft-tissue healing is unclear