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Genetically determined susceptibility to COX‐2 inhibitors – a report of exaggerated responders to diclofenac 3% gel in the treatment of actinic keratoses
Author(s) -
Patel M.J.,
Ulrich C.,
Forschner T.
Publication year - 2007
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2007.07858.x
Subject(s) - diclofenac , actinic keratoses , dermatology , medicine , contact dermatitis , skin reaction , pharmacology , immunology , allergy , basal cell
Summary Diclofenac 3% gel is an effective treatment for actinic keratoses (AKs) and is reported to be generally well tolerated with only mild local reactions. However, there is a subset of patients that seem to be susceptible to developing severe local reactions following application of diclofenac 3% gel. Although some of these reactions can be explained as being allergic contact dermatitis and/or photoallergic contact dermatitis, others cannot. We report a series of 10 patients who all developed severe local reactions following application of diclofenac 3% gel, despite negative diclofenac patch testing. This raises the question as to whether there is a subset of patients with skin cancer or AK lesions that are highly/more susceptible to local reactions caused by cyclo‐oxygenase‐2 (COX‐2) inhibitors and peroxisome proliferator‐activated receptor (PPAR) agonists? We speculate that underlying molecular differences exist in these patients that make the skin more susceptible to COX‐2 inhibitors.