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The letter by Mir et al (Gut 2004;53:154) caught our attention and seems to have caught the editorial staff dozing.
Mir et al present a patient who had been regularly taking conventional non-steroidal anti-inflammatory drugs (NSAIDs) for 26 years for axial spondylarthropathy and ascribe the presence of distal ileal stricturing and ulceration solely to the use of a cyclooxygenase 2 (COX 2) selective inhibitor that had been taken for two years. The differential diagnosis of ileal lesions in spondylarthropathy is quite clear. Firstly, as the authors themselves stated, strictures are associated with long term use of conventional NSAIDs.1 The 26 year use of NSAIDs by the patient is most significant. While such lesions are usually more proximal, slow release formulations of NSAIDs can give rise to distal disease such as in this circumstance. The authors do not specify if this is the case. NSAID induced ulcers, when established, may take years to heal, such that the two year time lag between stopping NSAIDs and clinical symptoms is not unexpected.
Secondly, spondylarthropathy is itself associated with ileitis in 30–70% of cases, irrespective of NSAID intake. Most cases are asymptomatic but some cases proceed to stricturing disease.2 De Keyser et al, in particular, have made a case for spondylarthropathic ileitis being a form of subclinical Crohn’s disease.3 Finally, axial spondylarthropathy may be an extraintestinal manifestation of 5–10% of cases of inflammatory bowel disease.2 It is difficult to exclude this as the cause of both the recent ulceration and stricturing because histology does not always show typical (for example, granulomatous) changes. To date, the only small bowel pathology reported from selective COX 2 inhibition (or absence) is of ileocaecal inflammation and perforation (not stricturing) in animal studies.4 Hence, while it is a remote possibility that COX 2 inhibition may have given rise to the lesions in this patient, these are far more likely to be due to other factors.