Abstract
Patients with inflammatory bowel disease (IBD) often have associated conditions, for which anti-inflammatory medication with cyclo-oxygenase (COX) inhibitors may be helpful. The current evidence is conflicting regarding the role of COX-inhibitors in causing relapse in IBD. This case-control study examined the association between the use of COX inhibitors and relapse of IBD. Logistic regression was used to analyse the relationship between COX-inhibitors and IBD relapse. Overall COX inhibitor use (combined non-steroidal anti-inflammatory drugs (NSAIDs) and selective COX-2 agents) had a negative association with relapse of IBD (adjusted OR 0.26, 95% CI 0.09–0.80). This negative association was confined to ulcerative colitis (UC) (adjusted OR = 0.06, 95% CI 0.01–0.50) and no association was found in Crohn’s disease (CD) patients (adjusted OR 1.25, 95% CI 0.18–7.46). The significant negative association between UC relapse and medication use was also seen with non-specific NSAIDs. Selective COX-2 inhibitor use was rare but non-significantly more common in stable patients. There was no association between low-dose aspirin or paracetamol use and relapse of CD or UC. We conclude that COX-inhibitor use was not associated with an increased risk of relapse in UC or CD, and may be protective in UC. Where indicated, NSAIDs should not be withheld from IBD patients.
Highlights
Inflammatory bowel disease (IBD) is a significant health problem, with a reported incidence of 24.3/100000/year for ulcerative colitis (UC) and 12.7/100000/year for Crohn’s disease (CD) [1].In 2011, it was thought that there were approximately 240000 patients in the UK with IBD, of which146000 had UC, 87000 had CD and the remaining 7000 had an unspecified colitis [2].IBD typically follows a relapsing and remitting pattern, with approximately a third of patients experiencing a relapse each year [3]
Despite the well know effects on the upper GI tract acid-suppressive drugs were uncommonly taken in this cohort, whilst it remains possible that acid-suppressive drugs, co-prescribed with COX-inhibitors, leading to changes in the GI microbiome may influence relapse of IBD, our study shows no such effect, albeit with small numbers
Any other variable found to be statistically significant was adjusted for. It was pre-planned to perform subgroup analysis of CD and UC and to examine both overall COX-inhibitor use and overall non-steroidal anti-inflammatory drug (NSAID) use. This case control study shows that COX- inhibitor use was not associated with an increased risk of relapse of inflammatory bowel disease
Summary
Inflammatory bowel disease (IBD) is a significant health problem, with a reported incidence of 24.3/100000/year for ulcerative colitis (UC) and 12.7/100000/year for Crohn’s disease (CD) [1].In 2011, it was thought that there were approximately 240000 patients in the UK with IBD, of which146000 had UC, 87000 had CD and the remaining 7000 had an unspecified colitis [2].IBD typically follows a relapsing and remitting pattern, with approximately a third of patients experiencing a relapse each year [3]. Inflammatory bowel disease (IBD) is a significant health problem, with a reported incidence of 24.3/100000/year for ulcerative colitis (UC) and 12.7/100000/year for Crohn’s disease (CD) [1]. In 2011, it was thought that there were approximately 240000 patients in the UK with IBD, of which. IBD typically follows a relapsing and remitting pattern, with approximately a third of patients experiencing a relapse each year [3]. The cause of relapse in disease can be due to medication issues, but it has been linked to many different factors, such as smoking, exposure to allergens, infection and in some cases, NSAIDs (non-steroidal anti-inflammatory drugs) [4]. NSAIDs act by inhibiting cyclo-oxygenase (COX) which is the key enzyme by which prostaglandins are formed from arachidonic acid [5]. Prostaglandins are mediators of pain, inflammation and fever; NSAIDs commonly exhibit anti-inflammatory and analgesic properties. COX has two isozymes, COX-1 and COX-2, of which COX-2 is the inducible form mainly responsible for inflammation, whilst the constitutive COX-1 isoform is more involved in a variety of general “household” activities including mucosal defence in the upper GI tract [6]
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