Do NSAIDs, Antibiotics, Infections, or Stress Trigger Flares in IBD?

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs), antibiotics, enteric or other systemic infections, and stress have all been reported to be potential triggers of inflammatory bowel disease (IBD). Although a mechanism of triggering a flare of IBD can be hypothesized for each factor, the associations of these factors with flares of IBD remains confusing. In this review, we analyze the literature that explores these associations. There is some evidence to support an association between NSAID use and flares but little data to associate antibiotic use directly with flares. An important connection between antibiotic use and an exacerbation of symptoms is through the development of Clostridium difficile infections. However, for all enteric infections, including C. difficile, it is unclear whether these infections simply trigger symptoms in patients with IBD that resolve on resolution of the infection, or whether they truly trigger a flare of intestinal inflammation that outlasts the infection. There is a paucity of evidence that other systemic infections trigger flares of IBD. Although there is strong evidence for an association between perceived stress levels and flares, there is a weaker association between a simple accounting of stressful life events and flares. Much of the literature is limited by a lack of adequate control groups and failure to report on base rates in the population under study (i.e., NSAIDs and antibiotic use, occurrence of infections, and stress levels). More large population-based matched cohort or case crossover studies and a continued emphasis on prospective designs are needed to better explore these potential associations. Clinical implications given the current state of knowledge are discussed.

Exacerbation of inflammatory bowel diseases associated with the use of nonsteroidal anti-inflammatory drugs: myth or reality?

“…If NSAIDs administration is necessary, there is a need for careful follow-up of IBD patients, mainly those in remission, during the first few days of treatment, as disease aggravation or clinical relapse requires drug discontinuation. Further randomized, double-blind trials should be performed to address this issue [74]. As far as the mechanisms of relapse are concerned, although the reduction of prostaglandins appears to be the hallmark of their adverse effects, more in vitro studies to identify other pathways involved are required.…”

Role of Corticotropin-releasing Factor in Gastrointestinal Permeability

“…Enhanced intestinal permeability in this population is considered an initial event because it is increased in first-degree relatives of Crohn's disease patients. 140,141 Several observations link clinical relapses to the increase in intestinal permeability 142,143 and to life stress, 144,145 partly through mast cell activation 146 and the release of CRF from eosinophils 83 and neighboring nerves. 68 Moreover, inflammatory Public speech and CRF administration increased intestinal permeability and salivary cortisol.…”

Colitis after polytrauma

“…It involves the rectum and may extend proximally to the colon [7]. Typical presentation includes rectal bleeding, frequent stools, and tenesmus with a mean onset of symptoms to diagnosis of 10 mo [8].…”