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Unlabelled: Recently non-steroidal anti-inflammatory drugs have seemed to reduce the frequency of post-ERCP pancreatitis in some prospective controlled trials, but the results have to be confirmed by further studies., Aim: To evaluate the efficacy of rectally administered indomethacin for the reduction of incidence of post-ERCP pancreatitis., Method: A prospective randomized placebo-controlled study was conducted in 228 patients who underwent ERCP. Patients were randomized to receive a suppository containing 100 mg indomethacin or an inert placebo 10 mins before ERCP. Patients were evaluated clinically and biochemically by using serum amylase levels measured 24 h after the procedure., Results: Pancreatitis and hyperamylasemia occurred more frequently in the placebo group, but the difference was not significant. In respect to the rate of pancreatitis, this tendency could particularly be observed in females, in patients older than 60 years and in patients with BMI lower than 25; however, it completely failed in cases with pancreatic duct filling or in those with pancreatic EST., Conclusions: Rectal indomethacin given before ERCP did not prove to be statistically effective in the reduction of the incidence of post-procedure pancreatitis. Further, controlled multicenter studies are required to assess safely the potential efficacy of indomethacin in the prevention of pancreatitis following ERCP.

Postinfectious irritable bowel syndrome (IBS) is a subgroup of IBS. Patients with an episode of bacterial gastroenteritis may have a 12-fold increased risk of developing IBS symptoms within the same year. The IBS can be manifested in each of its clinical types, but the diarrhea-predominant form occurs most commonly. The primary pathophysiologic factor in developing IBS after enteral infection may be defects in enteric nervous system which can produce abnormality in visceral hypersensitivity and intestinal motility. These patients also display exaggerated increases in mucosal immunocompetent T lymphocytes and an abnormally high pro- versus anti-inflammatory cytokine ratio, providing evidence to the contribution of the immune system in the development of postinfectious IBS. Via bi-directional brain-gut interactions both peripheral and central events can play a role in the development of clinical symptoms. Stress is associated with significant worsening of the complaints in IBS and may also result in a shift in the host-gut microbial relationship. IBS itself may predispose patients to acute bacterial gastroenteritis because of the altered intestinal motility. It needs further clarifying the relationship between IBS and small intestinal bacterial overgrowth syndrome. Upon the data so far the altered intestinal flora in IBS would merely reflect developments due to altered motility and not a causal relationship. The treatment of postinfectious IBS does not differ principally from that of the idiopathic IBS. Antibiotics or probiotics may lead to temporary symptomatic improvement, but, given the lack of evidence based data, they cannot be advised for routine use so far.