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Clostridium difficile infection (CDI), most common cause of hospital acquired infectious diarrhea, has been reported to be increasing in incidence, severity, and mortality over the past several decades throughout the world. Several risk factors for CDI have been demonstrated including antibiotics exposure, old age, prolonged hospital and intensive care unit (ICU) stay, previous CDI episode, co-morbidities, and acid suppression therapy such as proton pump inhibitors (PPIs), and histamine 2 receptor antagonists (H2RAs), and so forth. Among them, acid suppression therapy has recently received an increased attention as a risk factor for CDI. Several epidemiologic studies have suggested increased CDI risk is associated with both PPIs and H2RAs. Meanwhile, PPIs and H2RAs have been commonly used for prophylaxis and treatment of stress ulcers in critically ill patients. Several randomized controlled trials (RCTs) and metaanalyses demonstrated that PPIs were more effective than H2RA in preventing gastrointestinal (GI) bleeding, while others reported no significant difference between PPIs and H2RAs. Furthermore, some meta-analyses revealed no mortality benefit in patients with stress ulcer prophylaxis (SUP) than those without SUP. Although critically ill patients are at high risk of developing stress related ulcerations, the prevalence of overt GI bleeding in these patients has been reported to be relatively low, around 5%. Several guidelines have recommended SUP just in patients with high risk factors for clinically important GI bleeding such as mechanical ventilation, coagulopathy, acute renal injury, and hepatic failure, and so forth. However, inappropriate use of gastric acid suppressants appear to be common in clinical practice. In some studies, 63% of ICU patients and 60% of hospitalized general ward patients, who prescribed SUP, had no appropriate indication and one-third of these patients were discharged without discontinuation of the medication. Several studies have demonstrated that both PPIs and H2RAs are associated with an increased risk of CDI occurrence. Although precise mechanisms of CDI occurrence by gastric acid suppression are not clear, loss of gastric acidic environment caused by PPIs or H2RAs has been suggested to induce bacterial overgrowth and altered distal gut microbiome with decreased bacterial diversity, which may contribute to CDI occurrence. The meta-analysis by Tleyjeh et al., which included 35 observational studies with a total of 201,834 participants, demonstrated a relative risk of 1.44 (95% confidence interval, 1.22 to 1.70) for CDI occurrence among patients with H2RA therapy. On the contrary, several meta-analyses have showed pooled odds ratios of 1.65 to 2.15 for CDI occurrence among patients with PPIs therapy. In addition, U.S. Food and Drug Administration recently warned CDI can be associated with PPIs use. However, it is unclear whether the relation of gastric acid suppression (PPIs and H2RAs) and CDI occurrence is causal or mere association, suggesting that future well-organized prospective RCTs would be warranted. To date, there has been little data of meta-analyses directly comparing CDI occurrence risk between PPIs and H2RA among patients with stress ulcer treatment and prevention. In this issue of Gut and Liver, Azab et al. investigated the comparative

gut and liver

Does Proton Pump Inhibitor Increase the <i>Clostridium difficile</i> Infection Risk in the Treatment and Prophylaxis of Stress Ulcers than Histanime-2 Receptor Antagonist?

Does Proton Pump Inhibitor Increase the Clostridium difficile Infection Risk in the Treatment and Prophylaxis of Stress Ulcers than Histanime-2 Receptor Antagonist?