LAUSR

Inflammatory bowel disease (IBD) is regarded as a lifelong, relapsing–remitting inflammatory disorder of the gastrointestinal (GI) tract, with an unknown etiology and unpredictable clinical course [1]. GI infections commonly trigger relapse in patients with IBD; among these infections, Clostridioides (formerly Clostridium) difficile infection (CDI) is reported as the most common GI infection in patients with IBD, with recurrence in up to one-third of patients. CDI frequently complicates the subsequent course of IBD, delays IBD remission, and increases the need for colectomy, and even increases mortality rates [2]. Risk factors contributing to the acquisition and severity of CDI in IBD are preexisting colonic inflammation, especially in ulcerative colitis (UC), concomitant immunosuppression, prolonged hospitalization, and long-term antibiotic use. Though the clinical manifestations of an IBD flare and CDI have considerable overlap, the treatment strategies are markedly different with escalation of immunosuppression for an IBD flare compared with reduction in immunosuppression and antibiotics for active CDI [3]. Although IBDassociated inflammation could predispose patients to CDI, CDI may exacerbate IBD by triggering a mucosal inflammatory response or by reducing the diversity of the luminal microbiota [4]. Accordingly, whether IBD disease severity predisposes to the development of the CDI or whether CDI exacerbates IBD has often been presented as a problem of origin and first cause. In this issue of Digestive Diseases and Sciences, Varma and colleagues [5] retrospectively evaluated patients hospitalized for ≥ 2 IBD flares at New York–Presbyterian Columbia University Irving Medical Center from January 2010 to September 2019. The authors compared the time to IBD flare between patients who were hospitalized for a flare complicated by CDI and subsequently for a CDInegative flare (± ; cohort A) versus patients who were hospitalized for two CDI-negative flares (−/−; cohort B). They also determined the time between flares among the subset of cohort A patients who had three flares (−/± ; cohort C) before and after CDI. As a result, they reported that patients with prior CDI had significantly shorter time to IBD relapse compared with those without any history of CDI. On the contrary, among patients with IBD who had CDI, the interval between flares was similar before CDI compared with afterward. Their findings suggest that the acquisition of CDI may not inevitably influence the course of IBD, but rather, the shorter time to disease relapse among patients with CDI may be related to the intrinsic disease and/or patient characteristics that predispose patients to CDI, and ultimately impact the time to flare. Also, the authors found that patients with IBD who acquired CDI had a significantly lower BMI and higher Charlson comorbidity index at baseline, consistent with augmented illness severity and GI inflammation in these patients. In contrary, CDI-negative patients were more likely to have received budesonide and less likely to have received biologics prior to their first IBD-related hospitalization. Moreover, CDI-negative patients were more likely to have an escalation in IBD therapy after hospitalization. Therefore, these findings corroborate the hypothesis that patients with severe IBD are more likely to develop CDI. Some previous studies have indicated that IBD itself is a risk factor for acquiring CDI, particularly among patients with colonic involvement [6]. Moreover, patients with IBD regularly receive broad-spectrum antibiotics as a part of the treatment of disease exacerbations or have complications from immunosuppressive therapy. Hence, these patients are * Abbas Yadegar [email protected]; [email protected]