Increased rate of spontaneous bacterial peritonitis among cirrhotic patients receiving pharmacologic acid suppression.

BACKGROUND & AIMS: Patients with cirrhosis frequently receive proton pump inhibitor (PPI) or H2-receptor antagonist therapies. We investigated whether acid-suppressive therapy is associated with spontaneous bacterial peritonitis (SBP) in cirrhotic patients with ascites. METHODS: We compared data from 65 hospitalized cirrhotic patients with paracentesis-proven SBP, collected from 2006 to 2009, with those of 65 contemporaneous, hospitalized cirrhotic patients without SBP (controls). We evaluated PPI use and analyzed the effects of covariates. RESULTS: Patients with SBP had a significantly higher incidence of recent (past 7 days) PPI use (71%) than controls (42%). Of patients with SBP, 68% had no documented indication for PPI therapy. Based on multivariable logistic regression analysis, subjects who had not taken PPIs in the past 90 days were almost 70% less likely to develop SBP than those who had taken PPIs in the previous 7 days. Subjects who took PPIs within 8 to 90 days before hospitalization were 79% less likely to develop SBP than those who took PPIs within 7 days before hospitalization. There was no significant difference between patients who received no PPI therapy in the previous 90 days versus those who had taken PPIs in the previous 8 to 90 days (P = .58). Hyponatremia was associated significantly with SBP. There were no significant differences in length of hospital stay or 30-day survival for the SBP and control groups. CONCLUSIONS: Pharmacologic acid suppression is associated with SBP in patients with advanced cirrhosis. Prospective studies are needed to determine the mechanism of this association and to determine whether reduced use of PPIs and H2-receptor antagonists reduce the incidence of SBP.

Molecular pathways underlying IBD-associated colorectal neoplasia: therapeutic implications.

Chronic inflammatory diseases, depending upon the duration and severity, are frequently associated with an increased risk of developing cancer. A classic paradigm is the enhanced risk of colorectal cancer (CRC) in patients with inflammatory bowel disease (IBD). Carcinogenesis is a multifactorial process that involves accumulation of genetic defects, protein modification, and cell-matrix interaction. In this review, we discuss aspects of chronic inflammation in IBD that influence the development of CRC and highlight the key molecular mediators involved in this process. Also, we identify potential targets that could facilitate earlier detection of dysplasia. The targeted manipulation of specific molecules or pathways could provide opportunities for the development of therapeutic and chemopreventive interventions, which may prove effective in arresting the progression of colitis-associated cancer (CAC), with clinical implications.