J S Bajaj1, S M Ratliff, D M Heuman, K L Lapane. 1. Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, VA, USA. jsbajaj@vcu.edu
Abstract
BACKGROUND: There is increasing evidence that proton pump inhibitors (PPIs) increase the rate of infections in patients with decompensated cirrhosis. AIMS: To estimate the extent to which proton pump inhibitors (PPIs) increase the rate of infections among patients with decompensated cirrhosis. METHODS: We conducted a retrospective propensity-matched new user design using US Veterans Health Administration data. Only decompensated cirrhotic patients from 2001 to 2009 were included. New PPI users after decompensation (n = 1268) were 1:1 matched to those who did not initiate gastric acid suppression. Serious infections, defined as infections associated with a hospitalisation, were the outcomes. These were separated into acid suppression-related (SBP, bacteremia, Clostridium difficile and pneumonia) and non-acid suppression-related. Time-varying Cox models were used to estimate adjusted hazard ratios (HR) and 95% CIs of serious infections. Parallel analyses were conducted with H2 receptor antagonists (H2RA). RESULTS: More than half of persons with decompensated cirrhosis were new users of gastric acid suppressants, with most using PPIs (45.6%) compared with H2RAs (5.9%). In the PPI propensity-matched analysis, 25.3% developed serious infections and 25.9% developed serious infections in the H2RA analysis. PPI users developed serious infections faster than nongastric acid suppression users (adjusted HR: 1.66; 95% CI: 1.31–2.12). For acid suppression-related serious infections, PPI users developed the outcome at a rate 1.75 times faster than non-users (95% CI: 1.32–2.34). The H2RA findings were not statistically significant (HR serious infections: 1.59; 95% CI: 0.80–3.18; HR acid suppression-related infections: 0.92; 95% CI: 0.31–2.73). CONCLUSION: Among patients with decompensated cirrhosis, proton pump inhibitors but not H2 receptor antagonists increase the rate of serious infections.
BACKGROUND: There is increasing evidence that proton pump inhibitors (PPIs) increase the rate of infections in patients with decompensated cirrhosis. AIMS: To estimate the extent to which proton pump inhibitors (PPIs) increase the rate of infections among patients with decompensated cirrhosis. METHODS: We conducted a retrospective propensity-matched new user design using US Veterans Health Administration data. Only decompensated cirrhotic patients from 2001 to 2009 were included. New PPI users after decompensation (n = 1268) were 1:1 matched to those who did not initiate gastric acid suppression. Serious infections, defined as infections associated with a hospitalisation, were the outcomes. These were separated into acid suppression-related (SBP, bacteremia, Clostridium difficile and pneumonia) and non-acid suppression-related. Time-varying Cox models were used to estimate adjusted hazard ratios (HR) and 95% CIs of serious infections. Parallel analyses were conducted with H2 receptor antagonists (H2RA). RESULTS: More than half of persons with decompensated cirrhosis were new users of gastric acid suppressants, with most using PPIs (45.6%) compared with H2RAs (5.9%). In the PPI propensity-matched analysis, 25.3% developed serious infections and 25.9% developed serious infections in the H2RA analysis. PPI users developed serious infections faster than nongastric acid suppression users (adjusted HR: 1.66; 95% CI: 1.31–2.12). For acid suppression-related serious infections, PPI users developed the outcome at a rate 1.75 times faster than non-users (95% CI: 1.32–2.34). The H2RA findings were not statistically significant (HR serious infections: 1.59; 95% CI: 0.80–3.18; HR acid suppression-related infections: 0.92; 95% CI: 0.31–2.73). CONCLUSION: Among patients with decompensated cirrhosis, proton pump inhibitors but not H2 receptor antagonists increase the rate of serious infections.
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