Division of Gastroenterology, Hepatology and Nutrition, Virginia Commonwealth University and McGuire Veterans Affairs Medical Center, Richmond, VA, USA.
Aliment Pharmacol Ther. 2012 Nov;36(9):866-74. doi: 10.1111/apt.12045.
There is increasing evidence that proton pump inhibitors (PPIs) increase the rate of infections in patients with decompensated cirrhosis.
To estimate the extent to which proton pump inhibitors (PPIs) increase the rate of infections among patients with decompensated cirrhosis.
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).
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).
Among patients with decompensated cirrhosis, proton pump inhibitors but not H2 receptor antagonists increase the rate of serious infections.
越来越多的证据表明质子泵抑制剂（PPIs）会增加失代偿性肝硬化患者的感染率。
评估质子泵抑制剂（PPIs）在多大程度上增加失代偿性肝硬化患者的感染率。
我们使用美国退伍军人健康管理局的数据进行了回顾性倾向评分匹配新用户设计。仅纳入 2001 年至 2009 年期间的失代偿性肝硬化患者。失代偿后开始使用 PPI 的新患者（n=1268）与未开始胃酸抑制的患者按 1:1 匹配。严重感染定义为与住院相关的感染，作为结局。这些感染分为酸抑制相关（SBP、菌血症、艰难梭菌和肺炎）和非酸抑制相关。采用时变 Cox 模型估计严重感染的调整后危险比（HR）和 95%CI。同时进行了 H2 受体拮抗剂（H2RA）的平行分析。
超过一半的失代偿性肝硬化患者是胃酸抑制剂的新使用者，其中大多数（45.6%）使用 PPI，而 H2RA 仅占 5.9%。在 PPI 倾向评分匹配分析中，25.3%的患者发生严重感染，在 H2RA 分析中，25.9%的患者发生严重感染。与未使用胃酸抑制的患者相比，PPI 使用者发生严重感染的速度更快（调整后 HR：1.66；95%CI：1.31–2.12）。对于酸抑制相关的严重感染，PPI 使用者发生该结局的速度比非使用者快 1.75 倍（95%CI：1.32–2.34）。H2RA 的结果无统计学意义（严重感染的 HR：1.59；95%CI：0.80–3.18；酸抑制相关感染的 HR：0.92；95%CI：0.31–2.73）。
在失代偿性肝硬化患者中，质子泵抑制剂而非 H2 受体拮抗剂会增加严重感染的发生率。
