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INTRODUCTION: The aims of this study were to investigate the risk factors for bacterial infections (BIs) and the association of BIs with the progression to acute-on-chronic liver failure (ACLF) in patients with hepatitis B virus (HBV)-related compensated liver cirrhosis and severe hepatitis flares. METHODS: A total of 237 patients were retrospectively reviewed. Baseline biochemical characteristics were compared between patients with and without the occurrence of BIs and progression to ACLF. Univariate and multivariate logistic regression analyses were used to identify independent risk factors for ACLF before and after 1:1 propensity score matching. RESULTS: Forty-eight (20.3%) patients progressed to ACLF after admission. Additionally, 136 (57.4%) patients progressed to hepatic decompensation (HD) and 52 (21.9%) patients had BIs before the development of ACLF. Patients with BIs had significantly higher incidences of HD (84.6%) and ACLF (46.2%) than those without BIs (49.7% and 13.0%, respectively; P < 0.01). CTP score (OR 1.660, 95% CI 1.267-2.175) and MELD-Na score (OR 1.082, 95% CI 1.010-1.160) were independent risk factors for BIs. BIs (OR 4.037, 95% CI 1.808-9.061), CLIF-SOFA score (OR 2.007, 95% CI 1.497-2.691), and the MELD-Na score (OR 1.167, 95% CI 1.073-1.260) were independent risk factors for the progression to ACLF. BIs (OR 4.730, 95% CI 1.520-14.718) were also an independent risk factor for the progression to ACLF after propensity score matching. CONCLUSION: High CTP and MELD-Na scores are risk factors for BIs, and BIs are risk factors for the progression to ACLF in patients with HBV-related compensated liver cirrhosis and severe hepatitis flares.
RESUMO
Background and Aim: To investigate the short-term dynamic changes and the factors associated with regression of glucose metabolism disorders in patients with hepatitis flare of chronic hepatitis B virus (HBV) infection. Methods: In this study, 118 patients with severe hepatitis flare of chronic HBV infection were prospectively studied. Oral glucose tolerance test was performed on admission and during follow-up to evaluate dynamic changes in glucose metabolism disorders. The factors associated with regression of glucose metabolism disorders were identified using univariate and multivariate logistic regression analyses. Results: The prevalence of diabetes was significantly higher in 70 (47.1%) patients with liver cirrhosis than that in 48 (16.8%) patients without liver cirrhosis. The prevalence of impaired glucose tolerance in patients with liver cirrhosis (35.7%) was significantly lower than that in patients without liver cirrhosis (47.8%). After a follow-up of 20.0 ± 18.7 days, 28 of 31 (90.3%) patients without liver cirrhosis experienced regression of glucose metabolism disorders. Additionally, 30 (54.5%) patients with liver cirrhosis experienced regression of glucose metabolism disorders after 42.0 ± 36.2 days. In patients with liver cirrhosis, those with regression of glucose metabolism disorders had significantly higher levels of homeostasis model assessment-ß-cell function, albumin (ALB), and a significantly lower level of fibrosis-4 score. ALB was identified as an independent factor associated with the regression of glucose metabolism disorders in patients with liver cirrhosis. Conclusion: Severe acute liver inflammation aggravates glucose metabolism disorders in patients with hepatitis B-related liver cirrhosis and high ALB level is associated with regression of glucose metabolism disorders upon resolution of acute liver inflammation.