Bruno Savino, Zuin Massimo, Crosignani Andrea, Rossi Sonia, Zadra Felice, Roffi Luigi, Borzio Mauro, Redaelli Alessandro, Chiesa Alberto, Silini Enrico Maria, Almasio Piero Luigi, Maisonneuve Patrick
Department of Internal Medicine, AO Fatebenefratelli e Oftalmico, Milan, Italy.
Am J Gastroenterol. 2009 May;104(5):1147-58. doi: 10.1038/ajg.2009.31. Epub 2009 Apr 7.
The identification of prognostic factors associated with mortality is crucial in any clinical setting.
We enrolled in a prospective study 352 patients with compensated hepatitis C virus (HCV)-induced cirrhosis, consecutively observed between 1989 and 1992. At entry, patients underwent upper endoscopy to detect esophageal varices, and were then surveilled by serial clinical and ultrasonographic examination. The model for end-stage liver disease (MELD) score was calculated with information collected at enrollment. Baseline predictors and intercurrent events associated with mortality were assessed using the Cox regression model.
During a median follow-up of 14.4 years, 194 subjects received a single course of interferon monotherapy, 131 patients developed decompensation (ascites, bleeding, hepatic encephalopathy), 109 patients had hepatocellular carcinoma (HCC), 9 had liver transplant, and 158 died. Esophageal varices were associated with development of decompensation (hazard ratio (HR), 2.09; 95% confidence interval (CI), 1.33-3.30) and liver-related death (HR, 2.27; 95% CI, 1.41-3.66). A MELD score of > 10 predicted overall mortality (HR, 2.15; 95% CI, 1.50-3.09). Overall survival of patients with MELD < or = 10 was 80% at 10 years. HCC occurrence increased the risk of decompensation fivefold (HR, 5.52; 95% CI, 3.77-8.09). Hepatic and overall mortality hazard ratios were 8.62 (95% CI, 5.57-13.3) and 3.80 (95% CI, 2.67-5.42), respectively, for patients who developed HCC, and 16.9 (95% CI, 9.97-28.6) and 7.08 (95% CI, 4.88-10.2) for those who experienced decompensation.
In patients with compensated HCV-induced cirrhosis, the presence of esophageal varices at baseline predicted decompensation and mortality. The development of HCC during follow-up strongly hastens the occurrence of decompensation, which is the main determinant of death. Patients with a MELD score < or = 10 at study entry had a prolonged life expectancy.
在任何临床环境中，识别与死亡率相关的预后因素都至关重要。
我们纳入了一项前瞻性研究，该研究纳入了352例丙型肝炎病毒（HCV）引起的代偿期肝硬化患者，于1989年至1992年期间连续观察。入组时，患者接受上消化道内镜检查以检测食管静脉曲张，然后通过系列临床和超声检查进行监测。使用入组时收集的信息计算终末期肝病模型（MELD）评分。使用Cox回归模型评估与死亡率相关的基线预测因素和并发事件。
在中位随访14.4年期间，194名受试者接受了单一疗程的干扰素单药治疗，131例患者出现失代偿（腹水、出血、肝性脑病），109例患者发生肝细胞癌（HCC），9例接受肝移植，158例死亡。食管静脉曲张与失代偿的发生相关（风险比（HR），2.09；95%置信区间（CI），1.33 - 3.30）和肝脏相关死亡（HR，2.27；95%CI，1.41 - 3.66）。MELD评分>10预测总体死亡率（HR，2.15；95%CI，1.50 - 3.09）。MELD≤10的患者10年总生存率为80%。HCC的发生使失代偿风险增加五倍（HR，5.52；95%CI，3.77 - 8.09）。发生HCC的患者肝脏和总体死亡风险比分别为8.62（95%CI，5.57 - 13.3）和3.80（95%CI，2.67 - 5.42），而发生失代偿的患者分别为16.9（95%CI，9.97 - 28.6）和7.08（95%CI，4.88 - 10.2）。
在HCV引起的代偿期肝硬化患者中，基线时存在食管静脉曲张可预测失代偿和死亡率。随访期间HCC的发生强烈加速失代偿的发生，失代偿是死亡的主要决定因素。研究入组时MELD评分≤10的患者预期寿命延长。
