Arterial blood pressure is closely related to ascites development in compensated HCV-related cirrhosis.

BACKGROUND: Arterial blood pressure (BP) is a reliable marker of circulatory dysfunction in cirrhotic patients. There are no prospective studies evaluating the association between different levels of arterial BP and ascites development in compensated cirrhotic patients. Therefore, we evaluated the relationship between arterial BP and ascites development in compensated cirrhotic patients. MATERIALS AND METHODS: A total of 402 patients with compensated HCV-related cirrhosis were prospectively followed during 6 years to identify ascites development. At baseline, patients underwent systolic, diastolic and mean arterial pressure (MAP) measurements. Any history of arterial hypertension was also recorded. The occurrence of events such as bleeding, hepatocellular carcinoma, death and liver transplantation prior to ascites development were considered as competing risk events. RESULTS: Over a median of 156 weeks, ascites occurred in 54 patients (13%). At baseline, MAP was significantly lower in patients with ascites development (75.9 mm/Hg [95%CI, 70.3-84.3]) than those without ascites (93.6 mm/Hg [95% CI: 86.6-102.3]). After adjusting for covariates, the 6-year cumulative incidence of ascites was 40% (95%CI, 34%-48%) for patients with MAP<83.32 mm/Hg. In contrast, cumulative incidences of ascites were almost similar among patients with MAP values between 83.32 mm/Hg and 93.32 mm/Hg (7% [95% CI: 4%-12%]), between 93.32 mm/Hg and 100.31 mm/Hg (5% [95% CI: 4%-11%]) or higher than 100.31 mm/Hg (3% [95% CI: 1%-6%]). The MAP was an independent predictor of ascites development. CONCLUSIONS: The MAP is closely related to the development of ascites in compensated HCV-related cirrhosis. The risk of ascites development increases in 4.4 fold for subjects with MAP values <83.32 mm/Hg.

The natural history of HCV-related cirrhosis and its temporal progression across the different clinical stages.

PURPOSE: The clinical course of hepatitis C virus-related cirrhosis and its temporal progression across the different clinical stages has not been completely investigated. Our study evaluated the cumulative incidences (CIs) of clinical outcomes marking disease progression across the different clinical stages. METHODS: At baseline, 660 patients were classified as compensated [absence (294), or presence (108) of gastroesophageal varices] or decompensated [ascites (144), variceal bleeding alone (45) or in combination with ascites (17) and encephalopathy alone or together with bleeding and/or ascites (52)]. Subjects were followed for 312 weeks to identify time to a first event marking disease progression. RESULTS: Among compensated patients without varices, the 312-week CIs for developing varices, ascites, and encephalopathy were 37.4, 13.6 and 3.5 %, respectively. The 312-week CIs of development of ascites, bleeding and encephalopathy were 24, 12.5 and 9.9 % for compensated subjects with varices, respectively. Among patients with ascites, the 312-week CIs of bleeding, liver-related deaths/transplant and encephalopathy were 23.5, 27.8, and 47.3 %, respectively. The 312-week CIs of ascites, liver-related deaths/transplant and encephalopathy were 22.5, 14.7 and 5.7 % among patients with bleeding; however, CIs of liver-related deaths were significantly higher in those with ascites plus bleeding (77.6 %). Patients with encephalopathy alone or in combination with ascites and/or bleeding displayed the highest rates of deaths (312 weeks, 90 %). CONCLUSIONS: Among compensated patients, the presence of varices suggests a more accelerated course of the disease. Decompensated patients show the most severe clinical course, particularly in those with a combination of two or more clinical events.

The natural history of compensated HCV-related cirrhosis: a prospective long-term study.

BACKGROUND & AIMS: The natural history of HCV-related compensated cirrhosis has been poorly investigated in Latin-American countries. Our study evaluated mortality and clinical outcomes in compensated cirrhotic patients followed for 6 years. METHODS: Four hundred and two patients with compensated HCV-related cirrhosis were prospectively recruited in a tertiary care academic center. At the time of admission, patients were stratified as compensated (absence [stage 1] or presence [stage 2] of esophageal varices) as defined by D'Amico et al. Subjects were followed to identify overall mortality or liver transplantation and clinical complication rates. RESULTS: Among 402 subjects, 294 were categorized as stage 1 and 108 as stage 2. Over a median of 176 weeks, 42 deaths occurred (10%), of which 30 were considered liver-related (7%) and 12 non-liver-related (3%); eight individuals (2%) underwent liver transplantation; 30 patients (7%) developed HCC, 67 individuals in stage 1 (22%) developed varices and any event of clinical decompensation occurred in 80 patients (20%). The 6-year cumulative overall mortality or liver transplantation was 15% and 45%, for stages 1 and 2, respectively (p<0.001). The cumulative 6-year HCC incidence was significantly higher among patients with varices (29%) than those without varices (9%), p<0.001. Similarly, the cumulative 6-year incidence of any clinical liver-related complication was higher in patients with stage 2 (66%) as compared to 26% in those with stage 1, respectively (p<0.001). CONCLUSIONS: Our results indicate significant morbidity and mortality and clinical outcome rates in compensated cirrhotic patients with varices (stage 2).