Decompensated cirrhosis was defined as stage 3 or 4. 14: stage 1, no ascites and varices stage 2, esophageal varices without hemorrhage and no ascites stage 3, ascites without a history of esophageal variceal hemorrhage and stage 4, gastrointestinal bleeding with or without ascites. 1 The following four clinical stages were defined according to the classification by D'Amico et al. HS-1 was classified as follows according to HVPG grades based on previously reported cutoffs: group 1, 6–9 mmHg group 2, 10–12 mmHg group 3, 13–16 mmHg group 4, 17–20 mmHg and group 5, > 20 mmHg. HVPG subgroup, clinical stage, and MELD score The follow-up was performed up to December 31, 2013. Especially in case of alcohol related cirrhosis patients, alcohol abstinence for at least 6 months prior to participating in this study were considered eligible for the study to avoid the influence of inflammation by recent alcohol consumption. Finally, 572 non-critically-ill cirrhotic patients were analyzed ( Fig. Gastric varices are not correlated with HVPG level and patients who have recent esophageal variceal bleeding could be critically ill patients. The exclusion criteria were HVPG 5 mg/dL (41 patients) and recent esophageal variceal bleeding within 2 weeks (168 patients), serum creatinine levels > 1.5-fold the upper normal limit (7 patients), portal vein thrombosis (1 patient), and loss to follow-up within 28 days (51 patients). The patients were enrolled after confirming the presence of an HVPG of ≥ 6 mmHg. 21 HVPG measurements were used to establish the diagnosis of cirrhosis or to assess baseline portal pressure, prior to primary prophylaxis or secondary prophylaxis of variceal bleeding. Active drinkers were defined as patients who drink alcohol more than 140 grams/week (women), or 210 grams/week (men). 20 All of the patients had stable hemodynamic parameters and were not active drinkers. All of the patients had a previous histological confirmation of cirrhosis 19 or a diagnosis of cirrhosis suspected on the basis of standard clinical, ultrasonographic, and biochemical parameters. The present study investigated the current real-life setting in which patients with cirrhosis receive standard therapies for the different complications, with the aim of quantifying survival according to the HVPG grade and the prognostic value of HVPG grades and other prognostic factors.īetween January 2008 and June 2013, 1,025 cirrhotic patients were consecutively collected at 4 academic hospitals. 16, 17 However, considering that there are various causes of cirrhosis, regional and gender differences, and dynamic disease progression such as acute-on-chronic liver failure, few studies have evaluated survival prediction according to clinical characteristics and HS using the HVPG score in patients with PHT. 6, 14, 15 Previous reports have suggested that HS utilizing the HVPG score is closely associated with the clinical stage according to the presence of clinical complications. 6, 12, 13 For example, a hemodynamic stage (HS) with HVPG ≥ 6 mmHg indicates PHT (stage 1), while HVPG ≥ 10 mmHg represents clinically significant PHT (stages 2–4). 9Ī previous report suggested that specific stages within the classification of chronic liver disease can be associated with histological, clinical, hemodynamic, and biological stages. 11 The HVPG has been shown to have an independent role in survival in addition to the model for end-stage liver disease (MELD) score, with each 1-mmHg increase contributing to a 3% increase in mortality. 4, 5, 6, 7, 8, 9, 10 An HVPG of > 20 mmHg in acute variceal hemorrhage is indicative of a high probability of 1-year mortality. 2, 3 Measuring the hepatic venous pressure gradient (HVPG) is safe and has been found to be useful in the diagnosis of PHT and for risk stratification, assessment of prognosis, monitoring of treatment, and identification of patients with hepatocellular carcinoma (HCC) who are candidates for liver resection. 1 Portal hypertension (PHT) is a clinical syndrome characterized by a pathologically elevated portal perfusion gradient. The natural history of cirrhosis is related to elevated portal pressure.
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