In a prospective study of 444 patients with HCV and compensated cirrhosis, HCV eradication reduced risk for liver decompensation, HCC, and death, regardless of whether the patients had EVs.

Modified spleen stiffness measurement by transient elastography is associated with presence of large oesophageal varices in patients with compensated hepatitis C virus cirrhosis 1

P ortal hypertension (PH), defined by a hepatic venous pressure gradient (HVPG) greater than 6 mmHg, 1 is a common complication of cirrhosis. The presence and the development of esophageal varices (EV) is a clinical manifestation of PH, 2,3 with a prevalence that can range from 40% to 80% in patients with cirrhosis. This prevalence increases progressively in relation to the severity of liver damage. 4,5 The presence of EV is also a clear indicator of a certain stage of cirrhosis. 6 The development of EV in patients with cirrhosis occurs when the HVPG is greater than 10 mmHg, 3,7 with an incidence of approximately 5% per year and a yearly rate of progression to larger varices of 5% to 15%. 4,5,8 The clinical relevance of EV is linked to the risk of bleeding that occurs when HVPG is greater than 12 mmHg, 7-9 with a mortality rate that exceeds 20% within 6 weeks from the bleeding episode, despite aggressive treatment. 10 The Baveno IV 2005 Consensus Workshop 11 and the American Association for the Study of Liver Diseases 2007 single-topic symposium on portal hypertension 12 recommended that endoscopic screening for esophageal and gastric varices should always be performed when a diagnosis of cirrhosis is made. Upper endoscopy should be repeated at 2-year to 3-year intervals in patients without varices, and at 1-year to 2-year intervals in those with small varices, to evaluate their development or progression. 11,12 These guidelines might not be ideal for clinical

Summary Background It is unclear whether the course of cirrhosis and its prognosis are related to the amount of collagen in the liver. Aim To determine whether fibrosis, assessed by collagen proportionate area (CPA) in patients with compensated cirrhosis, is associated with the presence of oesophageal varices, and predict disease decompensation during the follow‐up period. Methods We prospectively evaluated 118 consecutive patients with compensated cirrhosis to correlate fibrosis, assessed by CPA in liver biopsies, with the presence of oesophageal varices (OV) and with the rate of liver decompensation (LD) development during a median follow‐up of 72 months. Results At baseline 38 (32.2%) patients had OV and during the follow‐up (median 72 months, IQR 47–91), 17 patients (14.4%) developed LD. The mean CPA value was different in patients with and without OV (14.8 ± 5.9% vs. 21.6 ± 9.5%, P < 0.001). The best CPA cut‐off for OV by area under the receiver operating characteristic (AUROC) was ≥14% and with multivariate logistic analysis CPA was the only variable associated with OV (OR: 28.32, 95% CI: 6.30–127.28; P < 0.001). By AUROC analysis the best CPA cut‐off to predict LD was 18.0%. By Cox regression multivariate analysis CPA ≥18% (HR: 3.99, 95% CI: 1.04–11.45; P = 0.036), albumin (HR: 0.12, 95% CI: 0.04–0.43; P = 0.001) and presence of OV (HR: 8.15, 95% CI: 2.31–28.78; P = 0.001) were independently associated with LD. Conclusion Quantification of fibrosis by collagen proportionate area allows identification of patients with compensated HCV cirrhosis with a higher likelihood of clinically relevant portal hypertension and a higher risk of decompensation.

Oesophagogastroduodenoscopy in patients with cirrhosis undergoing endoscopy for screening diagnosed pathologic lesions unrelated to portal hypertension requiring a change in management in 39.4% of asymptomatic subjects.