Cryptogenic cirrhosis: Metabolic liver disease due to insulin resistance.

Objective: Etiopathogenesis of cryptogenic cirrhosis (CC) is not yet well established. Up to 20% of non-alcoholic fatty liver disease (NAFLD) may progress to cirrhosis, mostly termed as cryptogenic. Insulin resistance and altered metabolic parameters form a major pathogenic link between NAFLD and CC. CC may thus be actually a metabolic liver disease. Materials and Methods: Thirty-four patients of CC and 32 patients having cirrhosis due to chronic hepatitis B (Hep B) were assessed in a cross-sectional study in a tertiary hospital for insulin resistance, % β-cell activity, obesity indices, plasma glucose, lipid profiles, and many other parameters. Results: CC patients had higher homeostasis model assessment (HOMA)-IR compared to Hep B group (P = 0.000016). A positive correlation between IR values and Child-Pugh score among CC patients was found ("r" = 0.87; P < 0.00001). Out of 34 CC patients, 15 (44.1%) had obesity contrary to 6 (18.8%) in the control group (P = 0.0022). Differences were observed in subcutaneous fat (P = 0.0022), intra-abdominal fat (P = 0.0055), waist circumference (P = 0.014), and percentage body fat (P = 0.047) between the two groups. Significant differences were observed in the levels of triglyceride, total cholesterol, and very low density lipoprotein (VLDL). Conclusion: Most of the CC patients showed significantly higher prevalence of HOMA-IR, obesity indices, and various parameters of "lipotoxicity" and metabolic syndrome, suggesting that CC may be the long-term consequence of a type of "metabolic liver disease." Further studies are required to evaluate the role of therapeutic interventions to enhance insulin sensitivity in such patients.

Quality of life assessment of patients with chronic liver disease in eastern India using a Bengali translation chronic liver disease questionnaire.

Aims The aim of this study was to translate and validate chronic liver disease questionnaire (CLDQ) into Bengali using a standard protocol and use it to assess the impact of socioeconomic factors, etiology, disease severity and complications on the quality of life of patients. Methods Formal translation of CLDQ to Bengali was done. Cronbach’s alpha and test-retest was performed for reliability analysis. Patients with clinically stable chronic liver disease (CLD) without significant associated co-morbid states were administered Bengali CLDQ in the Liver Clinic. The clinical, biochemical and disease parameters were recorded for analysis. Results Bengali CLDQ was administered to 100 patients with CLD. Cronbach’s alpha of overall scores was 0.90 and test-retest correlation coefficient of average CLDQ was 0.86 (P<0.001). Patients with history of decompensation (96.51 vs. 109.61; P=0.039) and Child’s C status (92.24 vs. 105.71; P=0.028) had significantly lower CLDQ scores. CLDQ scores showed a moderate inverse correlation with Child’s status (r=−0.35) and a poor correlation with MELD score (r=−0.09). Conclusion Bengali translation of CLDQ was found to be reliable. History of decompensation, Child’s C status was associated with worse CLDQ scores. Child’s status may have some role in predicting quality of life of patients with CLD. MELD score had poor predictability of quality of life.

Hemodynamic effect of spironolactone in liver cirrhosis and propranolol-resistant portal hypertension.

OBJECTIVE: In a proportion of patients with liver cirrhosis, portal pressure does not decrease adequately with propranolol. These patients may benefit from another drug that may reduce portal pressure. We evaluated the role of spironolactone, alone or with propranolol, in such patients. METHODS: Patients with cirrhosis, with or without ascites, with esophageal varices and with hepatic venous pressure gradient exceeding 12 mmHg, which did not show a 20% reduction after an 80-mg oral dose of propranolol, were studied. They were allocated to receive spironolactone 100 mg orally once daily either alone (group 1, n=10) or with propranolol 40 mg orally twice daily (group 2, n=10), for 7 days, after which the hemodynamic study was repeated. RESULTS: Hepatic venous pressure gradient decreased in those receiving spironolactone and propranolol (p=0.007); 5 patients in group 1 and 7 in group 2 showed a reduction in hepatic venous pressure gradient by more than 20%. However, the reduction produced by spironolactone alone (20.5 [31.3]%) was not significantly different from that produced by combination therapy (30.3 [25.9]%; p=0.46). CONCLUSION: Spironolactone in combination with propranolol achieves adequate reduction (> or = 20%) in hepatic venous pressure gradient in propranolol-resistant portal hypertension in patients with liver cirrhosis. Spironolactone alone was also effective in some patients.