Purpose Adiponectin is an adipocytokine suggested to have a hepatoprotective effect. To date, little information is available in the literature regarding changes in serum adiponectin levels in cirrhosis and cholestasis and the associated metabolic disturbances. In order to elucidate the role of adiponectin in chronic liver disease our aim was to determine serum adiponectin in patients with different grades of cirrhosis and cholestasis and to correlate it with markers of liver injury, inflammation and cholestasis. We also aimed to correlate adiponectin with markers of metabolic syndrome such as body mass index and insulin resistance. Methods Forty patients with cirrhosis; 30 patients with cirrhosis and cholestasis; and 20 matched controls were studied. They were subjected to clinical assessment, laboratory investigations: serum bilirubin, ALT, AST, alkaline phosphatase, GGT, albumin, C-reactive protein, prothrombin activity, fasting blood sugar, insulin. HOMA index was calculated. Abdominal ultrasonography and upper GI endoscopy were performed. Results Adiponectin was elevated in patients with cirrhosis and cirrhosis/cholestasis and was significantly higher in Child A and B. Adiponectin showed correlation with liver cell injury, marker of inflammation, synthetic liver function and markers of cholestasis. Adiponectin did not correlate with complications of cirrhosis as ascites and esophageal varices nor did it correlate with BMI or HOMA. Conclusions Adiponectin is elevated in cirrhosis and shows correlation with degree of hepatocellular injury and cholestasis. Finally, adiponectin levels in cirrhosis do not correlate with parameters of body composition or metabolism but exclusively with reduced liver function.

Background and aim In the era of hepatitis C virus eradication, Egypt had to pay attention to the two million infected with chronic hepatitis B. This study aimed to observe the current characteristics of chronic hepatitis B virus (HBV) infection in Egypt. Patients and methods This cross-sectional study was conducted on 183 patients with chronic HBV infection. The demographic, epidemiologic, clinical, laboratory, and treatment data were collected from patient registries. Results Positive hepatitis B e-antigen (HBeAg) cases represented 18.04%. They were younger (31.09±8.542–38.22±10.6 years) (P<0.05), with higher alanine aminotransferase (84.91±67.855–53.75±55.575 U/l) (P<0.05) and viral loads (3.58×108±16.49×108–1.74×106±10.1×106 IU/ml) (P<0.05), particularly in chronic active carrier states. Unsafe hygienic procedures (sharing toothbrushes and razors) were the main infective routes (73.7%). Coinfection with hepatitis C virus was documented in 14.7%, along with 16.3% with schistosomal infestation. HBV and hepatitis D virus coinfection was reported in 8.9% of the studied cohort. Radiologically, liver cirrhosis was detected in 44% of cases, with associated splenomegaly in 20.7%. Histologically, 40.2% were found to have significant pathology (A2, F2>2). Thirty (16.3%) cases were outside international guidelines of treatment, only for follow-up. Overall, 70.5% were subjected to lamidine therapy, with unfair responses mainly detected in the HBeAg-positive group (71.4%), who responded marvelously to interferon finite regimens. HBeAg-positive status and schistosomiasis were found to be associated with poor response to oral antivirals by multivariate analysis (P<0.05). Conclusion More classified governmental censorship efforts, notably on private organizations, along with awareness levitation are promptly mandated. Additionally, the poor response to oral antivirals in HBeAg-positive patients signifies sticking to interferon as a first-line treatment option.

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