ABSTRACT
Liver cirrhosis leads to decreased production of clotting factors that are generally all produced in the liver except factor VIII and von Willebrand factor. However, cirrhotic patients are not protected from thrombosis. The present study aimed to assess the procoagulant and anticoagulant factors in cirrhotic patients with and without bleeding and/or thrombotic events. A total of 102 adult subjects were enroled: 51 cirrhotic patients and 51 healthy controls. After full history taking with special attention given to thromboembolic and haemorrhagic events, platelet count, serum albumin, bilirubin, international normalised ratio [INR], PT, partial thromboplastin time [PTT], hepatitis B surface antigen [HBsAg], hepatitis B core [HBc] antibodies, hepatitis C virus [HCV] antibodies, factor VIII, protein C, Protac-induced coagulation inhibition percentage [PICI%] assay and abdominal ultrasound were performed for patients and controls. Upper gastrointestinal endoscopy was conducted for the patients. Compared with control subjects, factor VIII and factor VIII/protein C were significantly higher, while protein C and PICI% were significantly lower among patients. Patients with liver cirrhosis may have a tendency for bleeding or thrombosis according to the balance of coagulant and anticoagulant status. PICI%, the assay that evaluated the functionality of the protein C anticoagulant system, was significantly lower in patients compared to control subjects. Accordingly, low PICI% and high factor VIII/protein C ratio can be taken as an index of hypercoagulability in cirrhotic patients
ABSTRACT
Nonalcoholic fatty liver disease [NAFLD] is a major cause of liver-related morbidity and mortality. Insulin resistance is believed to be a key factor in the development of fatty liver. Moreover, insulin resistance states characterized by elevated expression and production of several cytokines have been implicated in the pathogenesis and progression of NAFLD but direct evidence of the role of resistin in NAFLD is lacking. To determine the circulating resistin level in patients affected by NAFLD and to correlate resistin level with insulin sensitivity, liver functions and histological features. This study included 100 subjects divided into: forty patients with NAFLD, forty obese persons with BMI >30 having normal transaminases and normal liver ultrasound and twenty controls with BMI < 20. For all subjects serum resistin was measured. Homeostasis model assessment [HOMA] was calculated and liver profile was assessed. Liver biopsy was done in NAFLD patients. Serum resistin was higher in patients with NAFLD [16.2 +/- 4 ng/ml] compared to obese and control groups [6.8 +/- 4.1 and 3.4 +/- 1.1 [ng/ml]] respectively [p <0.01]. Serum resistin was higher in histologically advanced cases of NAFLD compared to simple steatosis [19.2 +/- 3.6 vs. 13.5 +/- 2.7] respectively [p < 0.01]. Moreover serum resistin correlated positively with 8M I, HOMA, highly sensitive CRP, AST and ALT. Resistin has a role in pathogenesis of NAFLD. Its level is a predictive of histology in NAFLD. So The use or serum resistin assay as a simple diagnostic biomarker for NAFLD is recommended