![]() | Only 14 pages are availabe for public view |
Abstract Chronic liver diseases (CLD) are the 10th leading cause of death for men and the 12th for women in the United States. In Egypt, it was found that approximately 7% of all Egyptian deaths annually are associated with liver cirrhosis. Features of wound healing process causing cirrhosis include the presence of an inflammatory state, due to infiltrating leukocytes and activated liver-resident macrophages, and activation of extra-cellular matrix producing cells (hepatic stellate cells; HSCs). Persistence of the cause of injury leads to progressive scarring and eventually to liver cirrhosis. Obesity and insulin resistance have been found to accelerate this wound healing progression in different types of chronic liver diseases. Because of this observation, attention has been recently directed to the possible role of adipokines in the hepatic wound healing process, linking obesity and insulin resistance with fibrosis progression. Adipokines are polypeptide hormones which are expressed mainly, but not exclusively, by adipose tissue. Resistin is polypeptide hormone belonging to adipokines. It was reported that resistin reduces insulin sensitivity in adipocytes, skeletal muscles and hepatocytes. Resistin expression was found in mononuclear leucocytes and in inflamed tissues, suggesting a pro-inflammatory properties for resistin or its regulation by inflammatory mediators as interleukin-6 (IL-6) and tumor necrosis factor –α (TNF-α). The aim of this work is to evaluate the potential clinical and prognostic relevance of serum resistin in patients with various stages of chronic liver diseases; focusing on its relation with hyperinsulinemia and insulin resistance and whether it is correlated with the inflammatory markers. This may help to evaluate the prognosis of hepatic patients more efficiently. This study was conducted at Ain-Shams University Hospital on 31 patients with chronic liver disease CLD (Patients’ group) and 13 healthy subjects (healthy control group). The patients’ group is further classified into A, B and C subgroups according to Child classification. Class A has a favorable prognosis, while class C is at high risk of death. Patients with overt diabetes mellitus, received or receiving oral anti-diabetic medications, having spontaneous bacterial peritonitis, concurrent infection, received Interferon or antiviral therapy and alcoholic patients were excluded from the study. All the individuals will be subjected to careful history, clinical examination and laboratory investigations including liver function tests (serum transaminases, albumin, total bilirubin, and INR), serological markers (HBsAg, anti-HCV), fasting blood sugar, fasting insulin level, serum IL6 serum resistin assay. The results of the present study revealed a significantly lower serum albumin and total cholesterol level in patients of CLD when compared to control group. Patients with CLD had a significantly higher serum IL-6. Fasting insulin increases and HOMA score (insulin sensitivity) decreases significantly in CLD patients. Chronic hyperinsulinemia is thought to be the main cause of insulin resistance in cirrhosis. Resistin also shows a significant increase in patients of CLD when compared with healthy controls. On comparing the patients’ subgroups, non-significant difference of IL-6 between patients’ subgroups is founded. Fasting insulin and HOMA score revealed non-significant difference. Resistin showed a significant increase in Child C patients in comparison to Child A and in Child C in comparison to Child B patients. As regards the impact of CLD complications on resistin level in patients’ groups, patients with hematemesis (as an example for CLD complications) showed a significant increase in resistin when compared to those without hematemesis. No significant correlation between resistin level in patients’ groups in one hand and IL-6, fasting insulin, HOMA score and albumin in the other hand. The favorable cutoff value of serum resistin was 5.1 μg /L distinguishing liver diseased patients from healthy controls with a sensitivity of 51.2% and a specificity of 89.5%. The prognostic performance of resistin for discriminating patients of group C from group A, group B and control group collectively showed a cutoff for resistin of 6.00μg/L. This had a diagnostic sensitivity of 77.8%, specificity 85.7%. |