الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 32 |  |  |
| | | from | 32 | | |
Abstract
Hepatitis C infection is a disease with a significant global impact. It causes chronic liver disease in 70–80% of patients and leads to severe complications such as fibrosis, cirrhosis and liver cancer after many years. Fibrosis can no longer be considered as a simple deposition of fibrillar extracellular matrix. Rather, hepatic remodeling should be considered as a process in which neoformed vessels are embedded in an active evolving scar tissue, where a complex interplay occurs between several cell types and soluble substances Apelin is a peptide isolated from bovine stomach extracts act as an endogenous ligand APJ receptor which is expressed in endothelial cells of liver sinusoids and hepatic stellate cells. Apelin behave as a hepatic paracrine substance in the cirrhotic liver, secreted by the activated stellate cells. Apelin induce profibrogenic genes in the HSC and contributed to platelet derived growth factor induced proliferation and it is an important mediator of the profibrogenic gene induction promoted AII and ET-1 in HSC and apelin-APJ signaling may promote Fas-induced liver injury, also apelin stimulate angiogenesis by stimulating directly or by VEGF synthesis in fibrotic liver. A strong association between HCV and IR was identified. Hyperglycemia and hyperinsulinaemia, the formation of advanced glycation end products, increase the release of non-esterified fatty acids and their metabolites glycerol, hormones and proinflammatory cytokines from adipose tissue were implicated in contributing to the development of the insulin-resistant state in hepatocytes The current study evaluated apelin serum level & insulin resistance in CLD and fatty liver patients. It was conducted on (75) subjects aged from 21 years to 48 years. The selected subjects were classified into 5 groups: group (I) fifteen subjects served as healthy control of matched sex and age, group (II) fifteen patients had steatosis without HCV infection, group (III) fifteen patients had steatosis due to HCV infection, group (IV) fifteen patients have liver fibrosis due to HCV infection and group (V) fifteen patients have liver cirrhosis due to HCV infection. Care was taken to exclude patients with other causes of chronic liver diseases such as causes of hepatitis as hepatitis B virus, autoimmune hepatitis, Wilson disease, Budd Chiari syndrome, hemochromatosis, hepatocellular carcinoma, cholestatic disorders, diabetic mellitus patients and patients with cardiovascular disorders and neurological disorders. All patients were subjected to thorough history taking, physical examination, investigations including complete blood count, liver profile, hepatitis C virus antibodies, hepatitis B s ag, HIV antibodies, abdominal ultrasound, serum apelin level by ELISA and insulin resistance was determined by HOMA.The present study revealed that: - All groups had been matched with no significant differences between as regard age and sex (P>0.05). - There was a statistically significant relationship between the serum apelin & IR and fibrosis degree. - There was a statistically significant relationships between the serum apelin & IR and steatosis.