الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Thrombophilia is an inherited or acquired predisposition to thrombosis. It is a multifactorial disease that manifests when a person with an underlying predisposition to thrombosis (i.e., thrombophilia) is exposed to clinical risk factors. Thrombophilia is not a disease per se, but may be associated with a disease (e.g cancer), drug exposure (e.g., oral contraceptives) or condition (e.g. pregnancy or postpartum) or thrombophilia may be inherited. This concept is important because susceptibility to a disease does not imply an absolute requirement for primary or secondary prevention, or for treatment, the presence of a thrombophilic defect is only one of many elements that determine risk.
Liver fibrosis is the excessive accumulation of extracellular matrix proteins (ECM) including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension. Liver fibrosis results from chronic damage to the liver in conjunction with the accumulation of ECM proteins that distorts the hepatic architecture by forming a fibrous scar, and the subsequent development of nodules of regenerating hepatocytes defines cirrhosis. The main causes of liver fibrosis include chronic HCV infection, Bilharziasis, alcohol abuse, nonalcoholic steatohepatitis (NASH), Autoimmune diseases e.g primary billiary cirrhosis, primary sclerosing cholangitis and auto immune hepatitis.
Hepatic stellate cells (HSCs) are the main ECM-producing cells in the injured liver. In the normal liver, HSCs reside in the space of Disse and are the major storage sites of vitamin A. Following chronic injury, HSCs activate or trans differentiate into myofibroblast-like cells, acquiring contractile, proinflammatory, and fibrogenic properties. Activated HSCs migrate and accumulate at the sites of tissue repair.