الفهرس 
Liver anatomy and histologyOnly 14 pages are availabe for public view
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Abstract
The liver has a special susceptibility to damage by chemical agents. This susceptibility is a consequence of its primary role in metabolism and biotransformation of both injected and ingested foreign chemicals, so even if the original chemical is nontoxic, at a time, its metabolite may be toxic. The concentration of foreign chemicals in the liver, the position of the liver as a portal to other body organs and tissues, also contribute to this special vulnerability. Of course, the most clear setting of xenobiotic induced liver injury and most relevant to clinicians is drugs, next, occupational and household chemicals. In this review, we have been concerned with the occupational and household settings. Chemical injury to the liver, including drugs and other chemicals, has become a rising problem nowadays. It is responsible for about 5% of cases of jaundice or acute hepatitis in the community and about 10%–40% (depending on age) of cases of hepatitis admitted to hospitals. It is also an important cause of acute liver failure (>50% of cases in the United States). This represents the magnitude of chemical injury to the liver. Chemical induced liver injury is either intrinsic or idiosyncratic. In the intrinsic (predictable) type, the injury is dose related and is reproducible in animals and it can be due to the drug itself or to its metabolite. CCl4 is the prototype of direct hepatotoxins. On the other hand, idiosyncratic agents are not predictably hepatotoxic, but produce hepatic injury in only a small portion of exposed individuals, who are uniquely susceptible. In several instances, auto antibodies directed against normal cellular constituents are detected. The injury does not appear to be dose related and is not reproducible in experimental animals and appears after a variable latent period. Hepatotoxic chemicals can virtually lead to any variety of liver disease ranging from mild biochemical and clinical injury up to hepatic malignancies. These include necroinflammatory injury (e.g. aliphatic hydrocarbons and TNT), cholestatic injury (e.g. methylene dianiline), steatosis (e.g. tetrachloroethane and dimethylacetamide), granulomas (e.g. beryllium and copper), cirrhosis (e.g. arsenic and PCBs), veno-occlusive disease (e.g. pyrrolizidine alkaloids) and even hepatocellular carcinoma and angiosarcoma (e.g. vinyl chloride). This variability is also noticed with workers involved in the same industry and the different routes of exposure. Whereas some chemicals (like tetrachloroethane and carbon tetrachloride) can lead to mass affection of all workers with the same clinicopathological pattern, other chemicals (like dimethylacetamide) affect only few workers. Furthermore, while hepatotoxicity in most of the workers occurs through inhalation, yet, this hepatotoxicity in some other workers occurs through skin contact during handling and storage of chemicals. Lastly, it seems clear that this field has not gained adequate effort in research studies in comparison to other branches in hepatology inspite of its great importance. So we recommend more efforts to be applied by researchers in this field in collaboration with occupational specialists and industrial safety authorities.