Abstract
Alcoholic liver disease is characterized with excess consumption of alcohol for long term and variable hepatic injury. Chronic alcohol consumption often leads to a disease called alcoholic liver disease [ALD]. It is generally with an accompaning iron accumulation. Increased plasma iron levels and tissue iron overload stimulate synthesis of hepcidin, resulting with release of iron from macrophages and duodenal enterocytes to the plasma. This homeostasis ensures that plasma iron level is maintained within a constant range and excess absorption and accumulation of iron in tissues are prevented. Alcohol-induced oxidative stress in hepatocytes is one of the main mechanisms by which hepcidin expression in the liver is down-regulated by alcohol. The decrease in liver hepcidin synthesis leads to an increase in intestinal iron transport and liver iron content. We report a case hemosiderosis secondary to chronic alcoholism.
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