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Abstract
Cholestasis is not a disease; rather, it is a symptom of many diseases. It is defined as a pathologic state of reduced bile formation or flow. This definition applies more to the experimental situation, where the rates of bile formation and flow can be measured, than to human cholestasis, where neither can be assessed. Therefore, the clinical definition of cholestasis is any condition in which substances normally excreted into bile are retained. The serum concentrations of conjugated bilirubin and bile salts are the most commonly measured [1].
The mechanisms of cholestasis can be broadly classified into hepatocellular, where an impairment of bile formation occurs, and obstructive, where impedance to bile flow occurs after it is formed. The typical histopathologic features of hepatocellular cholestasis include the presence of bile within hepatocytes and canalicular spaces, in association with generalized cholate injury. Typical of obstructive cholestasis is bile plugging of the interlobular bile ducts, portal expansion, and bile duct proliferation in association with centrilobular cholate injury [2].
Bile is a highly complex water-based medium containing inorganic ions and many classes of organic amphiles, the formation of which involves multiple mechanisms and levels of regulation. The transport of solute into the canaliculus by specific transporters creates chemical and osmotic gradients and promotes water flow by a paracellular pathway. Several of these specific transporters have been identified, and their function has been characterized. The identification of defective transporters in some familial cholestatic disorders has led to improved understanding of the molecular mechanisms of human cholestasis. This subject was recently reviewed in depth [3].