Abstract

There is an increasing tendency to think that liver biopsy is of little value in the assessment and management of alcoholic liver disease (ALD). The argument that clinical evaluation with biochemical investigation and noninvasive imaging have replaced the need for a histological assessment appears to hold sway (Talley et al, 1988). Although much of the pathology of ALD is understood, there are still many processes that are not fully explained. Many of these can only be adequately investigated using material obtained from patients with ALD. The basis for interindividual susceptibility to alcohol is not fully understood, but it is likely to be complex and to involve both environmental and genetic mechanisms (Day and Bassendine, 1992). Although a number of sublethal and lethal forms of injuries are recognized, the former including hydropic (cloudy) swelling and steatosis and the latter including alcoholic hepatitis and progressive fibrosis, these changes are interdependent and both may occur in varying proportions. The structural basis of precirrhotic portal hypertension and other pathophysiological changes is only now being recognized. Even when liver function tests are normal or only minimally disturbed the biopsy may show quite advanced changes of ALD (Baptista et al, 1981; Popper et al, 1981; Scheuer, 1982; MacSween and Burt, 1986; Hall, 1987). There is also evidence that some patients have been labelled as having ALD but on biopsy and subsequent serological information or polymerase chain reaction have been shown to have hepatitis C virus infection; the implications for management, therapy and possible liver transplantation are clear. Additional useful information can be acquired when the biopsy is obtained at laparoscopy where a direct view of the liver allows choice of biopsy site (or sites) and subsequent correlation with histological appearances. Specialist histopathological examination of the liver is therefore still an important part of the full assessment of any patient thought to have ALD.

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