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Until recently, the subject of parenchymal liver disease presenting in elderly patients had received little specific attention. Many studies have examined changes in morphology and function in the aging liver, initially in rodents and subsequently in humans. In summary, there are no age specific alterations in conventional liver biochemistry (serum bilirubin, serum aminotransferases, hepatic alkaline phosphatase, and other liver blood tests) but a number of dynamic measurements of liver function do decline from early adulthood to senescence.1 Liver size, liver blood flow and liver perfusion decline between the third and tenth decades by 30–40%.2 Most reflections of dynamic liver function—galactose elimination, aminopyrine demethylation, or caffeine clearance—fall pari passu with the reduction in liver volume and blood flow.3 ,4 Conceivably, some specific liver functions—for example, hepatic nitrogen clearance, are independently impaired, in this case by up to 50% with advancing age.5 It is probably in the area of liver regeneration, however, that reduction in functional capacity of the liver is most apparent and important. A number of studies have suggested increased susceptibility to stress insult in aged experimental animals6 but there are no comparable human studies. A clue to the possible mechanism of impaired liver cell proliferation with advanced age has been provided by the demonstration of an age related decline in mitogen activated protein kinase activity in epidermal growth factor stimulated rat hepatocytes.7 The above factors, combined with the influence of lifetime variation in diet, alcohol consumption and smoking, nutritional status, co-existent disease, and genetic influences, form the background for the age related features of parenchymal liver disease described in this article.
Although there are no specific age related diseases of the liver, it is increasingly recognised that consideration of special features and differences between old and young are important in respect of …