Morphological Issues of Drug Induced Liver Disease

Abstract

Drug-induced liver disease is a multifaceted phenomenon which has a varied morphological spectrum that mimics other patterns of liver damage both in cases of acute drug exposure and in cases of chronic exposure to drugs. Those patients who are idiosyncratically susceptible at the therapeutic dose or to intrinsic toxicity may also be affected by other factors including genetic factors, age, sex, nutritional status, exposure to other drugs and the existence of an underlying disease. The only clinical manifestation of the disease may be the adverse effect of a drug, but it can also be accompanied by systemic manifestations and manifestations in other organs, and it can even be fatal (1).

The incidence of drug-induced liver disease is not well defined, but some studies claim that its overall annual incidence varies between 1/100,000 people and 15/100,000 people. In the United States, twenty new cases per 100,000 inhabitants occur every year. More than 900 natural and pharmaceutical drugs, herbal medicines, homeopathic products, dietary supplements and toxins have been reported to cause liver damage. This can occur whether or not they are used at normal therapeutic doses. These cases are responsible for about 15% of consultations and hospitalizations for jaundice, acute hepatitis, and chronic hepatitis in adults above the age of 50, and in up to 40% of all cases of hepatitis.  Drug-induced liver disease also accounts for 11% to 50% of all cases of acute liver failure. Published data indicate that antibiotics are responsible for between 27% and 46% of cases, that drugs for diseases of the central nervous system are responsible for between 13% and 17%, anti-inflammatory and analgesic agents are responsible for between 5% and 17%, and herbal products are responsible for 9%. New biomarkers and the use of microRNA are being studied and may become promising alternatives in the near future for identifying patients susceptible to drug-induced hepatotoxicity.

There are so many types of liver damage attributed to these agents that only give some examples can be provided in this article. These examples have been chosen on the basis ofn the patterns of liver damage with emphasis on the importance of proper and thorough clinical correlation (2, 3).