Numerous drugs and environmental chemicals are capable of influencing the clinical expression of human hepatic porphyria primarily by interfering with the orderly regulation of heme synthesis in the liver. Some agents trigger the disease in otherwise normal individuals whereas others exacerbate an underlying genetic abnormality leading to disease expression. In both instances careful avoidance of exposure to these drugs and chemicals can largely prevent the development of manifest disease. The mechanisms whereby these agents impair the normal regulation of hepatic heme synthesis have been carefully studied in recent years and have provided valuable new insights into this form of drug-induced hepatotoxicity.
