Drug-induced fatty liver disease: An overview of pathogenesis and management.

Drug-induced liver diseases (DILD) are clinico-pathologic patterns of liver injury caused by drugs or other foreign com- pounds. Steatohepatitis is a rare form of DILD, and drugs account for fewer than 2% of non-al- coholic steatohepatitis (NASH). Drugs known to be capable of inducing steatosis and steato- hepatitis can be divided into three broad groups: those that cause steatosis and steato- hepatitis independently (e.g., amiodarone, per- hexiline maleate); drugs which can precipitate latent NASH (e.g., tamoxifen); drugs which in- duce sporadic events of steatosis/steatohepati- tis (e.g., carbamazepine). Clinical DILD syn- dromes include acute viral hepatitis-like injury, acute liver failure, cholestatic hepatitis, liver disease with signs of hypersensitivity, autoim- mune hepatitis-like injury, acute venous-out- flow obstruction, chronic cholestasis, cirrho- sis, steatosis and steatohepatitis. The clinical picture is by no means dependent on the mech- anism of injury (direct hepatotoxicity, idiosyn- cratic reactions, hypersensitivity reactions). Reliable diagnosis of drug-induced liver dis- ease requires demonstration of close correla- tion between the patient history and clinical, laboratory, and histological data.

/pdf/fatty-liver-and-drugs-4k0tz6he5i.pdf

Fatty liver and drugs.

Liver steatosis is a common human disease, most often caused by long-term alcohol consumption. Non-alcoholic steatohepatitis (NASH) is characterized by similar histopathological features to those observed in alcoholic liver disease, but occurs in the absence of significant alcohol consumption. Several aetiological factors contribute to NASH: obesity, type 2 diabetes mellitus, hyperlipidaemia, pregnancy, different chemical intoxications, parenteral nutrition, jejeuno-ileal bypass, chronic inflammatory bowel disease, nutritional protein deficiency and congenital metabolic disorders. Biochemically, oxidative stress and lipid peroxidation and their ensuing damage are implicated in the pathogenesis of NASH and alcoholic steatohepatitis (probably resulting from free fatty acids in the mitochondria, and induction of the cytochrome P450 isoform CYP2E1 in hepatocytes and Kupffer's cells). This paper deals with the pathomechanisms, clinical findings and currently available therapies for NASH. The potential use of metadoxine in the treatment of NASH is also discussed.

https://journals.sagepub.com/doi/pdf/10.1177/147323000303100610

A new approach to drug therapy in non-alcoholic steatohepatitis (NASH).

Effects of the antiepileptic drug carbamazepine on human erythrocytes

Inhibition of mitochondrial fatty acid oxidation in drug-induced hepatic steatosis

A 42-year-old woman presented with acute bullous skin lesions and angio-oedema that had developed 3 months after initiation of treatment with carbamazepine for epilepsy. Chromatographic analysis of urinary porphyrins was compatible with variegate porphyria. This was manifested initially by neurological symptoms that were mistaken for epilepsy and later by cutaneous symptoms also. Histological findings excluded hepatic porphyria, but revealed severe fatty changes thought to be caused by idiosyncratic metabolism of carbamazepine. While the porphyrinogenicity of carbamazepine is well known, the presence of variegate porphyria has not been reported. The toxic hepatic effects of the drug on hepatic cytochrome P-450, which is involved in haem metabolism, could have aggravated the pre-existent porphyria, provoking the onset of skin lesions.

Non-alcoholic steatohepatitis induced by carbamazepine and variegate porphyria.

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Non-alcoholic steatohepatitis induced by carbamazepine and variegate porphyria.