Niacin‐Induced Anicteric Microvesicular Steatotic Acute Liver Failure. Issue 11 (25th September 2018)

• Record Type: Journal Article
• Authors: Leung, Kenneth; Quezada, Michael; Chen, Zhengshan; Kanel, Gary; Kaplowitz, Neil
• Is Part Of: Hepatology communications. Volume 2:Issue 11(2018)
• Page Start: 1293
• Page End: 1298
• Publication Date: 2018-09-25
• Subjects: Hepatology -- Periodicals; Liver -- Diseases -- Periodicals; Liver Diseases; Gastroenterology; Periodicals; Fulltext; Internet Resources; Periodicals; 616.36
• DOI: 10.1002/hep4.1253
• Languages: English
• ISSNs: 2471-254X

Abstract

Abstract : Niacin (vitamin B3) is available as a prescription medication and over‐the‐counter supplement. Although it is well known for its vasodilatory effect, it has also been associated with mild hepatotoxicity and, rarely, acute liver failure. We present the case of a 74‐year‐old Hispanic woman who developed acute liver failure (anicteric encephalopathy and coagulopathy) after her home dose of immediate‐release niacin was replaced with an extended‐release formulation during an inpatient hospital stay. This is the first reported case of niacin toxicity associated with a histopathologic finding of diffuse microvesicular steatosis. This unique phenotype strongly implicates mitochondrial impairment as a mechanism of niacin‐induced hepatotoxicity. Abstract : This is the first description of niacin‐induced ALF due to microvesicular steatosis and a presumed mitochondrial toxicity. The case is temporally associated with switch from immediate release to extended release niacin at the same total dose and is characterized by hepatic encephalopathy, coagulopathy, mild liver test abnormalities and autopsy finding revealing only microvascular steatosis. This may be an underecognized complication of extended and slow release formulation.