Niacin‐Induced Anicteric Microvesicular Steatotic Acute Liver Failure

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.

Profiles for identifying problematic dietary habits in a sample of recreational Spanish cyclists and triathletes

“…Excessive vitamin B3 intake could provoke flushing, headaches, light-headedness, itching, nausea and vomiting. In addition, liver injury can occur in rare cases and progress to fulminant hepatic failure 49 . As the indiscriminate use of vitamin and mineral supplements may adversely affect physiological function and impair health 50 , it is recommended to consume high nutrient density food rather than nutritional supplements.…”

Profiles for Identifying Problematic Dietary Habits in a Sample of Recreational Spanish Cyclists and Triathletes

“…Excessive vitamin B3 intake could provoke ushing, headaches, light-headedness, itching, nausea and vomiting. In addition, liver injury can occur in rare cases and progress to fulminant hepatic failure 39 . As the indiscriminate use of vitamin and mineral supplements may adversely affect physiological function and impair health 40 , it is recommended to consume high nutrient density food rather than nutritional supplements.…”

NAD+ and its possible role in gut microbiota: Insights on the mechanisms by which gut microbes influence host metabolism

“…It has been reported that NA had no impact on diet-induced NAFLD development in C57BL/6J mice but potentiated hepatic steatosis in HFD-fed B6129SF2/J mice ( Fang et al., 2020 ). Additionally, NA usually causes liver toxicity at doses higher than 3 g/day, which may be caused by mitochondrial damage ( Leung et al., 2018 ). The most obvious known side effect of NA administration is flushing, which is caused by the production of prostaglandins D2 and E2 by subcutaneous Langerhans cells through GPR109A ( Kamanna and Kashyap, 2008 ).…”