Vitamin A Toxicity from over the Counter Health Supplements

Abstract

Introduction: The growing popularity and availability of over the counter (OTC) health products is of concern. In United States, about 25% of adults ingest vitamin A containing supplements and 5% take supplements of vitamin A alone. We report a case of cirrhosis associated with habitual daily ingestion of OTC dietary supplement of vitamin A. Case: A 59-year-old white man was referred from primary care physician for massive ascites of six-months duration. He was abstinent from alcohol since 15 years and had been taking variety of unsupervised OTC multivitamin tablets containing an aggregate of 160,000 IU/d vitamin A for two years (Recommended Daily Amount is 5000 IU/d for adults). Laboratory workup was significant for total bilirubin of 0.5 mg/dL, ALP of 154 IU/L, ALT of 40 IU/L, AST of 45 IU/L, albumin of 2.7 g/dL, INR of 1.1, serum ascitic albumin gradient of 1.5, vitamin A level of 21 micrograms/L (normal 30–95 mcg/L) with normal serum levels of ceruloplasmin, ferritin, transferrin, alpha 1 antitrypsin and negative hepatitis and autoimmune serology. Echocardiogram showed ejection fraction of 55% with normal right ventricular systolic pressure. Ultrasonogram revealed a mildly shrunken liver. Grade I esophageal varices were present on esophagogastroduodenoscopy. Liver biopsy showed chronic hepatitis grade II stage II with hypertrophied stellate cells and perisinusoidal fibrosis consistent with vitamin A toxicity. Vitamin supplements were discontinued. At two year follow-up patient had minimal ascites with improved liver functions. Discussion: Symptoms may occur with too much or too little of vitamin A. Vitamin A hepatotoxicity is rare; ranging from elevated liver enzymes to cirrhosis and may be observed in the absence of extra hepatic signs of vitamin A intoxication or increase in serum vitamin A concentration like in our case. Hyperplasia and hypertrophy of perisinusoidal stellate cells and perisinusoidal fibrosis on liver biopsy is consistent with hepatic storage of excess vitamin A. Concomitant alcohol use further potentiates the intrinsic hepatotoxicity of vitamin A. This case highlights the collateral damage caused by OTC vitamin supplements and indicates the need for regulation of medically unsupervised use of such products. As a consequence of increasing use of OTC vitamin A supplements, physicians need to provide information regarding relative safety of such products and elicit history of vitamin A supplements use in evaluation of liver dysfunction.