Vitamin A toxicity has been reported to cause severe liver disease and, occasionally, liver failure. Herein we present the case of a 60-year-old male with symptoms of muscle soreness, alopecia, nail dystrophy, and ascites. He continued to deteriorate with the development of refractory ascites, renal insufficiency, encephalopathy, and failure to thrive. In this era of natural supplements, medication toxicity remains a major cause of concern. Biotransformation of drugs is a major function of the liver. Drug-induced liver injury can be serious enough to cause fulminant hepatic failure resulting in death or liver transplantation. We report a case of liver injury from subacute vitamin A toxicity leading to liver transplantation. To our knowledge, there is no prior published report of liver transplantation for vitamin A toxicity in the United States.
CASE REPORTThe case was that a 60-year-old gentleman whose initial complaint was muscle soreness of 1-month duration. He also noticed increased shedding of his scalp hair (Fig. 1). He developed cold intolerance, chapped lips, dystrophy of his fingernails, and a skin rash with pruritus within 2 months (Figs. 2 and 3) His past medical history was significant for dyslipidemia, hypertension, and possibly celiac sprue, which was untreated. A comprehensive metabolic profile showed liver injury with aminotransferases elevated to 2 times the upper limit of normal, with alkaline phosphatase slightly above normal. Total bilirubin was normal. The patient was on atorvastatin at that time, and it was discontinued. His alcohol intake was minimal, and he stopped soon after the development of symptoms. When the liver injury tests remained persistently abnormal, he underwent an evaluation for chronic liver disease. This evaluation was essentially normal with a ferritin 26 g/mL, iron serum 43 g/dL, iron binding capacity 348 g/dL, iron saturation 12%, and lactate dehydrogenase 177 U/L. His serologies for hepatitis A, B, and C were negative. Antinuclear antibody and antimitochondrial antibody were negative, and ceruloplasmin and alpha-1 antitrypsin levels and phenotype were normal as well. In the meantime, the patient developed ascites. He was afebrile and anicteric with an erythematous skin rash on the abdomen and extremities. He also had nonscarring alopecia, decreased pubic and axillary hair, and dystrophic nail changes.An abdominal Doppler ultrasound showed ascites and normal Doppler waveforms of the hepatic artery and portal veins. The echogenicity and appearance of the liver were within normal limits. The spleen was normal in size. The patient's laboratory values at this time were as follows: hemoglobin, 11.6 mg/dL; white
