Body. Non-alcoholic fatty liver disease (NAFLD), which can progress to cirrhosis in 10-15% of patients, is usually associated with metabolic syndrome. Hypopituitarism has recently been identified as a risk for NAFLD. Case report: A 53 year old Hispanic woman was referred to the hepatology clinic for evaluation of abnormal serum liver profile, hepatocellular type. She had morbid obesity, type 2 diabetes mellitus (DM), rheumatoid arthritis (RA), hypothyroidism, and had been on hormone replacement for central hypothyroidism and hypocortisolinemia from panhypopituitarism after craniopharyngioma resection 16 months prior to this evaluation. Months after surgery, she developed acute liver failure (ALF), days after infusion of infliximab for treatment of RA. Liver histology revealed portal and periportal fibrosis with focal early bridging. Drug-induced liver injury and autoimmune hepatitis were considered as causes of ALF, and she was treated with steroids for the latter, in association with recovery. Physical exam was notable for obesity and absence of stigmata of chronic liver disease, for which work up was unrevealing. Repeat liver biopsy revealed micro and macro vesicular steatosis, steatohepatitis and cirrhosis (figures 1 & 2). Life style modifications and adjustment of hormone replacement were associated with improved DM control, and normalization of thyroid function and serum liver profile.Figure: Hematoxylin and eosin stain of liverbiopsy, A: Fibrous septa showing predominantly polymorphonuclear cells B: Balloon degeneration of hepatocytes, steatosis.Figure: Arrow: Trichrome stain showing thick fibrous septa.Discussion: Cirrhosis was documented after ALF; however, this patient was at risk for NAFLD because of metabolic syndrome and panhypopituitarism; thus, a role of fat as an accelerator of her liver disease cannot be excluded. Hypopituitarism has been recognized as an etiologic factor of NAFLD possibly via low cortisol, TSH, GH, IGF-1, and insulin resistance, which impair transport of bile acids, hepatic lipid metabolism, and cell wall integrity. In children with panhypopituitarism, degree of liver disease decreased within 6 weeks of hormone replacement; however, its delay was associated with portal hypertension and cirrhosis (1). Accordingly, the threshold to consider a central etiologic component in patients with suspected NAFLD should be low, as timely identification of hormonal deficiencies and replacement may prevent progression of disease in association with hepatic steatosis. (1) Spray CH et al Acta Paed, 2000.