LAUSR

An obese 64-year-old pre-diabetic Navajo woman (BMI: 36) was initially treated for hypoxemic respiratory failure due to interstitial lung disease (ILD) and cryptogenic organizing pneumonia (COP). She was begun on long-term treatment with prednisone 20 mg/day and, due to an allergy to sulfa drugs, was also given atovaquone 1.5 g/day as prophylaxis for Pneumocystis jirovecii pneumonia. Two months later, she was admitted to hospital with asymmetrical leg swelling due to deep venous thrombosis (DVT) in her left leg with concurrent right pulmonary artery embolism: there was no evidence of right ventricular dysfunction; left ventricular ejection fraction was normal. A basic metabolic panel showed normal electrolytes, blood urea nitrogen and serum creatinine. A complete blood count demonstrated a slightly elevated white cell count of 12,000/μl (4000–11000 cells/ μl), consistent with steroid use, a hemoglobin of 11 mg/dl, and a platelet count of 210 × 103 (150–405 × 103 cells/μl). She was started on a therapeutic dose of apixaban in order to prevent additional thromboses. During the same admission, scleral icterus was noted on physical examination but no stigmata of chronic liver disease, e.g., palmar erythema, spider nevi, telangiectasia, ascites, hepatosplenomegaly, or asterixis were present. She denied any history of previous chronic liver disease, excessive alcohol use, family history of liver disease, or use of over-the-counter medications, herbal or nutritional supplements, or recreational drugs. She had had no exposure to fumes or other chemicals in the course of occupational or recreational activities. At her first admission, prior to initiation of systemic steroid and atovaquone therapies, she had normal liver test results, with serum concentrations of alanine aminotransferase (ALT) 32 U/L (14–67 U/L), aspartate aminotransferase (AST) 29 U/L (6–58 U/L), alkaline phosphatase (ALP) 86 U/L (38–150 U/L), total bilirubin 0.8 mg/dl (0.3–1.2 mg/dl), direct bilirubin 0.2 mg/dl (0.1–0.4 mg/dl), albumin 4.1 mmol/l (3.5–5.1 mmol/l) and internationalized normalized ratio (INR) of 1.0. Nevertheless, during her recent admission, abnormal tests included serum concentrations of AST 530 U/L, ALT 970 U/L, ALP 245 U/L, total bilirubin 2.1 mg/dl, direct bilirubin 1.8 mg/ dl, albumin 3.7 mmol/L and INR 1.3. The R factor was calculated to be 11.9, consistent with hepatocellular injury. Additional investigations revealed the following: serum TSH was mildly elevated (5.70 μU/mL [normal range: 0.5–5 μU/ mL]) and normal values of free T3 and T4; serum salicylate and acetaminophen were undetectable. Urine toxicology was unremarkable. Serologic tests for HCV Ab, CMV IgM, HBsAg, HBc Ab, HBsAb, HAV IgM, HIV, HSV IgM, EBV IgM were all negative. Serum ferritin was markedly elevated at 4079 ng/ml (20–200 ng/ml), possibly due to an acute phase reaction, though iron saturation was normal at 24%. Serum A1AT was 162 mg/dl (90–200 mg/dl) with a normal MM phenotype, and serum ceruloplasmin was 24 mg/ dl (17–46 mg/dl). Serum lactic dehydrogenase concentration of 346 units/L (117–224 units/L) was mildly elevated and her ANA titer of 1:40 (homogenous pattern) was weakly positive, but tests for anti-smooth muscle antibody, soluble anti-liver/kidney microsomal antibody and IgG concentrations were all normal. Computerized tomographic (CT) scan of abdomen and pelvis (with contrast) revealed calcified gallstones in the gallbladder without evidence of cholecystitis, and a common bile duct diameter of 3 mm, but no splenomegaly, liver parenchymal changes, abnormalities of * Aamer Abbass [email protected]