Taglietti et al. Journal of Medical Case Reports 2010, 4:332 http://www.jmedicalcasereports.com/content/4/1/332 previously, while on treatment with ramipril, the patient consulted his general practitioner because of recent onset of high systolic arterial pressure value. Treatment with ramipril was stopped, and olmesartan 10 mg and HCTZ 12.5 mg were started. At this time, our patient’s clinical and routine laboratory findings were normal. On admission to our hospital, the patient appeared asthenic. On physical examination, we found the patient to have a normal body mass index, vague right upper quadrant abdominal pain, sclera icterus and mild hepa- tomegaly. The remainder of the clinical examination was unremarkable. Other than the arterial hypertension, he had no medical history of note. Liver function test results showed: alanine aminotrans- ferase (ALT) 346 U/L (normal < 40 U/L), aspartate ami- notransferase (AST) 158 U/L (< 40 U/L), gamma glutamine transferase (GGT) 250 U/L (< 64 U/L), C-reactive protein 0.70 mg/dL (< 0.60 mg/dL), alkaline phosphatase 1.091 U/L (normal range 91 to 258 U/L), total bilirubin 6.28 mg/dL (0.2 to 1 mg/dL), direct bilir- ubin 4.26 mg/dL (0.01 to 0.2 mg/dL), ferritin 647 ng/dL (15 to 400 ng/dL). Results of red and white blood cell counts, platelet counts, and other laboratory tests were normal. Results of tests for possible infectious causes of hepati- tis showed that our patient was negative for cytomegalo- virus (CMV) IgM, parvovirus B19 IgM and IgG, and Epstein-Barr viral capsid antigen (EBV VCA) IgM, and positive for CMV IgG and EBV VCA IgG positive. Blood cultures, and antibody tests for human immuno- deficiency virus, hepatitis A, B, C and E viruses, hepatitis surface antigen, and leptospira were negative. Our patient’s immunoglobulin levels were normal. Antinuc- lear autoantibody, anti-microsomal antibodies, anti- smooth muscle antibodies, anti-liver-kidney-microsomal antibodies, anti-neutrophil cytoplasmic antibody, and anti-glomerular basement membrane were undetectable. Screening for tumor-associated antigens was also negative. Abdominal untrasonography, abdomen computed tomography, and magnetic resonance cholangiography were performed to assess the presence of solid tumors or bile duct obstruction; the results revealed only a mild hepatomegaly. By day 18, our patient was still jaundiced and had scleral icterus. His clinical condition was unchanged. Repeat laboratory investigations showed an increase in total bilirubin (14.7 mg/dL), with direct bilirubin at 12.6 mg/dL. AST and ALT values were slightly diminished (100 and 170 U/L respectively), and alkaline phospha- tase and GGT had decreased to 428 U/L and 170 U/L, respectively (Table 1). Because of our patient’s persistent higher transaminase and bilirubin values, and the negative findings on Page 2 of 4 Table 1 Trend of liver function tests Blood test ALT (U/L)2 AST (U/L)2 Total bilirubin (mg/dL) Direct bilirubin (mg/dL) Alkaline phosphatase (U/L) GGT (U/L)2 Day Day 0 346 158 6.28 4.26 1.09 250 181 170 100 14.7 12.6 428 170 22 100 96 10.6 8.4 340 140 30 76 58 6 4.1 298 98 90 20 14 0.2 0.1 146 12 1HCTZ therapy stopped. 2ALT = alanine amino-transferase; AST = aspartate amino-transferase; GGT = gamma glutammin transferase. laboratory and radiologic testing, the clinical picture was attributed to primary toxic damage by HCTZ. Therapy with olmesartan plus HCTZ was then stopped; enalapril 10 mg twice daily was started. Using percutaneous nee- dle biopsy, a liver sample was obtained, fixed in 10% buffered formalin, and embedded in paraffin wax for routine histologic examination. Slides were stained with hematoxylin and eosin, periodic acid-Schiff (PAS), PAS diastase, Perl, reticulin silver impregnation, and Masson trichrome. Histologic evaluation of the liver sample was per- formed by two pathologists. There was evidence of acute cholestatic hepatitis. The perivenular hepatocytes were swollen, with feathery degeneration. Bile thrombi in dilated canaliculi (canalicular cholestasis) were also seen throughout the acinus (Figure 1). Doubling of the hepatic trabeculae with anisokaryosis and formation of several liver cell rosettes, features that were most appar- ent in zone three, were considered features of regenera- tion. A mild hepatic necroinflammatory mixed infiltrate was present in all three zones of the acinus, in the form of spotty necrosis and occasionally confluent necrosis. There was accumulation and enlargement of Kupffer Figure 1 Marked cytoplasmic canalicular cholestasis (hematoxylin and eosin).