Abstract

INTRODUCTION: Hepatic atrophy, although rare, may be a potential confounder of transient elastography results. Atrophy can result from tumor or cirrhosis but can also be due to etiologies associated with diversion of portal venous blood flow. We present a case of overestimation of fibrosis by transient elastography in a patient with left hepatic lobe atrophy. CASE DESCRIPTION/METHODS: A 60 year old overweight male with hypertension and hyperlipidemia was referred for evaluation of elevated transaminases. Initial laboratory investigation noted AST 62 U/L, ALT 110 U/L, alkaline phosphatase (ALP) 160 U/L, total bilirubin 0.7 mg/dL, platelet count 172,000/microliter and albumin 4.2 g/dL. He was advised to stop taking high intensity atorvastatin and abstain from alcohol consumption, though alcohol intake was one glass of wine nightly. Repeat testing demonstrated AST 39 U/L, ALT 58 U/L, ALP 98 U/L and total bilirubin 0.9mg/dL. An abdominal ultrasound was obtained and showed cavernous transformation of the portal vein (PV) with gastrosplenic varices. Computed tomography of the abdomen (Image 1) confirmed these findings and also revealed atrophy of the left hepatic lobe. The etiology of chronic PV thrombus was explored. Protein C and S, and antithrombin III were within reference range. Anticardiolipin antibody was negative. JAK2 and Factor V Leiden mutations were negative. Given risk factors for non-alcoholic fatty liver disease, we decided to evaluate the extent of fibrosis with transient elastography during the patient's office visit. FibroScan measured liver stiffness at 21.1 kPa, correlating with F4 fibrosis. No overt confounders were identified. To confirm the diagnosis of cirrhosis, the patient underwent a percutaneous liver biopsy. The sample obtained was from the right liver lobe and was adequate for interpretation, over 2cm in length. It showed minimal macrovesicular steatosis without features of steatohepatitis and no significant portal or lobular inflammation. Trichrome stain revealed stage 1 fibrosis with patchy perisinusoidal fibrosis. DISCUSSION: We concluded that the patient did not have cirrhosis, and that chronic PV thrombus contributed to left hepatic lobe atrophy. The etiology of chronic PV thrombus remains elusive. FibroScan results were likely confounded by the atrophic left hepatic lobe. Our case highlights the importance of confirming cirrhosis with liver biopsy in particular subsets of patients given the many implications in the patient’s monitoring and prognosis with a diagnosis of cirrhosis.Image 1.: Atrophy of the Left Hepatic Lobe.

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