An Unusual Case of Intermittent Fever With Multiple Liver Lesions

Abstract

Question: A 46-year-old man with a history of hypertension presented to our hospital with a chief compliant of intermittent fever for 2 weeks. He denied a history of nausea, vomiting, abdominal pain, diarrhea, abdominal distention, loss of appetite, or weight loss. Physical examination on admission was unremarkable. Laboratory studies showed white blood cells 15.32 × 109/L (reference 3.5–9.5 × 109/L) with 38.3% (reference 0.4%–8.0%) eosinophils, C-reactive protein 49.72 mg/L (reference 0–10 mg/L), and erythrocyte sedimentation rate 44 mm/h (reference 0–15 mm/h). No parasite eggs or larvae were found in microscopic examination of direct smears of the stool. Liver function tests revealed alanine transaminase 50.5 IU/L (reference 9–50 IU/L), alkaline phosphatase 134 IU/L (reference 15–40 IU/L), gamma-glutamyltransferase 224 IU/L (reference 10–60 IU/L), total protein 40.1 g/L (reference 65–85 g/L), and albumin 21.6 g/L (reference 40–55 g/L). His renal function and tumor markers, such as alpha-fetoprotein, carcino-embryonic antigen, and carbohydrate antigen 19-9 were all within normal ranges. Tests for hepatitis B, hepatitis C, antinuclear antibodies, extractable nuclear antigen antibodies, and anti–neutrophil cytoplasm antibodies were all negative. No significant abnormalities were detected on electrocardiography, echocardiography, and chest computed tomography (CT). Routine ultrasound revealed multiple hypoechoic areas with unclear borders in the left lobe and right posterior lobe of the liver. Magnetic resonance imaging (MRI) of the liver was subsequently performed and showed multiple nodular or clumpy lesions as low signal intensity on T1-weighted imaging (WI) (Figure A) and high signal intensity on fat-suppressed T2-WI (Figure B) and diffusion WI (Figure C). Contrast-enhanced scan exhibited slightly heterogeneous enhancement (Figure D) or annular enhancement (Figure E). MRI did not indicate any anatomic malformations or intrahepatic or extrahepatic bile duct dilation. Positron emission tomography–computed tomography (PET-CT) revealed increased 18F-fluorodeoxyglucose uptake in the liver lesions (maximum standardized uptake value 3.8–5.2) (Figure F). The patient subsequently underwent CT-guided liver biopsy. Histopathology demonstrated chronic hepatic inflammation with prominent eosinophilic infiltration in portal areas and some acinar areas (Figure G).