A 55-year-old woman with progressive hepatic region discomfort was referred to a hematological department in May 2006. Her previous medical history was significant for chronic aplastic anemia and she was treated with stanozolol and intermittent γ-globulin infusion. Full blood and bone marrow examination on a regular time schedule showed significant remission.
On admission, the patient had a body temperature of 36.5 °C, pulse of 75 beats per minute, blood pressure of 120/80 mmHg, respiratory rate of 16 per minute, and oxygen saturation of 98% on room air. Her abdomen was soft to palpation. Full blood test showed leukocyte count of 3.0 × 109/L, hemoglobin 110 g/L and platelet 23 × 109/L. Immunological studies, including quantitative immunoglobulins analysis, CD4/CD8 T lymphocyte ratio, and delayed hypersensitivity skin tests, were all normal. No predisposing disease associated with immunosuppression, such as diabetes mellitus, was found. Her human immunodeficiency virus status was negative, indicating the patient was in a non-immunocompromised condition. Abdominal ultrasonography and magnetic resonance imaging (MRI) showed multiple heterogeneous solid nodules in the right lobe of the liver (). No abdominal lymphadenopathy or effusions were visible.
Horizontal abdominal MRI image in May 2006 shows multiple solid nodules in the right lobe of the liver (arrows indicated).
Malignant ailments and metastatic diseases were initially suspected, but serum tumor marker screening (including CEA, CA-125, CA-199, PSA, AFP, etc.) was within normal limits. Her aspartate aminotransferase (AST) was 80 U/L (normal range <40 U/L) and alanine aminotransferase (ALT) was 65 U/L (normal range <40 U/L). Other laboratory investigations, including erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), galactomannan antigenemia (GM) test, and autologous antibody, performed twice a week, were not specific. Complete liver disease studies, including hepatitis virology, cytomegalovirus, Epstein-Barr virus serology, urinary copper, serum ceruloplasmine failed to lead a significant result.
Two weeks after admission, ultrasound-guided fine needle aspiration was performed. On histopathological examination, abundant fungal hyphae were observed in the background of necrosis and chronic inflammation (). A. fumigatus was subsequently isolated and cultured from the biopsy aspirate. Bacterial and acid-fast smears and cultures were negative. Pulmonary aspergillosis with liver dissemination was suspected, but the patient denied relevant infectious and occupational exposure history. A comprehensive whole body evaluation, including chest and paranasal sinus computed tomography (CT), did not indicated aspergillosis lesions. Regular GM tests continued to be negative. On the basis of these findings, we concluded the diagnosis of liver aspergilloma.
Profound Aspergillus hyphae were observed in the necrotic liver specimen. Magnification at 400×, bar = 200 μm.
The patient was prescribed caspofungin acetate (Cancidas®, Merck Sharp & Dohme Pty. Ltd., Australia) according to the minimal inhibitory concentrations (MICs) tests. An antifungal regimen was started with caspofungin acetate 70 mg on day 1 and 50 mg daily from day 2 to day 10. Serum liver enzymes were monitored to interrupt potential adverse effects. The patient received one course of caspofungin acetate first-line therapy every month and responded well in the clinical symptoms. Two months after the initial diagnosis, repeated MRI images showed a significant reduction in the sizes and number of the liver nodules (). Our patient underwent caspofungin acetate therapy for six months and was discharged. During our last time follow-up in May 2012, she was stable without signs of progression or recurrence.
After receiving two courses of caspofungin acetate first-line therapy, follow-up horizontal abdominal MRI image showed evident remission.