A 69-year-old man was diagnosed with post-hepatitis B cirrhosis for 20 years and presented with 2 weeks of fever. Two weeks before his admission, he developed pyrexia without obvious predisposing causes, and his highest temperature recorded was 39.6 C, with fever ocurring mainly in the afternoons. Furthermore, the patient suffered from asthenia, anorexia, mild cough, whitish sputum, and pain in the anterior chest wall without chills or abdominal pain. He had undergone a splenectomy for hypersplenism 16 years ago. During a physical examination, his temperature was 38.8 C. There were many spider angiomas in the anterior thoracic wall and decreased respiratory sound in both lungs, combined with shifting dullness and fist percussion over the liver. Laboratory tests revealed a C-reactive protein level of 84.36 mg/L (normal range <5 mg/L) and an erythrocyte sedimentation rate (ESR) level of 69 mm/h (normal range 0-43 mm/h). Liver function tests demonstrated a slight elevation of aspartate aminotransferase (AST) at 59.7 U/L, total bilirubin (TBIL) at 39.7 mmol/L, and a slight decrease of albumin at 31.4 g/L. Additionally, serum alpha-fetoprotein (AFP) level was markedly elevated to 1210 ng/ml (normal range 0-20 ng/mL). The serum adenosine deaminase (ADA) was mildly elevated to 24.4 U/L. However, an ascitic fluid examination demonstrated that ADA was normal. Negative test results were observed for purified protein derivative (PPD) and mycobacterium TB DNA. An interferon-gamma release assay (IGRA) test was positive. The results of coagulation function tests expressed that prothrombin time (PT) was 19.9 s (normal range 10-15 s), the international normalized ratio (INR) was 1.71, and there was 47.7% prothrombin time activity (PTA). An ultrasound (US) of the abdomen revealed signs of cirrhosis, a filling defect in the portal vein, and a large hypoechoic lesion with an irregular border and non-uniform internal echoes in the left lobe of the liver. Abdominal CT plain scans depicted a decompensated period of cirrhosis, a lobulated and inhomogeneous mass with a slightly lower density in the left lobe, measuring 13.5 cm x 6.8 cm, and the presence of ascites and bilateral pleural effusion (Figure 1). MRI, including T1- and T2-weighted imaging and contrast-enhanced with fat saturation and subsequent subtraction, revealed signs of cirrhosis and a huge mass in the left liver lobe, characterized by slightly higher non-uniform intensity, which was not significantly enhanced in the arterial phase, and mild to moderate delayed enhancement was found in the perifocal and internal septum of the venous phase and the delayed phase. In addition, the mass presented without a capsule surrounding it. The mass was hyperintense in DWI mapping. Moreover, a filling defect in the trunk of the portal vein was observed (Figure 2). The results led us to consider primary liver cancer and main portal vein tumor thrombus combined with decompensated cirrhosis.
Although discovering a space-occupying lesion of the liver on MRI and that the AFP level in the peripheral blood was extremely elevated, the first diagnosis was probably HCC. Biopsy and histology may be considered the ultimate diagnostic tests, but needle biopsy was excluded because of a high risk of bleeding; in addition, the patient declined the procedure.
To cope with fever, the patient was initially given broad-spectrum antibiotic treatment (3.0 g of cefoperazone-sulbactam every 8 h for 6 days and 0.5 g of levofloxacin every 24 h for 3 days, followed by 0.5 g of intravenous vancomycin every 12 h and 1 g of meropenem every 8 h via intravenous drip infusion for 3 days). After 12 days, the fever persisted (the highest temperature recorded was 38.2 C.). Although there was no direct evidence of TB infection, primary hepatic TB was suspected based on clinical symptoms, and an anti-TB therapeutic diagnosis was given. The patient was treated with 0.75 g of anti-TB oral ethambutol every 24 h and 0.6 g of amikacin every 24 h via intravenous drip infusion for 10 days; after that, the patient maintained a normal temperature (36.5 C). Anti-TB treatment continued at the same dosage for the following 15 days, with supplemental isoniazid at 0.3 g/24 h. In the days and weeks following the patient's coagulopathy correction, we repeatedly offered him a biopsy, but he declined it. The patient was then discharged from the hospital.
The patient received tuberculostatic therapy with amikacin, isoniazid, and ethambutol for 6 months. The level of AFP had completely normalized upon review after stopping the medication for 20 weeks, and the imaging displayed that the mass on the left liver lobe had disappeared, the portal vein filling defect had markedly reduced, and ascites and bilateral pleural effusion reduced in the patient (Figure 3). At the 2-year follow-up, no evidence of recurrence was observed (Figure 4), and the patient had recovered well. The final diagnosis was predominantly that of hepatic TB based on the disappearance of the lesions, and the level of AFP gradually returned to normal after the patient had been given anti-TB therapy for 6 months.