Clinical record

A 26-year-old recently married Filipino-born woman was referred to our hospital with left upper quadrant pain, vomiting and abnormal liver function test (LFT) results. There was nothing significant in her family history or past medical history. She described being unwell, and had lost 5 kg over 3 months, but had no respiratory symptoms or fever. On examination, she had slightly tender hepatomegaly palpable 3 cm below the right costal margin without any clinical stigmata of chronic liver disease. A BCG scar was noted. Her chest was clear and there were no other abnormal clinical findings. Her LFT results revealed elevated levels of alkaline phosphatase (345 U/L; normal range, 32–91 U/L) and γ-glutamyl transferase (215 U/L; normal range, < 38 U/L); other LFT results were normal. Findings of a full blood examination and urea, electrolytes and creatinine levels were all within normal limits. A triple-phase computed tomography scan of the liver was performed which showed hepatomegaly with multiple small, low-density lesions within the liver, which the reporting radiologist suggested may possibly be simple cysts. The appearance of the bowel, pancreas and lung bases were all normal. There was no intra-abdominal lymphadenopathy. Results of serological tests for hepatitis A, B and C were negative, as were results of tests for Wilson’s disease and α-1-antitrypsin deficiency, and antinuclear antibody, antimitochondrial antibody and antismooth muscle antibody.

The patient subsequently underwent a liver biopsy, which revealed florid, non-caseating granulomatous reaction with aggregates of epithelioid histiocytes and Langerhans-type giant cells in a predominantly portal and periportal distribution (Figures A and B). The bile ducts were all intact and no evidence of malignancy was seen. Special stains, including Ziehl–Neelsen stain for acid-fast bacilli, were negative. The pathologist concluded that the histological appearance and distribution of granulomas was most consistent with the diagnosis of hepatic sarcoidosis.

However, because of the patient’s ethnic background, further tests were undertaken to exclude tuberculosis (TB). A chest x-ray revealed clear lung fields and a normal mediastinal outline, with no indication of previous or current TB infection. A tuberculin skin test (TST) produced 12 mm of transverse induration. A QuantiFERON-TB Gold test (Cellestis International, Melbourne, Vic) was positive. As the TST and QuantiFERON-TB Gold test results were more in keeping with TB than sarcoidosis, the patient was treated for primary hepatic TB with quadruple therapy (isoniazid, rifampicin, pyrazinamide and ethambutol). Her clinical condition improved dramatically within a month of starting therapy, with a marked reduction in her hepatomegaly and normalisation of liver biochemistry.

A retrospective polymerase chain reaction on the paraffin embedded tissue from the liver biopsy confirmed the presence of active TB within the liver specimens. Five months after completing the 9-month course of antituberculosis therapy, she was well and had recently become pregnant.