Massive Primary Hepatic Tuberculoma Mimicking Hepatocellular Carcinoma in an Immunocompetent Host

Matthew J. Brookes, MB ChB; Melanie Field, MB ChB; Dee M. Dawkins, MB ChB; Joan Gearty, MB ChB; Paul Wilson, MB ChB

Disclosures

July 18, 2006

Discussion

Hepatic TB has been classified by Levine[2] into: (a) miliary TB; (b) pulmonary TB with hepatic involvement; (c) primary liver TB; (d) focal tuberculoma or abscess; or (e) tuberculous cholangitis. The most common form of hepatic involvement is the miliary form of TB, in which hematogenous spread is through the hepatic artery.[1] Hepatic involvement can be seen in up to 80% of disseminated cases of TB. Isolated tuberculous involvement of the liver is considered rare because of the low oxygen tension within the liver, making it unfavorable for mycobacterial growth. Primary hepatic TB in the absence of immunocompromise is extremely rare.

Tuberculous cholangitis may present with jaundice and fever.[3] However, the presentation of a focal liver abscess is often much less specific, with right upper quadrant abdominal pain, fever, night sweats, anorexia, and weight loss. The most frequent examination findings include abdominal tenderness with or without a palpable mass and occasional jaundice.

Laboratory investigations often reveal an elevated alkaline phosphatase in the presence of normal alanine transaminase and aspartate transaminase.[1] Less specific findings include anemia, hypoalbuminemia, and hyponatremia.[1]

Imaging studies can pose a diagnostic challenge, with a number of potential differential diagnoses, including primary hepatocellular carcinoma. Hypoechoic nodules are usually seen at ultrasonography,[4] though rarely the appearances may appear hyperechoic. CT findings usually reveal a round hypodense lesion with slight peripheral enhancement and, occasionally, areas of focal calcification.[4] Noninvasive diagnosis is therefore difficult, and up to 90% of cases require a laparotomy to make the diagnosis.[5] Despite the rarity of this condition, primary hepatic tuberculoma should be considered among the differential diagnoses of space-occupying lesions of the liver.

The histologic findings often achieve the diagnosis, with features of caseating granulomatous necrosis. Langhans-type giant cells are often present with a mixed inflammatory infiltrate including plasma cells, eosinophils, and lymphohistiocytic cells.

It is clear from the literature that a histologic diagnosis is imperative in these cases, but avoiding laparotomy is ideal. In the reported case, a guided biopsy of the lesion was performed, and the resulting histology and cultures confirmed the diagnosis of hepatic tuberculoma without the need for a laparotomy.

Low sensitivity of both acid-fast staining (from 0% to 45%) and culture (from 10% to 60%) mean diagnosis can still be difficult.[2] However, the use of polymerase chain reaction to directly detect the presence of Mycobacterium tuberculosis is increasing and may improve sensitivity rates.

Treatment of hepatic TB is by quadruple therapy for 1 year, though there are often signs of clinical improvement within 2-3 months. The use of percutaneous drainage has also been advocated. Mustard and colleagues[6] suggested features associated with successful drainage included: (1) unilocular abscess; (2) safe access route for instillation of drainage catheter; and (3) a sterile uncontaminated compartment.

Hepatic tuberculoma are rare, but with the increasing worldwide incidence of TB, it is a diagnosis that must be considered, especially in patients considered at high risk. This case illustrates the minimally invasive investigation, diagnosis, and treatment of a primary hepatic tuberculoma.

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