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Primary tuberculous liver abscess: a case report and review of the literature.

Abstract: A 48-year-old diabetic man was admitted to our hospital with abdominal pain in the right upper quadrant, weight loss, night sweats, fatigue, and anorexia. Ultrasonography, computed tomography, and magnetic resonance imaging of the abdomen revealed multiple hemangiomas and a hypodense mass lesion in the posterior segment of the right hepatic lobe. Histopathologic examination of the specimens obtained by ultrasonography-guided percutaneous needle biopsy revealed caseating granulomas with epithelioid histiocytes and giant cells. Systemic antituberculous therapy led to improvement of the lesion in the liver without necessitating surgery or percutaneous drainage. Tuberculosis should be considered in the differential diagnosis of hepatic mass lesions, especially in the presence of immune-compromised states. Ruling out tuberculosis may avoid delay in initiation of specific therapy in some cases. A greater awareness of this rare clinical entity may prevent needless surgical interventions.

Key Words: tuberculosis, liver abscess, conservative therapy


Tuberculosis (TB) can affect the liver in two ways: as a diffuse involvement secondary to miliary or pulmonary TB (the most common form), and as a local process (primary miliary, tuberculoma or abscess) in which the hepatic involvement is the principal manifestation of the disease. (1)

Tuberculous liver abscess (TLA) is a rare clinical entity. It is usually associated with a focus of infection in the lung or gastrointestinal tract. (2) Primary TLA, with no evidence of infection elsewhere, is even less common. (3) It is usually seen in immunocompromised patients. The clinical diagnosis is difficult owing to the rarity of the disease, nonspecific clinical findings, and a subsequent low clinical index of suspicion. It is frequently confused with primary and metastatic necrotic hepatic malignancies, and pyogenic or amebic liver abscesses. (1)

The management of TLA is still a subject of debate. Early reports stressed the need for surgical exploration and drainage. (2,3) Later, ultrasound or CT-guided aspiration or drainage of TLA and percutaneous infusion of antituberculous agents were defined. (4,5) Treatment with systemic antituberculous chemotherapy without necessitating percutaneous drainage or laparotomy has also been reported. (6,7)

We report the case of a diabetic patient with primary tuberculous liver abscess. The TLA was initially confused with hemangioma, but was later treated successfully with antituberculous therapy after the diagnosis was established by histopathologic examination of the specimen obtained by ultrasonography-guided percutaneous biopsy of the lesion.

Case Report

A 48-year-old man was admitted to our hospital with a 3-month history of abdominal pain in the right upper quadrant, weight loss of 9 kg, night sweats, fatigue, and anorexia. He had a diagnosis of diabetes mellitus and had been regularly using acarbose for two years.

At admission, vital signs were normal other than a low grade fever of 37.8[degrees]C. The liver was palpable 7 cm under the right costal margin and was tender. Complete blood count revealed a hematocrit level of 32, white blood cell count of 7,800/[mm.sup.3] and a thrombocyte count of 671,000/[mm.sup.3]. Erythrocyte sedimentation rate was 96 mm/h. Biochemical analysis was normal other than increased levels of fasting blood glucose (200 mg/dL, N: 70-110), y-glutamyl transpeptidase (166 U/L, N: 8-61), alkaline phosphatase (556 U/L, N: 0-270) and a decreased level of serum albumin (3.2 g/dL, N: 3.5-4.8). Anti-HIV antibody was negative. Tuberculin skin test was 13 mm.

A thorax computed tomography (CT) revealed minimal pleural effusion unobtainable by thoracentesis. Abdominal ultrasonography revealed multiple hyperechoic lesions compatible with hemangiomas and a hypoechoic mass lesion in the posterior segment of the right hepatic lobe (Fig.). Contrast-enhanced abdominal CT revealed multiple nodular lesions in the liver which were 1 to 3 cm in diameter and compatible with hemangiomas. They were hypodense on initial images and contrasted from periphery to the center on later images. There was also a 7 cm hypodense mass lesion in the posterior segment of the right hepatic lobe and multiple conglomerated lympadenopathies of 3 cm in maximum diameter in the periportal, peripancreatic, and upper para-aortic regions. Magnetic resonance imaging (MRI) could not differentiate the hypoechoic lesion in the posterior segment of the right hepatic lobe from an atypical hemangioma.

An ultrasound-guided percutaneous biopsy was performed from the hypoechoic lesion in the posterior segment of the right hepatic lobe. The histopathologic examination revealed caseating granulomas with epithelioid histiocytes and giant cells. No acid-fast bacilli could be detected on direct examination. Culture of the specimen for M tuberculosis was not performed. Antituberculosis therapy with isoniazid 300 mg, rifampin 600 mg, morphazinamide 3,000 mg, and ethambutol 1,500 mg was initiated. The patient's symptoms resolved over 10 days. Follow-up ultrasound after 2 months of therapy revealed that the abscess was reduced to nearly half of its initial volume. Pleural effusion was also resolved. In the third month of treatment, morphazinamide and ethambutol were stopped and the therapy was continued with isoniazid and rifampin. Cure was achieved after 9 months of therapy without necessitating drainage. A control ultrasound at the end of treatment revealed an abscess sequelae in the posterior segment of the right hepatic lobe and hemangiomas.


Liver involvement is well recognized in generalized miliary tuberculosis. It is present in 50 to 80% of patients dying from pulmonary tuberculosis. (8) Primary TLA without involvement of other organs is an extremely rare clinical entity. However, an increase in the number of cases can be anticipated, especially in the presence of immune-compromised states, such as acquired immunodeficiency syndrome, diabetes mellitus, chronic renal failure, and corticosteroid therapy.

TLA is seen in 0.34% of patients with hepatic tuberculosis. (9) A literature review reported 23 cases of isolated tuberculoma or TLA between the years 1950 and 1990. (1) Demographic features of these patients revealed a male preponderance (14 male and 9 female) with an average age of 35 years. A literature review in 1994 reported 30 cases of TLA in the English and 14 cases in the Japanese literature. (10) Of these 44 patients, 22 had isolated TLA and 15 had coexisting pulmonary tuberculosis. Pulmonary tuberculosis was not documented in 5 patients and was suspicious in the remaining 2 patients. Although there was a male preponderance in all of the patients with TLA (28 male, 16 female), demographic features of the patients with isolated TLA revealed a female preponderance (12 female and 10 female) with an average age of 39 years.

The presenting symptoms of TLA are constitutional in nature and include abdominal pain, fever, weight loss, anorexia, fatigue, and night sweats. (11,12) Jaundice is rare and is usually due to extra- or intrahepatic obstruction of the bile ducts. (13) Fever, abdominal tenderness usually in the epigastrium or right upper quadrant, and enlarged liver on palpation are common physical findings. (1) Although the biochemical findings can vary, a disproportionate rise in alkaline phosphatase, a marginal elevation of aminotransferases, prolongation of prothrombin time, a reversal of the albumin/globulin ratio, and hyponatremia may occur. (12)

The ultrasonographic features vary from a normal ultrasound to a large, well-defined hypoechoic lesion, multiple septations or a solid hepatic mass. A large low attenuation lesion with no visible wall or enhancement, ring enhancement or multiseptate abscess can be seen on CT scan. (4,14-16)


Considering the rarity of the disease, protracted course, nonspecific clinical findings, and variable imaging appearances, the diagnosis of an isolated TLA is difficult. The clinical picture can mimic primary or secondary hepatic neoplasms. They are most often confused with amebic or pyogenic liver abscesses. TLA is diagnosed by demonstration of acid-fast bacilli either on smear of the aspirated material or in the culture. Unfortunately the diagnosis of TLA can not be reached by bacteriologic confirmation at all and the diagnosis can only be established by histologic examination of the samples obtained from the margin of the abscess wall. (16,17) But often the results of these aforementioned examinations are negative and the diagnosis is usually established at laparotomy or autopsy. (1,4,10)

Treatment of TLA is still a subject of debate. While there are cases treated with only systemic antituberculous drugs, (5-7) some reports emphasize the importance of open surgical drainage. (2,3,14) Recently, CT and ultrasound-guided percutaneous drainage and infusion of antituberculous agents have been found to be effective for the treatment of TLA. (4,5) Jain et al (15) claimed that direct infusion of antituberculous agents were more effective than systemic application when used in combination with simple needle aspiration or short-term catheter drainage of TLA, because the thick fibrous tissue around the abscess cavity and the large size of the lesion may prevent the antibiotics from reaching the target. (3) Mustard et al (5) also treated a patient by percutaneous drainage and direct instillation of antituberculous drugs into the abscess cavity without necessitating surgery. In our patient, we observed clinical improvement within 10 days of systemic antituberculous therapy. The abscess was reduced to half of its initial size after two months of treatment. Owing to the response, we thought that medical therapy could be sufficient for cure. If the systemic treatment with antituberculous agents proved insufficient, we could have considered placing an ultrasound-guided percutaneous catheter.

In conclusion, tuberculosis should be considered in the differential diagnosis of hepatic mass lesions, especially in the presence of immune-compromised states. Ruling out tuberculosis in the etiology may avoid delay in initiation of specific therapy in occasional cases. A greater awareness of this rare clinical entity may prevent needless surgical interventions. We suggest starting treatment with antituberculous therapy and considering placement of a percutaneous catheter when the systemic treatment proves insufficient.


1. Oliva A, Duarte B, Jonasson O, et al. The nodular form of local hepatic tuberculosis. J Clin Gastroenterol 1990;12:166-173.

2. Leader SA. Tuberculosis of the liver and gallbladder with abscess formation: a review and case report. Ann Intern Med 1952;37:594-606.

3. Gracey L. Tuberculous abscess of the liver. Br J Surg 1965;52:442-443.

4. Reed DH, Nash AF, Valabjhi P. Radiological diagnosis and management of solitary hepatic abscess. Br J Radiol 1990;63:902-904.

5. Mustard RA, Mackenzie RL, Gray RG. Percutaneous drainage of a tubercular liver abscess. Can J Surg 1986;29:449-450.

6. Desmidt P, Apfelbaum M, Holvoet J, et al. Tuberculous (peri) hepatic abscesses. Acta Clin Belg 1988;43:378-380.

7. Weinberg JJ, Cohen P, Malhotra R. Primary tuberculous liver abscess associated with the human immunodeficiency virus. Tubercle 1988;69:145-147.

8. Morris E. Tuberculosis of the liver. Am Rev Tuberc 1930;22:585-592.

9. Essop AR, Segel I, Posen J, et al Tuberculous abscess of the liver: a case report. S Afr Med J 1983;63:825-826.

10. Kubota H, Ageta M, Kubo H, et al. Tuberculosis liver abscess treated by percutaneous infusion of antituberculous agents. Intern Med 1994;33:351-356.

11. Alvarez SZ, Carpio R. Hepatobiliary tuberculosis. Dig Dis Sci 1983;28:193-200.

12. Essop AR, Posen JA, Hodkinson JH, et al. Tuberculosis hepatitis: a clinical review of 96 cases. QJ Med 1984;212:465-477.

13. Abascal J, Martin F, Abreu L, et al. Atypical hepatitis tuberculosis presenting as obstructive jaundice. Am J Gastroenterol 1988;83:1183-1186.

14. Spiegel CT, Tuazon CU. Tuberculous liver abscess. Tubercle 1984;65:127-131.

15. Jain R, Sawhney S, Gupta RG, et al. Sonography appearances and percutaneous management of primary tuberculous liver abscess. J Clin Ultrasound 1999;27:159-163.

16. Wilde CC, Kueh YK. Tuberculosis hepatic and splenic abscess. Clin Radiol 1991;43:215-216.

17. Zipser RD, Rau JE, Ricketts RR, et al. Tuberculous pseudotumors of the liver. Am J Med 1976;61:946-951.

Deniz Koksal, MD, Aydin Seref Koksal, MD, Seyfettin Koklu, MD, Bahattin Cicek, MD, Emin Altiparmak, MD, and Burhan Sahin, MD

From the Department of Chest Diseases and Tuberculosis, Ataturk Chest Diseases and Chest Surgery Education and Research Hospital, and the Department of Gastroenterology, Turkiye Yuksek Ihtisas Hospital, Ankara, Turkey.

Reprint requests to Seyfettin Koklu, MD, TIp Fakultesi caddesi, 259 / 3, Mamak, Ankara, Turkey. Email:

Accepted January 5, 2006.


* A tuberculous liver abscess is the end result of a tuberculoma that has undergone extensive caseous and liquefaction necrosis.

* A high index of suspicion is required for diagnosis of tuberculous liver abscess, since it may mimic common hepatic diseases including primary and metastatic carcinoma of the liver, and amebic or pyogenic liver abscesses.

* In patients presenting with a febrile course, upper abdominal tenderness and abnormalities on imaging studies of liver, the diagnosis of tuberculous involvement should be considered.

* The prognosis of tuberculous liver abscess is usually good for the majority of patients if diagnosed early and prompt effective treatment is administered.

* A greater awareness of this rare clinical entity may prevent needless surgical interventions.
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Author:Sahin, Burhan
Publication:Southern Medical Journal
Geographic Code:1USA
Date:Apr 1, 2006
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