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CASE REPORT Table of Contents   
Year : 2010  |  Volume : 53  |  Issue : 4  |  Page : 763-766
Pseudotumoral hepatic tuberculosis with pericardial abscess

1 Department of Pathology, 12 Air Force Hospital, Air Force Station, Gorakhpur - 273 002, India
2 Command Hospital Central Command, Lucknow - 226 002, India

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Date of Web Publication27-Oct-2010


We report the postmortem findings in a 28-year-old immunocompetent male patient, a rare case of tuberculous liver abscesses with concomitant pericardial abscess in the absence of pleuropulmonary or splenic involvement, who continued to be a diagnostic dilemma. This case report illustrates the difficulty in reaching the correct diagnosis in case of hepatic masses, which are most often confused with carcinoma of the liver, primary or metastatic and, hence, have been aptly referred to as pseudotumoral hepatic tuberculosis in the past.

Keywords: Pericardial abscess, pseudotumoral masses liver, tuberculous liver abscesses

How to cite this article:
Mutreja D, Nangia R, Mishra P. Pseudotumoral hepatic tuberculosis with pericardial abscess. Indian J Pathol Microbiol 2010;53:763-6

How to cite this URL:
Mutreja D, Nangia R, Mishra P. Pseudotumoral hepatic tuberculosis with pericardial abscess. Indian J Pathol Microbiol [serial online] 2010 [cited 2021 Aug 5];53:763-6. Available from: https://www.ijpmonline.org/text.asp?2010/53/4/763/72082

   Introduction Top

Tubercular liver abscesses are usually associated with an immunocompromised state, with a focus of infection in the lungs or in the gastrointestinal tract. Localization to the liver without active pulmonary or miliary tuberculosis presenting as pseudotumoral masses is a rare entity. [1]

Concomitant involvement of the pericardium with hepatic tuberculous abscesses in the absence of pleuropulmonary and peritoneal involvement has never been reported. We present a rare case of tuberculous liver abscesses that spread contiguously to involve the pericardium in the form of tubercular pericardial abscess where the diagnosis was established on postmortem examination.

   Case Report Top

A 28-year-old male was referred from a peripheral hospital with a provisional diagnosis of hepatic amoebic abscesses. Examination revealed a febrile pale individual with tender hepatomegaly 3 cm below the costal margin. Other systemic examinations were unremarkable. Investigations showed hemoglobin - 10.2 g/dL, white blood cell count - 10,800 (P 80, L 13, E 05, M 02) and erythrocyte sedimentation rate 12 mm after the first hour. The peripheral smear showed normocytic normochromic anemia. Serum alkaline phosphatase was 1,503 IU/L. Serum bilirubin, transaminases, chest X-ray PA view, upper gastro-intestinal (UGI) endoscopy renal profile and tumor maker studies (Carcino embryonic antigen (CEA) - 2.6 ng/ml, Alfa feto protein (AFP) - 5.15 ng/ml, CA - 19.9-23.3) were normal. A tuberculin skin test was negative. Serology was negative for malaria, enteric fever and tuberculosis. Detection of human immunodeficiency virus by enzyme-linked immunosorbent assay was negative and blood culture was sterile. An ultrasound of the abdomen showed multiple hypoechoeic space-occupying lesions (SOLs) in the liver and contrast-enhanced computed tomography (CECT) scans of the abdomen showed multiple hepatic SOLs in both lobes of the liver with splenomegaly [Figure 1]. Radiological differential diagnoses of metastases to the liver and organized pyogenic liver abscesses were entertained. CT-guided fine needle aspiration of the liver parenchymal nodules was performed and 5 ml of yellowish pus was aspirated. Microscopy showed necrotic debris only; no amoebic trophozoites/acid fast bacilli (AFB) were seen on ZN stain. Polymerase chain reaction (PCR) for mycobacteria, amoebic serology and mycobacterial cultures were negative. On continued parental antibiotics, the patient became afebrile after 4 weeks of admission. A repeat ultrasound showed resolving abscesses and the patient was discharged to home with advice to abstain from alcohol and to consume hematinics and a protein-rich diet.
Figure 1: Contrast-enhanced computed tomography of the abdomen showing multiple hepatic space-occupying lesions and splenomegaly

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He reported after 6 weeks with complaints of fever, pain in the upper abdomen, jaundice and loss of appetite. On examination at readmission, he was found to be sick looking with pallor and marked icterus. Systemic examination revealed tender hepatomegaly and ascites. There was evidence of liver cell failure in the form of deranged PT/INR (control - 13/test - 42 s, INR - 5.31) with markedly elevated liver enzymes (ALT - 2,345 U/L, AST - 754 U/L, ALP - 680 U/L ). A repeat CECT of the abdomen showed multiple hypoechoic lesions in the liver, ascites and pleural effusion. Diagnostic ascitic tap showed high serum ascitic albumin gradient (SAAG); the deposit was negative for malignant cells. Adenosine deaminase (ADA) levels in the ascitic fluid were normal. Repeat tumor marker studies showed raised AFP of 46.5 ng/dL. CEA and CA 19.9 were within normal limits. Chest X-ray PA view showed cardiomegaly and bilateral pleural effusions. A colonoscopy showed grade II/III internal piles and no mucosal growth/abnormality were detected. Clinical possibilities of gastrointestinal malignancy with hepatic metastases, disseminated tuberculosis and lymphoma were considered and the patient was managed with supportive therapy to correct coagulopathy and was started on modified anti-tubercular therapy (ATT) empirically. However, he showed a progressive downhill course, becoming stuporose with features of hepatic encephalopathy and died 10 days after admission. A complete autopsy was performed.

   Pathological Findings Top

At autopsy, the most significant findings were confined to the liver and heart. The liver weighed 1,050 g and, on sectioning, showed thickened capsule with multiple yellowish, well-circumscribed, septate parenchymal nodules varying in size from 1.0 to 4.5 cm, involving all liver lobes with central yellowish-green necrotic material. Blotchy bile staining and cirrhosis of liver parenchyma were seen [Figure 2]a and b.
Figure 2: a: Cirrhotic liver with multiple well-circumscribed parenchymal nodules
b: Cirrhotic liver with multiple well-circumscribed parenchymal nodules, slice through hilum

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The heart weighed 500 g and the pericardial cavity was obliterated with adherent pericardium on the myocardium, anteriorly. Multiple necrotic foci in the pericardium were seen around the aortic root, right ventricle, right AV groove and left ventricle [Figure 3]. The myocardium, valves, chordae tendinae and papillary musculature were unremarkable. Both the lungs were heavy and subcrepitant on gross morphology, but did not reveal any focal parenchymal lesions or military nodules. The spleen weighed 350 g and did not show any focal or military nodules on gross morphology. The pleural and peritoneal cavities showed hemorrhagic effusions. No military nodules were seen. Multiple pretracheal, paratracheal, diaphragmatic and peripancreatic nodes showing central caseation were dissected. The adrenals, kidneys, testes and brain were unremarkable.
Figure 3: Pericardial abscess around the root of aorta

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Hematoxylin and eosin (H and E) stained liver sections showed confluent caseating necrotic granulomas with complete contiguous destruction of liver architecture and cirrhosis [Figure 4]a and b. PCR for mycobacteria from the wall of liver nodules was positive. Similar granulomas were demonstrated in sections from the pericardium [Figure 5] and lymph nodes. The lungs and spleen showed features of chronic passive congestion. Numerous sections through the lungs/pleura/peritoneum/adrenals/intestines/kidneys or brain did not reveal any tuberculous pathology.
Figure 4: a: Liver necrotic area showing granulomas with caseation and Langhans giant cells (H and E, ×100)
b: Liver necrotic area adjacent to cirrhotic parenchymal nodules (H and E, ×100)

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Figure 5: Pericardium, necrotic area with tubercular granulomas (H and E, ×100)

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   Discussion Top

Tuberculous involvement of the liver as a part of disseminated tuberculosis is seen in up to 50-80% of the cases, but localized hepatobiliary tuberculosis is uncommonly described. [2] Tuberculous pericarditis is found approximately in 1% of all autopsied cases of tuberculosis and in 1-2% instances of pulmonary tuberculosis. [3] 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 tuberculosis in the absence of immunocompromise is extremely rare. [4]

Tuberculous liver abscess is usually secondary to primary pulmonary or gastrointestinal involvement. The tubercle bacilli gain access to the portal vein from a microscopic or small tubercular focus in the bowel. Subsequent healing at the site of entry leaves behind no trace of the primary lesion whatsoever. [5] Our case in consideration was an immunocompetent individual who developed rapidly progressing hepatic insufficiency progressing to acute hepatic failure following untreated extrapulmonary tuberculous liver abscesses, which disseminated to involve the pericardium and contiguous lymph nodes in the form of tubercular constrictive pericarditis and lymphadenitis.

Three forms of tuberculous liver involvement are described; diffuse involvement associated with miliary or pulmonary tuberculosis, diffuse parenchymal involvement without any evidence of existing tuberculosis anywhere and focal or nodular lesion in the liver, which may be multiple or solitary and present as tuberculoma or abscess. [6] Our case had only hepatic tuberculosis without pulmonary infection, we accept as the third type.

Pericardial involvement develops by retrograde lymphatic spread of Mycobacterium tuberculosis from the peritracheal, peribronchial or mediastinal lymph nodes or by hematogenous spread from the primary tuberculous infection. The pericardium is infrequently involved by breakdown and contiguous spread from a tuberculous lesion in the lung or by hematogenous spread from distant secondary skeletal or genitourinary infection. [3] The involvement of the heart in this patient was a possible contiguous spread across the diaphragm as the patient remained untreated for long.

On imaging, tubercular liver abscess or tuberculoma may be detected as an SOL on ultrasound (hypoechoic lesions with hyperechoic rims and complex masses) and CT (hypodense lesions). [6] Radiological findings can be confounding; only a fine needle aspiration cytology or a trucut biopsy can confirm the diagnosis.

Histopathological examination of the specimens from lesions is essential for the exact diagnosis. Low sensitivity of both acid-fast staining (from 0% to 45%) and culture (from 10% to 60%) mean diagnosis can still be difficult. [6] In this case, the aspirate from liver SOL was negative for AFB on staining, culture and PCR, adding to the diagnostic dilemma. Diaz et al. found that at least 57% of the hepatic granulomas caused by tuberculosis gave positive PCR test results. [8]

This case report illustrates the difficulty in arriving at a correct diagnosis in case of hepatic masses most often confused with carcinoma of the liver, primary or metastatic; hence, have been aptly referred to pseudotumoral hepatic tuberculosis in the past. Tubercular liver abscess is a diagnosis that must be considered especially in young patients with non-specific symptoms residing in areas with a high prevalence of TB. Vigorous attempts at obtaining histological diagnosis should be made where bacteriological diagnosis has been inconclusive.

   References Top

1.Bangaroo AK, Malhotra AS. Isolated hepatic tuberculosis. J Indian Assoc Pediatr Surg 2005;10:105-7.   Back to cited text no. 1
2.Amarapurkar DN, Patel ND, Amarapurkar AD. Hepatobiliary tuberculosis in western India. Indian J Pathol Microbiol 2008;51:175-81.   Back to cited text no. 2
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3.Mayosi BM, Burgess LJ, Doubell AF. Tuberculous pericarditis. Circulation 2005;112:3608-16.  Back to cited text no. 3
4.Brookes MJ, Field M, Dawkins DM, Gearty J, Wilson P. Massive primary hepatic tuberculoma mimicking hepatocellular carcinoma in an immunocompetent host. MedGenMed 2006;8:11.   Back to cited text no. 4
5.Hersch C. Tuberculosis of the Liver: A study of 200 cases. S Afr Med J 1964;38:857-63.   Back to cited text no. 5
6.Levine C. Primary macronodular hepatic tuberculosis: US and CT appearances. Gastrointest Radiol 1990;15:307-9.  Back to cited text no. 6
7.Cherian G. Diagnosis of tuberculous aetiology in pericardial effusions. Postgrad Med J 2004;80:262-6.  Back to cited text no. 7
8.Diaz ML, Herrera T, Lopez-Vidal Y, Calva JJ, Hernandez R, Palacios GR, et al. Polymerase chain reaction for the detection of Mycobacterium tuberculosis DNA in tissue and assessment of its utility in the diagnosis of hepatic granuloma. J Lab Clin Med 1996;127:359-63.  Back to cited text no. 8

Correspondence Address:
Deepti Mutreja
Department of Pathology, 12 Air Force Hospital, Air Force Station, Gorakhpur - 273 002
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0377-4929.72082

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  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]

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