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Granulomatous Liver Diseases
Granulomatous liver diseases are a common finding which may be precipitated by infectious microbes or in response to systemic inflammatory or autoimmune processes. Granulomatous hepatitis may occasionally be idiopathic in origin in context of a fever of unknown origin. Granulomas of the liver are believed to originate from macrophages that are transformed into epithelioid cells after stimulation by antigens and may be composed of multinucleated giant cells. Granulomas are further classified into caseating and noncaseating granulomas, which may help distinguish between etiologic agents such as tuberculosis (which are often associated with caseating granulomas) and autoimmune or inflammatory processes (which are associated with noncaseating granulomas).
Infectious Processes
The most common organisms associated with granulomas are bacteria such as Mycobacterium tuberculosis (MTB), Mycobacterium avium-intracellulare (MAI), brucellosis, listeriosis, and tularemia. Other infections associated with granuloma development include schistosomiasis, leishmaniasis, and visceral larva migrans. Rickettsial diseases, viruses (e.g., cytomegalovirus), and protozoal infections less commonly may be associated with granulomas.
Hepatic Tuberculosis
Primary hepatic tuberculosis may occur in the extremely rare congenital form, but it is usually secondary to miliary tuberculosis ( Fig. 175.1 ). The most frequent lesion is the small miliary granuloma (tubercle), which may be scattered over the liver in all forms of active organ tuberculosis. Granuloma formation begins with a focal proliferation of Kupffer cells, which form small histiocytic nodules located throughout the parenchyma. Subsequently, liver cells surrounded by the histiocytes become necrotic, and in some cases, smaller or larger foci of hepatocellular necrosis with minimal mesenchymal reaction develop. In the nodules, some cells become larger and develop into epithelioid cells, the nuclei of which can divide without division of the cytoplasm, resulting in large giant cells (Langerhans). A lymphocytic infiltrate can be seen on the periphery of the granuloma. As the tubercle enlarges, central caseation necrosis may develop. Eventually, the histiocytes may transform into fibroblasts and form a capsule around the tubercle. Finally, the entire lesion becomes transformed into a nodule of collagenous connective tissue.
Acid-fast bacilli (AFB) are usually not seen in the scar, and tubercle bacilli are also difficult to culture from liver biopsy specimens. In addition, the morphologic picture of the tubercles is nonspecific because other granulomatous diseases may produce similar lesions in the wall of the central vein. Tuberculous granulomas are spread throughout the lobule, frequently close to the portal triads where they tend to coalescence.
In miliary tuberculosis (TB), the tubercles are densely spread, as readily seen on gross inspection, and they appear as white, pinhead-sized nodules best recognized through the capsule on inspection of the inferior surface of the left lobe. Hepatic miliary TB may precede pulmonary involvement, or the lungs may remain unaffected. Fever may be prolonged, and chest x-ray findings may be negative; the diagnosis is typically confirmed by liver biopsy.
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