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Tuberculous hepatitis
Last reviewed: 07.07.2025
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Tuberculous hepatitis is usually detected at autopsy or laparoscopy in patients with abdominal tuberculosis. Liver tuberculosis accompanies intestinal tuberculosis in 79-99% of cases.
Isolated liver damage is quite rare; more often, several anatomical structures are simultaneously involved in a specific process. However, the clinical picture of the disease is dominated by symptoms characteristic of damage to any organ, which allows us to distinguish the disease as an independent nosological unit.
Pathomorphology
Tuberculosis mycobacteria penetrate the liver through the hematogenous or lymphogenous route; the process can also spread through the bile ducts.
Granulomatous specific hepatitis, myeloid and focal liver tuberculosis, tuberculous cholangitis and tuberculous pylephlebitis are most frequently observed. With prolonged tuberculosis, liver steatosis and amyloidosis develop.
The main morphological substrate is granuloma. After its disintegration, healing occurs without the formation of scar tissue; focal fibrosis and calcification are observed less frequently.
Pseudotumoral liver tuberculomas may develop. Tuberculomas are white, heterogeneous caseous masses surrounded by a fibrous capsule. Tuberculomas may be multiple.
Rarely, tuberculous cholangitis is observed, caused by the entry of caseous masses from the portal tracts into the bile ducts. Tuberculous pylephlebitis develops as a result of the rupture of caseous masses into the portal vein. As a rule, it quickly leads to a fatal outcome, although sometimes it can be the cause of the development of chronic portal hypertension. Tuberculous lesions of the lymph nodes in the portals of the liver can rarely lead to stricture of the bile ducts.
Symptoms of tuberculous hepatitis
Clinical manifestations of tuberculous hepatitis are often scanty or absent. Patients may experience anorexia, general malaise, weakness, increased sweating, subfebrile temperature, pain in the right hypochondrium. The liver is enlarged, its edge is dense, in some cases the surface is uneven (in the granulomatous form) or it is possible to palpate a node on its surface (tuberculoma). The spleen is often enlarged.
Liver tuberculosis may also be a manifestation of miliary tuberculosis. The literature describes the development of fulminant liver failure of tuberculosis etiology, including in patients undergoing hemodialysis treatment.
The clinical signs of tuberculous hepatitis are multifaceted, pathognomonic symptoms are absent. It usually occurs under the guise of other diseases and is detected only in some patients, and in most patients it remains unrecognized.
In modern conditions, tuberculosis of the abdominal organs in children is observed against the background of general symptoms associated with intoxication.
Tuberculous liver damage may manifest itself as fever, jaundice, which occurs in severe cases of miliary tuberculosis. In rare cases, multiple caseous granulomas lead to massive hepatosplenomegaly and death of the patient from liver failure.
In the blood serum, a decrease in the albumin/globulin ratio and an increase in alkaline phosphatase activity are observed.
Liver damage in extrahepatic tuberculosis
Chronic tuberculosis may be complicated by liver amyloidosis. Fatty liver disease may be caused by exhaustion and toxemia. Drug-induced jaundice may develop after completion of treatment, especially when using isoniazid, rifampicin.
Where does it hurt?
Diagnosis of tuberculous hepatitis
In general, the diagnosis of tuberculous hepatitis is difficult. Liver tuberculomas are difficult to differentiate from lymphomas. The determining role in diagnosis belongs to liver biopsy. In addition, computed tomography can be used, which reveals lobular formation or multiple filling defects in the liver and spleen.
On plain abdominal radiograph, multiple or discrete hepatic petrifications may be detected.
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