Hepatitis granulomatosa en paciente con tuberculosis miliar: presentación de un caso / Granulomatous hepatitis in a patient with Miliary Tuberculosis: presentation of a case

La hepatitis granulomatosa como elemento inicial de una enfermedad tuberculosa es muy poco frecuente. El rendimiento de las pruebas para el diagnóstico de tuberculosis hepática resulta baja, siendo las principales causas de granulomatosis hepática las infecciones (tuberculosis, brucelosis, hongos, parásitos, etc). En la tuberculosis miliar, durante la diseminación hemática, que ocurre en el desarrollo de la primoinfección, el hígado es capaz de recibir y albergar una carga considerable de bacilos por sus características anatomofuncionales que se agrupan en forma de granuloma, que es un patrón de reacción inflamatoria crónica en el que predomina un tipo especial de célula denominada macrófago. Esto es causa frecuente de síndrome febril prolongado de causa sistémica, puede debutar con manifestaciones clínicas poco precisas. Se presentó un caso del sexo masculino que ingresa en el servicio de Medicina del Hospital Militar Docente Dr Mario Muñoz Monroy, de Matanzas, que ingresa por cuadro de fiebre de origen desconocido, que resultó ser por esta causa.

Granulomatous hepatitis as initial element of a tubercular disease is few frequent; the efficacy of the tests for diagnosing hepatic tuberculosis is low, being infections (tuberculosis, brucellosis, fungi, parasites, etc). The main cause of hepatic granulomatosis. during the hematic dissemination in the miliary tuberculosis, occurring in the development of primo-infection, liver is able of receiving and dwelling a considerable charge of bacilli due to its anatomic functional characteristics; they group in the form of granulomas, a pattern of chronic inflammatory reaction, in which there is a predomination of an special kind of cells called macrophages; it frequently causes a prolonged febrile syndrome and may start with little precise clinical manifestations. We present the case of a male patient entering the Medicine Service of the Military Hospital Dr Mario Muñoz Monroy of Matanzas, with a picture of unknown origin fever, resulting being originated by this cause.

Tuberculosis and liver disease: management issues.

Tuberculosis is one of the most common diseases in India and has attained epidemic proportions. Tuberculosis and liver are related in many ways. Liver disease can occur due to hepatic tuberculosis or the treatment with various anti-tubercular drugs may precipitate hepatic injury or patients with chronic liver disease may develop tuberculosis and pose special management problems. Tuberculosis per se can affect liver in three forms. The most common form is the diffuse hepatic involvement, seen along with pulmonary or miliary tuberculosis. The second is granulomatous hepatitis and the third, much rarer form presents as focal/local tuberculoma or abscess. Tubercular disease of liver occurring along with pulmonary involvement as in disseminated tuberculosis is treated with standard regimen for pulmonary tuberculosis. Granulomatous hepatitis and tubercular liver abscess are treated like any other extra-pulmonary tubercular lesions without any extra risk of hepatotoxicity by anti-tubercular drugs. Treatment of tuberculosis in patients who already have a chronic liver disease poses various clinical challenges. There is an increased risk of drug induced hepatitis in these patients and its implications are potentially more serious in these patients as their hepatic reserve is already depleted. However, hepatotoxic anti-tubercular drugs can be safely used in these patients if the number of drugs used is adjusted appropriately. Thus, the main principle is to closely monitor the patient for signs of worsening liver disease and to reduce the number of hepatotoxic drugs in the anti-tubercular regimen according to the severity of underlying liver disease.

A case of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis / 대한간학회지

Allopurinol-induced hypersensitivity syndrome is characterized by an idiosyncratic reaction involving multiple-organs, which usually begins 2 to 6 weeks after starting allopurinol. In rare cases, the adverse reactions to allopurinol are accompanied by a variety of liver injury, such as reactive hepatitis, granulomatous hepatitis, vanishing bile duct syndrome, or fulminant hepatic failure. Here we report a case with granulomatous hepatitis and ductopenia. A 69-year-old man with chronic renal failure, hyperuricemia, and previously normal liver function presented with jaundice, skin rash, and fever 2 weeks after taking allopurinol (200 mg/day). In histopathology, a liver biopsy specimen showed mild spotty necrosis of hepatocytes, marked cholestasis in parenchyma, and some granulomas in the portal area. There were vacuolar degeneration in the interlobular bile ducts and ductopenia in the portal tracts. Pathologic criteria strongly suggested the presence of allopurinol-induced granulomatous hepatitis with ductopenia and cholestasis. The patient fully recovered following the early administration of systemic corticosteroid therapy.

A Case of Granulomatous Hepatitis Associated with Common Variable Immunodeficiency / 대한간학회지

A granuloma is a compact, organized collection of chronic inflammatory cells, predominantly consisting of mature mononuclear phagocytes. Clinical manifestations of hepatic granulomas vary widely from asymptomatic elevation of serum alkaline phosphatase activity to liver cirrhosis. The hepatic granuloma is nonspecific and represents a pathologic reaction induced by any of a number of factors. Although the causes of hepatic granuloma vary considerably according to geographic site, sarcoidosis and tuberculosis are the two leading causes. Here we present a 20-year-old female with a long history of recurrent otitis media, upper respiratory infection, and unexplained hepatosplenomegaly. A diagnosis of common variable immunodeficiency was made, based on the decreased levels of serum immunoglobulins. A liver biopsy revealed chronic granulomatous inflammation, but neither caseous necrosis nor acid-fast bacillus was found. Her liver disease progressed despite a nine-month course of antituberculous medication. Hypogammaglobulinemia should be included in the differential diagnosis of granulomatous liver disease.