A Case of Tuberculosis-associated Hemophagocytic Syndrome during Antituberculosis Medication for Tuberculous Pericarditis

Abstract

A 63-year old woman was admitted to our hospital for an evaluation of thrombocytopenia. She had been diagnosed with tuberculous pericarditis three months earlier in a local clinic and treated with anti-tuberculosis medication. Two months later, thrombocytopenia developed. The medication was subsequently stopped because it was suspected that the anti-tuberculosis medication, particularly rifampin, might have caused the severe platelet reduction. However, the thrombocytopenia was more aggravated. A bone marrow biopsy was performed, which showed moderate amounts of histiocytes with active hemophagocytosis. This finding strongly suggested that the critical thrombocytopenia had been caused by hemophagocytic syndrome, not by the side effects of the anti-tuberculosis medication. Furthermore, the development of hemophagocytosis might have been due to an uncontrolled tuberculosis infection and its associated aberrant immunity. Therefore, she was started with both standard anti-tuberculosis medication and chemotherapy using etoposide plus steroid. One month after the initiation of treatment, the thrombocytopenia had gradually improved and she was discharged in a tolerable condition. At the third month of the follow-up, her platelet level and ferritin, the activity marker of hemophagocytic syndrome, was within the normal range. (Tuberc Respir Dis 2008;65:522-526)

Disseminated tuberculosis presenting with secondary haemophagocytic lymphohistiocytosis and Poncet's disease in an immunocompetent individual

“…Pertinently, the patient suffered only mild pancytopenia, and liver function was unaffected, permitting immediate institution of first-line antitubercular drugs. This was also the case with a patient described by No et al ,9 who was administered full antitubercular treatment along with etoposide and dexamethasone, and subsequently made a complete recovery. Brastianos et al 10 reviewed 36 cases of tuberculosis-associated HLH.…”