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Bcr-abl-tyrosine-kinase-inhibitors/hydroxycarbamide/methylprednisolone Tuberculous peritonitis: case report

A 59-year-old woman developed tuberculous peritonitis following treatment with dasatinib, bosutinib, hydroxycarbamide and methylprednisolone [dosages and routes not stated]. The woman was hospitalised in Japan with leucocytosis, thrombocytosis, loss of appetite, dyspnoea on exertion and weight loss. Her medical history was significant for cervical cancer. Following investigations, granulocytic and megakaryocytic hyperplasia with significant fibrosis were noted. No findings showed lung tuberculosis. On hospitalisation day 1, she received hydroxycarbamide [hydroxyurea] for approximately 8 days for cytoreduction. On day 9, a diagnosis of chronic myelogenous leukaemia (CML) was made, and she received dasatinib approximately until day 10. However, dasatinib was again started approximately on day 17. Following the therapy, the leukocyte counts rapidly decreased. Concurrently, she was on various medications. Following the therapy, she developed renal function impairment and decreased BP. On day 18, her serum soluble interleukin-2 receptor (sIL-2R) level was found to be elevated to 4251 U/mL. Ascites was diagnosed eventually. On day 22, abdominal paracentesis revealed translucent and yellow fluid with adenosine deaminase (ADA) level of 83.5 U/L. Laboratory findings showed ascitic fluid along with LDH level of 731 U/L and albumin level of 1.3 g/dL. The polymerase chain reaction test of the ascitic fluid was negative for Mycobacterium tuberculosis. The dasatinib therapy was stopped approximately on day 25 [reason for stopping dasatinib not stated]. On day 29, she received bosutinib; however, the serum sIL-2R eventually increased to 7369 U/mL despite the improvement of leucocytosis and thrombocytosis. She also developed cardiopulmonary deterioration. She received methylprednisolone pulse therapy due to a suspected lymphoma. None of the other findings except elevated sIL-2R were suggestive of tuberculosis. She had a family history of tuberculosis. Based on these findings and based on the clinical presentation, tuberculous peritonitis was suspected. The woman was treated with anti-tuberculosis therapy with isoniazid, levofloxacin and streptomycin due to concern of tuberculous peritonitis. She also received continuous renal replacement therapy with a vasopressor agent. On day 39, ascitic fluid culture resulted positive for Mycobacterium tuberculosis. She was thus diagnosed with tuberculous peritonitis (seven days after initiation of the anti-tuberculosis therapy). Later, her bosutinib therapy was stopped approximately on day 43 [reason for discontinuation of drug not stated]. She received anti-tuberculosis therapy with levofloxacin, isoniazid and ethambutol. The use of steroid therapy and immunosuppressants were considered as a risk factor for development of tuberculous peritonitis. Following the anti-tuberculosis therapy, the serum sIL-2R levels significantly decreased to 1810 U/mL on day 67 and to 1225 U/mL on day