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Various toxicities: case report An approximately 55-year-old man developed rash and itchy skin during treatment with imatinib, Additionally, he developed primary gastric diffuse large B cell lymphoma (PGDLBCL) during treatment with imatinib and nilotinib [routes not stated; not all dosages stated]. The man, who was diagnosed with chronic myelogenous leukaemia chronic phase (CML-CP) nearly 8 years prior to the presentation, started receiving imatinib in June 2011. Three months later, his treatment with imatinib was switched to nilotinib due to rash and itchy skin. Subsequently, he was diagnosed with acute cerebral infarction in the right temporal lobe and was treated with unspecified symptomatic treatment at the age of 63 years. He complained of gastric discomfort for several months. A gastroscopic biopsy was performed and he initially diagnosed with small cell gastric cancer. On 15 March 2018, he was moved to the department of internal medicine and neurology. An MRI scan of the brain revealed acute cerebral infarction of right cerebral hemisphere and multiple sulcus in the brain. His unspecified symptomatic treatment was continued and gastric biopsy was re-examined. He was diagnosed with a non-germinal centre DLBCL. Immunohistochemistry showed followings: CD34 (+), CD10 (-), Mum-1 (a few cells were positive), BCL-6 (approximately 80%+), BCL-2 (-), C-MYC (approximately 80%+), CD5 (-), CD30 (-), P53 (several cells were positive), LCA (+), CD3 (-), CD7 (-), CD20 (+), EBER (-), Ki67 (approximately 80%+), CD3 (-), CD20 (±), CD79a (±), PAX5 (+), CD45RO (-), LCA (+), panCK (-). On 2 April 2018, he was moved to the haematology department. Physical examination revealed no enlarged superficial lymph nodes, splenomegaly or hepatomegaly. Laboratory findings were as follows: WBC count of 4.09 × 109/L, RBC count of 2.74 × 1012/L, haemoglobin of 90 g/L, platelet count of 124 × 109/L; β2 microglobulin of 2.07 mg/L and lactic dehydrogenase of 236 IU/L. Bone marrow smear demonstrated the positive rate of neutrophil alkaline phosphatase (NAP) staining was 54% and the score was 66 points but did not find primordial cells. The BCR/ABL fusion gene was observed in the bone marrow cells by fluorescence in situ hybridisation, which showed the presence of the transcript for BCR/ABL P210. Positron emission tomography revealed no evidence of lymphoma infiltration except for malignant lesions at the bottom of the stomach. A diagnosis of CML-CP, PG-DLBCL and acute cerebral infarction was made. Thereafter, the man was treated with RCOP regimen including rituximab, cyclophosphamide, vindesine, dexamethasone, lenalidomide from April 2018 to July 2018. He received nilotinib 400mg once daily to reduce the risk of bone marrow suppression. After three cycles, positron emission tomography revealed complete remission from PGDLBCL. Subsequently, the dose of nilotinib was increased to 400mg twice daily to achieve a better therapeutic efficacy for CML. The regimen was adjusted to rituximab and dexamethasone (RP) due to the low blood cell count during