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Myelotoxicity and lack of drug effect: 2 case reports A case series described 2 men, one man aged 54-years was described who exhibited lack of drug effect during treatment with erythropoietin and cytarabine for normocytic anaemia; the second man (aged 79 years) developed myelotoxicity during treatment with azacitidine [Azacytidine] for chronic myelomonocytic leukemia-II [not all routes and dosages stated]. Case 1: The man, who had a history of arterial hypertension, diabetes type-I, bilateral cataract, coronary heart disease and splenorrhaphy due to traumatic splenic rupture 15 years ago, presented with normocytic anaemia. Examinations indicated myelodysplastic syndrome ring sideroblasts (MDS-RS) and multilineage dysplasia (RCMD-RS). After further examinations, he was classified as low risk by both IPSS and age-adjusted age-adjusted IPSS-R systems. Subsequently, he was referred for allogeneic transplantation; however, it was not performed due to high HCT-CI score. Due to heavy transfusion requirement of three packed RBC per month, he was started on recombinant erythropoietin 40000 IU/week. After 2 months, the dose of erythropoietin was increased to 80000 IU/week for four months; however, the treatment was stopped as no response was observed. Thereafter, he started receiving treatment with azacitidine. However, due to lack of response after 8 cycles, azacitidine therapy was stopped. During re-evaluation, findings similar to the initial assessment were noted. Despite sequential treatment with unspecified androgens and valproic acid with deferasirox, he remained transfusion dependent. After 50 months, he developed massive splenomegaly with low grade fever. Biopsy examination showed grade-III fibrosis. Therefore, treatment with azacitidine was reinitiated. Improvement was noted after the second cycle. The size of spleen and his transfusion requirements reduced after 24 cycles, but erythroid response was not noted. Later, he developed an acute myocardial infarction, and azacitidine therapy was withheld. After two months, azacitidine therapy was again started; however, the disease progressed after one cycle, and the therapy was stopped. After 3 months, low dose cytarabine [AarC] was started due to persistent systemic symptoms. After two cycles, it was stopped due to no response. After one month of cytarabine discontinuation, he died due to heart attack. Case 2: The man, who had a history of congestive heart failure, arterial hypertension and coronary heart disease with a coronary angioplasty 12 years prior, presented with severe transfusion-dependent anaemia and thrombocytopenia. Following examinations, a diagnosis of chronic myelomonocytic leukaemia-2 (CMML-2) was made. Subsequently, his treatment was started with SC azacitidine 75 mg/m2 for 7 days in a cycle of 28 days. Subsequent improvement was noted in his condition, but the azacitidine therapy was discontinued on cycle 6 due to transfusion requirements and severe anaemia. Additionally, development of azacitidine therapy related severe myelotoxicity was noted.