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Various toxicities: 4 case reports

In a retrospective study involving 179 patients followed up for β-thalassemia at a hospital in Oman from 2007 through 2017, four patients (3 boys and 1 girl) aged 7–14 years were described, who developed agranulocytosis during treatment with deferiprone. Two of these patients also developed febrile neutropenia during treatment with deferiprone, and one of these 2 patients additionally developed eye toxicity in the form of optic disc pallor with decreased visual acuity during treatment with deferoxamine, as well as an anaphylactic reaction and acute kidney injury during treatment with deferasirox for β-thalassemia [not all dosages, times to reactions onsets and outcomes clearly stated]. Case 1: A 14-year-old boy started receiving oral deferiprone 100 mg/kg for β-thalassemia. However, after 8 weeks, he developed agranulocytosis, which was attributed to the treatment with deferiprone. He was treated with filgrastim; however, the course was complicated bu the development of lymphopenia, pneumonia and parapneumonic effusion, further complicated by rupture of pulmonary artery aneurysm, massive haemoptysis and cardiopulmonary arrest. He was admitted to the paediatric ICU and managed with catheter coil embolisation. The agranulocytosis resolved after 8 days. Thereafter, he was treated with a combination of deferoxamine and deferasirox, with poor response. Case 2: A 9-year-old boy started receiving oral deferiprone 100 mg/kg for β-thalassemia. However, after 6 years, he experienced agranulocytosis, which was attributed to the treatment with deferiprone. He also developed facial cellulitis and deferiprone-related febrile neutropenia. The facial cellulitis was treated with unspecified antibiotics, whereas the agranulocytosis and febrile neutropenia were managed with filgrastim. However, the treatment with filgrastim was complicated by the development of frequent premature ventricular contractions, which were conservatively managed. The agranulocytosis resolved after 12 days. Thereafter, he was treated deferasirox, with a good response. Case 3: A 12-year-old girl started receiving oral deferiprone 100 mg/kg for β-thalassemia. However, after 4 years and 3 weeks, she developed agranulocytosis, which was attributed to the treatment with deferiprone. She also developed lymphopenia, extensive mucositis and herpes simplex infection, which necessitated admission to the paediatric ICU for inotropic support. The agranulocytosis was treated with filgrastim and resolved after 7 days. Thereafter, she was treated with deferasirox, with poor response. Case 4: A 7-year-old boy started receiving oral deferiprone 75 mg/kg for β-thalassemia. However, after 6 weeks, he developed agranulocytosis, which was attributed to the treatment with deferiprone. He also developed deferiprone-related febrile neutropenia. Therefore, deferiprone was discontinued, and he was treated with filgrastim for the agranulocytosis. He also received unspecified antibiotics. The agranulocytosis resolved after 7 days. The febrile ne