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Evolution of iron burden in acquired aplastic anemia: a cohort study of more than 3-year follow-up
Peng Jin1, Jinhuan Wang, Xingxin Li
1Severe Aplastic Anemia Studying Program, State Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, 288 Nanjing Road, Tianjin, 300020, People's Republic of China.
Acquired aplastic anemia (AA) is the most common condition linked to transfusion dependence. We conducted a cohort study to explore patterns of the dynamic evolution of iron burden, and to identify the risk factors for iron overload (IO) in 550 AA patients. Of the participants, 13 % presented with IO when diagnosed, including 7 % of patients without a history of transfusion and 22 % of those receiving transfusions. Male patients [hazard ratio (HR) = 3.85, 95 % confidence interval (CI) 1.77-8.36], adults (HR = 3.04, 95 % CI 1.21-7.63), and patients with high transfusion burdens (more than eight units; HR = 11.30, 95 % CI 4.45-28.70) experienced a significantly higher risk of IO. Furthermore, we found a sharply increasing risk of IO within the first 2 years, especially in males, patients with large number of lifetime transfusions, and patients not responding to treatment. More interestingly, after transfusion independence, a significant seesaw effect between erythropoiesis and iron burden was not noted until 6 months later, which continued over 3 years. In contrast to female patients, children, and patients with lower transfusion burdens, male subjects, adults, and subjects with high transfusion burdens experienced a pattern of slow decline in iron burden. AA incurred a high risk of progression to IO and showed distinct patterns in the evolution of iron burden. In light of these data, we offer suggestions for decision-making regarding who should undergo iron chelation and when.
Acquired aplastic anemia (AA) is the most common condition linked to transfusion dependence. We conducted a cohort study to explore patterns of the dynamic evolution of iron burden, and to identify the risk factors for iron overload (IO) in 550 AA patients. Of the participants, 13 % presented with IO when diagnosed, including 7 % of patients without a history of transfusion and 22 % of those receiving transfusions. Male patients [hazard ratio (HR) = 3.85, 95 % confidence interval (CI) 1.77-8.36], adults (HR = 3.04, 95 % CI 1.21-7.63), and patients with high transfusion burdens (more than eight units; HR = 11.30, 95 % CI 4.45-28.70) experienced a significantly higher risk of IO. Furthermore, we found a sharply increasing risk of IO within the first 2 years, especially in males, patients with large number of lifetime transfusions, and patients not responding to treatment. More interestingly, after transfusion independence, a significant seesaw effect between erythropoiesis and iron burden was not noted until 6 months later, which continued over 3 years. In contrast to female patients, children, and patients with lower transfusion burdens, male subjects, adults, and subjects with high transfusion burdens experienced a pattern of slow decline in iron burden. AA incurred a high risk of progression to IO and showed distinct patterns in the evolution of iron burden. In light of these data, we offer suggestions for decision-making regarding who should undergo iron chelation and when.
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