Lovric V A, Beal P J, Lammi A T
J Pediatr. 1975 Feb;86(2):194-7. doi: 10.1016/s0022-3476(75)80466-5.
Compensatory mechanisms in children with iron-deficiency anemia were evaluated by measuring erythrocytic organic phosphates and, in some cases, shifts in the P50 of the oxygen dissociation curve. In 19 children with nutritional anemia (hemoglobin values of 3.2 to 8.2 gm/dl) there was a calculated improved oxygen delivery to tissues equivalent to a hemoglobin level of at least 7.5 gm/dl. Transient decompensation was observed during acidosis. In five children with iron-deficiency anemia due to blood loss and in one child with rheumatoid arthritis no such compensatory changes were observed.
通过测量红细胞有机磷酸盐，并在某些情况下测量氧解离曲线P50的变化，对缺铁性贫血患儿的代偿机制进行了评估。在19名营养性贫血患儿（血红蛋白值为3.2至8.2克/分升）中，经计算，组织的氧输送改善程度相当于血红蛋白水平至少为7.5克/分升。酸中毒期间观察到短暂失代偿。在5名因失血导致缺铁性贫血的患儿和1名类风湿性关节炎患儿中，未观察到此类代偿性变化。
