Solmaz Soner, Özdoğu Hakan, Boğa Can
Department of Hematology, Sivas Numune Hospital, Sivas, 58000 Turkey.
Department of Haematology, Adana Hospital of Başkent University, Adana, Turkey.
Indian J Hematol Blood Transfus. 2015 Jun;31(2):255-8. doi: 10.1007/s12288-014-0417-x. Epub 2014 Jun 14.
Vitamin B12 deficiency impairs DNA synthesis and causes erythroblast apoptosis, resulting in anaemia from ineffective erythropoiesis. Iron and cobalamin deficiency are found together in patients for various reasons. We have observed that cobalamin deficiency masks iron deficiency in some patients. We hypothesised that iron is not used by erythroblasts because of ineffective erythropoiesis due to cobalamin deficiency. Therefore, we aimed to demonstrate that depleted iron body reserves are masked by cobalamin deficiency. Seventy-five patients who were diagnosed with cobalamin deficiency were enrolled in this study. Complete blood counts and serum levels of iron, unsaturated iron binding capacity (UIBC), ferritin, vitamin B12, and thyroid stimulant hormone were determined at diagnosis and after cobalamin therapy. Patients who had a combined deficiency at diagnosis and after cobalamin therapy were recorded. Before cobalamin therapy, we found increased serum iron levels (126.4 ± 63.4 µg/dL), decreased serum UIBC levels (143.7 ± 70.8 µg/dL), increased serum ferritin levels (192.5 ± 116.4 ng/mL), and increased transferrin saturation values (47.2 ± 23.5 %). After cobalamin therapy, serum iron levels (59.1 ± 30 µg/dL), serum ferritin levels (44.9 ± 38.9 ng/mL) and transferrin saturation values (17.5 ± 9.6 %) decreased, and serum UIBC levels (295.9 ± 80.6 µg/dL) increased. Significant differences were observed in all values (p < 0.0001). Seven patients (9.3 %) had iron deficiency before cobalamin therapy, 37 (49.3 %) had iron deficiency after cobalamin therapy, and a significant difference was detected between the proportions of patients who had iron deficiency (p < 0.0001). This study is important because insufficient data are available on this condition. Our results indicate that iron deficiency is common in patients with cobalamin deficiency, and that cobalamin deficiency can mask iron deficiency. Therefore, we suggest that all patients diagnosed with cobalamin deficiency should be screened for iron deficiency, particularly after cobalamin therapy.
维生素B12缺乏会损害DNA合成并导致成红细胞凋亡,进而因无效造血导致贫血。由于多种原因,患者常同时存在铁和钴胺素缺乏的情况。我们观察到,在一些患者中,钴胺素缺乏会掩盖缺铁情况。我们推测,由于钴胺素缺乏导致无效造血,成红细胞无法利用铁。因此,我们旨在证明钴胺素缺乏会掩盖体内铁储备的减少。本研究纳入了75例被诊断为钴胺素缺乏的患者。在诊断时及钴胺素治疗后,测定全血细胞计数以及血清铁、未饱和铁结合能力(UIBC)、铁蛋白、维生素B12和促甲状腺激素水平。记录诊断时及钴胺素治疗后合并缺乏的患者情况。在钴胺素治疗前,我们发现血清铁水平升高(126.4±63.4μg/dL)、血清UIBC水平降低(143.7±70.8μg/dL)、血清铁蛋白水平升高(192.5±116.4ng/mL)以及转铁蛋白饱和度值升高(47.2±23.5%)。钴胺素治疗后,血清铁水平(59.1±30μg/dL)、血清铁蛋白水平(44.9±38.9ng/mL)和转铁蛋白饱和度值(17.5±9.6%)降低,而血清UIBC水平(295.9±80.6μg/dL)升高。所有数值均观察到显著差异(p<0.0001)。7例患者(9.3%)在钴胺素治疗前存在缺铁,37例(49.3%)在钴胺素治疗后存在缺铁,缺铁患者比例之间存在显著差异(p<0.0001)。本研究具有重要意义,因为关于这种情况的数据不足。我们的结果表明,缺铁在钴胺素缺乏患者中很常见,并且钴胺素缺乏会掩盖缺铁情况。因此,我们建议所有被诊断为钴胺素缺乏的患者都应进行缺铁筛查,尤其是在钴胺素治疗后。