Yokusoglu Mehmet, Nevruz Oral, Baysan Oben, Uzun Mehmet, Demirkol Sait, Avcu Ferit, Koz Cem, Cetin Turker, Hasimi Adnan, Ural Ali Ugur, Isik Ersoy
Department of Cardiology, Gulhane Military Medical School, Ankara, Turkey.
Tohoku J Exp Med. 2007 Aug;212(4):397-402. doi: 10.1620/tjem.212.397.
Autonomic function is impaired in anemic patients with various etiologies such as vitamin B12 deficiency, sickle cell trait, and thalassemia major. However, there are insufficient data about autonomic functions in patients with iron deficiency anemia, the leading cause for anemia in the general population. In the present study we aimed to investigate the autonomic status in iron deficiency anemia by analyzing the heart rate variability (HRV). Age- and gender-matched 43 patients with iron deficiency anemia and 39 healthy subjects were undertaken into 24-hr Holter monitoring for assessing the HRV. We used serum levels of iron, iron binding capacity, C-reactive protein, vitamin B12, and folate to exclude other causes of anemia. While age, gender, vitamin B12 and folate levels were not different between the groups, HRV values were lower in patients with iron deficiency anemia compared to control group, which reflects parasympathetic withdrawal. Blood hemorheological factors such as decreased viscosity and/or altered red cell deformability may be responsible for this decreased parasympathetic activity. However, these components do not display remarkable contribution in iron deficiency anemia. Therefore, we speculated a probable link between anemia and the accentuated sympathetic activity that may be triggered by hypoxia sensed through carotid bodies. Despite lacking adequate convincing evidence concerning exact mechanism of carotid body activation, it is assumed as due either to hypoxia-related mitochondrial respiratory chain inhibition or potassium channel suppression that leads to intracellular calcium accumulation. In conclusion, the present study demonstrates an altered autonomic balance in patients with true iron deficiency anemia.
自主神经功能在患有各种病因的贫血患者中会受损，这些病因包括维生素B12缺乏、镰状细胞性状和重型地中海贫血。然而，关于缺铁性贫血患者自主神经功能的数据不足，缺铁性贫血是一般人群中贫血的主要原因。在本研究中，我们旨在通过分析心率变异性（HRV）来研究缺铁性贫血患者的自主神经状态。对年龄和性别匹配的43例缺铁性贫血患者和39例健康受试者进行了24小时动态心电图监测，以评估HRV。我们使用血清铁、铁结合能力、C反应蛋白、维生素B12和叶酸水平来排除其他贫血原因。虽然两组之间的年龄、性别、维生素B12和叶酸水平没有差异，但缺铁性贫血患者的HRV值低于对照组，这反映了副交感神经活动减弱。血液流变学因素，如粘度降低和/或红细胞变形性改变，可能是导致副交感神经活动降低的原因。然而，这些因素在缺铁性贫血中并没有显著作用。因此，我们推测贫血与可能由颈动脉体感知的缺氧引发的交感神经活动增强之间可能存在联系。尽管缺乏关于颈动脉体激活的确切机制的充分确凿证据，但推测其原因要么是与缺氧相关的线粒体呼吸链抑制，要么是钾通道抑制导致细胞内钙积累。总之，本研究表明真正缺铁性贫血患者的自主神经平衡发生了改变。
