The Altered Autonomic Nervous System Activity in Iron Deficiency Anemia

Abstract

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.