Investigating the Role of Serum Hepcidin and Interleukin-6 in Non-Anemic Women with Acute Ischemic Stroke

Abstract

Background: Hepcidin (HP) is an important regulator of iron homeostasis. Iron status and IL-6 have been shown to regulate the expression of HP. Serum iron (SI), HP, and IL-6 have a highly significant role in inflammation since inflammation elevates the levels of HP for expressing the ischemic condition. The present study was carried out to investigate the impact of an interactive association between HP, SI, and IL-6 in non-anemic women with acute ischemic stroke (AIS). Methods and Results: The present case-control, descriptive study comprised 25 non-anemic women with AIS and 25 healthy non-anemic women controls. The age range of AIS and control subjects was 50 to 54 years. Non-anemic AIS women within 8 hours after AIS onset (AIS<8 hrs) and 72 hours after onset of AIS (AIS-72 hours) were examined. The patients underwent assessment of traditional risk factors, physical examination, CBC, blood biochemistry test, 12-lead ECG, CT scans, MRI, CT or MR angiogram, carotid ultrasound of the arteries, transcranial doppler ultrasound, and EEG. Office blood pressure was measured using a mercury sphygmomanometer. Significantly increased values were obtained for systolic blood pressure and diastolic blood pressure in AIS women, compared to the control subjects: 137.44±12.35 vs. 130.88±7.30 mmHg (P=0.0267) and 86.72± 8.48 vs. 81.80± 5.42 mmHg (P=0.0183), respectively. Serum CRP and LDL-C levels in AIS were significantly higher than in healthy control women (P<0.0001). A significant increase in serum HP, SI, and IL-6 for AIS<8 hrs was found, compared to AIS-72 hrs (P<0.001 in all cases). Comparison for AIS<8 hrs vs. controls showed a highly significant increase in serum HP, SI, and IL-6 for AIS<8 hrs (P<0.001 in all cases). On the other hand, AIS-72 hrs vs. controls indicated a significant increase in SI (P=0.0028) and IL-6 (P=0.0065) but a non-significant increase in serum HP (P>0.05) in AIS-72 hrs. Linear regression expressed a high strength of the relationship between serum HP and SI for AIS<8 hrs (R2=0.82, P<0.0001) and AIS-72 hrs (R2=0.73, P<0.0001), but a negligible linear association for controls (R2=0.01, P=0.5990). There was a high relationship between HP and IL-6 for AIS<8 hrs (R2=0.67, P<0.0001) and AIS-72 hrs (R2=0.67, P<0.0001), but a small linear association for controls (R2=0.28, P=0.0063). The R2 value of 0.47 (P<0.0002) and 0.42 (P<0.0004) was found between SI and IL-6 for AIS<8 hrs and AIS-72 hrs, and a negligible linear association (R2=0.006, P=0.7250) for controls. Conclusion: The present study provides evidence of the association of AIS in non-anemic women with increased hepcidin. The interactive pathophysiological role of HP, IL-6, and SI in non-anemic women with AIS has also been shown.