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Assessment of serum hepcidin levels in patients with non-ST elevation myocardial infarction
Burak Altun1, Mehzat Altun, Gürkan Acar
1Department of Cardiology, Faculty of Medicine, Ministry of Health, Çanakkale Onsekiz Mart University; Çanakkale-Turkey. hakantasolar@gmail.com.
Insights
Serum hepcidin levels did not increase in patients with non-ST elevation myocardial infarction (NSTEMI) during the acute phase. Hepcidin is not a reliable marker for myocardial necrosis in NSTEMI patients.
Area of Science:
- Cardiology
- Biochemistry
- Inflammation Research
Background:
- Hepcidin, an acute-phase reactant with antimicrobial properties, is produced in the liver.
- Limited research exists on hepcidin as an inflammatory marker in acute coronary syndromes.
- Non-ST elevation myocardial infarction (NSTEMI) represents an acute inflammatory exacerbation of chronic atherosclerosis.
Purpose of the Study:
- To investigate elevated hepcidin levels in the acute phase of NSTEMI.
- To assess hepcidin's role as an acute and chronic inflammatory marker in NSTEMI patients.
Main Methods:
- Observational cross-sectional study involving 70 NSTEMI patients and 20 healthy controls.
- Serum hepcidin and troponin levels measured at admission and 6 hours later using ELISA and standard methods.
- Statistical analysis included Student t-test, Mann-Whitney U test, and paired t-test.
Main Results:
- No significant difference in hepcidin levels between NSTEMI patients and controls at admission.
- Hepcidin levels remained stable in NSTEMI patients 6 hours post-admission.
- Troponin levels significantly increased from baseline in NSTEMI patients.
Conclusions:
- Hepcidin does not appear to be a useful marker for myocardial necrosis in the acute phase of NSTEMI.
- Current findings suggest hepcidin cannot be used similarly to troponin for NSTEMI assessment.
Objective:
Hepcidin is an acute-phase reactant produced in the liver displaying intrinsic antimicrobial activity. There are few studies about hepcidin considered to be acute and chronic inflammatory marker in acute coronary syndromes patients. We investigated in our study whether the level of hepcidin has increased in the acute phase of non-ST elevation myocardial infarction patients (NSTEMI) known as acute inflammatory aggravation of chronic atherosclerotic process.
Methods:
Seventy patients with NSTEMI and twenty healthy people were recruited as controls in this observational cross-sectional study. Serum hepcidin levels were determined by ELISA, and troponin levels were measured by standard laboratory methods. Levels of hepcidin and troponin were measured at admission and 6 hours later. Mean values of continuous variables were compared between groups using the Student t-test or Mann-Whitney U test, according to whether normally distributed or not, as tested by the Kolmogorov-Smirnov test. Serum troponin and hepcidin levels measured at admission and after 6th hours were compared using paired t-test.
Results:
Hepcidin level was similar between NSTEMI and controls at admission (24.55±32.13, 23.67±33.62 ng/mL, p>0.05, respectively). Also, serum hepcidin levels did not change significantly from baseline in blood samples taken after 6 hour from admission in NSTEMI patients (24.55±32.13 ng/mL, 29.75±31.48 ng/mL, p=0.62, respectively). However, serum troponin levels were increased significantly compared to baseline (0.29±3.56, 2.92±7.2 ng/mL, p<0.01).
Conclusion:
Our findings suggest that hepcidin could not be use as a marker of myocardial necrosis in acute phase such as troponin in patients with NSTEMI.
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