Correlation of hepcidin level with insulin resistance and endocrine glands function in major thalassemia.
BACKGROUND
Hepcidin is a master regulator of iron metabolism that inhibits the transport of iron out of enterocytes and macrophages. Thalassemia major (TM) is associated with some of the endocrine disorders. However, studies have yet to be conducted on the correlation of hepcidin with hormone levels and insulin resistance (IR) in patients with TM.


OBJECTIVE
In the present study, the correlation of hepcidin level with some endocrine and biochemical parameters was investigated to determine the factors that mainly affect hepcidin correlation in patients with thalassemia. These factors include hormones, iron status, and IR parameters.


METHODS
Hepcidin and other measured biochemical parameters were compared between the TM patients (100) and healthy children (37).


RESULTS
Serum thyroid-stimulating hormone (TSH) was positively correlated (p < 0.05) with hepcidin, iron, and ferritin. T4 hormone was correlated with ferritin only. Other hormones showed different correlation patterns with iron status parameters but were statistically insignificant (p > 0.05). The percentage of β-cell function was the only parameter among the IR parameters that showed a significant difference between thalassemic and control groups.


CONCLUSIONS
Thyroid and β-cells dysfunctions are common in TM patients with frequent blood transfusions. In addition, hepcidin and TSH levels can be predicted significantly using the most correlated factors with hepcidin. These factors, including ferritin, insulin and TSH were used to construct predicting equations: S. Hepcidin = 0.003*Ferritin + 3.02*TSH + 0.12*Insulin + 16.85 (± 7.78) and TSH = 0.0083 × Insulin + 0.0042 × Ferritin + 0.0937 × Hepcidin + 1.91 (± 1.373).
Department of Chemistry, College of Science, Kufa University, Iraq.
Hussein K
HK
Al-Hakeim
Department of Chemistry, College of Science, Kufa University, Iraq.
Manal M
MM
Al-Khakani
Department of Internal Medicine, College of Medicine, Kufa University, Iraq.
Mahmood A
MA
Al-Kindi
D015415:Biomarkers / Q000097:blood; D002452:Cell Count; D002648:Child; D002675:Child, Preschool; D005260:Female; D005293:Ferritins / Q000097:blood / Q000235:genetics; D015870:Gene Expression; D064451:Hepcidins / Q000097:blood* / Q000235:genetics; D006801:Humans; D007328:Insulin / Q000097:blood* / Q000235:genetics; D007333:Insulin Resistance; D050417:Insulin-Secreting Cells / Q000378:metabolism / Q000473:pathology; D007501:Iron / Q000097:blood; D019190:Iron Overload / Q000097:blood* / Q000209:etiology / Q000503:physiopathology; D008297:Male; D013961:Thyroid Gland / Q000378:metabolism / Q000503:physiopathology; D013972:Thyrotropin / Q000097:blood / Q000235:genetics; D013974:Thyroxine / Q000097:blood / Q000235:genetics; D065227:Transfusion Reaction; D017086:beta-Thalassemia / Q000097:blood* / Q000235:genetics / Q000503:physiopathology / Q000628:therapy
D015415:Biomarkers; D064451:Hepcidins; D007328:Insulin; D013972:Thyrotropin; D005293:Ferritins; D007501:Iron; D013974:Thyroxine