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ORIGINAL ARTICLE
Year : 2019  |  Volume : 31  |  Issue : 1  |  Page : 31-37

Serum macrophage migration inhibitory factor levels in Hashimoto’s thyroiditis


1 Department of Internal Medicine, Zagazig University, Zagazig, Egypt
2 Department of Clinical Pathology, Zagazig University, Zagazig, Egypt

Correspondence Address:
MN Ayman Abd Elrahman
Department of Internal Medicine, Zagazig University, Zagazig
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejim.ejim_64_18

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Background Hashimoto’s thyroiditis (HT) is the most common autoimmune thyroid disease. The actual mechanism by which the immunological factors lead to HT has remained obscure. Macrophage migration inhibitory factor (MIF) is recently recognized as a cytokine that has a broad range of inflammatory and immune effects. The aim of this study is to assess the role of MIF in the pathogenesis of HT. Patients and methods One hundred and twenty-nine patients were classified into three groups: (a) overt hypothyroidism, (b) subclinical hypothyroidism, and (c) the control group. A complete history taking, clinical examination, and laboratory investigations were done. Laboratory investigations included thyroid function tests [thyroid-stimulating hormone (TSH), triiodothyronine, and thyroxine], antithyroid antibodies (antithyroid peroxidase antibodies and thyroglobulin antibodies), and MIF level. Results There is highly statistically significant difference between the three groups regarding MIF, the highest level being in group 1>group 2>group 3. In both hypothyroid groups (1 and 2), there are statistically significant positive correlations between MIF with TSH, thyroid peroxidase antibodies, and thyroglobulin antibodies, but there is no statistically significant correlation between MIF with thyroid functions tests and antithyroid antibodies in the control group. Conclusion Serum MIF levels increased in overt and subclinical hypothyroidism and its levels were positively correlated to TSH and thyroid-specific autoantibodies. Serum MIF levels play a role in the pathogenesis of thyroid autoimmune responses in patients with HT. We recommend further larger studies to assess the MIF role in the prognosis of the HT and its treatment by a new strategy.


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