Mohammad Hossein Feiz Haddad
Ahvaz Jundishapur University of Medical Sciences, Iran
Title: Effects of toxoplasmosis on thyroid hormones in diabetic patients
Biography
Biography: Mohammad Hossein Feiz Haddad
Abstract
Background: Evidence suggests the involvement of autoimmune mechanisms in pathogenesis of diabetes mellitus and thyroid gland dysfunction. The role of Toxoplasma gondii in diabetes and autoimmune diseases has been separately discussed. In this regard, the present study aimed to evaluate the effects of Toxoplasmosis on thyroid hormones in diabetic patients.
Material & Methods: In this cross-sectional and descriptive study 582 patients, referred to Endocrine and Diabetes Clinics, were enrolled in the study by an endocrinologist. Thyroperoxidase antibodies (TPOAb), Serum thyroid stimulating hormone (TSH), and free thyroxine (FT4 & FT3) were assessed to detect Toxoplasma status by the anti-Toxoplasma IgG and IgM enzyme-linked immunosorbent assay (ELISA). The collected data were analyzed using SPSS version 20.
Results: Generally, 21.7% of the subjects were positive for Toxoplasma infection and 15.3% were indicated for TPOAb. Subjects with toxoplasma infection showed a higher TPOAb than negative subjects (p=0.005), and there was a positive association between the index of anti-Toxoplasma IgG antibodies (p=0.033) and FT4, FT3, and it was seen even more stronger in TPOAb-positive Toxoplasma-positive subjects, (p=0.014). Totally, anti- Toxoplasma gondii IgG immunoglobulin showed the highest mean in subjects. The mean and standard deviation of anti- Toxoplasma gondii IgG and IgM in diabetic patients with and without thyroid dysfunction showed a significant difference (p<0.05). Furthermore, the proportion of patients with acute and chronic Toxoplasma gondii infection was significantly different in diabetic patients with and without thyroid disorders (p=0.005). The highest correlation was observed between anti- Toxoplasma gondii IgG and IgM antibodies and TPOAb and TSH test.
Conclusion: The results thus indicated that toxoplasmosis as such might have a stimulatory compact on thyroid gland hormone production in diabetic patients. We presume that an initial shift of Th1 to Th2 immune reactions arises in diabetic subjects which may initiate a recrudescence for Toxoplasma infection, because under regular circumstances, Toxoplasma infection is mostly controlled through Th1 immune cells. The parasite in this alteration could probably have a limited capability to escape from immune responses and subsequently there is autoimmune mechanisms activation to progress the release of thyroid hormones. Meanwhile, the role of NK cells should be considered in the interaction between thyroid autoimmunity and Toxoplasma infection due to their capacity in parasite replication restraint and parasite clearance by a robust IFN-c-mediated effect. Therefore, the NK cell deficiency in autoimmune thyroiditis could led to a higher risk of recrudescence of T. gondii infection in diabetic patients. The results of this study showed that Toxoplasma was associated with the increase of thyroid hormones and enhance the risk of thyroid problems in diabetes subjects; so, screening tests are recommended for detecting of toxoplasmosis in diabetic patients with thyroid disorders to provide new indications for preventive measures in the triad pathogenesis complex.