ArticleActa parasitologica2025
Impact of Experimental Congenital Toxoplasmosis on the Thyroid Gland: Histopathological and Immunobiochemical Indices Assessment.
Article in Acta parasitologica, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
purposeThe thyroid gland is one of the most vital endocrine organs. It is responsible for the synthesis and secretion of hormones principally triiodothyronine (T3) and thyroxine (T4). These hormones play a significant role in the functions and the metabolism of the body. The thyroid gland could be affected by several infections, among them Toxoplasma gondii. Congenital toxoplasmosis took place when the parasite reached the developing fetus and infected any nucleated cells within it. This study assessed the effect of experimental congenital toxoplasmosis on the thyroid gland structure and function.
methodsWe used 34 Wistar rats and allocated them into two groups: normal control group (17 rats) and congenital toxoplasmosis group (17 rats). After euthanasia, the brain and the thyroid gland was assessed through histopathological examination. Thyroid functions examination was performed through measuring the serum levels of T3, thyroxine T4, and thyroid stimulating hormone (TSH). Moreover, serum levels of thyroid antibodies [thyroid-peroxidase antibody (TPO-Ab) and anti-thyroglobulin (TG-Ab)] were examined.
resultsThe examination of thyroid tissues of the congenital toxoplasmosis group showed decreased or absent colloid secretion. About 47.1% of follicles showed degeneration with different grades. Parafollicular cells hyperplasia were observed in 23.6% of specimens. The serum concentrations of T3, T4, and TSH were significantly higher in congenital toxoplasmosis group than the control group. The congenital toxoplasmosis group had lower serum concentrations of TPO-Abs than the control group.
conclusionThese results indicated that congenital Toxoplasma infection could result in a central hyperthyroidism state with alteration of thyroid gland structure in offspring.
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