Organ-Specific Autoimmune Disease, That Eventually Leads To Hypothyroidism

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Description

Hashimoto's thyroiditis and Graves’ disease are autoimmune diseases of the thyroid gland, and both diseases are diagnosed with ultrasound findings and autoantibody height. However, ultrasound (US) findings may be normal in both diseases rarely. In some pediatric studies, it was reported that shear wave velocity values in autoimmune thyroiditis were significantly higher than normal thyroid parenchyma and it was recommended to be used as a diagnostic method. Our study will address the evaluation of patients with Hashimoto's thyroiditis and Graves’ disease by thyroid elastography and the role of this method in diagnosis. The synchronous development of a medullary and papillary carcinoma as two different tumors has only been reported very rarely. The aim of the current report is to describe an extremely rare occurrence of medullary carcinoma, papillary microcarcinoma, and Hashimoto thyroiditis.

Cell destruction in Hashimoto's thyroiditis (HT) involves autoantibodies and cytotoxic T lymphocytes. Thyrocytes maintenance occurs by pro-apoptotic, anti-apoptotic and cell proliferation balance. Left ventricular noncompaction (LVNC) is a structural abnormality of the left ventricular myocardium of unknown cause. Cardiovascular system involvement is an important manifestation in juvenile systemic lupus erythematosus (jSLE) and is a leading cause of morbidity and mortality. Hashimoto’s thyroiditis (HT) is an organ-specific autoimmune disease that eventually leads to hypothyroidism. XBP1s is an endoplasmic reticulum stress related protein and participates in the pathogenesis of several diseases. Nevertheless, the potential role of XBP1s in amiodarone (AMIO)-treated HT patients remains unknown. In this study, AMIO aggravated the endoplasmic reticulum stress responses in HT patients and thyroid epithelial follicular cells. Moreover, MTT assay and flow cytometer analysis revealed that knockdown of XBP1s suppressed AMIO-induced thyroid epithelial follicular cells apoptosis. Mechanically, the Chromatin Immunoprecipitation (ChIP) and luciferase activity assay proved that XBP1s enhanced LINC00842 expression in HT patients and thyroid epithelial follicular cells via binding to LINC00842 promoter. LINC00842 functioned as a miR-214 sponge in HT patients and thyroid epithelial follicular cells. Besides, LINC00842 up-regulated Fas ligand (FASL) expression via inhibition of miR-214. In rescue experiments, overexpression of FASL reversed shXBP1s-induced suppression of cell apoptosis in AMIO-treated thyroid epithelial follicular cells. These findings concluded that AMIO-drove XBP1s aggravated endoplasmic reticulum stress and apoptosis in HT via modulating LINC00842/miR-214/FASL axis, providing a new sight for the therapeutic strategy of AMIO-induced HT.

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With Regards
Merssy

Journal Coordinator
Journal of Reproductive Endocrinology & Infertility