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Published on: December 27, 2016
Value of Apoptotic, Antiapoptotic, and Cell Proliferation Markers in the Treatment of Graves' Disease
Jessica Castro de Vasconcelos1, Icléia Siqueira Barreto2, Patrícia Sabino Matos2
1Endocrinology Division, Department of Internal Medicine, University of Campinas, Campinas, SP, Brazil.
Abstract:
To better understand the genesis of autoimmunity in Graves' disease (GD), it is essential to study the mechanism of apoptosis and cell proliferation in thyroid cells and intrathyroidal lymphocytic infiltrate of GD patients. Methods. A cross sectional, observational study performed by evaluating histopathological samples of thyroidectomy products from GD patients using immunohistochemistry. New histological sections were prepared for immunohistochemical analysis with markers of cell proliferation, antiproliferation, apoptosis, and antiapoptosis. Results. Patients with GD who underwent radioiodine therapy (RIT) had a lower lymphocytic expression level of p27Kip1, and those who took beta-blockers had higher expression levels of BID (BH3-interacting domain) and a lower Ki-67 expression level in thyrocytes than those who did not. The association of a shorter diagnostic time with a lower expression level of MCL-1 in thyroid cells suggests that the hyperthyroid state was related to a lower antiapoptotic effect on thyrocytes. In comparison to patients with GD not using antithyroid drugs (ATD), we found a lower expression level of BID in lymphocytes for those who used ATD. Conclusion. In GD, the hyperthyroid state was associated with a lower antiapoptotic effect on thyroid cells. RIT, beta-blockers, and thionamide act by stimulating apoptosis of thyrocytes by intrathyroidal lymphocytes.
Insights
Graves' disease involves reduced apoptosis in thyroid cells. Treatments like radioiodine therapy and beta-blockers may enhance this apoptosis, offering insights into managing autoimmune thyroid disease.
Area of Science:
- Endocrinology
- Immunology
- Cell Biology
Background:
- Graves' disease (GD) pathogenesis involves complex interactions between thyroid cells and immune cells.
- Understanding apoptosis and cell proliferation is crucial for elucidating GD autoimmunity.
- Thyroid cell and intrathyroidal lymphocyte dynamics in GD require further investigation.
Purpose of the Study:
- To investigate the mechanisms of apoptosis and cell proliferation in Graves' disease.
- To analyze the expression of key proteins related to cell cycle and apoptosis in thyroid and immune cells of GD patients.
Main Methods:
- Cross-sectional, observational study utilizing immunohistochemistry on thyroidectomy samples from GD patients.
- Evaluation of markers for cell proliferation (Ki-67), antiproliferation (p27Kip1), apoptosis (BID), and antiapoptosis (MCL-1).
Main Results:
- Radioiodine therapy (RIT) correlated with lower lymphocytic p27Kip1 levels.
- Beta-blocker use was associated with higher BID and lower thyrocyte Ki-67 expression.
- Shorter diagnostic time linked to lower MCL-1 in thyroid cells, suggesting reduced antiapoptotic effect in hyperthyroidism.
- Antithyroid drug (ATD) users showed lower lymphocytic BID expression compared to non-users.
Conclusions:
- The hyperthyroid state in Graves' disease is associated with decreased antiapoptotic effects on thyroid cells.
- Radioiodine therapy, beta-blockers, and thionamides appear to promote thyrocyte apoptosis mediated by intrathyroidal lymphocytes.
Related Concept Videos
01:28Graves' Disease I: Introduction
01:24Graves Disease II: Pathophysiology