1. Chronic iodine overload and apoptosis in cold nodules from endemic multinodular goiters.
- Author
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El May MV, Zekri S, Boubaker S, Ladgham A, and El May A
- Subjects
- Antigens, CD34 analysis, Capillaries chemistry, Capillaries drug effects, Chronic Disease, Deficiency Diseases complications, Deficiency Diseases epidemiology, Deficiency Diseases prevention & control, Drug Administration Schedule, Genes, bcl-2, Goiter, Endemic epidemiology, Goiter, Endemic etiology, Goiter, Endemic surgery, Humans, Immunoenzyme Techniques, Iodides administration & dosage, Iodine deficiency, Necrosis, Preoperative Care, Thyroglobulin analysis, Tunisia epidemiology, bcl-2-Associated X Protein analysis, Apoptosis drug effects, Goiter, Endemic drug therapy, Goiter, Endemic pathology, Iodides poisoning
- Abstract
As apoptosis and necrosis are known to exist during experimental goiter development and involution, we studied them in ten Tunisian multinodular endemic goiters, five of them having received a chronic excess of iodine during six months. Apoptotic thyrocyte nuclei have been counted on hematoxylin-eosin stained semi-thin sections. Using immunoperoxidase on paraffin sections, bcl-2 and bax immunoreactivities have been evidenced, and CD34 positive microvessels counted; ultra-thin sections have also been observed. After six months of iodine overload, apoptotic thyrocytes were ten times more numerous; CD34 positive endothelial cells were diminished by one half bcl-2 immunoreactivity disappeared in thyrocytes and a bax one appeared in thyroid follicular and endothelial cells. Presence of numerous apoptotic follicular and endothelial cells was confirmed using electron microscopy. Chronic iodine excess induces apoptosis and necrosis of thyroid follicular and endothelial cells, leading to thyroglobulin accumulation in connective tissue.
- Published
- 2005