地方性多结节性甲状腺肿冷结节的慢性碘超载和细胞凋亡。

M V El May, S Zekri, S Boubaker, A Ladgham, A El May
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引用次数: 0

摘要

由于已知细胞凋亡和坏死存在于实验性甲状腺肿的发展和复发过程中,我们对10例突尼斯多结节地方性甲状腺肿进行了研究,其中5例在6个月内接受了慢性过量碘治疗。苏木精-伊红染色半薄切片上可见凋亡甲状腺细胞核。利用免疫过氧化物酶对石蜡切片检测bcl-2和bax的免疫反应,计数CD34阳性微血管;超薄切片也被观察到。碘超载6个月后,凋亡的甲状腺细胞数量增加了10倍;CD34阳性内皮细胞减少一半,甲状腺细胞bcl-2免疫反应性消失,甲状腺滤泡和内皮细胞bcl-2免疫反应性减弱。电镜下可见大量凋亡的滤泡细胞和内皮细胞。慢性碘过量诱导甲状腺滤泡和内皮细胞凋亡和坏死,导致结缔组织中甲状腺球蛋白积聚。
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Chronic iodine overload and apoptosis in cold nodules from endemic multinodular goiters.

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.

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