贵州医科大学学报

1982, (02) 84-100

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缺碘性甲状腺肿演化过程的实验研究
EXPERIMENTAL STUDIES OF THE EVOLUTION OF IODINE-DEFICIENCY GOITER (Abstract)

曹序茂;刘家骝;
Postgraduate of Pathology: Cao Xumao Advisor: Associate Professor Liu Jialiu

摘要(Abstract):

<正> 地方甲状腺肿是一种分布广泛,发病率高,危害很大的地方病。此病除在少数海滨地区及某些病区是由高碘及致甲状腺肿物质引起外,主要的原因是缺碘。这一点巳由大量流行病学资料所证实。虽然地方甲状腺肿的病因比较明确,但病变发生和演化过程目前仍不十分清楚。目前国外多用人工配制的低碘饮食在实验动物中复制甲状腺肿的模型,来研究甲状腺肿的发生、发展过程及发病机制。国内有关甲状腺肿病变发展的资料,主要是来自手术标本的病理检查,实验研究的报告不多。于志恒及李彦等分别用地方
Although low dietary supply of iodine has been known as a main etiologic factor in the development of endemic goiter, the evolution and pathogenesis of iodine-deficincy goiter are not yet clearly understood. In order to make a further study on this problem, the author has performed experiments in rats. Wistar rats of both sexes, weighing 110-170 g initially before beginning the experiments, were fed a low-iodine diet (LID) containing 20-45 ng of iodine per g and deionized water. Control animals were on the same diet with 0.3 μg/ml of KI added to the drinking water. After feeding the LID for 17 days, the thyroid showed marked conges- tion and early hyperplastic changes microscopically though not increased in size and weight. The Serum T_4 was within the normal range. The anterior pituitary exhibited hypertrophy and hyperplasia of thyrotrophs. The early hyperplastic changes of the thyroid represented a compensatory response of the thyroid to the need for more thyroid hormone, resulted from an increased TSH stimulation by a feed-back ~nechanism. The increased TSH secretion might be indicated indirectly by hypertrophy and hyperplasia of thyrotrophs. On the 35th day and 97th day of fhe L!D feeding, the thyroid was markedly enlarged and showed a typical microscopic pattern of hyperplastic goiter with an enhancement of tbs epithelial peroxidase activity. The Serum T4 concentration was decreased. Hypertophy and hyperplasia of thyrotrophs were still seen in t~ anterior pituitary. To study the pathogenesis of colloid goiter, experimental animals fed fhe LIE for 97 days were divided again into 3 subgroups and each was given one of the following regimens respectively for a further 30 days. ( 1 ) LID with 0.$ /tg of KI added to each mi of drinking water (iodine-sufficient diet) , (2) LID for 7 days alternated with iodine-sufficient diet for 2 days (cyclic diet) ~ (3) LID. In the animals refed the iodine-sufficient diet, colloid goiter was produced. The average thyroid weight was 1.6 times that of control animals and show- ed under microscope primarily eolloid-fillec[ PAS-positive follicles with lining cells reverted fro u the hyperplastic appearance to a relatively flat appearance. There were a few slightly hyperplastic areas scattered throughout the gland. The vascularity of the gland was much less than that seen in the rats fed the LID persistently. The peroxidase activity had already decereased. The serum T_4 had reverted to normal. Hypertrophy and hyperplasia of pituitary thyrotro- phs disappeared. These findings suggested that feeding the iodine sufficient diet would supply enough raw material to enable the rats make sufficient thyroid hormone to suppress the TSH production. The above data might demonstrate that the most important etiologic factor in the production of colloid goiter was a reduction of TSH stimulation of a thyroid previously kept hyperplastic for a prolonged period. In the animals fed the cyclic diet on the basis of "Mariae's cycle", a typical colloid goiter was also produced. The average thyroid weight was 1.7 times that of control rats. The histologic feature of thyroid :was similar to that prod uced by refeeding the iodine-sufficient diet. The serum T_4 level was still lower than normal. Hypertrophy and hyperplasia of thyrotrophs had disappeared. These above findings suggested that a hyperplastic thyroid was involuting to a colloid goiter state. It is worthy to note that in the rats fed the LID persistently for 127 days, the thyroid showed also a tendency to develop into colloid goiter on the basis of hyperplastic lesion. Some of the follicles did not remain continually in a state of hyperlasia but underwent involution, tending to enlarge and to reacc- umulate colloid. At the same time, the serum T_4 concentration was still lowe- red, the increment of the pituitary weight was remarkable and hypertrophy and hyperplasia of thyrotrophs had still been present. These data showed that under a prolonged severe iodine-deficiency condition, despite the presence of an enhan- ced TSH stimulation, colloid goiter might gradually develop from a hyperplastic thyroid due to decreased reactivity of the follicular epithelia to the TSH stimu- lation.

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作者(Author): 曹序茂;刘家骝;
Postgraduate of Pathology: Cao Xumao Advisor: Associate Professor Liu Jialiu

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