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Thyroid atrophy in myxedematous endemic cretinism: possible role for growth-blocking immunoglobulins.

作者信息

Tsuboi K, Lima N, Ingbar S H, Medeiros-Neto G

机构信息

Beth-Israel Hospital, Thorndike Laboratory, Harvard Medical School, Boston, MA.

出版信息

Autoimmunity. 1991;9(3):201-6. doi: 10.3109/08916939109007645.

Abstract

We have examined the ability of IgGs obtained from 8 endemic cretins to inhibit TSH-stimulated thyroid cell growth in culture. Clinical and laboratory evidence for hypothyroidism was present in six subjects; the two remaining patients had borderline low serum T4, normal T3 and exaggerated TSH response to TRH. In six patients 2 mg IgG exhibited an inhibitory effect in the cellular growth expressed by a diminished incorporation of 3H-thymidine into the DNA of TSH-stimulated FRTL-5 cells (range: 26-87% inhibition). Seven patients presented clinically with thyroid atrophy of relatively small thyroid enlargements for the degree of chronic iodine deficiency that was present in the area. The remaining subject had a large multinodular goiter and IgG purified from this patient had no inhibitory effect in the FRTL-5 cellular growth. A direct relationship was noted between the degree of thyroid growth inhibition (%) and the basal serum TSH concentration. We conclude that the presence of thyroid growth inhibiting immunoglobulin may be related to the absence of thyroid growth or even thyroid atrophy in endemic cretins.

摘要

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