摘要
我们对地方性克汀病(地克病)病人血清中 IgG 对甲低和甲状腺萎缩的病因发病学进行了研究。在新疆阿克苏地区检测了20例无甲状腺肿大的地克病病人,粘肿型8例,神经型5例,混合型7例,其中7例粘肿型,1例混合型病人血清中 TSH 水平增高,T_4降低(?)1例混合型病人高 TSH,而 T_4值在正常范围(亚临床甲低),其余病人为甲状腺功能正常或怀疑甲亢者。通过对病人血清 IgG 纯化后,按4mg/ml 在大鼠甲状腺细胞(FRTL-5)中抑制~3H-胸腺嘧啶核苷掺入DNA 的作用,测定甲状腺生长抑制免疫球蛋白(TGII),结果在上述9例病人血清中有6例(66.7%)TGII 阳性,其它各种类型的病人均为阴性。此外也测定了其它抑制生长的 IgG,如对IGF-I 抑制~3H-胸腺嘧啶核苷掺入 DNA 的作用。结果在上述9例病人中有5例(55.6%)有抑制胰岛素样生长因子 I 的(IGF-I blocking)IgG。上述结果指出,尽管血清中 TSH 水平升高,TGII 确是引起甲状腺萎缩的原因之一,同时抑制 IGF-I 诱发甲状腺生长的 IgG。
The role of circulating serum immunoglobulins (IgG) inhibiting the growth ofthyroid was evaluated in the etiology of hypothyroidism and thyroid atrophy in en-demic cretinism. Serum T_4, T_3 and TSH levels in twenty nongoitrous subjects wereexamined. 8 subjects were of myxedematous form, 7 mixed form, and 5 neurologicalform. They were born and living in iodine deficient areas Xinjiang, northwest of China.Anti-thyroid autoantibody titers were negative in all seram. Eight subjects hadhigh thyrotropin levels and low T_4 levels, one had high TSH and normal T_4 levels(subclinical hypothyroidism). Others were euthyroid or hyperthyroid.TGII that was measured as inhibitory effect of 4mg/ml IgG on TSH-induced^3H-thymidine incorporation into DNA of rat thyroid follicular cell line, FRTL_5 cellswas studied. Of the nine patients with primary hrpothyroidism, six (66.7%) hadTGII. None of the patients with other thyroid status had TGII. Other growth inhi-biting IgG that inhibits ~3H-thymidine incorporation into DNA stimulated by insu-lin-like growth factor-Ⅰ (IGFI), a growth factor that works through cAMP-inde-pendent pathway was measured. Five patients(55.6%)with hypothyroidism had IGFI-blocking IgG.The results indicated that TGII was a cause of atrophy of the thyroid in spiteof elevated serum TSH concentrations, and IgG which inhibited IGFI-induced thy-roid growth might play a role in thyroid atrophy in endemic cretins. An autoim-mune process might be involved in the pathogenesis of hypothyroidism secondary tothyroid atrophy, though severe iodine deficiency in a course of endemic cretin.
出处
《天津医药》
CAS
1990年第11期656-658,共3页
Tianjin Medical Journal
