McGregor A M, Petersen M M, Capiferri R, Evered D C, Smith B R, Hall R
Clin Endocrinol (Oxf). 1979 Oct;11(4):437-44. doi: 10.1111/j.1365-2265.1979.tb03095.x.
We have studied the effects of 131I therapy on thyrotrophin binding inhibiting immunoglobulins (TBII) in fifty-five patients with Graves' disease and five patients with toxic multinodular goitre (MNG). A group of forty patients with Graves' disease and four patients with toxic MNG were treated with drugs and acted as controls. In 78% of patients treated with 131I there was a marked increase in the serum TBII activity during the 3 months following therapy, whereas drug-treated patient showed a decrease (77%) or no change in TBII activity over the same period. TBII activity was not detectable in patients with toxic MNG before or after drug or 131I therapy. Consideration of the mechanisms involved in the changes in serum TBII activity after 131I treatment or during drug treatment provide insight into the basic defects responsible for the development of hyperthyroid Graves' disease and suggest that both the thyroid and immune system are involved.
我们研究了131I治疗对55例格雷夫斯病患者和5例毒性多结节性甲状腺肿(MNG)患者促甲状腺素结合抑制性免疫球蛋白(TBII)的影响。一组40例格雷夫斯病患者和4例毒性MNG患者接受药物治疗并作为对照。接受131I治疗的患者中,78%在治疗后的3个月内血清TBII活性显著增加,而接受药物治疗的患者在同一时期TBII活性下降(77%)或无变化。在药物治疗或131I治疗前后,毒性MNG患者均未检测到TBII活性。对131I治疗后或药物治疗期间血清TBII活性变化所涉及机制的考虑,有助于深入了解导致甲状腺功能亢进格雷夫斯病发生的基本缺陷,并提示甲状腺和免疫系统均参与其中。