Wenzel K W, Lente J R
J Endocrinol Invest. 1983 Oct;6(5):389-94. doi: 10.1007/BF03347623.
Among 48 Graves' patients treated with antithyroid drugs there were 8 patients with a further growth of an already enlarged goiter and a persistence of thyroid stimulating immunoglobulins (TSI). TSI activity did not persist in a comparison group of patients with less severe initial symptoms and an uncomplicated course during a similar regimen of drug treatment. Thyrotoxicosis was difficult to control in this subgroup of patients as low serum T4 was accompanied by borderline high T3 levels although TSH in serum remained undetectable. In spite of comparable low doses of antithyroid drugs serum T4 in the complicated group remained significantly lower (58 +/= 15 nmol/I SD vs. 97 +/- 19 nmol/I SD, p less than 0,001) and serum T3 stayed significantly higher (3,66 +/- 0,49 nmol/I SD vs. 2,15 +/- 0,50 nmol/I SD, p less than 0,001) than in the group with uncomplicated treatment. It is discussed that the promotion of goiter growth could be due to growth stimulating antibodies, and that a local intrathyroidal iodide depletion during antithyroid drug treatment might cause the shift from T4 to T3 production in this entity of Graves' patients.
在48例接受抗甲状腺药物治疗的格雷夫斯病患者中,有8例患者已增大的甲状腺肿进一步增大,且甲状腺刺激免疫球蛋白(TSI)持续存在。在药物治疗方案相似的情况下,初始症状较轻且病程无并发症的患者对照组中,TSI活性并未持续存在。在该亚组患者中,甲状腺毒症难以控制,因为尽管血清促甲状腺激素(TSH)仍无法检测到,但血清总甲状腺素(T4)水平较低,而三碘甲状腺原氨酸(T3)水平处于临界高水平。尽管抗甲状腺药物剂量相当,但复杂组的血清T4仍显著低于对照组(58±15nmol/L标准差 vs. 97±19nmol/L标准差,p<0.001),血清T3显著高于对照组(3.66±0.49nmol/L标准差 vs. 2.15±0.50nmol/L标准差,p<0.001)。讨论认为,甲状腺肿生长的促进可能归因于生长刺激抗体,并且在抗甲状腺药物治疗期间甲状腺内碘的局部消耗可能导致该格雷夫斯病患者群体中甲状腺激素从T4向T3生成的转变。