Takasu N, Yamada T, Takasu M, Komiya I, Nagasawa Y, Asawa T, Shinoda T, Aizawa T, Koizumi Y
Department of Gerontology, Endocrinology, and Metabolism, Shinshu University School of Medicine, Japan.
N Engl J Med. 1992 Feb 20;326(8):513-8. doi: 10.1056/NEJM199202203260803.
Hypothyroidism may result from the production of antibodies that block the actions of thyrotropin. How often these thyrotropin-blocking antibodies are a cause of hypothyroidism and whether their production may cease, causing hypothyroidism to disappear, have not been extensively studied.
We determined the frequency with which thyrotropin-blocking antibodies were present in 172 hypothyroid patients with goitrous autoimmune thyroiditis (Hashimoto's disease) and 64 hypothyroid patients with atrophic autoimmune thyroiditis (idiopathic primary hypothyroidism). For 6 to 11 years we then followed 21 of these patients who were found to have thyrotropin-blocking antibodies. They received levothyroxine therapy for 3.5 to 8 years, after which it was discontinued. At frequent intervals during this time we measured the patients' serum concentrations of thyroxine, triiodothyronine, thyrotropin, and thyrotropin-blocking antibodies (measured as immunoglobulins that inhibit thyrotropin binding and immunoglobulins that inhibit thyrotropin bioactivity).
Thyrotropin-blocking antibodies were detected in 9 percent of the patients with goitrous autoimmune thyroiditis and in 25 percent of those with atrophic autoimmune thyroiditis. Among the 21 patients studied serially while receiving levothyroxine, thyrotropin-blocking antibodies disappeared in 15 (group 1), 7 of whom had goiter initially, and persisted in 6 (group 2), none of whom had goiter initially. Levothyroxine therapy was subsequently discontinued in these 21 patients. Six of those in group 1 (four with goiter) remained euthyroid (mean follow-up after discontinuation of therapy, 2.1 years), and nine became hypothyroid again within 3 months. All six patients in group 2 remained hypothyroid.
Hypothyroidism in some patients with autoimmune thyroiditis may be due to thyrotropin-blocking antibodies. The production of thyrotropin-blocking antibodies may subside, producing remissions of hypothyroidism. Chronic autoimmune thyroiditis may therefore cause transient as well as permanent hypothyroidism.
甲状腺功能减退可能是由于产生了阻断促甲状腺激素作用的抗体所致。这些促甲状腺激素阻断抗体导致甲状腺功能减退的频率以及它们的产生是否可能停止从而使甲状腺功能减退消失，尚未得到广泛研究。
我们测定了172例患有甲状腺肿性自身免疫性甲状腺炎（桥本氏病）的甲状腺功能减退患者和64例患有萎缩性自身免疫性甲状腺炎（特发性原发性甲状腺功能减退）的甲状腺功能减退患者中促甲状腺激素阻断抗体的存在频率。然后，我们对其中21例被发现有促甲状腺激素阻断抗体的患者进行了6至11年的随访。他们接受左甲状腺素治疗3.5至8年，之后停药。在此期间，我们定期测量患者血清中的甲状腺素、三碘甲状腺原氨酸、促甲状腺激素以及促甲状腺激素阻断抗体（以抑制促甲状腺激素结合的免疫球蛋白和抑制促甲状腺激素生物活性的免疫球蛋白来衡量）。
在患有甲状腺肿性自身免疫性甲状腺炎的患者中，9%检测到促甲状腺激素阻断抗体；在患有萎缩性自身免疫性甲状腺炎的患者中，25%检测到该抗体。在接受左甲状腺素治疗期间接受连续研究的21例患者中，15例（第1组）的促甲状腺激素阻断抗体消失，其中7例最初有甲状腺肿；6例（第2组）的抗体持续存在，这些患者最初均无甲状腺肿。随后这21例患者停用左甲状腺素治疗。第1组中的6例（4例有甲状腺肿）仍保持甲状腺功能正常（停药后平均随访2.1年），9例在3个月内再次出现甲状腺功能减退。第2组的所有6例患者仍为甲状腺功能减退。
一些自身免疫性甲状腺炎患者的甲状腺功能减退可能是由于促甲状腺激素阻断抗体所致。促甲状腺激素阻断抗体的产生可能会消退，从而使甲状腺功能减退得到缓解。因此，慢性自身免疫性甲状腺炎可能导致暂时性以及永久性甲状腺功能减退。
