卡比马唑与格雷夫斯病中的自身免疫反应。

Carbimazole and the autoimmune response in Graves' disease.

作者信息

McGregor A M, Petersen M M, McLachlan S M, Rooke P, Smith B R, Hall R

出版信息

N Engl J Med. 1980 Aug 7;303(6):302-7. doi: 10.1056/NEJM198008073030603.

DOI:10.1056/NEJM198008073030603

Abstract

Microsomal antibodies and antibodies directed toward the receptor for thyroid-stimulating hormone (TSH) decreased in parallel while patients with Graves' disease were taking carbimazole, whereas no significant changes were observed during treatment with placebo or propranolol. The changes in autoantibody levels during carbimazole treatment were independent of changes in serum thyroxine and could have been due to a direct effect of the drug on autoantibody synthesis. Evidence for this suggestion was provided when low doses of methimazole (the active metabolite of carbimazole) were found to inhibit thyroid-autoantibody production in cultured lymphocytes. Since thyroid lymphocytes are probably a major site of thyroid-antibody synthesis in Graves' disease and methimazole is concentrated in the thyroid during treatment, a local action of the drug on antibody production seems likely. This possibility could be important in the use of carbimazole to control hyperthyroidism.

摘要

在格雷夫斯病患者服用卡比马唑期间，微粒体抗体和针对促甲状腺激素（TSH）受体的抗体水平平行下降，而在服用安慰剂或普萘洛尔治疗期间未观察到显著变化。卡比马唑治疗期间自身抗体水平的变化与血清甲状腺素的变化无关，可能是药物对自身抗体合成的直接作用所致。当发现低剂量的甲巯咪唑（卡比马唑的活性代谢产物）可抑制培养淋巴细胞中甲状腺自身抗体的产生时，为这一推测提供了证据。由于甲状腺淋巴细胞可能是格雷夫斯病中甲状腺抗体合成的主要部位，且治疗期间甲巯咪唑在甲状腺中浓集，药物对抗体产生的局部作用似乎很可能存在。这种可能性在使用卡比马唑控制甲状腺功能亢进症方面可能很重要。