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格雷夫斯病及抗甲状腺药物治疗期间自然杀伤细胞活性降低。

Depressed natural killer activity in Graves' disease and during antithyroid medication.

作者信息

Wang P W, Luo S F, Huang B Y, Lin J D, Huang M J

机构信息

Department of Internal Medicine, Chang Gung Memorial Hospital, Taiwan, R.O.C.

出版信息

Clin Endocrinol (Oxf). 1988 Feb;28(2):205-14. doi: 10.1111/j.1365-2265.1988.tb03657.x.

Abstract

To investigate the natural killer (NK) cell mediated immunity in Graves' disease (GD) and the effect of antithyroid drugs upon NK cell activity, 51Cr release assay for NK cytotoxicity against K562 cells was examined in patients with GD before and during antithyroid medication and after drug withdrawal. Fifty-eight patients were divided into three groups: the untreated thyrotoxic patients (n = 33), the euthyroid patients under antithyroid treatment (n = 19) and the euthyroid patients after drug withdrawal (n = 6). The results of the three groups were compared to 23, 15 and 5 sex- and age-matched controls, respectively. The data revealed a significant NK dysfunction in the untreated hyperthyroid patients, although the number of the NK cells was not decreased. NK function was normal when patients were no longer taking antithyroid medication and in euthyroid state. However, euthyroid patients under antithyroid medication had markedly depressed NK activity, suggesting an immunosuppressive effect of the antithyroid drugs. This study demonstrated that both the hyperthyroid state and the antithyroid drugs exerted immunosuppressive effects upon the NK cells. Since such an immunosuppressive effect on NK cells might be associated with a decreased immune surveillance against tumour growth, this study implies that a long-term follow up of GD patients treated with antithyroid drugs may be indicated to guard against a possible increased incidence of malignancy.

摘要

为研究格雷夫斯病(GD)中自然杀伤(NK)细胞介导的免疫以及抗甲状腺药物对NK细胞活性的影响,我们检测了51例GD患者在抗甲状腺药物治疗前、治疗期间及停药后的NK细胞对K562细胞的细胞毒性,采用51Cr释放试验进行检测。58例患者分为三组:未经治疗的甲状腺毒症患者(n = 33)、接受抗甲状腺治疗的甲状腺功能正常患者(n = 19)和停药后的甲状腺功能正常患者(n = 6)。三组结果分别与23例、15例和5例性别及年龄匹配的对照组进行比较。数据显示,未经治疗的甲亢患者存在明显的NK细胞功能障碍,尽管NK细胞数量未减少。当患者不再服用抗甲状腺药物且处于甲状腺功能正常状态时,NK功能正常。然而,接受抗甲状腺治疗的甲状腺功能正常患者的NK活性明显降低,提示抗甲状腺药物具有免疫抑制作用。本研究表明,甲亢状态和抗甲状腺药物均对NK细胞产生免疫抑制作用。由于对NK细胞的这种免疫抑制作用可能与对肿瘤生长的免疫监视降低有关,本研究提示,可能需要对接受抗甲状腺药物治疗的GD患者进行长期随访,以预防恶性肿瘤发病率可能增加的情况。

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