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甲状腺功能亢进型格雷夫斯病患者干细胞因子水平升高。

An elevation of stem cell factor in patients with hyperthyroid Graves' disease.

作者信息

Yamada T, Sato A, Aizawa T, Ootsuka H, Miyahara Y, Sakai H, Terao A, Onuma S, Ito Y, Kanamori A, Nakamura Y, Tejima E

机构信息

Department of Medicine, Kashiwa City Hospital, Chiba, Japan.

出版信息

Thyroid. 1998 Jun;8(6):499-504. doi: 10.1089/thy.1998.8.499.

Abstract

Graves' disease is an autoimmune disorder characterized by the presence of antibodies against thyrotropin receptor (TRAb). Stem cell factor (SCF), derived from bone marrow, is known to promote lymphohematopoiesis. To investigate the relation between the alteration in plasma levels of SCF, thyroid hormone status, and TRAb measured by thyrotropin binding inhibition (TBI), 13 untreated, 21 treated, and 4 relapsed hyperthyroid Graves' disease patients, 21 patients with Hashimoto's thyroiditis, 6 patients with subacute thyroiditis, and 11 control subjects were examined. In untreated hyperthyroid Graves' disease patients, serum levels of thyroxine (T4) and triiodothyronine decreased rapidly by methimazole treatment, and TBI decreased progressively, but variably. Simultaneously, the elevated plasma levels of SCF decreased gradually and progressively. The plasma levels of SCF correlated curvilinearly with the serum levels of T4. In 4 patients with relapsed hyperthyroid Graves' disease, TBI was marginally positive in 3 patients and negative in 1, but plasma levels of SCF were elevated significantly in all 4 patients. In patients with subacute thyroiditis and Hashimoto's thyroiditis with or without T4 replacement, plasma levels of SCF did not differ from that of controls. These findings indicate that the elevation of plasma levels of SCF relates to the longstanding thyrotoxic state and that short-term thyrotoxicosis does not significantly affect plasma levels of SCF. It remains to be determined whether the elevation in plasma levels of SCF is induced by excess thyroid hormone, reflecting the hypermetabolic state, or whether the elevation of plasma levels of SCF contributes to stimulation of lymphocytes producing TRAb.

摘要

格雷夫斯病是一种自身免疫性疾病,其特征是存在抗促甲状腺素受体(TRAb)抗体。已知源自骨髓的干细胞因子(SCF)可促进淋巴细胞生成。为了研究通过促甲状腺素结合抑制(TBI)测量的SCF血浆水平变化、甲状腺激素状态和TRAb之间的关系,对13例未经治疗、21例接受治疗和4例复发的甲状腺功能亢进格雷夫斯病患者、21例桥本甲状腺炎患者、6例亚急性甲状腺炎患者和11名对照受试者进行了检查。在未经治疗的甲状腺功能亢进格雷夫斯病患者中,甲巯咪唑治疗使血清甲状腺素(T4)和三碘甲状腺原氨酸水平迅速下降,TBI逐渐下降,但存在差异。同时,升高的SCF血浆水平逐渐下降。SCF血浆水平与T4血清水平呈曲线相关。在4例复发的甲状腺功能亢进格雷夫斯病患者中,3例患者的TBI呈弱阳性,1例呈阴性,但所有4例患者的SCF血浆水平均显著升高。在亚急性甲状腺炎患者以及接受或未接受T4替代治疗的桥本甲状腺炎患者中,SCF血浆水平与对照组无差异。这些发现表明,SCF血浆水平升高与长期甲状腺毒症状态有关,而短期甲状腺毒症对SCF血浆水平无显著影响。尚有待确定SCF血浆水平升高是由过量甲状腺激素引起,反映高代谢状态,还是SCF血浆水平升高有助于刺激产生TRAb的淋巴细胞。

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