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桥本病甲状腺功能正常患者的脑紊乱。

Brain disorders in euthyroid Hashimoto's thyroiditis patients.

机构信息

Department of Medical and Molecular Biology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia in Katowice, Jordana 19 Zabrze 41-800, Poland.

Division of Endocrinology, Department of Pathophysiology and Endocrinology, Silesian Medical University, Ceglana 35, Katowice 40-514, Poland.

出版信息

Clin Neurol Neurosurg. 2024 Oct;245:108519. doi: 10.1016/j.clineuro.2024.108519. Epub 2024 Aug 26.

Abstract

Hashimoto's thyroiditis (HT) is an autoimmune disorder characterized by the destruction of thyroid follicular cells by thyroid peroxidase antibodies (TPOAb) and thyroglobulin antibodies (TgAb), leading to hypothyroidism. Hashimoto's encephalopathy (HE) is associated with elevated levels of antithyroid antibodies. An important question is whether brain alterations precede the development of HE and are present in euthyroid patients with HT, and what pathomechanisms could be responsible for these changes. A PubMed search was conducted to identify studies addressing this issue. Numerous questionnaire studies confirmed impairments in cognitive functioning, mental and physical health, and overall well-being in euthyroid HT patients. Additionally, some imaging and mouse model studies indicate that euthyroid patients with HT likely have central nervous system alterations. Antibodies may be involved in the development of these changes. Some research suggests the role of TPOAb and TgAb, while other studies highlight the involvement of coexisting antibodies. Determining whether antibodies are assessed in serum or cerebrospinal fluid (CSF) is crucial. Antibody-specific indices (ASIs) can differentiate between antibodies passively diffusing from the serum and brain-derived antibodies, and could serve as biomarkers for brain alterations in HT patients. Much more research is needed to identify reliable biomarkers and treatments that could improve the quality of life for these patients.

摘要

桥本甲状腺炎(HT)是一种自身免疫性疾病,其特征是甲状腺过氧化物酶抗体(TPOAb)和甲状腺球蛋白抗体(TgAb)破坏甲状腺滤泡细胞,导致甲状腺功能减退。桥本脑病(HE)与抗甲状腺抗体水平升高有关。一个重要的问题是,脑改变是否先于 HE 的发生,以及在甲状腺功能正常的 HT 患者中是否存在,以及哪些病理机制可能导致这些变化。我们进行了 PubMed 检索,以确定解决这个问题的研究。许多问卷调查研究证实,甲状腺功能正常的 HT 患者在认知功能、心理和身体健康以及整体幸福感方面存在损害。此外,一些影像学和小鼠模型研究表明,甲状腺功能正常的 HT 患者可能存在中枢神经系统改变。抗体可能参与了这些变化的发生。一些研究表明 TPOAb 和 TgAb 起作用,而其他研究则强调了共存抗体的参与。确定抗体是在血清中还是脑脊液(CSF)中评估至关重要。抗体特异性指数(ASIs)可以区分被动从血清扩散的抗体和脑源性抗体,并可作为 HT 患者脑改变的生物标志物。需要进行更多的研究来确定可靠的生物标志物和治疗方法,以提高这些患者的生活质量。

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