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系统性红斑狼疮患者伴有相关器官损害,发生甲状腺功能减退症的风险较高。

Systemic Lupus Erythematosus Patients With Related Organic Damage Are at High Risk of Hypothyroidism.

机构信息

Department of Endocrinology, Shandong Provincial Hospital, Shandong University, Jinan, China.

Department of the Health Management Center, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.

出版信息

Front Endocrinol (Lausanne). 2022 Jul 15;13:920283. doi: 10.3389/fendo.2022.920283. eCollection 2022.

DOI:10.3389/fendo.2022.920283
PMID:35909519
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9335194/
Abstract

PURPOSE

The aim of this study included determining the prevalence of hypothyroidism in patients with systemic lupus erythematosus (SLE), clarifying the clinical characteristics of SLE patients with hypothyroidism, and identifying the relationship between hypothyroidism and SLE-related organic damage. Another purpose was to analyze the relationship between SLE and thyroid autoantibody. We also intended to discuss the pathogenesis of hypothyroidism in SLE patients, which would provide clues for further investigation.

METHODS

This study recruited 856 SLE patients and 856 age- and sex-matched healthy population and compared the prevalence of hypothyroidism between the cases and controls. Univariate and multivariate logistic analyses were applied to identify risk factors for hypothyroidism in SLE patients.

RESULTS

SLE patients had higher prevalence of clinical hypothyroidism (9.10%) and TgAb+TPOAb- (10.40%) than controls. The prevalence of hypothyroidism was the highest in SLE patients aged 16-26 years (18.9%) and decreased with age. The prevalence of autoimmune hypothyroidism in SLE group was higher than that in the control group (64.4% vs. 51.5%, =0.042), which was mainly due to TgAb; the prevalence of non-autoimmune hypothyroidism in SLE group was also significantly higher than that in the control group (67.3% vs. 47.8%, <0.001). Based on multivariate analysis, the use of glucocorticoids/immunosuppressants, liver abnormality, lupus nephritis (LN), and cardiac insufficiency were independently associated with hypothyroidism in SLE patients.

CONCLUSION

The prevalence of hypothyroidism in SLE patients was higher than that in controls and decreased with age. The results suggested that young SLE patients combined with LN, liver abnormality and cardiac insufficiency were at higher risk of hypothyroidism. According to the results of this study, we speculated that SLE might have impact on thyroid, and SLE might be one of the causes of hypothyroidism.

摘要

目的

本研究旨在确定系统性红斑狼疮(SLE)患者中甲状腺功能减退症的患病率,阐明甲状腺功能减退症 SLE 患者的临床特征,并确定甲状腺功能减退症与 SLE 相关器官损害之间的关系。另一个目的是分析 SLE 与甲状腺自身抗体之间的关系。我们还旨在讨论 SLE 患者甲状腺功能减退症的发病机制,这将为进一步研究提供线索。

方法

本研究纳入了 856 例 SLE 患者和 856 名年龄和性别匹配的健康人群,并比较了病例组和对照组中甲状腺功能减退症的患病率。应用单因素和多因素 logistic 分析来确定 SLE 患者甲状腺功能减退症的危险因素。

结果

SLE 患者临床甲状腺功能减退症(9.10%)和 TgAb+TPOAb-(10.40%)的患病率高于对照组。16-26 岁 SLE 患者甲状腺功能减退症的患病率最高(18.9%),并随年龄降低。SLE 组自身免疫性甲状腺功能减退症的患病率高于对照组(64.4%比 51.5%,=0.042),这主要是由于 TgAb;SLE 组非自身免疫性甲状腺功能减退症的患病率也明显高于对照组(67.3%比 47.8%,<0.001)。基于多因素分析,使用糖皮质激素/免疫抑制剂、肝功能异常、狼疮肾炎(LN)和心功能不全与 SLE 患者甲状腺功能减退症独立相关。

结论

SLE 患者甲状腺功能减退症的患病率高于对照组,且随年龄降低。结果表明,伴有 LN、肝功能异常和心功能不全的年轻 SLE 患者发生甲状腺功能减退症的风险更高。根据本研究结果,我们推测 SLE 可能对甲状腺有影响,并且 SLE 可能是甲状腺功能减退症的原因之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/d946dcab3793/fendo-13-920283-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/9c1300323ac9/fendo-13-920283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/7fc775ea774f/fendo-13-920283-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/697f34dc2a38/fendo-13-920283-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/82ddf7551f87/fendo-13-920283-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/d946dcab3793/fendo-13-920283-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/9c1300323ac9/fendo-13-920283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/7fc775ea774f/fendo-13-920283-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/697f34dc2a38/fendo-13-920283-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/82ddf7551f87/fendo-13-920283-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2107/9335194/d946dcab3793/fendo-13-920283-g005.jpg

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