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Article(id=1241025212314080011, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241025201983508979, articleNumber=null, orderNo=null, doi=10.20043/j.cnki.MPM.202410074, pmid=null, cstr=null, oa=null, hot=null, price=null, onlineType=0, articleFormat=0, articleType=null, articleTypeStr=null, receivedDate=1728230400000, receivedDateStr=2024-10-07, revisedDate=null, revisedDateStr=null, acceptedDate=null, acceptedDateStr=null, onlineDate=1773813067749, onlineDateStr=2026-03-18, pubDate=1744214400000, pubDateStr=2025-04-10, doiRegisterDate=null, doiRegisterDateStr=null, onlineIssueDate=1773813067749, onlineIssueDateStr=2026-03-18, onlineJustAcceptDate=null, onlineJustAcceptDateStr=null, onlineFirstDate=null, onlineFirstDateStr=null, sourceXml=null, magXml=null, createTime=1773813067749, creator=13701087609, updateTime=1773813067749, updator=13701087609, issue=Issue{id=1241025201983508979, tenantId=1146029695717560320, journalId=1227665162245664772, year='2025', volume='52', issue='7', pageStart='1153', pageEnd='1344', issueExtLink='null', onlineDate='null', pubDate='null', beforeIssueId=null, nextIssueId=null, price=null, status=1, issueComplete=1, articleOrder=1, issueType=-1, specialIssue=null, createTime=1773813065285, creator=13701087609, updateTime=1773815493878, updator=13701087609, preIssue=null, nextIssue=null, ext={EN=IssueExt(id=1241035388320543403, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241025201983508979, language=EN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=), CN=IssueExt(id=1241035388320543404, tenantId=1146029695717560320, journalId=1227665162245664772, issueId=1241025201983508979, language=CN, specialIssueTitle=, coverIllustrator=null, specialIssueEditor=, specialIssueAbout=)}, issueFiles=null}, startPage=1335, endPage=1344, ext={EN=ArticleExt(id=1241025212607681322, articleId=1241025212314080011, tenantId=1146029695717560320, journalId=1227665162245664772, language=EN, title=Mendelian randomization analysis of Sjögren’s syndrome and thyroid diseases, columnId=1228016569138213037, journalTitle=Modern Preventive Medicine, columnName=Clinical Medicine and Prevention, runingTitle=null, highlight=null, articleAbstract=
Objective

To explore the potential causal relationship between Sjögren’s syndrome (SS) and thyroid diseases using a two-sample bidirectional Mendelian randomization (MR) approach.

Methods

Data were sourced from genome-wide association studies (GWAS), obtaining samples and single nucleotide polymorphisms (SNPs) related to SS and thyroid diseases, which included hyperthyroidism, hypothyroidism, goiter, Hashimoto thyroiditis (HT), Graves’ Disease (GD), and thyroid carcinoma (THCA). The inverse variance weighting (IVW) method was employed as the primary analysis approach, supplemented by the weighted median method (WME) and MR-Egger regression model for MR analysis, along with sensitivity analyses to ensure the robustness of results. The Bonferroni method was used to correct for multiple testing, with a correction threshold set at P=0.008(0.05/6), considering P-values between 0.008 and 0.05 as potentially relevant.

Results

Genetically predicted SS was found to have a positive causal relationship with the risk of hypothyroidism (IVW: OR=1.372, 95%CI: 1.124-1.674) and HT (IVW: OR=1.254, 95%CI: 1.142-1.377). SS was not associated with an increased or decreased risk of hyperthyroidism (IVW: OR=1.435,95%CI: 1.012-2.036), goiter (IVW: OR=0.933, 95%CI: 0.838-1.040), GD (MR-Egger: OR=4.094, 95%CI: 2.818-5.947), or THCA (IVW: OR=1.057, 95%CI: 0.866-1.29). Hyperthyroidism (IVW: OR=1.950, 95% CI: 0.776-1.163), hypothyroidism (IVW: OR=1.149, 95%CI: 0.93-1.42), goiter (IVW: OR=0.992, 95%CI: 0.85-1.157), HT (IVW: OR=1.532, 95%CI: 1.055-2.225), GD (IVW: OR=1.041, 95%CI: 0.728-1.488), and THCA (IVW: OR=0.987, 95%CI: 0.874-1.114) were not found to increase or decrease the risk of SS.

Conclusion

Genetically predicted SS is a risk factor for hypothyroidism and HT. There is no association between SS and the risk of hyperthyroidism, goiter, GD, or THCA.

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目的

采用两样本双向孟德尔随机化（Mendelian randomization，MR）方法探索干燥综合征（Sjögren syndrome，SS）与甲状腺疾病间的潜在因果关系。

方法

数据来自全基因组关联研究（genome-wide association studies，GWAS），获取SS及甲状腺疾病数据样本及单核苷酸多态性（aingle nucleotide polymorphism，SNP），甲状腺疾病包括甲状腺功能亢进、甲状腺功能减退、甲状腺肿（goiter）、桥本甲状腺炎（Hashimoto thyroiditis，HT）、毒性弥漫性甲状腺肿（Graves disease，GD）、甲状腺癌（thyroid carcinoma，THCA）。采用逆方差加权法（inverse variance weighting，IVW）为主要分析方法，补充加权中位数法（weighted median，WME）、MR-Egger回归模型进行MR分析，并进行敏感性分析以确保结果稳健性。采用Bonferroni法对多次检验的结果进行矫正，其校正标准为P=0.008（0.05/6），当P值在0.008和0.05之间时被认为是潜在相关。

结果

遗传预测的SS与甲状腺功能减退（IVW：OR=1.372，95%CI：1.124～1.674）和HT（IVW：OR=1.254，95%CI：1.142～1.377）的发病风险存在正向因果关系。SS不会增加或降低甲状腺功能亢进（IVW：OR=1.435，95%CI：1.012～2.036）、甲状腺肿（IVW：OR=0.933，95%CI：0.838～1.040）、GD（MR-Egger：OR=4.094，95%CI：2.818～5.947）、THCA（IVW：OR= 1.057，95%CI：0.866～1.29）的发病风险。甲状腺功能亢进（IVW：OR=1.950，95%CI：0.776～1.163）、甲状腺功能减退（IVW：OR=1.149，95%CI：0.93～1.42）、甲状腺肿（IVW：OR=0.992，95%CI：0.85～1.157）、HT（IVW：OR=1.532，95%CI：1.055～2.225）、GD（IVW：OR=1.041，95%CI：0.728～1.488）、THCA（IVW：OR=0.987，95%CI：0.874～1.114）不会增加或降低SS的发病风险。

结论

遗传预测SS是甲状腺功能减退、HT的危险因素。SS与甲状腺功能亢进、甲状腺肿、GD、THCA之间的发病风险没有关联。

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罗静，E-mail:；
陶庆文，E-mail:；
, copyrightStatement=本刊刊出的所有文章不代表中华预防医学会和本刊编委会的观点，除非特别声明。, copyrightOwner=中华预防医学会和四川大学华西公共卫生学院, extLink=null, articleAbsUrl=null, sourceXml=AHd/ttekWqHQYAn8nGrxrw==, magXml=ekTIavbN6pedO9Df1Gd/JA==, pdfUrl=null, pdf=geGYkBG/lO1kJrP0qu3kfg==, pdfFileSize=1407454, pdfExtLink=null, richHtmlUrl=null, mobilePdfUrl=null, reviewReport=null, pdfFirstPage=null, abstractGraph=K6Z4Mf4rs2e2VcCfRx2bfw==, abstractGraphContent=null, abstractVideo=null, citation=null, cebUrl=null, magXmlContent=5tbea0Y2r1gh9kKIE1LElg==, mapNumber=null, authorCompany=null, fund=null, authors=

罗静与陶庆文为共同通信作者

雷淳心（2000—），女，硕士在读，研究方向：风湿免疫学

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雷淳心（2000—），女，硕士在读，研究方向：风湿免疫学

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雷淳心（2000—），女，硕士在读，研究方向：风湿免疫学

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注：图A为正向研究中，设置暴露因素为与SS相关的SNP，甲状腺疾病作为结局；图B为反向研究中，设置暴露因素为与甲状腺疾病相关的SNP，SS作为结局。

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注：图A为甲状腺功能亢进对SS的MR分析散点图；图B为SS对甲状腺功能亢进的MR分析散点图；图C为甲状腺功能减退对SS的MR分析散点图；图D为SS对甲状腺功能减退的MR分析散点图；图E为甲状腺肿对SS的MR分析散点图；图F为SS对甲状腺肿的MR分析散点图；图G为HT对SS的MR分析散点图；图H为SS对HT的MR分析散点图；图I为GD对SS的MR分析散点图；图J为SS对GD的MR分析散点图；图K为THCA对SS的MR分析散点图；图L为SS对THCA的MR分析散点图。

, figureFileSmall=38EhpSbUqohTRLDb6KEtNQ==, figureFileBig=QEyqdPZUfCNiSvQ1h4GGYA==, tableContent=null), ArticleFig(id=1241025221965173082, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=EN, label=Figure 5, caption=Leave-one-out sensitivity analysis of the Mendelian randomization study on SS and thyroid diseases, figureFileSmall=evxMeMo1txCHs0ra/f/mYA==, figureFileBig=Pi21srSPjDIsf0Pw7YRsZg==, tableContent=null), ArticleFig(id=1241025223328321888, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=CN, label=图5, caption=“leave-one-out”敏感性分析结果

注：图A为甲状腺功能亢进对SS的MR留一分析；图B为SS对甲状腺功能亢进的MR留一分析；图C为甲状腺功能减退对SS的MR留一分析；图D为SS对甲状腺功能减退的MR留一分析；图E为甲状腺肿对SS的MR留一分析；图F为SS对甲状腺肿的MR留一分析；图G为HT对SS的MR留一分析；图H为SS对HT的MR留一分析；图I为GD对SS的MR留一分析；图J为SS对GD的MR留一分析；图K为THCA对SS的MR留一分析；图L为SS对THCA的MR留一分析。

, figureFileSmall=evxMeMo1txCHs0ra/f/mYA==, figureFileBig=Pi21srSPjDIsf0Pw7YRsZg==, tableContent=null), ArticleFig(id=1241025223420596578, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=EN, label=Table 1, caption=

Information of datasets in the MR study

, figureFileSmall=null, figureFileBig=null, tableContent=
暴露/结局数据集ID数据来源试验组（n）对照组（n）SNPs样本种族来源公布年份
甲状腺功能亢进ebi-a-GCST90018860MRC IEU Open GWAS3 557456 94224 189 279欧洲人2021
甲状腺功能减退ebi-a-GCST90018862MRC IEU Open GWAS30 155379 98624 138 872欧洲人2021
甲状腺炎ebi-a-GCST90018853MRC IEU Open GWAS2 711456 94224 190 615欧洲人2021
HTebi-a-GCST90018855MRC IEU Open GWAS15 654379 98624 146 037欧洲人2021
GDebi-a-GCST90018847MRC IEU Open GWAS1 678456 94224 189 816欧洲人2021
THCAebi-a-GCST90018929MRC IEU Open GWAS1 054490 92024 198 226欧洲人2021
SSfinn-b-M13_SJOGRENFINNGEN RESEARCH PROJECT1 290213 14516 380 454欧洲人2021
), ArticleFig(id=1241025223496094058, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=CN, label=表1, caption=

MR研究中的数据来源信息

, figureFileSmall=null, figureFileBig=null, tableContent=
暴露/结局数据集ID数据来源试验组（n）对照组（n）SNPs样本种族来源公布年份
甲状腺功能亢进ebi-a-GCST90018860MRC IEU Open GWAS3 557456 94224 189 279欧洲人2021
甲状腺功能减退ebi-a-GCST90018862MRC IEU Open GWAS30 155379 98624 138 872欧洲人2021
甲状腺炎ebi-a-GCST90018853MRC IEU Open GWAS2 711456 94224 190 615欧洲人2021
HTebi-a-GCST90018855MRC IEU Open GWAS15 654379 98624 146 037欧洲人2021
GDebi-a-GCST90018847MRC IEU Open GWAS1 678456 94224 189 816欧洲人2021
THCAebi-a-GCST90018929MRC IEU Open GWAS1 054490 92024 198 226欧洲人2021
SSfinn-b-M13_SJOGRENFINNGEN RESEARCH PROJECT1 290213 14516 380 454欧洲人2021
), ArticleFig(id=1241025223621923187, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=EN, label=Table 2, caption=

Heterogeneity and pleiotropy analysis

, figureFileSmall=null, figureFileBig=null, tableContent=
暴露因素结局因素异质性检验水平多效性检验
QP值截距P值
SS甲状腺功能亢进2.5150.113-0.2010.231
SS甲状腺功能减退25.3464.792×10-7*-0.0080.962
SS甲状腺肿0.5250.469-0.0400.530
SSHT2.2410.134-0.0380.516
SSGD5.5440.063-0.3800.031*
SSTHCA0.2530.615-0.0940.469
甲状腺功能亢进SS10.5000.162-0.0750.309
甲状腺功能减退SS2.2920.682-0.0590.421
甲状腺肿SS8.3690.9080.0830.016*
HTSS42.4104.336×10-7*0.0560.587
GDSS15.4940.001*-0.0440.763
THCASS0.1430.705-0.0870.417
), ArticleFig(id=1241025223710003572, tenantId=1146029695717560320, journalId=1227665162245664772, articleId=1241025212314080011, language=CN, label=表2, caption=

异质性检验及水平多效性检验

, figureFileSmall=null, figureFileBig=null, tableContent=
暴露因素结局因素异质性检验水平多效性检验
QP值截距P值
SS甲状腺功能亢进2.5150.113-0.2010.231
SS甲状腺功能减退25.3464.792×10-7*-0.0080.962
SS甲状腺肿0.5250.469-0.0400.530
SSHT2.2410.134-0.0380.516
SSGD5.5440.063-0.3800.031*
SSTHCA0.2530.615-0.0940.469
甲状腺功能亢进SS10.5000.162-0.0750.309
甲状腺功能减退SS2.2920.682-0.0590.421
甲状腺肿SS8.3690.9080.0830.016*
HTSS42.4104.336×10-7*0.0560.587
GDSS15.4940.001*-0.0440.763
THCASS0.1430.705-0.0870.417
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干燥综合征与甲状腺疾病的孟德尔随机化分析
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雷淳心 1 , 张燕 1 , 张曦亚 1 , 黄子玮 1 , 罗静 2 , 陶庆文 2
现代预防医学 | 临床与预防 2025,52(7): 1335-1344
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现代预防医学 | 临床与预防 2025, 52(7): 1335-1344
干燥综合征与甲状腺疾病的孟德尔随机化分析
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雷淳心1, 张燕1, 张曦亚1, 黄子玮1, 罗静2 , 陶庆文2
作者信息
  • 1.北京中医药大学研究生院，北京 100029
  • 2.中日友好医院中医风湿病科，免疫炎性疾病北京市重点实验室，北京 100029

    • 雷淳心（2000—），女，硕士在读，研究方向：风湿免疫学

通讯作者:

罗静，E-mail:；
陶庆文，E-mail:；
Mendelian randomization analysis of Sjögren’s syndrome and thyroid diseases
Chun-xin LEI1, Yan ZHANG1, Xi-ya ZHANG1, Zi-wei HUANG1, Jing LUO2 , Qing-wen TAO2
Affiliations
  • Graduate School of Beijing University of Chinese Medicine, Beijing, 100029, China
出版时间: 2025-04-10 doi: 10.20043/j.cnki.MPM.202410074
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摘要
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目的

采用两样本双向孟德尔随机化（Mendelian randomization，MR）方法探索干燥综合征（Sjögren syndrome，SS）与甲状腺疾病间的潜在因果关系。

方法

数据来自全基因组关联研究（genome-wide association studies，GWAS），获取SS及甲状腺疾病数据样本及单核苷酸多态性（aingle nucleotide polymorphism，SNP），甲状腺疾病包括甲状腺功能亢进、甲状腺功能减退、甲状腺肿（goiter）、桥本甲状腺炎（Hashimoto thyroiditis，HT）、毒性弥漫性甲状腺肿（Graves disease，GD）、甲状腺癌（thyroid carcinoma，THCA）。采用逆方差加权法（inverse variance weighting，IVW）为主要分析方法，补充加权中位数法（weighted median，WME）、MR-Egger回归模型进行MR分析，并进行敏感性分析以确保结果稳健性。采用Bonferroni法对多次检验的结果进行矫正，其校正标准为P=0.008（0.05/6），当P值在0.008和0.05之间时被认为是潜在相关。

结果

遗传预测的SS与甲状腺功能减退（IVW：OR=1.372，95%CI：1.124～1.674）和HT（IVW：OR=1.254，95%CI：1.142～1.377）的发病风险存在正向因果关系。SS不会增加或降低甲状腺功能亢进（IVW：OR=1.435，95%CI：1.012～2.036）、甲状腺肿（IVW：OR=0.933，95%CI：0.838～1.040）、GD（MR-Egger：OR=4.094，95%CI：2.818～5.947）、THCA（IVW：OR= 1.057，95%CI：0.866～1.29）的发病风险。甲状腺功能亢进（IVW：OR=1.950，95%CI：0.776～1.163）、甲状腺功能减退（IVW：OR=1.149，95%CI：0.93～1.42）、甲状腺肿（IVW：OR=0.992，95%CI：0.85～1.157）、HT（IVW：OR=1.532，95%CI：1.055～2.225）、GD（IVW：OR=1.041，95%CI：0.728～1.488）、THCA（IVW：OR=0.987，95%CI：0.874～1.114）不会增加或降低SS的发病风险。

结论

遗传预测SS是甲状腺功能减退、HT的危险因素。SS与甲状腺功能亢进、甲状腺肿、GD、THCA之间的发病风险没有关联。

干燥综合征  /  甲状腺疾病  /  孟德尔随机化分析  /  因果关系
Objective

To explore the potential causal relationship between Sjögren’s syndrome (SS) and thyroid diseases using a two-sample bidirectional Mendelian randomization (MR) approach.

Methods

Data were sourced from genome-wide association studies (GWAS), obtaining samples and single nucleotide polymorphisms (SNPs) related to SS and thyroid diseases, which included hyperthyroidism, hypothyroidism, goiter, Hashimoto thyroiditis (HT), Graves’ Disease (GD), and thyroid carcinoma (THCA). The inverse variance weighting (IVW) method was employed as the primary analysis approach, supplemented by the weighted median method (WME) and MR-Egger regression model for MR analysis, along with sensitivity analyses to ensure the robustness of results. The Bonferroni method was used to correct for multiple testing, with a correction threshold set at P=0.008(0.05/6), considering P-values between 0.008 and 0.05 as potentially relevant.

Results

Genetically predicted SS was found to have a positive causal relationship with the risk of hypothyroidism (IVW: OR=1.372, 95%CI: 1.124-1.674) and HT (IVW: OR=1.254, 95%CI: 1.142-1.377). SS was not associated with an increased or decreased risk of hyperthyroidism (IVW: OR=1.435,95%CI: 1.012-2.036), goiter (IVW: OR=0.933, 95%CI: 0.838-1.040), GD (MR-Egger: OR=4.094, 95%CI: 2.818-5.947), or THCA (IVW: OR=1.057, 95%CI: 0.866-1.29). Hyperthyroidism (IVW: OR=1.950, 95% CI: 0.776-1.163), hypothyroidism (IVW: OR=1.149, 95%CI: 0.93-1.42), goiter (IVW: OR=0.992, 95%CI: 0.85-1.157), HT (IVW: OR=1.532, 95%CI: 1.055-2.225), GD (IVW: OR=1.041, 95%CI: 0.728-1.488), and THCA (IVW: OR=0.987, 95%CI: 0.874-1.114) were not found to increase or decrease the risk of SS.

Conclusion

Genetically predicted SS is a risk factor for hypothyroidism and HT. There is no association between SS and the risk of hyperthyroidism, goiter, GD, or THCA.

Sjögren’s syndrome  /  Thyroid diseases  /  Mendelian randomization analysis  /  Causal relationship
雷淳心, 张燕, 张曦亚, 黄子玮, 罗静, 陶庆文. 干燥综合征与甲状腺疾病的孟德尔随机化分析. 现代预防医学, 2025 , 52 (7) : 1335 -1344 . DOI: 10.20043/j.cnki.MPM.202410074
Chun-xin LEI, Yan ZHANG, Xi-ya ZHANG, Zi-wei HUANG, Jing LUO, Qing-wen TAO. Mendelian randomization analysis of Sjögren’s syndrome and thyroid diseases[J]. Modern Preventive Medicine, 2025 , 52 (7) : 1335 -1344 . DOI: 10.20043/j.cnki.MPM.202410074
正文
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干燥综合征（Sjögren syndrome，SS）是一种以淋巴细胞浸润外分泌腺为特征的慢性炎症性自身免疫病，起病隐匿，以口干、眼干为主要临床表现，严重者可伴有血液、肺、肾等脏器受累[1]。流行病学调查显示，SS的世界发病率为0.5%～1.5%，其发病率在风湿病中仅次于类风湿关节炎[2]。近年来，SS与甲状腺疾病间的关系备受关注，临床常见SS患者存在甲状腺疾病。临床多个回顾性研究[3-6]亦提示，SS常合并甲状腺疾病，特别是自身免疫性甲状腺疾病（autoimmune thyroid diseases，AITD），包括毒性弥漫性甲状腺肿（Graves disease，GD）和桥本甲状腺炎（Hashimoto thyroiditis，HT）。AITD发病隐匿，主要病理特征为免疫系统失调介导的甲状腺实质淋巴细胞浸润，临床主要表现为甲状腺毒症与甲状腺功能减退[7]。SS和AITD均以淋巴细胞浸润为主要病理特点，但二者的关系尚不清楚。孟德尔随机化（Mendelian randomization， MR）研究是一种利用遗传变异作为工具变量来评估变量之间潜在因果关系的统计方法，被视为天然的随机对照试验，可较大程度的避免混杂因素及反向因果关系的影响[8]。因此，本研究采用两样本双向MR方法探索SS与甲状腺疾病间的潜在因果关系，为SS伴随甲状腺疾病的临床诊疗及二者间的关系研究提供参考。
1　资料与方法
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1.1　数据来源
本研究严格按照MR研究报告指南进行。采用两样本双向MR探索SS与甲状腺疾病之间发病风险的潜在因果关系。甲状腺疾病包括甲状腺功能亢进（hyperthyroidism）、甲状腺功能减退（hypothyroidism）、甲状腺肿（goiter）、HT、GD、甲状腺癌（thyroid carcinoma,THCA）。
甲状腺功能亢进（“ebi-a-GCST90018860”）、甲状腺功能减退（“ebi-a-GCST90029022”）、甲状腺肿（“ebi-a-GCST90018853”）、HT（“ebi-a-GCST90018855”）、GD（“ebi-a-GCST90018847”）、THCA（“ebi-a-GCST 90018929”）的遗传工具变量来自于欧洲生物信息中心（European Bioinformatics Institute，EBI），其全基因组关联研究（genome-wide association studies，GWAS）的汇总数据可在MRC IEU Open GWAS项目数据中找到。其中甲状腺亢进的GWAS研究包含了3 557例病例和456 942例对照；甲状腺功能减退的GWAS研究包含了30 155例病例和379 986例对照；甲状腺肿的GWAS研究包含了2 711例病例和456 942例对照；HT的GWAS研究包含了15 654例病例和379 986例对照；GD的GWAS研究包含了1 678例病例和456 942例对照；THCA的GWAS研究包含了1 054例病例和490 920例对照。
SS的汇总数据来自芬兰研究项目（FINNGEN RESEARCH PROJECT），这项GWAS研究包含了1 290例病例和213 145例对照。见表1。
1.2　研究设计
为了保证研究结果的可靠性，工具变量（instrumental variables，IVs)的选择需要符合MR研究的三个重要假设[9]，（1）相关性假设：所选择的IVs与暴露因素显著相关；（2）独立性假设：所选择的IVs与暴露和结局之间无混杂因素；（3）排他性假设：IVs仅通过暴露因素影响结局。见图1。
将SS作为暴露因素、甲状腺疾病作为结局事件的MR正向分析，严格筛选单核苷酸多态性（single nucleotide polymorphisms，SNP）作为IVs。提取暴露因素数据集中与暴露因素强相关的SNP（P<5×10-8）；设定阈值为r2<0.01和kb=10 000，以去除连锁不平衡（linkage disequilibrium，LD），从而保证获得与暴露因素独立的SNP；为了排除混杂因素影响，通过检索PhenoScannerV2网站（http://www.PhenoScanner.medschl.cam.ac.uk/），逐个排除与结局因素直接相关的SNP。此外，需去除回文序列以严格筛选用于最终因果分析的SNP。为了避免弱工具偏倚，剔除统计量F<10[10]的SNPs。N代表样本量，k为遗传变异的数量，MAF为次要等位基因频率（minor allele frequency），β为SNP对暴露的效应量，为β的标准误。统计量F值、遗传工具解释的暴露方差R2、标准差（standard deviation，SD）计算公式如下：
对于以甲状腺疾病作为暴露因素、SS作为结局的反向MR分析，IVs的选择方法与正向MR分析的方法相同。
1.3　MR分析
以逆方差加权法（inverse variance weighting，IVW）作为主要分析方法，补充加权中位数法（weighted median，WME）与MR-Egger回归模型评估SS与甲状腺疾病（甲状腺功能亢进、甲状腺功能减退、甲状腺肿、HT、GD、THCA）之间发病风险的潜在因果关系。IVW法是使用多个SNPs获得MR估计的最简单方法，其特点是回归时不用考虑截距，是两样本MR研究的标准估计方法。当IVs满足相关性假设、独立性假设及排他性假设时，IVW法在统计上最有效[11]，当结果存在异质性而无多效性时，应采用IVW随机效应模型。此外，以MR-Egger回归模型及WME法作为补充分析。MR-Egger回归模型中当IVs与结局的直接效应独立于IVs与暴露因素的关联效应时，计算暴露对结局的因果效应，故当结果具有多效性时，应采用MR-Egger回归模型[12]。WME法在50%以上的SNPs为有效工具变量时，可提供有效的因果估计。采用RStudio 2023.9.0.0中的“TwoSampleMR、MR-PRESSO”进行统计分析。使用比值比（odds ratio，OR）及95%可信区间（confidence interval，CI）描述SS与甲状腺疾病之间发病风险的潜在因果关联。采用Bonferroni法对多次检验的结果进行矫正，认为P<0.008（0.05/6）是校正后的显著性阈值，而P值在0.008和0.05之间的结果被认为是暗示关联。
1.4　敏感性分析
采用Cochrane Q检验评估异质性，利用IVW和MR-Egger回归模型检验MR分析结果是否存在异质性，当P<0.05时，提示存在异质性。MR-Egger-intercept可帮助判断是否存在水平多效性，当MR-Egger回归截距的P<0.05时，提示存在水平多效性，则MR分析的结果不可靠，需要使用孟德尔随机多态性残差和离群值（Mendelian randomization pleiotropy residual sum and outlier，MR-PRESSO）分析，将P<0.05的SNPs剔除后再次进行MR分析[13]。使用“留一法”对结果进行敏感性分析，以评估MR结果是否受单个SNP影响。
2　结果
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2.1　SS与甲状腺疾病的两样本双向MR分析
对甲状腺功能亢进、甲状腺功能减退、甲状腺肿、HT、GD、THCA与SS之间的MR分析，见图2、图3。
遗传预测的SS会增加甲状腺功能减退（IVW：OR=1.372，95%CI：1.124～1.674，P=0.002）、HT（IVW：OR=1.254，95%CI：1.142～1.377，P=2.023×10-6)的发病风险。没有证据表明SS会增加或降低甲状腺功能亢进（IVW：OR=1.435，95%CI：1.012～2.036，P=0.043）、甲状腺肿（IVW：OR=0.933，95%CI：0.838～1.040，P=0.210）、THCA(IVW：OR=1.057，95%CI：0.866～1.29，P=0.586)、GD（MR-Egger：OR=4.094，95%CI：2.818～5.947，P=0.018）的发病风险。
IVW结果说明，没有证据表明甲状腺功能亢进（OR=1.950，95%CI：0.776～1.163，P=0.621）、HT（OR=1.532，95%CI：1.055～2.225，P=0.025）、THCA（OR=0.987， 95%CI：0.874～1.114，P=0.830）、GD（OR=1.041，95%CI：0.728～1.488，P=0.827）会增加或降低SS的发病风险。IVW结果说明，甲状腺功能减退与SS之间存在水平多效性，使用MR-PRESSO分析离群值，将P<0.05的SNPs剔除（rs1794280、rs2160215、rs385863、 rs4338740、rs6131010）后再次进行MR分析，IVW法显示没有证据表明甲状腺功能减退会增加或降低SS的发病风险（OR=1.149，95%CI：0.93～1.42，P=0.198），补充MR-Egger回归模型及WM法分析二者间的因果效应，MR-Egger回归模型（OR=1.555，95%CI：0.776～3.116，P=0.281）及WME法（OR=1.11，95%CI：0.849～1.45，P=0.445）结果支持IVW结果。甲状腺肿作为暴露因素，SS作为结局因素时，二者间存在水平多效性，使用MR-PRESSO分析离群值，将P<0.05的SNPs剔除，结果显示无离群SNP，采用IVW法分析，提示没有证据表明甲状腺肿会增加或降低SS的发病风险（OR=0.992，95%CI：0.85～1.157，P=0.914）。
2.2　敏感性分析
基于MR-Egger法的Cochran Q检验分析结果是否存在异质性，采用MR-Egger回归模型截距项检验水平多样性，见表2。
经MR-PRESSO检测并分析离群值，在发现离群值后将其剔除并重新分析（剔除rs1794280、rs2160215、rs385863、rs4338740、rs6131010）。基于MR-Egger法的Cochran Q检验结果显示，设置暴露因素为SS，结局因素为甲状腺功能亢进、甲状腺肿、HT、GD、THCA时，二者间异质性分析结果提示P>0.05，表明数据不存在异质性；结局因素为甲状腺功能减退（Q=25.439，P=4.792×10-7）时，提示二者间存在异质性，使用IVW随机效应模型分析二者间因果效应。设置结局因素为SS，暴露因素为甲状腺功能亢进、甲状腺功能减退、甲状腺肿、THCA，二者间异质性分析结果提示P>0.05，表明数据不存在异质性。暴露因素为HT（Q=42.410，P=4.336×10-7）、GD（Q= 15.494，P=0.001）时，提示二者间存在异质性，使用IVW随机效应模型分析二者间因果效应。
对结局进行水平多效性检验，设置暴露因素为SS，结局因素为甲状腺功能亢进、甲状腺功能减退、甲状腺肿、HT、THCA的MR-Egger截距P>0.05，表明二者间不存在水平多效性；结局因素为GD时MR-Egger截距P=0.031，表明其间存在水平多效性MR-PRESSO分析结果显示无离群SNP，应用MR-Egger回归模型分析二者间的因果效应。设置结局因素为SS，暴露因素为甲状腺功能亢进、甲状腺功能减退、HT、GD、THCA的MR-Egger截距P>0.05，表明二者间不存在水平多效性；暴露因素为甲状腺肿时截距P=0.016，表明其间存在水平多效性MR-PRESSO分析结果显示无离群SNP，应用MR-Egger回归模型分析二者间的因果效应。本研究采用leave-one-out检验逐个剔除单个SNP，总体结果不受单独SNP影响，进一步支持分析结果的稳健性及准确性，散点图及leave-one-out检验分别见图4、图5。
3　讨论
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本研究采用两样本双向MR设计研究遗传学预测甲状腺疾病对SS发病风险的潜在因果效应，经过严格筛选IVs及两样本双向MR分析发现，遗传预测SS是甲状腺功能减退、HT的危险因素。SS与甲状腺功能亢进、甲状腺肿、GD、THCA之间的发病风险没有关联。
临床研究方面，既往多个回顾性研究对SS常见的合并疾病进行探索。Baldini C[14]认为SS是HT合并疾病中最常见的自身免疫病，反之亦然。齐海宇等[3]回顾性分析了73例原发性干燥综合征（pSS）合并甲状腺疾病患者的临床资料，发现pSS合并甲状腺疾病特别是HT和/或甲状腺功能减退的比例高于正常人群。仲彬等[4]回顾性分析了118例p SS患者的临床资料，发现pSS患者中HT发病明显增多（27.1%），其次为甲状腺功能减退（16.9%），SS合并HT的患者口干、乏力症状的发生率明显增高，同时可能伴见甲状腺肿大、Ig G升高和浆膜腔积液。何静等[5]回顾性分析了64例pSS患者，发现其中有23例患者伴有甲状腺功能异常，其中有17例患者为HT，就发病特征而言，17例SS合并HT的患者中，4例HT早于SS确诊，8例HT晚于SS确诊，剩余5例SS与HT几乎同时发生。与本研究分析结果相一致，遗传预测SS与HT会相互增加其发病风险。Ha YJ等[15]纳入196例pSS患者进行横断面研究，探索甲状腺相关自身抗体对隐匿性甲状腺疾病的pSS患者的临床意义，结果发现，其中23例（11.7%）患者伴有亚临床甲状腺功能减退，抗促甲状腺激素受体抗体（TRAb）阳性的隐匿性甲状腺疾病患者ESSDAI评分更高。吴迪等[6]回顾性分析了210例p SS患者， 发现有70例患者伴有甲状腺能异常，其中包括19例亚临床甲状腺功能减退（27.1%）、15例甲状腺功能减退（21.4%），超声结果显示其中28例患者发生甲状腺肿（40%），对患者临床表现进行比较，发现pSS伴有甲状腺功能异常的患者发生雷诺现象和淋巴结肿大的可能显著增高（P<0.05），结合本研究分析结果，该临床回顾性研究与遗传预测的SS显著增加甲状腺功能减退的发病风险相一致，但没有证据显示SS会增加或降低甲状腺肿的发病风险。
生物机制方面，SS是一种以侵犯外分泌腺为主的自身免疫病，主要表现为唾液腺和泪腺功能受损，出现口干、眼干等症状[16-17]。甲状腺疾病中，如HT、GD等也受自身免疫机制介导[18-19]，导致机体免疫系统错误地攻击自身组织。在这两种疾病中，免疫系统对特定的组织或器官都产生了异常的免疫应答。在疾病过程中，SS和甲状腺相关疾病以Th1/Th2 细胞比例失衡较为常见，可能导致炎症反应的持续和加重，且细胞因子如肿瘤坏死因子-α（TNF-α）、白细胞介素-6（Interleukin-6，IL-6）等也可能升高，促进炎症反应和组织损伤。Huang YM等[20]研究支持SS与自身免疫性甲状腺疾病均通过THαβ免疫途径发病，二者都涉及Toll样受体（TLR）信号通路的异常，TLR3、TLR7和TLR9在两种疾病中均有过度表达，这些受体在感知病毒抗原以触发THαβ免疫反应中发挥重要作用。转录因子如IRF7在GD中过表达，与I型干扰素表达相关，而在SS中，IRF5、STAT1和STAT3等转录因子也参与疾病过程，表明转录因子在两种疾病的免疫调节中均起重要作用。SS和甲状腺相关疾病具有部分共同的遗传易感基因，人类白细胞抗原（HLA）基因与SS和甲状腺疾病的发病风险密切相关。例如，HLA-DR3 等位基因在SS和GD患者中的频率较高。此外，一些非HLA 基因如细胞毒性T淋巴细胞相关抗原4（CTLA-4）、蛋白酪氨酸磷酸酶非受体型22（PTPN22）等基因的多态性也与这两种疾病的易感性有关[21]。遗传因素在疾病的发生发展中起到一定的作用，但通常不是单一基因决定疾病的发生，而是多个基因相互作用以及与环境因素共同影响疾病的易感性。HT通常被认为与甲状腺球蛋白抗体（TGAb）和甲状腺过氧化物酶抗体（TPOAb）相关[22]，T细胞攻击甲状腺，使得甲状腺抗原暴露，随后发生自身免疫，HT以Th1免疫应答为主要表现[23]，TGAb、TPOAb与抗原结合形成免疫复合物，淋巴细胞毒等直接作用在甲状腺滤泡上皮细胞，从而发生免疫炎性反应，导致补体成分减少[24]。在组织病理学上，HT患者甲状腺的淋巴细胞浸润情况与SS唾液腺的淋巴细胞浸润相似[25]。Clio P Mavragani等[26]认为SS早期与HT一样，也呈Th1应答，而随着疾病的发展逐渐转变为以Th2应答为主。且SS与AITD二者在淋巴细胞浸润、HLA II类分子上皮表达和B细胞克隆扩增间相似，此证据支持甲状腺疾病与pSS之间的关联[27]。Yang Y[28]等回顾性分析202例pSS患者并构建pSS患者甲状腺受累预测模型，提出抗Ro-52抗体阳性与甲状腺受累的关联，强调了自身免疫反应在pSS患者甲状腺功能障碍中的潜在作用。
本研究仍然存在一定局限性：（1）本研究纳入人群主要由欧洲个体组成，可能导致种族偏倚的潜在存在，研究结果推广至其他种族背景时需要保持谨慎。（2）GWAS汇总数据具有一定局限性，需要未来补充更多SNPs作为工具变量重复研究以提高分析结果稳健性。（3）GD中自身抗体的存在会导致甲状腺增生，而在HT中自身抗体的存在会导致甲状腺组织的破坏，故临床上常见继发甲状腺功能亢进和甲状腺功能减退[29]，本研究采用两样本双向MR分析，从遗传学层面探索SS与甲状腺相关疾病间的潜在联系，但MR无法全面展现真实世界中两疾病间可能存在的复杂关系。
概而言之，遗传预测的SS是甲状腺功能亢进、甲状腺功能减退、HT、GD的危险因素，HT是SS的危险因素。该研究结果和目前临床回顾性研究结果相一致，生物机制研究结果支持SS与自身免疫性甲状腺疾病相关。目前仍然缺乏SS和甲状腺肿、THCA之间的生物机制研究，其机制需要未来进一步实验室探索，以及更大样本量的临床研究提供证据支持。
基金
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  • 首都卫生发展科研专项(首发2024-1-4065)
  • 中日友好医院“菁英计划”人才培育工程资助(ZRJY2024-GG08)
  • 中华中医药学会风湿病分会青年培英计划(202327-007)
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2025年第52卷第7期
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doi: 10.20043/j.cnki.MPM.202410074
  • 接收时间：2024-10-07
  • 首发时间：2026-03-18
  • 出版时间：2025-04-10
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  • 收稿日期：2024-10-07
基金
首都卫生发展科研专项(首发2024-1-4065)
中日友好医院“菁英计划”人才培育工程资助(ZRJY2024-GG08)
中华中医药学会风湿病分会青年培英计划(202327-007)
作者信息
    1.北京中医药大学研究生院，北京 100029
    2.中日友好医院中医风湿病科，免疫炎性疾病北京市重点实验室，北京 100029

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Number of
genus		 种数
Number of
species		 占总种数比例
Percentage of
total species (%)		 属
Genus		 种数
Number of
species		 占总种数比例
Percentage of total
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鹅膏菌科Amanitaceae 2 11 5.26 鹅膏菌属 Amanita 10 4.78
小菇科 Mycenaceae 2 12 5.74 丝盖伞属 Inocybe 5 2.39
多孔菌科 Polyporaceae 8 14 6.70 蜡蘑属 Laccaria 5 2.39
红菇科 Russulaceae 3 23 11.00 小皮伞属 Marasmius 6 2.87
小菇属 Mycena 11 5.26
光柄菇属 Pluteus 5 2.39
红菇属 Russula 17 8.13
栓菌属 Trametes 5 2.39
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