Parity and the risk of autoimmune thyroid disease: A community-based study
Parity and the risk of autoimmune thyroid disease: A community-based study
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DOI：
10.1210/jc.2005-0771
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发表时间：
2005-09-01
影响因子：
5.8
通讯作者：
Michelangeli, V
中科院分区：
文献类型：
--
作者：
Walsh, JP;Bremner, AP;Michelangeli, V
背景：最近的研究表明，胎儿微嵌合（胎儿细胞经胎盘传代后植入母体组织）可能在自身免疫性甲状腺疾病的发病机制中发挥作用。如果这是真的，那么胎次应该是自身免疫性甲状腺疾病的一个危险因素。目的：本研究的目的是检查胎次作为自身免疫性甲状腺疾病的危险因素。设计、环境和参与者：1981年在西澳大利亚州Busselton进行的一项社区健康调查中，对1045名女性参与者的存档血清中TSH、甲状腺过氧化物酶抗体和甲状腺球蛋白抗体浓度进行了测量。结果测量：采用甲状腺抗体阳性（任一抗体浓度升高）或甲状腺功能障碍（血清TSH异常）的优势比（ORs）。结果：在调整年龄后，曾经怀孕的妇女甲状腺抗体阳性的风险没有显著增加[OR， 1.20；95%置信区间（CI）， 0.74-1.97；P = 0.46]，与从未怀孕过的妇女相比，TSH升高（OR, 0.93; 95% CI, 0.46-1.87; P = 0.84），或TSH降低（OR, 0.87; 95% CI, 0.33-2.30; P = 0.79）。每增加一次妊娠，抗体阳性的OR为1.02 (95% CI, 0.94-1.11, P = 0.57)， TSH升高的OR为1.02 (95% CI, 0.91-1.14, P = 0.67)， TSH升高的OR为1.03 (95% CI, 0.87-1.22)；P = 0.73)表示TSH降低。使用活产数进行分析得出了类似的结果。结果在年轻女性和老年女性中是相似的。结论：胎次不是甲状腺自身免疫或甲状腺功能障碍的危险因素。这些数据不支持胎儿微嵌合在慢性自身免疫性甲状腺疾病中的关键致病作用。
Context: Recent studies have suggested that fetal microchimerism ( transplacental passage of fetal cells followed by engraftment into maternal tissues) may play a role in the pathogenesis of autoimmune thyroid disease. If that is true, then parity should be a risk factor for autoimmune thyroid disease.Objective: The objective of this study was to examine parity as a risk factor for autoimmune thyroid disease.Design, Setting, and Participants: TSH, thyroid peroxidase antibody, and thyroglobulin antibody concentrations were measured on archived sera from 1045 female participants in a 1981 community health survey in Busselton, Western Australia.Outcome Measures: Odds ratios (ORs) for positive thyroid antibodies (increased concentration of either antibody) or thyroid dysfunction (abnormal serum TSH) were used.Results: After adjustment for age, women who had previously been pregnant did not have a significantly increased risk of positive thyroid antibodies [OR, 1.20; 95 % confidence interval (CI), 0.74-1.97; P = 0.46], raised TSH (OR, 0.93; 95 % CI, 0.46-1.87; P = 0.84), or reduced TSH (OR, 0.87; 95 % CI, 0.33-2.30; P = 0.79) compared with women who had never been pregnant. For each additional pregnancy, the OR was 1.02 (95 % CI, 0.94-1.11; P = 0.57) for positive antibodies, 1.02 (95 % CI, 0.91-1.14; P = 0.67) for raised TSH, and 1.03 95% CI, 0.87-1.22; P = 0.73) for reduced TSH. Analysis using number of live births gave similar results. The results were similar in younger and older women.Conclusions: Parity is not a risk factor for thyroid autoimmunity or thyroid dysfunction. These data do not support a key pathogenic role for fetal microchimerism in chronic autoimmune thyroid disease.