Association between family history, early growth and the risk of beta cell autoimmunity in children at risk for type 1 diabetes.
Association between family history, early growth and the risk of beta cell autoimmunity in children at risk for type 1 diabetes.
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DOI：
10.1007/s00125-020-05287-1
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发表时间：
2021-01
期刊：
影响因子：
8.2
通讯作者：
TRIGR investigators
中科院分区：
文献类型：
--
作者：
Pacaud D;Nucci AM;Cuthbertson D;Becker DJ;Virtanen SM;Ludvigsson J;Ilonen J;Knip M;TRIGR investigators
这项工作的目的是研究1型糖尿病家族史、出生体重、头两年的生长发育与儿童多种β细胞自身抗体的发展之间的关系，这些儿童与1型糖尿病和人类白细胞抗原相关疾病的易感性有一级亲属。在减少IDDM遗传风险(TRIGR)试验的第二次分析中，比较了2074名来自单一受影响家庭成员的儿童的临床特征和β细胞自身抗体的发展与1型糖尿病家族史(母亲与父亲与兄弟姐妹)的关系。在277名(13%)儿童中发生了多种自身抗体(≥2/5)：母亲、父亲或兄弟姐妹中分别有107名(10%)、114名(16%)和56名(18%)患有1型糖尿病(p <； 0.001)。与患有1型糖尿病的同胞相比，患病母亲的子女(n = 10 7/10 46，p <； 0.001)和患病父亲的子女(n = 114/72 2，p = 0.19)的多重自身免疫所需时间的HR分别为0.5 4(95%CI 0.39，0.75)和0.81(95%CI 0.5 9，1.11)(n = 5 6/30 6)。三组首次自身抗体出现的时间相似(对胰岛素、GAD、酪氨酸磷酸酶相关的胰岛素瘤相关分子、胰岛细胞或锌转运蛋白8)。前24个月的身高速度(z分数/年)与总队列中出现多种抗体独立相关(HR 1.31[95%CI 1.01，1.70]，p = 0.04)。患病母亲所生孩子的出生体重高于患病父亲或患病兄弟姐妹的出生体重，与多重自身免疫的风险无关。患有母体1型糖尿病的儿童发生多种自身抗体的风险较低。对于整个小组来说，患上多种自身抗体的风险与出生体重无关，但在出生后头两年身高速度增加的人中，风险更大。然而，与父亲1型糖尿病相关的风险与出生体重或早期生长的差异无关。ClinicalTrials.gov NCT00179777图形摘要本文的在线版本(10.1007/s00125-020-17977-1)包含经过同行评审但未经编辑的补充材料，授权用户可以使用。
The aim of this work was to examine the relationship between family history of type 1 diabetes, birthweight, growth during the first 2 years and development of multiple beta cell autoantibodies in children with a first-degree relative with type 1 diabetes and HLA-conferred disease susceptibility. In a secondary analysis of the Trial to Reduce IDDM in the Genetically at Risk (TRIGR), clinical characteristics and development of beta cell autoantibodies were compared in relation to family history of type 1 diabetes (mother vs father vs sibling) in 2074 children from families with a single affected family member. Multiple autoantibodies (≥2 of 5 measured) developed in 277 (13%) children: 107 (10%), 114 (16%) and 56 (18%) born with a mother, father or sibling with type 1 diabetes, respectively (p < 0.001). The HR for time to multiple autoimmunity was 0.54 (95% CI 0.39, 0.75) in offspring of affected mothers (n = 107/1046, p < 0.001) and 0.81 (95% CI 0.59, 1.11) (n = 114/722, p = 0.19) in offspring of affected fathers, compared with participants with a sibling with type 1 diabetes (comparator group n = 56/306). The time to the first autoantibody present (to insulin, GAD, tyrosine phosphatase-related insulinoma-associated 2 molecules, islet cell or zinc transporter 8) was similar in the three groups. Height velocity (z score/year) in the first 24 months was independently associated with developing multiple antibodies in the total cohort (HR 1.31 [95% CI 1.01, 1.70], p = 0.04). A higher birthweight in children born to an affected mother vs affected father or an affected sibling was not related to the risk of multiple autoimmunity. The risk of developing multiple autoantibodies was lower in children with maternal type 1 diabetes. For the whole group, this risk of developing multiple autoantibodies was independent of birthweight but was greater in those with increased height velocity during the first 2 years of life. However, the risk associated with paternal type 1 diabetes was not linked to differences in birthweight or early growth. ClinicalTrials.gov NCT00179777 Graphical abstract The online version of this article (10.1007/s00125-020-05287-1) contains peer-reviewed but unedited supplementary material, which is available to authorised users.
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