Disease concurrence in type 1 diabetes

描述（由申请人提供）：本研究通过研究疾病并发模式，特别是与其他自身免疫性疾病（AD）的并发模式，探索1型糖尿病（T1 D）的病因。疾病并发症-在一个个体中发生两种或多种疾病-是自身免疫的一个突出特征，特别是T1 D。在初步研究中，我们建立了获得第一个真实的基于人群的疾病并发症患病率的方法，以及量化疾病并发症模式的程度的方法，长期以来一直被认为是自身免疫性疾病的特征。AD之间的关系实际上构成了一系列相互关联的疾病，并且被认为反映了共同的潜在致病因素，这是由于遗传环境（包括感染因子），性别相关和早期生活条件因素的相互作用。这些因素对T1 D的相对重要性的澄清可以通过AD并发症的研究来揭示和量化。将对基于全国人群的瑞典健康数据库进行统计分析，包括两个糖尿病登记处、住院出院登记处、出生登记处和癌症登记处，以揭示T1 D疾病并发模式的相似性和对比。登记研究中个体的关联将允许评估T1 D疾病并发症和有影响力的辅助因素，如出生体重。通过检查最常住院的AD，将定义成对疾病并发的总体模式。统计上确定的过剩和赤字并存模式都将提供信息。免疫、内分泌和产前事件将为解释发病年龄、疾病发病顺序、性别和感染性疾病效应与T1 D并发症的关系提供功能背景。

DESCRIPTION (provided by applicant): This research explores the etiology of Type 1 Diabetes (T1D) through study of patterns of disease concurrence, especially with other autoimmune diseases (AD). Disease concurrence--the occurrence in an individual of two or more diseases--is a prominent feature of autoimmunity, and of T1D in particular. In preliminary studies we establish the methods to obtain the first true population based disease concurrence prevalence rates, and of quantifying the extent of disease concurrence patterns, long thought to be a characteristic feature of autoimmune disease. The relationships among ADs actually constitute a constellation of interrelated diseases, and are thought to reflect common underlying causative factors, due to the interplay of genetic environmental (including infectious agents), sex-related and early life conditional factors. Clarification of the relative importance of these factors for T1D can be revealed and quantified by the study of AD concurrence. Statistical analysis of the national population-based Swedish health data bases, including two diabetes registries, the hospitalization discharge registry, the birth registry and the cancer registry, will be used to uncover similarities and contrast in patterns of disease concurrence in T1D. Linkage of individuals across registries will permit an assessment of T1D disease concurrence and influential cofactors such as birth weight. By examining the ADs most subject to hospitalization, overall patterns of pairwise disease concurrence will be defined. Both statistically established excess and deficit concurrence patterns will be informative. Immune, endocrine and prenatal events will supply the functional background for interpreting age of onset, order of disease onset, gender and the relationship of infectious disease effects relative to T1D concurrence.