背景：第一型糖尿病是基因與環境因子交互作用所致。隨著世界各國第一型糖尿病發生率呈現上升趨勢，環境因子被許多研究指向是導致發生率上升的因素，其中包括周產期因子和微生物感染。西方研究指出，控制了干擾因子後，新生兒出生體重≥4000 克或懷孕週數≦37 週，日後發生第一型糖尿病風險較高，但台灣的研究在控制了干擾因子後，出生體重≦3000 克或懷孕週數≦37 週嬰兒，日後發生第一型糖尿病風險較高。另外，衛生假說（hygiene hypothesis）指出，兒童早期生活暴露微生物感染可降低日後第一型糖尿病發生，但有些研究認為並非所有微生物感染都有保護作用，甚至指出暴露病毒量和感染時間才是造成第一型糖尿病發生風險高低的關鍵。為此有關周產期因子和感染症與第一型糖尿病發生風險的關係，需進一步探討。
目的：本研究將探討台灣地區 2000-2005 年出生世代其兒童周產期因子、母親周產期因子、父親因子以及投保所在地人口密度與第一型糖尿病發生風險的相關。此外，本研究也會分析兒童不同時期感染症住院事件與發生第一型糖尿病的相關，以及母親懷孕期間感染與兒童罹患第一型糖尿病之間的相關。
方法：本研究將採用巢式病例對照研究法，資料來源為健保資料庫中 2002-2008 年承保資料檔（ID）、2000-2008 年糖尿病特定主題門診分檔（DB） 和 2000-2008 年住院醫療費用清單明細檔（DD）。病例組為 2000-2005 年出生世代追蹤至 2008 年罹患第一型糖尿病之兒童（n=632）；對照組則為剩下 2000-2005 年出生世代至 2008 年無罹患第一型糖尿病且無罹患第二型糖尿病者，以 1:10 匹配出生年之個案（N=6320）。確認病例組與對照組後，回溯其周產期因子、感染症住院事件等暴露資料；並以邏輯斯迴歸模式在控制潛在干擾因子後，計算調整後勝算比及其 95% 信賴區間，以分析上述因子與第一型糖尿病發生風險是否存在相關性。
結果：低出生體重早產兒相較於足月重足月產兒童罹患第一型糖尿病的校正風險是 1.73 倍（95% CI=1.10-2.72）。母親生育年齡<25 歲其兒童罹患第一型糖尿病的校正風險是 25-29 歲母親的 1.98 倍（95% CI=1.37-2.87），但母親生育年齡≥35 歲其兒童罹患第一型糖尿病的校正風險是 25-29 歲母親 0.61 倍（95% CI=0.40-0.93）。另外，採剖腹產方式出生（校正 OR=3.5，95% CI=2.61-4.70）、父親生育年齡越大（30-34 歲、≥35 歲比 25-29 歲的校正 OR，分別是 1.57 倍（95% CI=1.19-2.05）、1.56 倍（95% CI=1.16-2.10））、投保所在地人口密度越高（趨勢檢定 P 值<0.05），兒童得到第一型糖尿病的風險越高。父母親罹患糖尿病類型均會影響兒童發生第一型糖尿病風險。控制了兒童發病年齡、兒童性別、出生體重、懷孕週數、投保所在地人口密度，若兒童在發病前，曾罹患急性呼吸道感染（校正 OR=1.74，95% CI=1.30-2.33）、肺炎及流行性感冒（校正 OR=1.80，95% CI=1.35-2.41）、結膜及角結膜炎（校正 OR=30.87，95% CI=3.18-299.35）、中耳炎（校正 OR=4.43，95% CI=1.72-11.42）任一住院感染事件，以及母親懷孕期間因感染而住院（校正 OR=1.16，95% CI=0.25-5.51），均會增加兒童發生第一型糖尿病機會。
結論：低出生體重與早產會增加第一型糖尿病發生風險。不同於西方國家，在台灣，低出生體重兒童易罹患第一型糖尿病。部分父母親周產期因子與兒童發生第一型糖尿病有關。本研究部分數據支持衛生假說，唯嚴重感染之住院反而會增加兒童罹患第一型糖尿病之風險。

Background： Type 1 diabetes is considered to result from the interaction between gene susceptibility and environment exposure. Given the rising incidence of type 1 diabetes worldwide, some environment factors, including perinatal factors and microbial infections, are considered to be responsible for such rising trend in many studies. Western studies reported that a birth weight of 4000 grams (g) or higher or a gestational age of 37 weeks or less was associated with an increased risk of developing type 1 diabetes, after controlling for confounding factors. However, domestic studies reported that a birth weight of 3000g or less or a gestional age of 37 weeks or less may experience a higher risk of type 1 diabetes. Additionally, according to the hygiene hypothesis, microbial exposure in one’s early life shows a protective role in the development of type 1 diabetes, but not all studies support this hypothesis, arguing that the development of type 1 diabetes determined by the viral exposure level and exposure duration. Given the above inconsistency and argument, the associations of type 1 diabetes with exposure to adverse perinatal factors and microbial organism warrants further investigations.

Objectives：This study sought to investigate the effects of selected perinatal factors, maternal factors, patenal factors and population density of residential area on incidence of type 1 diabetes among 2000-2005 birth cohort in Taiwan. We also investigated the associations of infection occurring to children and mothers during pregnancy with type 1 diabetes onset.

Methods：The study is conducted by a population-based nested case-control design.
The data were retrieved from the claims of the National Health Insurance Research Database (NHIRD), including beneficiary registry from 2002 to 2008, claims of ambulatory care for diabetes from 2000 to 2008, and inpatient claims from 2000 to 2008. Cases were the 2000-2005 birth cohort members who were diagnosed as type 1 diabetes between birth and the last day of 2008 (n=632)；The control subjects were matched to cases on year of birth and randomly selected, with a case/control ratio of 1:10, from in the rest of the 2000-2005 birth cohort members without type 1 diabetes and type 2 diabetes throughout the entire follow-up period (n=6320). We then tracked cases and controls back for their information on perinatal factors and admission due to infectious. We used multivariate logistic regression model adjusting potential confounders to estimate the adjusted odds ratio (AOR) and the corresponding 95% confidence interval (CI) to indicate the associations of the above mentioned factors and risk of type 1 diabetes.

Results： Compared to the term birth with normal birth weight, preterm births with low birth weight had a significantly increased risk of developing type 1 diabetes, with an AOR of 1.73（95% CI=1.10-2.72）. The AOR associated with maternal age less than 25 years were 1.98 （95% CI=1.37-2.87）, as compared to maternal ages of 25-29. On the other hand, maternal age >=35 years were associated with a significantly reduced AOR at 0.61(95% CI=0.40-0.93). In addtion, caesarean section（AOR=3.5,95% CI=2.61-4.70）, older fathers （30-34 years (1.57, 95% CI=1.19-2.05) and ≥35 years (1.56, 95% CI=1.16-2.10)）, higher population density（the p-value for trend test: <0.05） were all asscciated with a significantly increased risk of type 1 diabetes. Parents with diabetes also posed influences on risk of type 1 diabetes in offspring. After controlling for age at type 1 diabetes diagnosis, sex, birth weight, gestional age, population density of residential areas, admission due to certain infectious disease were found to be associated with increased risk of type 1 diabetes, including acute respiratory infections（AOR=1.74,95% CI=1.30-2.33）, pneumonia and influenza（AOR=1.80,95% CI=1.35-2.41）, keratitis and conjunctivitis（AOR=30.87,95% CI=3.18-299.35）, and otitis media（AOR=4.43,95% CI=1.72-11.42）. Moreover, maternal admitted for infection during pregnancy may also increase thr risk of type 1 diabetes（AOR=1.16,95% CI=0.25-5.51）.

Conclusion：Low birth weight and preterm children had a higher risk of developing type 1 diabetes. Unlike the finding noted in Western countries, our study suggested a higher risk of type 1 diabetes in preterm births with low birth weight. Certain parental perinatal factors were also related to the development of type 1 diabetes. Besides, our study showed some support for hygiene hypothesis; and admission for infectious disease posed an adverse effect on risk of type 1 diabetes in children under 10 years of old.

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