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研究生：	黃建程 Huang, Chien-Cheng
論文名稱：	台灣全國1999年至2012年一氧化碳中毒的流行病學與併發症研究 Carbon monoxide poisoning: epidemiology and subsequent complications between 1999 and 2012 in Taiwan
指導教授：	郭浩然 Guo, How-Ran
學位類別：	博士 Doctor
系所名稱：	醫學院 - 環境醫學研究所 Department of Environmental and Occupational Health
論文出版年：	2017
畢業學年度：	105
語文別：	英文
論文頁數：	147
中文關鍵詞：	一氧化碳中毒、糖尿病、高壓氧治療、甲狀腺低下、死亡、心肌受損、神經學後遺症、臺灣
外文關鍵詞：	carbon monoxide poisoning, diabetes, hyperbaric oxygen therapy, hypothyroidism, mortality, myocardial injury, neurological sequelae, Taiwan
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目的：一氧化碳中毒是公共衛生上一個很重要的問題，但是很多相關議題在目前的文獻裡仍未被釐清。我們進行一系列研究以探討：(1)臺灣自1999年至2012年全國一氧化碳中毒的流行病學，(2)一氧化碳中毒與心肌受損、糖尿病與甲狀腺低下的關聯性，(3)高壓氧治療對一氧化碳中毒後的死亡率、心肌受損及神經學後遺症的功效，(4)一氧化碳中毒後發生神經學後遺症的預測因子。
方法：我們採用了臺灣健保資料庫裡的二個子資料庫「全國中毒資料庫」與「2000年百萬歸人檔」進行資料分析，首先以描述性統計來呈現臺灣自1999年至2012年全國一氧化碳中毒的流行病學資料，其次以世代研究設計用存活分析比較一氧化碳中毒患者與對照族群發生心肌受損、糖尿病與甲狀腺低下的風險，最後再以一氧化碳中毒患者為對象探討高壓氧治療是否可減少一氧化碳中毒後的死亡率、心肌受損及神經學後遺症的風險。另外，我們在南部某醫學中心進行一個回溯性病例對照研究，以邏輯斯回歸分析比較一氧化碳中毒發生與未發生神經學後遺症的患者，探討其獨立預測因子。
結果：我們分析臺灣全國流行病學資料發現，大部分一氧化碳中毒病人年齡在50歲以下、平均是36歲，男女比例差不多，中等收入最多，約三分之一有精神疾病，而20.4%是自殺所致。一氧化碳中毒後會增加心肌受損的風險，但是主要是發生在急性期一個月內。一氧化碳中毒也會增加後罹患糖尿病的風險，尤其是在年輕（< 35歲）、高齡（≥ 65歲）、女性以及鬱血性心衰竭、甲狀腺亢進以及多囊卵巢綜合症的患者。一氧化碳中毒還會增加之後發生甲狀腺低下的風險，尤其是糖尿病、高血脂以及精神疾病的患者族群。高壓氧治療可減少短期及長期死亡率，尤其是在20歲以下及急性呼吸衰竭病人的功效更明顯。高壓氧治療也有減少心肌受損發生率的趨勢，但做高壓氧治療的病人中神經學後遺症的發生比例增加。在醫學中心的病例對照研究中，我們收案371位一氧化碳中毒患者，經過單變項與多變項邏輯斯迴歸分析後，發現「一氧化碳中毒暴露時間超過5小時」與「有高血壓病史」是預測神經學後遺症的獨立因子。
結論：本系列研究結果呈現了整個臺灣自1999年至2012年一氧化碳中毒的流行病學資料，另發現了一氧化碳中毒後心肌受損、糖尿病與甲狀腺低下的風險會上升，而高壓氧治療可減少死亡與心肌受損的風險，但可能因為增加存活率而導致神經學後遺症的風險增加。此外，本系列研究找到了二個神經學後遺症的獨立預測因子。這些結果可提供我們未來治療及預防一氧化碳中毒後遺症的重要參考，但仍須要後續研究去釐清其背後的機制。

Objectives: Carbon monoxide poisoning (COP) is an important problem in public health; however, many related issues remain unclear in the literature. We conducted a series of studies to investigate the follows: (1) epidemiology of COP between 1999 and 2012 in Taiwan; (2) associations of COP with myocardial injury, diabetes, and hypothyroidism; (3) effects of hyperbaric oxygen therapy (HBOT) on mortality, myocardial injury, and neurological sequelae (NS) after COP; and (4) independent predictors for the NS of COP.
Methods: We analyzed data from the Nationwide Poisoning Database (NPD) and Longitudinal Health Insurance Database 2000 (LHID 2000), two sub-datasets from Taiwan National Health Insurance Research Database (NHIRD). We first studied the epidemiology of COP between 1999 and 2012 in Taiwan using descriptive analysis. And then, through a cohort study design, we compared the incidence of myocardial injury, diabetes, and hypothyroidism between patients of COP and reference patients groups using survival analysis. Finally, we evaluated whether HBOT can reduce mortality, myocardial injury, and NS. In addition, we conducted a retrospective hospital-based case-control study in a tertiary medical center in Southern Taiwan to identify the independent predictors for NS using logistic regression analysis.
Results: The nationwide epidemiological data in Taiwan showed that the COP patients were mostly less than 50 years old (with a mean age of 36.0 years), equally distributed in the two sexes, mostly in the middle income group, more likely to have had mental disorders (nearly one-third), and frequently (20.4%) resulted from suicide attempts. COP increased the risk of myocardial injury, but the increased risk was mainly observed in the first month after COP. COP increased the risk of diabetes, especially in participants with a younger (< 35 years) or older (≥ 65 years) age, female sex, and comorbidities of congestive heart failure, hyperthyroidism, and polycystic ovary syndrome. COP increased the risk of developing hypothyroidism, especially in participants with diabetes, hyperlipidemia, and mental disorders. HBOT was associated with lower short- and long-term mortalities in COP participants, especially in those who were less than 20 years old and those with acute respiratory failure. HBOT had a trend of reducing the risk of subsequent myocardial injury. The risk of developing NS was higher in the COP participants who received HBOT than in those who did not. A total of 371 COP participants were recruited into the hospital-based case-control study. After uni-variate and multi-variate logistic regression analyses, a duration of CO exposure > 5 hours and a past history of hypertension were independent predictors for NS.
Conclusions: These studies showed a whole picture of COP between 1999 and 2012 in Taiwan and found increased risks of subsequent myocardial injury, diabetes, and hypothyroidism after COP; a positive effect of HBOT on reducing mortality and myocardial injury after COP; and an increased risk of developing NS in COP patients who received HBOT, most likely due to the better survival. In addition, two independent predictors for NS were found. The results provide important references for the treatment and prevention of subsequent complications following COP; however, further studies are warranted to clarify the underlying mechanisms.

Certification………………………………………………………………………….……...I
Chinese abstract…………………………………………………………………………….II
Abstract……………………………………………………………………………………IV
Acknowledgement…………………………………………………………………………VI
Contents…………………………………………………………………………………..VII
List of tables……………………………………………………………………………….XI
List of figures…………………………………………………………………………….XIV
Chapter 1. Epidemiology……………………………………………………………………1
1	Background…………………………………………………………………………..1
2	Objective: demographic and clinical characteristics of COP between 1999 and 2012 in Taiwan……………………………………………………………………..............2
3	Materials and Methods……………………………………………………………….2
3.1	Data sources…………………………………………………………………...2
3.2	Identification of COP participants and definitions of variables……………….3
3.3	Ethics statement………………………………………………………………..5
3.4	Data analysis…………………………………………………………………...5
4	Results…………………………………………………………..……………………5
5	Discussion……………………………………………………………………………6
6	Conclusions…………………………………………………………………………..9
Chapter 2. Subsequent complications after COP………………………………………….10
1 Background…………………………………………………………………………10
2 Objectives…………………………………………………………………………...11
3 Materials and Methods……………………………………………………………...11
3.1 Association between COP and myocardial injury……………………………...11
3.1.1 Data sources………………………………………………………………..11
3.1.2 Definitions, variables, and outcomes………………………………………11
3.1.3 Comparison of the risk of myocardial injury between COP and non-COP 
participants………………………………………………………………...12
3.1.4 Ethics statement……………………………………………………………12
3.1.5 Statistical analyses…………………………………………………………12
3.2 Association between COP and diabetes………………………………………..13
3.2.1 Data source………………………………………………………………...13
3.2.2 Definition of study cohort (COP participants) and comparison cohort (non-
COP participants) and variables…………………………………………...13
3.2.3 Comparison of the risk for diabetes between the study and comparison cohorts……………………………………………………………………..14
3.2.4 Ethics statement……………………………………………………………14
3.2.5 Data analysis……………………………………………………………….14
3.3 Association between COP and hypothyroidism………………………………..15
3.3.1 Data source………………………………………………………………...15
3.3.2 Identification of COP and non-COP participants………………………….15
3.3.3 Definitions of included variables………………………………………….15
3.3.4 Ethics statement……………………………………………………………16
3.3.5 Data analysis……………………………………………………………….16
4 Results………………………………………………………………………………16
4.1 Association between COP and myocardial injury……………………………...16
4.2 Association between COP and diabetes………………………………………..17
4.3 Association between COP and hypothyroidism………………………………..18
5 Discussion…………………………………………………………………………..19
5.1 Association between COP and myocardial injury……………………………...19
5.2 Association between COP and diabetes………………………………………..22
5.3 Association between COP and hypothyroidism………………………………..24
6 Conclusions…………………………………………………………………………26
6.1 Association between COP and myocardial injury……………………………..26
6.2 Association between COP and diabetes………………………………………..27
6.3 Association between COP and hypothyroidism………………………………..27
Chapter 3. Effect of HBOT on the complications after COP………………...……………28
1 Background…………………………………………………………………………28
2 Objectives…………………………………………………………………………...29
3 Materials and Methods……………………………………………………………...29
3.1 Effect of HBOT on mortality………………….…………..…………………...29
3.1.1 Data source and identification of participants with COP and definitions of 
variables……………………………………………………………………29
3.1.2 Mortality risk and independent mortality predictors………………………30
3.1.3 Ethics statement……………………………………………………………30
3.1.4 Data analysis……………………………………………………………….30
3.2 Effect of HBOT on myocardial injury……………...….……………………….31
3.2.1 Data sources, identification of participants, and definitions of variables…31
3.2.2 Comparison of the risk for myocardial injury between participants with and 
without HBOT……………………………………………………………..31
3.2.3 Ethics statement……………………………………………………………32
3.2.4 Statistical analysis…………………………………………………………32
3.3 Effect of HBOT on NS………………….……………………………………...32
3.3.1 Data source and identification of participants with COP………………….32
3.3.2 Definitions of variables……………………………………………………33
3.3.3 Comparison of the risk for NS between the two cohorts and independent 
predictors for NS…………………………………………………………..33
3.3.4 Ethics statement……………………………………………………………34
3.3.5 Data analysis……………………………………………………………….34
4 Results………………………………………………………………………………34
4.1 Effect of HBOT on mortality………..……………….………………………...34
4.2 Effect of HBOT on myocardial injury…..………………….………………….36
4.3 Effect of HBOT on NS……..……………..……………………………………37
5 Discussion…………………………………………………………………………..38
5.1 Effect of HBOT on mortality………………….………………..……………...38
5.2 Effect of HBOT on myocardial injury………………….………..…………….41
5.3 Effect of HBOT on NS……………..…….……………………………………43
6 Conclusions…………………………………………………………………………45
6.1 Effect of HBOT on mortality…….….....………..……………………………..45
6.2 Effect of HBOT on myocardial injury……………..…..……………………….45
6.3 Effect of HBOT on NS…………..……….…………………………………….46
Chapter 4. Independent predictors for NS…………………………………………………47
1 Background and objective…………………………………………………………..47
2 Materials and Methods……………………………………………………………...47
2.1 Study design, setting, and enrollment of participants………………………….47
2.2 Data collection………………………………………………………………….48
2.3 Definition of variables………………………………………………………….48
2.4 Definition of primary outcome…………………………………………………48
2.5 Ethics statement………………………………………………………………...48
2.6 Data analysis……………………………………………………………………49
3 Results………………………………………………………………………………49
4 Discussion…………………………………………………………………………..50
5 Conclusions…………………………………………………………………………52
Chapter 5. Final conclusions………………………………………………………………53
References………….……………………………………………………………………...55
Tables………………………………………………………………………………………65
Figures……………………………………………………………………………………127
                                    

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