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研究生:杭良文
研究生(外文):Hang Liang-wen
論文名稱:正陽壓呼吸器治療阻塞性睡眠呼吸中止症效果與順應性之探討
論文名稱(外文):The Compliance and Effectiveness of Continuous Positive Airway Pressure on the Patient of Obstructive Sleep Apnea
指導教授:藍守仁藍守仁引用關係
指導教授(外文):Lan Shou-Jen
口試委員:徐武輝嚴成文黃明賢陳悅生曹世明藍守仁
口試委員(外文):Hsu Wu-HueiYen Chen-WenHuang Ming-HsienChen Yueh-ShengTsao Shih-MingLan Shou-Jen
口試日期:2013-07-11
學位類別:博士
校院名稱:亞洲大學
系所名稱:健康產業管理學系健康管理組
學門:商業及管理學門
學類:醫管學類
論文種類:學術論文
論文出版年:2013
畢業學年度:101
語文別:英文
論文頁數:82
中文關鍵詞:阻塞性睡眠呼吸中止症正陽壓呼吸器順應性睡眠品質人格肝炎
外文關鍵詞:obstructive sleep apnea hypopnea syndromecontinuous positive airway pressurecompliancesleep qualitypersonalityliver disease
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阻塞性睡眠呼吸中止症(obstructive sleep apnea hypopnea syndrome, OSAHS),其為睡眠障礙最常見之臨床診斷一般人口中,約有4%的中年男性與2%的中年女性患有睡眠呼吸中止。近年來阻塞性睡眠呼吸中止症已逐漸受到醫界的重視,由於睡眠呼吸中止症會引起心臟血管疾病及交通意外,它潛在影響多數人的身體健康,已是不容忽視的議題。
在治療方面,目前針對睡眠呼吸中止症並無有效藥物可供治療,因此需依賴介入性的治療方式,包括:睡眠時配戴連續陽壓呼吸器(continuous positive airway pressure apparatus, CPAP)、進行耳鼻喉科手術、裝置口腔矯正牙套等,其中陽壓呼吸器是此類患者的黃金標準治療法。使用持續性呼吸道陽壓治療是一種有效的治療方式,並且是對於中度至重度以上的阻塞性睡眠呼吸中止症候群患者,最被廣泛使用的治療方法。
過去許多的研究多著重於阻塞性睡眠呼吸中止症患者的病患衛教、疾病嚴重度、機器及配件設計等因素與持續使用的相關性,較少利用行為模式切入配戴連續陽壓呼吸器順應性之研究 本論文藉由分析健康認知模式Health believed model中的自我效能(Self efficacy)及人格特徵(personality)及瞭解得到疾病造成的嚴重性(perceived severity)進而產生行為(cues of action)使用呼吸器的影響因素。

本論文第一部研究自我效能(Self efficacy),希望藉由比較初次連續陽壓呼吸道正壓治療前,及治療壓力調整時多功能睡眠檢查生理變化,影響自我效能進而有動機持續使用呼吸道正壓治療, 收集睡眠醫學中心中度以上(apnea-hypopnea index; AHI>15/h)阻塞性睡眠呼吸中止症病患共312名患者進行回朔性分析研究, 依連續陽壓呼吸器繼續使用與否分為接受治療(n=146)與不接受治療(n=166)等二個群組。結果發現整體睡眠時間睡眠效率在兩組有統計學差異,所以在初次連續陽壓呼吸道正壓治療壓力調整時睡得愈好也就是自我效能愈好時, 就有動機持續使用呼吸道正壓治療。

第二部分利用人格特徵D型與否,提早解暸人格特徵, 是否就是影響接不接受持續性呼吸道正壓治療的因素, 讓臨床醫療人員提早預測順應性, 早些提供其他有效之治療, 避免等待連續陽壓呼吸道正壓治療壓力調整檢查時間之醫療浪費。收集睡眠醫學中心中度以上(apnea-hypopnea index; AHI>15/h)阻塞性睡眠呼吸中止症病患共202名患者進行前瞻性分析研究, 人格特徵D型與非D型以1:1比例配對,包括疾病嚴重度、性別、年齡、身體質量指數、頭頸圍及白天嗜睡程度。結果發現人格特徵D型不影響持續使用呼吸道正壓治療, 反而收入與有無睡眠伴侶影響較大,社會經濟因素反而更為重要。
本論文第三部分想藉由比較容易瞭解的疾病, 讓民眾能容易瞭解得到阻塞性睡眠呼吸中止症疾病造成疾病的嚴重性,藉由分析台灣健保資料庫肝炎與否, 了解肝炎盛行的台灣地區,肝炎與睡眠呼吸中止症的關係,並分析連續陽壓呼吸器是否對肝炎之改善有一定幫助, 分析哪些人比較容易接受連續陽壓呼吸器檢查。 收集自1995至2010年台灣健康保險資料庫中年齡二十歲以上, 共12745人有接受多功能睡眠生理檢查並診斷阻塞性睡眠呼吸中止症, 考慮年齡及性別1:3配對, 共18,516 人無阻塞性睡眠呼吸中止症為控制組, 分析發現不論共病是高血壓、糖尿病、高血脂、心臟衰竭、心房顫動等, 肝炎的發生風險都比控制組高, 使用持續性呼吸道正壓治療可以減低肝炎的發生的趨勢。

結 論
由自我效能、人格特徵及瞭解得到疾病造成的嚴重性三部分研究,使用呼吸器的順應性,可藉由對台灣民眾對肝炎的重視出發,從家人及經濟角度切入, 讓病人能自檢查過程中發現治療效果, 自然順應性就可以增加。

Part I Better Sleep Quality Improves the CPAP Compliance in Patients with OSA
Objectives: An extensive use of continuous positive airway pressure (CPAP) has been shown to have greater clinical benefit for most patients with obstructive Sleep apnea (OSA). Patient compliance remains a major limiting factor to the effectiveness of CPAP. This study sought to determine the potential and quantifiable factors affecting OSA patients to undertake CPAP treatment by comparing the polysomnographic parameters recorded during diagnosis and titration between persistent users and non-users of CPAP.
Methods: Patients with moderate-to-severe OSA attended diagnostic polysomnography (PSG) and CPAP titration at the sleep center of China Medical University Hospital were included for this study. A total of 312 patients were divided to persistent users and non-users of CPAP according to treatment with and without in-home CPAP following titration and a 7-day trial use. Patient characteristics and their polysomnographic parameters were analyzed for comparing sleep efficacy and quality between persistent users and non-users.
Results: Total sleep time, sleep efficiency, and minimum SaO2 were statistically significant different between persistent users and non-users during CPAP titration. The overall sleep quality was also improved among persistent users.
Conclusions: CPAP adherence was associated with longer Total sleep time (TST), better sleep efficiency, lower minimum SaO2, and improved sleep quality during CPAP titration. Appropriate CPAP devices, experienced sleep technicians, and comfortable environment were key elements potentially influencing patients' decision-making of CPAP adoption.

Part 2: Do Personality in OSA patients reduce motivation to purchase CPAP machine.
Objectives: Use of continuous positive airway pressure (CPAP) has been shown to be clinically beneficial for most patients with obstructive sleep apnea hypopnea syndrome (OSAHS). Patient compliance remains a major limiting factor to the effectiveness of CPAP. This study sought to determine the factors that may contribute to the decision of purchasing mechanical ventilation including personality.
Methods: Patients with moderate-to-severe OSAHS who attended diagnostic polysomnography (PSG) and CPAP titration were included in this study. After personality types were determined using a questionnaire, 101 OSAHS patients with Type-D personality were selected and matched at a ratio of 1:1 to OSAHS patients with Non type-D personality. The factors that might affect the decision of purchasing CPAP were analyzed using a conditional logistic regression model .
Results: Characteristic differences were only observed in income and sleep habit with or without a partner between the patients with Type-D and non Type-D personalities. Type-D personality was not significantly associated with the motivation of purchasing a CPAP machine, and EES was the only predicting variable in this study.
Conclusions: CPAP adherence was associated with Type-D personality. More studies using population-based and longitudinal designs with randomly selected OSAS patients are needed to correct the potential bias of participant inclusion and to assess the long term impacts of Type-D personality on health status among OSAS patients.

Part 3
In view of these relevant evidence supporting the association of OSAHS with NAFLD, this study aimed to determine the incidence of NAFLD among OSASH patients, to evaluate whether CPAP treatment contributes to those with these two disorders in a prospective and population-based study in Taiwan, followed-up over a period of 10 years, and to investigate the incidences and effects of comorbidities. To determine whether OSAHS is a risk factor for the development of NAFLD and to compare the relative risks between OSAHS patients with and without CPAP treatment, we measured the hazards ratios (HRs) of NAFLD by using the stratified Cox proportional hazards model adjusting for age, gender, and comorbidities. All data management and calculation of HRs was performed using the SAS System (version 9.3; SAS Institute, Cary, NC). Cumulative incidence was analyzed via the Statistical Package for the Social Sciences (version 10.0; SPSS Inc, Chicago, IL).Our observations from the cohort data suggested that the mechanisms thereby OSAHS increasing the incidence of NALFD are likely associated with the both settings, insulin resistance and intermittent hypoxia (nocturnal hypoxemia). This study also suggests that treatment of OSAHS with CPAP may delay the development or reduce the incidences of NALFD. More evidence is also needed on how to manage comorbidities in OSAHS. Comorbidities not only adds challenges to treatment, but also increases the complexity of patient care, as well as adding to the economic burden of disease. Further interventional studies are required to demonstrate whether CPAP treatment results in diminished severity of NASLD and/or other comorbidities.
綜論 4
目錄 7
1.Better Sleep Quality Improves the CPAP Compliance in Patients with OSA 15
2.Do Personality in OSA patients reduce motivation to purchase CPAP achine 40
3.CPAP Therapy Improved the Risk of Developing NAFLD in Patients with OSASH: A Nationwide Population-Based Cohort Study 63

Contents 1
Abbreviations 18
Introduction 19
Methods 21
Results 24
Discussions 26
Acknowledgement 28
References 29 
List of Table 1
Table 1. Analysis of patient characteristics 34
Table 2. Comparison of baseline characteristic differences between CPAP persistent users and non-users 35
Table 3. Comparison of polysomnographic parameters on the first night between persistent users and non-users of CPAP 36
Table 4. Comparison of polysomnographic parameters during CPAP titration between CPAP persistent users and non-users 37
Table 5. Comparison of sleep quality between CPAP Persistent users and Non-users at diagnosis and during CPAP titration, respectively 38
Table 6. Comparison of sleep quality between diagnosis and CPAP titration for CPAP Persistent users and Non-users) 39

Contents 2
Introduction 42
Material and Methods 44
Results 48
Discussion 49
References 52
List of Table 2
Table 1. Characteristics of patients with OSAHS at baseline 56
Table 2. Characteristics of patients with OSAHS at baseline 57
Table 3. Effects of variables on patients’ use of CPAP, analyzed by conditional logistic regression models (adjusted for variables among Type-D and Non Type-D groups) 58
List of Figure 2
Figure 1. Flow diagram of patient progress through phases of the study 55

Content 3
Introduction 64
Methods 66
Results 68
Discussion 70
Strengths and limitations 72
Conclusion 72
References 73
List of Table 3
Table 1. Baseline Characteristics of Patients in Non-CPAP, CPAP and CONTROL Cohorts 80
Table 2. Hazard ratios calculated for the relative risks of developing non-alcoholic fatty liver diseases (NAFLD) between the comparative OSAHS cohorts with and without CPAP treatment, adjusted by age and gender 81
Table 3. Hazard ratios of developing non-alcoholic fatty liver diseases (NAFLD) in OSAHS patients without and with CPAP treatment. Adjustments were made for various comorbidities 82

Part 1
1.Young T, Palta M, Dempsey J, et al. The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med. 1993;328(17):1230-1351.
2.Black J. Sleepiness and residual sleepiness in adults with obstructive sleep apnea. Respir Physiol Neurobiol. 2003;136(2-3): 211-220.
3.Ohayon MM. The effects of breathing-related sleep disorders on mood disturbances in the general population. J Clin Psychiatry. 2003;64(10):1195-1200; quiz, 274-276.
4.Beebe DW. Neurobehavioral effects of obstructive sleep apnea: an overview and heuristic model. Curr Opin Pulm Med. 2005;11(6): 494-500.
5.Weaver TE, Laizner AM, Evans LK, et al. An instrument to measure functional status outcomes for disorders of excessive sleepiness. Sleep. 1997;20(10): 835-843.
6.Wright J, Johns R, Watt I, et al. Health effects of obstructive sleep apnoea and the effectiveness of continuous positive airways pressure: a systematic review of the research evidence. BMJ. 1997;314(7084): 851-860.
7.Lanfranco F, Motta G, Minetto MA, et al. Neuroendocrine alterations in obese patients with sleep apnea syndrome. Int J Endocrinol. 2010;2010:474-518.
8.Henley DE, Russell GM, Douthwaite JA, et al. Hypothalamic-pituitary-adrenal axis activation in obstructive sleep apnea: the effect of continuous positive airway pressure therapy. J Clin Endocrinol Metab. 2009;94(11):4234-4242.
9.Jelic S, Le Jemtel TH. Inflammation, oxidative stress, and the vascular endothelium in obstructive sleep apnea. Trends Cardiovasc Med. 2008;18(7):253-260.
10.Punjabi NM, Shahar E, Redline S, et al. Sleep-disordered breathing, glucose intolerance, and insulin resistance: the Sleep Heart Health Study. Am J Epidemiol. 2004; 160(6):521-530.
11.Institute for Clinical Systems Improvement web site. Healthcare guideline: Diagnosis and treatment of obstructive sleep apnea in adults. 6th edition. 2008. Available at: http://www.icis.org/guidelines_and more/.
12.Young T, Evans L, Finn L, et al. Estimation of the clinically diagnosed proportion of sleep apnea syndrome in middle-aged men and women. Sleep. 1997;20(9): 705-706.
13.Jennum P, Riha RL. Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J. 2009;33(4):907-914.
14.Taiwan Society of Sleep Medicine Press conference statement, 2006. Available at: http://www.tssm.org.tw/old_page/2006conf/20060310NewsRelease.htm.
15.Barzi F, Patel A, Gu D, et al. Cardiovascular risk prediction tools for populations in Asia. J Epidemiol Community Health. 2007;61(2): 115-121.
16.Kushida CA, Chediak A, Berry RB, et al. Clinical guidelines for the manual titration of positive airway pressure in patients with obstructive sleep apnea. J Clin Sleep Med. 2008;4(2):157-171.
17.Patel SR, White DP, Malhotra A, et al. Continuous positive airway pressure therapy for treating sleepiness in a diverse population with obstructive sleep apnea: results of a meta-analysis. Arch Intern Med. 2003;163(5):565-571.
18.Giles T, Lasserson T, Smith B, et al. Continuous positive airway pressure for obstructive sleep apnea in adults. Cochrane Database of Systematic Reviews. 2006;(1):CD001106
19.Loube DI, Gay PC, Strohl KP, et al. Indications for positive airway pressure treatment of adult obstructive sleep apnea patients: a consensus statement. Chest. 1999;115(3):863-866.
20.Arias MA, Garcia-Rio F, Alonso-Fernandez A, et al. CPAP decreases plasma levels of soluble tumour necrosis factor-alpha receptor 1 in obstructive sleep apnoea. Eur Respir J. 2008;32(4):1009-1015.
21.Elshaug AG, Moss JR, Southcott AM, et al. An analysis of the evidence-practice continuum: is surgery for obstructive sleep apnoea contraindicated? J Eval Clin Pract. 2007;13(1): 3-9.
22.Chen MF, Ding H, Ho CW, et al. A preliminary investigation of CPAP compliance in patients with severe sleep-disordered breathing in central Taiwan. Annual Meeting of Taiwan Society of Sleep Medicine; 2007 2007/03/25; Taipei: the TSSM; 2007. p. 100.
23.Verse T, Pirsig W, Stuck BA, et al. Recent developments in the treatment of obstructive sleep apnea. Am J Respir Med. 2003;2(2):157-168.
24.Engleman HM, Wild MR. Improving CPAP use by patients with the sleep apnoea/hypopnoea syndrome (SAHS). Sleep Med Rev. 2003;7(1):81-89.
25.Hoffstein V, Viner S, Mateika S, et al. Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis. 1992;145(4 Pt 1):841-845.
26.Stepnowsky CJ, Jr. Marler MR, Ancoli-Israel S. Determinants of nasal CPAP compliance. Sleep Med. 2002;3(3):239-247.
27.Edinger JD, Carwile S, Miller P, et al. Psychological status, syndromatic measures, and compliance with nasal CPAP therapy for sleep apnea. Percept Mot Skills. 1994; 78(3 Pt 2):1116-1118.
28.Engleman HM, Martin SE, Douglas NJ. Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome. Thorax. 1994;49(3):263-266.
29.Sin DD, Mayers I, Man GC, et al. Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest. 2002;121(2):430-435.
30.Chou KT, Chang YT, Chen YM, et al. The minimum period of polysomnography required to confirm a diagnosis of severe obstructive sleep apnoea. Respirology, 2011; 16(7):1096-1102.
31.Johns MW. A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep. 1991;(6)14:540-545.
32.Johns MW. Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest. 1993;103(1):30-36.
33.Rechtschaffen A, Kales, A. A Manual of Standardized Terminology, Technique and scoring Systems for Sleep Stages of Human Subjects: NIH Publ; 1968.
34.Iber C, Ancoli_Israel S, Chesson A, et al. The AASM manual for the scoring of sleep and associated events: rules, terminology and technical specifications. Westchester, Illinois; 2007.
35.Mcardle N, Devereux G, Heidarnejad H, et al. Long-term use of CPAP therapy for sleep apnea/hypopnea syndrome. Am J Respir Crit Care Med. 1999; 159(4):1108-1114.
36.Weaver TE, Grunstein RR. Adherence to continuous positive airway pressure therapy: the challenge to effective treatment. Proc Am Thorac Soc. 2008;5(2):173-178.
37.Yetkin O, Kunter E, Gunen H. CPAP compliance in patients with obstructive sleep apnea syndrome. Sleep Breath. 2008;12(4):365-367.
38.McDaid C, Griffin S, Weatherly H, et al. Continuous positive airway pressure devices for the treatment of obstructive sleep apnoea-hypopnoea syndrome: a systematic review and economic analysis. Health Technol Assess. 2009;13(4): iii-iv, xi-xiv, 1-119, 43-274.
39.Pelletier-Fleury N, Rakotonanahary D, Fleury B. The age and other factors in the evaluation of compliance with nasal continuous positive airway pressure for obstructive sleep apnea syndrome. A Cox's proportional hazard analysis. Sleep Med. 2001; 2(3):225-232.
40.Aloia MS, Arnedt JT, Stanchina M, et al. How early in treatment is PAP adherence established? Revisiting night-to-night variability. Behav Sleep Med. 2007;5(3):229-240.
41.Damjanovic D, Fluck A, Bremer H, et al. Compliance in sleep apnoea therapy: influence of home care support and pressure mode. Eur Respir J. 2009;33(4):804-811.
42.Richards D, Bartlett DJ, Wong K, et al. Increased adherence to CPAP with a group cognitive behavioral treatment intervention: a randomized trial. Sleep. 2007;30(5):635-640.
43.Budhiraja R, Parthasarathy S, Drake CL, et al. Early CPAP use identifies subsequent adherence to CPAP therapy. Sleep. 2007;30(3):320-324.
44.Collen J, Lettieri C, Kelly W, et al. Clinical and polysomnographic predictors of short-term continuous positive airway pressure compliance. Chest. 2009;135(3):704-709.
45.Drake CL, Day R, Hudgel D, et al. Sleep during titration predicts continuous positive airway pressure compliance. Sleep. 2003;26(3):308-311.
46.Kribbs NB, Pack AI, Kline LR, et al. Objective measurement of patterns of nasal CPAP use by patients with obstructive sleep apnea. Am Rev Respir Dis. 1993;147(4):887-895.

Part 2
1.Gay, P., et al., Evaluation of positive airway pressure treatment for sleep related breathing disorders in adults. Sleep, 2006. 29(3): 381-401.
2.Marin, J.M., et al., Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. The Lancet, 2005. 365(9464): 1046-1053.
3.Engleman, H.M. and M.R. Wild, Improving CPAP use by patients with the sleep apnoea/hypopnoea syndrome (SAHS). Sleep Medicine Reviews, 2003. 7(1): 81-99.
4.Verse, T., et al., Recent developments in the treatment of obstructive sleep apnea. Am J Respir Med, 2003. 2(2): 157-168.
5.Hoffstein, V., et al., Treatment of obstructive sleep apnea with nasal continuous positive airway pressure. Patient compliance, perception of benefits, and side effects. Am Rev Respir Dis, 1992. 145(4 Pt 1): 841-845.
6.Stepnowsky, C.J., Jr., M.R. Marler, and S. Ancoli-Israel, Determinants of nasal CPAP compliance. Sleep Med, 2002. 3(3): 239-247.
7.Catcheside, P.G., Predictors of continuous positive airway pressure adherence. F1000 Med Rep, 2010. 2.
8.Lucas, R.E. and B.M. Baird, Extraversion and emotional reactivity. J Pers Soc Psychol, 2004. 86(3): 473-485.
9.Aldwin, C.M., et al., Longitudinal findings from the Normative Aging Study: III. Personality, individual health trajectories, and mortality. Psychol Aging, 2001. 16(3): 450-465.
10.Denollet, J., DS14: standard assessment of negative affectivity, social inhibition, and Type D personality. Psychosom Med, 2005. 67(1): 89-97.
11.Al-Ruzzeh, S., et al., Predictors of poor mid-term health related quality of life after primary isolated coronary artery bypass grafting surgery. Heart, 2005. 91(12): 1557-1562.
12.Johns, M.W., A new method for measuring daytime sleepiness: the Epworth sleepiness scale. Sleep, 1991. 14(6): 540-545.
13.Johns, M.W., Daytime sleepiness, snoring, and obstructive sleep apnea. The Epworth Sleepiness Scale. Chest, 1993. 103(1): 30-36
14.Therapy, C.P.A.P., f.T.S.i.a.D. Population, and W.O.S. Apnea, Continuous Positive Airway Pressure Therapy for Treating Sleepiness in a Diverse Population With Obstructive Sleep Apnea. American Medical Association, 2003.
15.Giles, T.L., et al., Continuous positive airways pressure for obstructive sleep apnoea in adults. Cochrane Database Syst Rev, 2006(3): p. CD001106.
16.Loube, D.I., et al., Indications for positive airway pressure treatment of adult obstructive sleep apnea patients: a consensus statement. Chest, 1999. 115(3): 863-866.
17.Elshaug, A.G., et al., An analysis of the evidence-practice continuum: is surgery for obstructive sleep apnoea contraindicated. J Eval Clin Pract, 2007. 13(1): 3-9.
18.Arias, M.A., et al., CPAP decreases plasma levels of soluble tumour necrosis factor-alpha receptor 1 in obstructive sleep apnoea. Eur Respir J, 2008. 32(4):1009-1015.
19.Horne, R., Adherence to treatment. Cambridge Handbook of Psychology, Health & Medicine,, ed. A. Baum, et al. 2007, Cambridge, UK: Cambridge University Press.
20.McCrae, R.R., et al., Sources of structure: genetic, environmental, and artifactual influences on the covariation of personality traits. J Pers, 2001. 69(4): 511-535.
21.Denollet, J., J. Vaes, and D.L. Brutsaert, Inadequate response to treatment in coronary heart disease : adverse effects of type D personality and younger age on 5-year prognosis and quality of life. Circulation, 2000. 102(6):630-635.
22.Williams, L., et al., Type D personality predicts poor medication adherence in myocardial infarction patients. Psychol Health, 2011. 26(6): 703-712.
23.Engleman, H.M., S.E. Martin, and N.J. Douglas, Compliance with CPAP therapy in patients with the sleep apnoea/hypopnoea syndrome. Thorax, 1994. 49(3): 263-266.
24.Sin, D.D., et al., Long-term compliance rates to continuous positive airway pressure in obstructive sleep apnea: a population-based study. Chest, 2002. 121(2): 430-435.
25.Billings, M.E., et al., Race and residential socioeconomics as predictors of CPAP adherence. Sleep, 2011. 34(12): 1653-1658.
26.Ethnicity and socioeconomic status predict initial continuous positive airway pressure compliance in New Zealand adults with obstructive sleep apnoea.Campbell, A., A. Neill, and R. Lory, Ethnicity and socioeconomic status predict initial continuous positive airway pressure compliance in New Zealand adults with obstructive sleep apnoea. Intern Med J, 2012. 42(6): e95-101.
27.Kupper, N., et al., Heritability of type-D personality. Psychosom Med, 2007. 69(7): 675-681.

Part 3
References
1.Punjabi NM, Caffo BS, Goodwin JL, Gottlieb DJ, Newman AB, O'Connor GT, Rapoport DM, Redline S, Resnick HE, Robbins JA, Shahar E, Unruh ML, Samet JM. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009;6(8):e1000132.
2.Young T, Palta M, Dempsey J, Skatrud J, Weber S, Badr S. The occurrence of sleep-disordered breathing among middle-aged adults. N Eng J Med 1993;328:1230-5.
3.Bearpark H, Elliott L, Grunstein R, Cullen S, Schneider H, Althaus W, et al. Snoring and sleep apnea. A population study in Australian men. Am J Respir Crit Care Med 1995:151:1459-65.
4.Smith IE, Shneerson JM. Is the SF 36 sensitive to sleep disruption? A study in subjects with sleep apnoea. J Sleep Res 1995;4:183-8.
5.Cartwright RD, Knight S. Silent partners: the wives of sleep apneic patients. Sleep 1987;10:244-8.
6.McNicholas WT, Bonsigore MR. Sleep apnoea as an independent risk factor for cardiovascular disease: current evidence, basic mechanisms and research priorities. Eur Respir J 2007; 29: 156–178.
7.Blankfield RP, Hudgel DW, Tapolyai AA, Zyzanski SJ. Bilateral leg edema, obesity, pulmonary hypertension, and obstructive sleep apnea. Arch Intern Med 2000; 160: 2357–2362.
8.Sajkov D, Wang T, Saunders NA, Bune AJ, Mcevoy RD.Continuous positive airway pressure treatment improves pulmonary hemodynamics in patients with obstructive sleep apnea. Am J Respir Crit Care Med 2002; 165: 152–158.
9.Marin JM, Carrizo SJ, Vicente E, et al. Long-term cardiovascular outcomes in men with obstructive sleep apnoea-hypopnoea with or without treatment with continuous positive airway pressure: an observational study. Lancet. 2005 Mar 19-25;365(9464):1046-53.
10.Engleman HM, Kingshott RN, Martin SE, Douglas NJ. Cognitive function in the sleep apnea/hypopnea syndrome (SAHS). Sleep 2000; 23: Suppl. 4, S102–S108.
11.George CF, Smiley A. Sleep apnea and automobile crashes. Sleep 1999; 22: 790–795.
12.Ulfberg J, Carter N, Edling C. Sleep-disordered breathing and occupational accidents. Scand J Work Environ Health 2000; 26: 237–242.
13.McDaid C, Griffin S, Weatherley H. The continuous positive airway pressure for the treatment of obstructive sleep apnoea–hypopnoea syndrome: a systematic review and economic analysis. Health Technol Assess 2009; 13: 1–142.
14.Douglas NJ, George CF. Treating sleep apnoea is cost effective. Thorax 2002; 57: 93.
15.Peker Y, Hedner J, Johansson A, Bende M. Reduced hospitalization with cardiovascular and pulmonary disease in obstructive sleep apnea patients on nasal CPAP treatment. Sleep 1997; 20: 645–653.
16.Mar J, Rueda JR, Dura´n-Cantolla J, Schechter C, Chilcott J. The cost-effectiveness of nCPAP treatment in patients with moderate-to-severe obstructive sleep apnoea. Eur Respir J 2003; 21: 515–522.
17.Hui DS, Shang Q, Ko FW, Ng SS, Szeto CC, Ngai J, Tung AH, To KW, Chan TO, Yu CM. A prospective cohort study of the long-term effects of CPAP on carotid artery intima-media thickness in obstructive sleep apnea syndrome. Respir Res. 2012 Mar 16;13:22.
18.de Araújo MT, Bissoli NS, Gouvêa SA, Pacheco MC, Meyer B, Vasquez EC, Fleury B. CPAP therapy prevents increase in blood pressure after upper airway surgery for obstructive sleep apnoea. Sleep Breath. 2013 May 6.
19.Marrone O, Salvaggio A, Bue AL, Bonanno A, Riccobono L, Insalaco G, Bonsignore MR. Blood pressure changes after automatic and fixed CPAP in obstructive sleep apnea: relationship with nocturnal sympathetic activity. Clin Exp Hypertens. 2011;33(6):373-80.
20.Iftikhar IH, Khan MF, Das A, Magalang UJ. Meta-analysis: Continuous Positive Airway Pressure Improves Insulin Resistance in Patients with Sleep Apnea without Diabetes. Ann Am Thorac Soc. 2013 Apr;10(2):115-20.
21.Robinson, G. V., Pepperell, J. C., Segal, H. C., Davies, R. J., and Stradling, J. R. (2004). Circulating cardiovascular risk factors in obstructive sleep apnoea:data from randomized controlled trials. Thorax 59, 777
22.Sharma, S. K., Agrawal, S., Damodaran, D., Sreenivas,V.,Kadhiravan,T. etal.(2011).CPAP for the metabolic syndrome in patients with obstructive sleep apnea. N. Engl.J. Med. 365, 2277
23.Lavie L, Lavie P. Smoking interacts with sleep apnea to increase cardiovascular risk. Sleep Med 2008; 9: 247–253.
24.Riha RL, Gislasson T, Diefenbach K. The phenotype, genotype of adult obstructive sleep apnoea/hypopnea syndrome. Eur Respir J 2009; 33: 646–655.
25.Grunstein RR, Stenlof K, Hedner JA, Peltonen M, Karason K, Sjostrom L. Two year reduction in sleep apnea symptoms and associated diabetes incidence after weight loss in severe obesity. Sleep 2007; 30: 703–710.
26.Newman AB, Foster G, Givelber R, Nieto FJ, Redline S, Young T. Progression and regression of sleep-disordered breathing with changes in weight: the Sleep Heart Health Study. Arch Intern Med 2005; 165: 2408–2413.
27.Spivak H, Hewitt MF, Onn A, Half EE. Weight loss and improvement of obesity-related illness in 500 U.S. patients following laparoscopic adjustable gastric banding procedure. Am J Surg 2005; 189: 27–32.
28.Tanne F, Gagnadoux F, Chazouilleres O, Fleury B, Wendu D., et al. Chronic liver injury during obstructive sleep apnea. Hepatology 2005; 41:1290–1296.
29.Jouet P, Sabate JM, Maillard D, Msika S, Mechler C, Ledoux S, et al. Relationship between obstructive sleepapnea and liver abnormalities in morbidly obese patients: a prospective study. Obes. Surg. 2007;17: 478-485.
30.Kallwitz ER, Herdegen J, Madura J, Jakate S, Cotler SJ. Liver enzymes and histology in obese patients with obstructive sleep apnea. J. Clin.Gastroenterol. 2007;41:918-921.
31.Polotsky VY, Patil SP, Savransky V, Laffan A, Fonti S, Frame LA, et al. Obstructive sleep apnea, insulin resistance, and steatohepatitis in severe obesity. Am.J.Respir. Crit.CareMed. 2009;179: 228
32.Drager LF, Lopes HF, MakiNunes C, Trombetta IC, Toschi-Dias E, Alves MJ, et al. The impact of obstructive sleep apnea on metabolic and inflammatory markers inconsecutive patients with metabolic syndrome. PLoSONE 2010; 5:e12065.
33.Bonsignore M R, Esquinas C, Barcelo A, et al. Metabolic syndrome, insulin resistance and sleepiness in real-life obstructive sleep apnoea. Eur.Respir. J. 2012;39:1136–1143.
34.Polotsky,V.Y., Rubin,A.E., Balbir, A., Dean,T., Smith,P.L.,Schwartz, A. R., et al. Intermittent hypoxia causes REM sleep deficits and decreases EEG delta power in NREMsleepintheC57BL/6Jmouse. SleepMed. 2006;7:7-
35.Aron-Wisnewsky, J., Minville, C., Tord- jman, J., Levy, P., Bouillot, J. L., Bas- devant, A., et al. Chronic intermittent hypoxia is a major TG for non-alcoholic alcoholic fatty liver disease in morbid obese. J. Hepatol. 2012;56, 225
36.Drager LF, Li J, Reinke C, Bevans-Fonti S, Jun JC, Polotsky VY. Intermittent hypoxia exacerbates metabolic effects of diet-induced obesity. Obesity (Silver Spring). 2011 Nov;19(11):2167-74.
37.Savransky V, Bevans S, Nanayakkara A, Li J, Smith PL, Torbenson MS, et al. Chronic intermittent hypoxia causes hepati- tis in a mouse model of diet- induced fatty liver. Am J Physiol Gastrointest Liver Physiol. 2007;293, G871
38.Bellentani S, Saccoccio G, Masutti F, Croce LS, Brandi G, Sasso F, et al. Prevalence of and risk factors for hepatic steatosis in Northern Italy. Ann Intern Med. 2000;132: 112-
39.Browning JD, Horton JD. Molecular mediators of hepatic steatosis and liver injury. J. Clin. Invest. 2004;114:147
40.Browning JD, Szczepaniak LS, Dobbins R, Nuremberg P, Horton JD, Cohen JC, et al. Prevalence of hepatic steatosis in a nurban population in the United States: impact of ethnicity. Hepatology 2004;40:1387
41.Clark JM. The epidemiology of nonalcoholic fatty liver disease in adults. J. Clin.Gastroenterol.2006; 40:S5
42.McCullough AJ. Pathophysiology of nonalcoholic steatohepatitis. J. Clin. Gastroenterol. 2006;40:S17
43.Diehl AM. Lessons from animal models of NASH. Hepatol.Res. 2005: 33:138
44.Clark JM, Diehl AM. Non alcoholic fatty liver disease: an underrecognized cause of cryptogenic cirrhosis. JAMA 2003;289:3000
45.Marchesini G, Bugianesi E, Forlani G, Cerrelli F, Lenzi M, Manini R, et al. Nonalcoholic fatty liver, steatohepatitis, and the metabolic syndrome. Hepatology 2003;37(4):917-923.
46.Jonathan C. Cohen, Jay D. Horton, Helen H. Hobbs. Human Fatty Liver Disease: Old Questions and New Insights, Science 2011:24, 1519-1523
47.Sass DA, Chang P, Chopra KB. Nonalcoholic fatty liver disease: a clinical review. Dig Dis Sci 2005;50(1):171-180.
48.Bugianesi, E., Leone, N., Vanni, E., Marchesini, G., Brunello, F.,Carucci, P., et al. (2002). Expanding the natural history of nonalcoholic steato- hepatitis: from cryptogenic cirrhosis to hepatocellular carcinoma. Gastroenterology 123, 134
49.Dixon,J.B.,Bhathal,P.S.,andO’Brien, P.E.(2001).Non alcoholic fatty liver disease: predictors of nonalcoholic steatohepatitis and liver fibrosis in the severely obese. Gastroenterology 121, 91
50.Jennum P, Riha RL. Epidemiology of sleep apnoea/hypopnoea syndrome and sleep-disordered breathing. Eur Respir J. 2009 Apr;33(4):907-14.
51.Mirrakhimov AE, Polotsky VY. Obstructive sleep apnea and non-alcoholic Fatty liver disease: is the liver another target? Front Neurol. 2012;3:149.
52.Younossi ZM, Diehl AM, Ong JP: Nonalcoholic fatty liver disease: an agenda for clinical research. Hepatology 35:746–752, 2002
53.Day CP: Pathogenesis of steatohepatitis. Best Pract Res Clin Gastroenterol 16:663–678, 2002
54.Donnelly KL, Smith CI, Schwarzenberg SJ, et al. Sources of fatty acids stored in liver and secreted via lipoproteins in patients with nonalcoholic fatty liver disease. J Clin Invest 2005;115(5):1343- 1351.
55.Madan K, Bhardwaj P, Thareja S, Gupta SD, Saraya A. Oxidant stress and antioxidant status among patients with nonalcoholic fatty liver disease (NAFLD). J Clin Gastroenterol 2006;40(10):930-935
56.Kohler M, Stradling JR. Mechanisms of vascular damage in obstructive sleep apnea. Nat Rev Cardiol 2010;7(12):677-685.
57.Neuschwander-Tetri BA, Caldwell SH. Nonalcoholic steatohepatitis: summary of an AASLD Single Topic Conference. Hepatology 2003; 37(5):1202-1219.
58.Edmison J, McCullough AJ. Pathogenesis of non-alcoholi alcoholic steatohepatitis: human data. Clin Liver Dis 2007;11(1):75-104.
59.Singh H, Pollock R, Uhanova J, Kryger M, Hawkins K, Minuk GY. Symptoms of obstructive sleep apnea in patients with nonalcoholic fatty liver disease. Dig Dis Sci 2005;50(12):2338-2343.
60.Türkay C, Ozol D, Kasapoğlu B, Kirbas I, Yıldırım Z, Yiğitoğlu R. Influence of obstructive sleep apnea on fatty liver disease: role of chronic intermittent hypoxia. Respir Care. 2012 Feb;57(2):244-9.
61.Pamidi S, Tasali E. Obstructive sleep apnea and type 2 diabetes: is there a link? Front Neurol. 2012;3:126.
62.Louis,M.,andPunjabi,N.M.(2009). Effects of acute intermittent hypoxia on glucose metabolism in awake healthy volunteers. J. Appl.Physiol. 106, 1538
63.Abdelmalek, M. F. and Diehl, A. M. (2007) Nonalcoholic fatty liver disease as a complication of insulin resistance. Med. Clin. North Am. 91, 1125–1149
64.Adams, L. A. and Lindor, K. D. (2007) Nonalcoholic fatty liver disease. Ann. Epidemiol. 17, 863–869
65.Charlton, M. (2004) Nonalcoholic fatty liver disease: a review of current understanding and future impact. Clin. Gastroenterol. Hepatol. 2, 1048–1058
66.Postic, C. and Girard, J. (2008) Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice. J. Clin. Invest. 118, 829–838
67.Harsch IA, Schahin SP, Bruckner K, Radespiel-Troger M, Fuchs FS, Hahn EG, Konturek PC, Lohmann T, Ficker JH. The effect of continuous positive airway pressure treatment on insulin sensitivity in patients with obstructive sleep apnoea syndrome and type 2 diabetes. Respiration 2004;71(3):252–9.
68.Brooks B, Cistulli PA, Borkman M, Ross G, McGhee S, Grunstein RR, Sullivan CE, Yue DK. Obstructive sleep apnea in obese noninsulin-dependent diabetic patients: effect of continuous positive airway pressure treatment on insulin responsiveness. J Clin Endocrinol Metab 1994;79(6): 1681–5.
69.Aronsohn RS, Whitmore H, Van Cauter E, Tasali E. Impact of untreated obstructive sleep apnea on glucose control in type 2 diabetes. Am J Respir Crit Care Med 2010;181(5):507–13.

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