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Metabolic Syndrome - Drug Management- Chih-Hsing Wu, MD Body Composition, Obesity and Osteoporosis Research Center, Department of Family Medicine, NCKUH.

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Presentation on theme: "Metabolic Syndrome - Drug Management- Chih-Hsing Wu, MD Body Composition, Obesity and Osteoporosis Research Center, Department of Family Medicine, NCKUH."— Presentation transcript:

1 Metabolic Syndrome - Drug Management- Chih-Hsing Wu, MD Body Composition, Obesity and Osteoporosis Research Center, Department of Family Medicine, NCKUH


3 Definition of Metabolic Syndrome in Taiwan (Central obesity) / BMI waist : 90 cm 80 cm BMI 27 (Central obesity) waist : 90 cm 80 cm (BP) SBP 130 mmHg /DBP 85 mmHg (BP) SBP 130 mmHg /DBP 85 mmHg (HDL-C) <40 mg/dl <50 mg/dl (HDL-C) <40 mg/dl <50 mg/dl (Fasting glucose) FG 110 mg/dl (Fasting glucose) FG 100 mg/dl (Triglyceride) TG 150 mg/dl (Triglyceride) TG 150 mg/dl

4 60 xx (90) 28% 136 / 86 (130/85) mmHg 72/min 105 mg/dl (100), 204 mg/dl, 156 mg/dl (150), 36 mg/dl (40), 8.1 mg/dl, 1.1 mg/dl,

5 Metabolic Syndrome = Pre-Disease MicrovascularComplicationsMicrovascularComplications MacrovascularDiseaseMacrovascularDisease Risk Relative To General Population Years of Diabetes Insulin Resistance Dyslipidemia Hypertension Hyperglycemia © 2001 International Diabetes Center. All rights reserved. Adapted from: Kendall DM. Am J Manag Care 7S327-S343, Pre-diabetes Type 2 Diabetes Metabolic syndrome

6 (1023) % % % % %

7 CVD Risks and Anthropometric Index in Male Elderly Taiwanese - Huang KC, et al. Obes Res 2005;13:170-8

8 CVD Risks and Anthropometric Index in Female Elderly Taiwanese - Huang KC, et al. Obes Res 2005;13:170-8

9 Obesity and Metabolic Syndrome: A Cluster of Coronary Heart Disease Risk Factors Adapted from Grundy SM. J Clin Endocrinol Metab. 2005;89: Raised Blood Pressure Autonomic Dysfunction Proinflammatory State Genetic Susceptibility Insulin Resistance Obesity Diet Physical Inactivity Stress Prothrombotic State Small Low-Density Small Low-Density Lipoprotein Particles High-Density Lipoprotein Cholesterol High-Density Lipoprotein Cholesterol Triglycerides Triglycerides Atherogenic Dyslipidemia


11 35 40 ( ) 30.0~ ~39.9 ( ) 27.0~ ~ ~34.9 ( ) 24.0~ ~ ~ ~ ~ ~ (2000) 1998 = ( ) ( ) ~ ~ ~ ~ (2005) 24.0~26.9

12 16 T P<0.05* Chen YJ, Wu CH, et al.Chin J Fam Med 2005; 15(4):


14 Drugs Approved by FDA for Treating Obesity Generic Name Trade Names DEA Schedule Approved Use Year Approved OrlistatXenicalNoneLong-term1999 SibutramineMeridiaIVLong-term1997 DiethylpropionTenulateIVShort-term1973 Phentermine Adipex, lonamin IVShort-term1973 Phendimetrazine Bontril, Prelu-2 IIIShort-term1961 BenzphetamineDidrexIIIShort-term1960 -Yanovski SZ, et al. N Engl J Med 2002;346:

15 15 (Xenical) 30% of triglycerides pass undigested and are excreted. 30%

16 Meta-analysis of RCTs Evaluating Effect of Orlistat Therapy on Weight Loss at 1-Year Study or Sub-category WMD (random) 95% CI Hollander 1998* Sjostrom 1998 Davidson 1999 Finer 2000 Heuptman 2000 Lindgarde 2000 Rossner 2000 Bakris 2002 Broom 2002 Kelley 2002* Miles 2002* Total (95% CI) Padwal et al. Int J Obes 2003;27:1437 *All subjects had type 2 diabetes WMD=weighted mean difference Favours Treatment Favours Control

17 FDA advisory committee approval for a low dose (60 mg) over-the-counter orlistat product (Alli) in 2007.

18 NA 5-HT Adapted from Ryan et al. Obesity Res. 1995;3(suppl 4):553S-559S. S = sibutramine = noradrenaline, = serotonin (Reductil) (Reductil) RELEASE S S S Catabolism Reuptake MAO Reuptake MAO S

19 Meta-analysis of RCTs Evaluating Effect of Sibutramine Therapy on Weight Loss at 1-Year Study or Sub-category WMD (random) 95% CI McMahon 2000 Smith 2001 McMahon 2002 * Total (95% CI) Padwal et al. Int J Obes 2003;27:1437 All subjects had hypertension WMD=weighted mean difference -10 Favours Treatment Favours Control

20 Sibutramine, Orlistat or Combination Therapy for 12 week in Turkey(n=86) -Aydin N, et al. Tohoku J Exp Med 2004;202:173-80

21 Similar Effects The body weight, BMI and body fat change between baseline and 6-month interval in NCKUH * * * * * Wu CH, et al. 2008: submitted

22 Average weight loss of subjects completing a minimum 1- year weight-management intervention; based on review of 80 studies (N=26,455; 18,199 completers [69%]). Franz MJ, et al. J Am Diet Assoc. 2007;107:

23 BMI (HbA 1c ) 5-6Kg 10% < 23 kg/M

24 Cardinal Behaviors of Successful Long- term Weight Management National Weight Control Registry Data Self-monitoring: –Diet: record food intake daily, limit certain foods or food quantity –Weight: check body weight >1 x/wk Low-calorie, low-fat diet: –Total energy intake: kcal/d –Energy intake from fat: 20%-25% Eat breakfast daily Regular physical activity: kcal/wk (eg, walk 4 miles/d) Klem et al. Am J Clin Nutr 1997;66:239. McGuire et al.Int J Obes Relat Metab Disord 1998;22:572.

25 Pathogenesis of Metabolic syndrome 2 major, interacting causes Obesity and abnormal body fat distribution disorders of adipose tissue. Endogenous metabolic susceptibility Insulin resistance A constellation of independent factors (e.g. molecules of hepatic, vascular, and immunologic origin) Contributors: aging, proinlfammatory state, hormonal change. Grundy SM et al: Circulation 2004;109:433-8 Grundy SM: Am J Clin Nutr 2006 Aug 1248


27 - Diabetologia 2003;(suppl 1):M30-M36 Mean Efficacy of Pharmacological Treatment Options in Type II DM

28 Side Effect of Oral Hypoglycemic Agents - Endocrinol Metab Clin North Am 2001; 30(4):

29 Placebo Metformin Lifestyle Metformin- Mean Weight Change The DPP Research Group, NEJM 346: , 2002

30 Weight Change of DM patients using Acarbose in Taiwan Patients Initial visitFirst follow-upSecond follow-upThird follow-up kg Hung YJ, et al. Clin Drug Invest 2006;26:559-65

31 Data from Henry. Endocrinol Metab Clin. 1997;26: Gitlin, et al. Ann Intern Med. 1998;129: Neuschwander-Tetri, et al. Ann Intern Med. 1998;129:38-41 Medical Management of Type 2 Diabetes. 4th ed. Alexandria, Va: American Diabetes Association; 1998: Fonseca, et al. J Clin Endocrinol Metab. 1998;83: Data from Bell & Hadden. Endocrinol Metab Clin. 1997;26: De Fronzo, et al. N Engl J Med. 1995;333: Bailey & Turner. N Engl J Med. 1996;334: Medical Management of Type 2 Diabetes. 4th ed. Alexandria, Va: American Diabetes Association; 1998: Goldberg, et al. Diabetes Care 21: to 1.7% 0/+ +++ HbA1 C reduction Action on insulin resistance Action on insulin secretion 1% to 2% Conventional Sulfonylureas 0/ % to 2% Biguanides % to 2% New SU % to 1.3% Glitazones % to 1% -glucosidase inhibitors 0 0 Glinides Similar Effect of Hypoglycemic Agents Postprandial Primary Goal Fasting Postprandial

32 Characters of individuals in MetS of NHANESIII - Jacobson TA, et al. Diabet Obes Metab 2004;6:353-62

33 Intra-abdominal adiposity promotes insulin resistance and increased CV risk Hepatic FFA flux (portal hypothesis) Secretion of metabolically active substances (adipokines) suppression of lipolysis by insulin FFA Insulin resistance Dyslipidaemia PAI-1 Adiponectin IL-6 TNF Intra-abdominal adiposity Net result: Insulin resistance Inflammation Pro-atherogenic Heilbronn et al 2004; Coppack 2001; Skurk & Hauner 2004

34 Metabolic Syndrome Pathology : Visceral Fat, Atherosclerosis Physiology : Insulin Resistance Assessment : Abdominal Obesity, CAD risk Regimen : Weight reduction, Insulin Sensitizer

35 Fat Topography in MetS and Diabetic Subjects High TG High FFA Intramuscular Fat Intrahepatic Fat Subcutaneous Fat Intraabdominal Fat Bays H, Mandarino L, DeFronzo RA. J Clin Endocrinol Metab. 2004;89:

36 Intramuscular Fat Intrahepatic Fat Intraabdominal Fat Subcutaneous Fat Effect of Thiazolidinediones on Fat Topography High TG High FFA TG FFA TZD Bays H, Mandarino L, DeFronzo RA. J Clin Endocrinol Metab. 2004;89:

37 StudyInterventionRR (%) ACT NOWPioglitazone vs placebo 78% DREAMRosiglitazone vs placebo 62% Finnish DPSIntensive lifestyle vs control 58% Da Qing studyIntensive lifestyle vs control 38% DPPIntensive lifestyle vs placebo Metformin vs placebo Troglitazone vs placebo 58% 31% 75% IDPPMetformin + lifestyle Metformin 31% 19% TRIPODTroglitazone (after gestational diabetes) 50% Fasting Hyperglycemic Study Gliclazide or intensive lifestyleNo effect STOP-NIDDMAcarbose vs placebo 25% XENDOSOrlistat + lifestyle vs placebo 37% Diabetes prevention trials Tuomilehto J, et al. N Engl J Med 2001; Pan XR, et al. Diabetes Care 1997; Knowler WC, et al. N Engl J Med 2002; Ramachandran A, et al. Diabetologia 2006; DREAM Trial Investigators. Lancet, N Engl J Med 2006; Buchanan TA, et al. Diabetes 2002; Karunakaran S, et al. Metabolism 1997; Chiasson JL, et al. Lancet 2002; Torgerson JS, et al. Diabetes Care ACTosNOW. Diabetologia 2008 DREAM Trial Investigators. Lancet 2006; 368:1096– Accessed October 2006.

38 ADOPT (A Diabetes Outcome Progression Trial) -Fasting Plasma Glucose Over Time- Rosiglitazone vs Metformin 9.8 ( 12.7 to 7.0), P<0.001 Rosiglitazone vs Glyburide 17.4 ( 20.4 to 14.5), P<0.001 mg/dl Glyburide Metformin Rosiglitazone Time (years)

39 Other Adverse Events 335 (23%) Weight gain, n (%) Gastrointestinal, n (%) Hypoglycaemia, n (%) Oedema, n (%) 557 (38%)316 (22%) 100 (7%)18 (1%)47 (3%) 142 (10%)168 (12%)557 (39%) 205 (14%)104 (7%)123 (9%) P<0.05 vs. rosiglitazone Rosiglitazone (N = 1456) Metformin (N = 1454) Glyburide (N = 1441)

40 NEJM 2007;356;437-40

41 Role of DPP-4, GLP-1, GIP in glucose homeostasis Herman GA, et al. Clin Pharmacol Ther. 2007;81:761-7

42 Amori RE, et al. JAMA 2007;298: Mean Difference in BW Change for Gliptins vs Control in Adults With Type 2 Diabetes

43 Major Targeted Sites of Oral Drug Classes Buse JB et al. In: Williams Textbook of Endocrinology. 10th ed. Philadelphia: WB Saunders; 2003:1427–1483; DeFronzo RA. Ann Intern Med. 1999;131:281–303; Inzucchi SE. JAMA 2002;287: ; Porte D et al. Clin Invest Med. 1995;18:247–254. DPP-4=dipeptidyl peptidase 4; TZDs=thiazolidinediones. Glucose absorption Hepatic glucose overproduction Impaired insulin secretion Insulin resistance Pancreas Glucose level Muscle and fat Liver Biguanides TZDs Biguanides Sulfonylureas Meglitinides TZDs α-Glucosidase inhibitors Gut DPP-4 inhibitors Biguanides (indirect) DPP-4 inhibitors (indirect)

44 Developing Avenue of Ideal OADs OADsGlycemic Effect B-cell Preserve Insulin Sensitizing Neutral Weight Low Hypoglycemia QD Dosage SU++++/- Non-SU+++ BG++++ A-GI+++ Glitazone Gliptins++ +/-++++

45 Modified from UKPDS 34. Lancet 1998; 352: Weight change (kg) Years from randomisation Insulin Metformin, Acarbose DPP-4 inhibitors (?) Diet alone Chlorpropamide Glibenclamide Weight gain with antidiabetic therapy UK Prospective Diabetes Study and Update Meglitinides (?) Glitazones (supposed)

46 Chiang CW, et al. J Clin Phar Therapeutics 2006;31:73-82 Trends in the prescribing patterns of OADs for outpatients in Taiwan, Combination = 62.9% Any three OAD = 10.9%

47 Reilly & Rader 2003; Eckel et al 2005 Plaque rupture/thrombosis Cardiovascular events Atherosclerosis Insulin resistance TG Metabolic syndrome HDL BP Inflammatory markers Pathophysiology of the metabolic syndrome leading to atherosclerotic CV disease Adipocyte Monocyte/ macrophage Genetic variationEnvironmental factors Abdominal obesity CytokinesAdipokines

48 Cardiovascular Disease Mortality Increased in the Metabolic Syndrome Lakka et al. JAMA. 2002;288:2709– RR (95% Cl), 3.55 (1.98–6.43) Metabolic syndrome Yes No Cumulative hazard, % Follow-up, y

49 Disability-adjusted life years (DALYs) attributable to high blood pressure in 2001 Lawes CCM, et al. Lancet 2008; 371: 1513–18 M/L F/L F/H

50 Effect of antihypertensive agents in patients with mild hypertension (TOMHS 4-year data) Neaton et al. JAMA 1993;270:713–724. SBP after 48 months (mmHg) DBP after 48 months *P<0.01 vs placebo * * * * * * * * Acebutolol (n=126) Amlodipine (n=114) Chlorthalidone (n=117) Doxazosin (n=121) Enalapril (n=119) Placebo (n=207) (mmHg) Neaton et al. JAMA 1993;270:713–724.

51 Elliott WJ, Meyer PM. Lancet 2007; 369: 201–207. New-onset DM with antihypertensives -143,153 subjects, network meta-analysis-

52 Conditions favouring use of some antihypertensive drugs-ESC 2007 Guideline Journal of Hypertension 2007, 25:1105–1187


54 Clinical efficacy and tolerability of alpha-blocker doxazosin as add-on therapy in patients with hypertension and impaired glucose metabolism Nutrition, Metabolism & Cardiovascular Diseases (2006) 16, weeks of combined therapy

55 ESH-ESC 2007 Guidelines a 1 -blockers… have been shown to adequately lower blood pressure and to also have favorable metabolic effects. As the only trial testing an a 1 -blocker (the doxazosin arm of the ALLHAT trial) was interrupted before crucial evidence could be obtained, the overall benefits or harm of a 1 -blockers for antihypertensive therapy remain unproved. However, all these agents have been frequently used as added drugs in trials documenting cardiovascular protection and can thus be employed for combination treatment. a1-blockers have a specific indication in the presence of benign prostatic hypertrophy. Journal of Hypertension 2007;25: P. 1141

56 AASK MAP <92 Target BP (mmHg) Multiple antihypertensive agents are needed to achieve target BP Number of antihypertensive agents 1 UKPDS DBP <85 ABCD DBP <75 MDRD MAP <92 HOT DBP <80 Trial 234 DBP, diastolic blood pressure; MAP, mean arterial pressure; SBP, systolic blood pressure IDNTSBP <135/DBP <85 ALLHATSBP <140/DBP <90 Bakris GL, et al. Am J Kidney Dis 2000;36: ; Lewis EJ, et al. N Engl J Med 2001;345: ; Cushman WC, et al. J Clin Hypertens 2002;4: DOX-EM-07004

57 Combination Therapy Emphasized in All Guidelines JNC 7 Most patients with hypertension will require 2 or more antihypertensive medications to achieve goal BP If BP is more than 20/10 mm Hg above goal BP, consideration should be given to initiating therapy with 2 agents, 1 of which usually should be a thiazide-type diuretic WHO/ISH Less than half of hypertension patients will attain target pressures with monotherapy; as many as 30% will need 3 or more drugs Diuretic should be a component of combination therapy ESH-ESC 2007 Regardless of the drug employed, monotherapy allows to achieve BP target in only a limited number of hypertensive patients Use of more than one agent is necessary to achieve target BP in the majority of patients. In several patients BP control is not achieved by two drugs and a combination of three of more drugs is required. Chobanian et al. JAMA. 2003;289: ; WHO Writing Group. J Hypertens. 2003;21: ESH-ESC J. Hypertens. Chobanian et al. JAMA. 2003;289: ; WHO Writing Group. J Hypertens. 2003;21: ESH-ESC J. Hypertens. 2007;25:

58 Model for Origins of Atherogenic Dyslipidemia of Obesity and MetS Adiposity Adiposity High carbohydrate diet High carbohydrate diet Insulin resistance Insulin resistance Genetic predisposition Genetic predisposition Pattern A Pattern B Adapted from Berneis KK, Krauss RM. J Lipid Res. 2002;43: Plasma TG TG pool High Small LDL Low Remnants Larger VLDL Smaller VLDL LDL-R LPL/HLLPL/HL LPLLPL CholChol CETPCETP TGTG IDL Large LDL Smaller LDL HDL Smaller HDL HL<90<90>175 LPL LPL CETP, cholesteryl ester transfer protein; Chol, cholesterol; HDL, high-density lipoprotein; HL, hepatic lipase; IDL, intermediate- density lipoprotein; LDL, low-density lipoprotein; LDL-R, LDL receptor; MetS, metabolic syndrome; TG, triglycerides; VLDL, very-low-density lipoprotein.

59 HDL Cholesterol, Very Low Levels of LDL Cholesterol, and Cardiovascular Events N Engl J Med 2007;(Sep 27)357:

60 BNHI Treatment Guideline - Taiwan 2 Risk Factors –TC 200 mg/dL or LDL 130 mg/dL TC < 200mg/dL LDL < 130mg/dL TG 200 mg/dL –TC/HDL >5 or HDL< 40 mg/dL TG < 200mg/dL TC 200mg/dL < 160mg/dL LDL 130mg/dL 100mg/dL TG 200 mg/dL - TC/HDL >5 or HDL< 40 mg/dL TG < 200mg/dL With CVD or DM Patients Without CVD Patients

61 Taiwan Association of Diabetes (n=7541) Source: TADE 2005 data (%) Total (n = 7541) A+B+C4.1 (n=310) A1C test >1x/year96.6 (n=7288) A1C> (n=1121) A1C >920.0 (n=1507) A1C (n=857) A1C<731.3 (n=2363) BP<140/ (n=4893) BP<130/ (n=2305) LDL-C< (n=4255) LDL-C<100 or TC< (n=2516) LDL test frequency79.8 (n=6018)

62 Trends of Higher Dosage of Statins

63 Statins dosage vs LDL-C reduction rate % Reduction in LDL-C Lovastatin 20/80 mg Fluvastatin 20/80 mg Simvastatin 20/80 mg Pravastatin 20/80 mg Atorvastatin 10/80 mg Response to Minimum/Maximum Statin Dose * Adapted from Illingworth. Med Clin North Am. 2000;84:23. *Pravachol ® (pravastatin) PI. *CRESTOR (rosuvastatin) for active control study PI. Rosuvastatin 10/40 mg 55

64 10 mg20 mg40 mg80 mg 0 0,5 1,0 1,5 2,0 2,5 20 mg40 mg80 mg % Patients of AEs 40 mg80 mg 4 x 1.7 x 2.3 x Atorvastatin Lovastatin Simvastatin Physicians Desk Reference (PDR) mg Statin LDL-Reduction (%) mg - 6% +20 mg - 6% +40 mg - 6% mg Statins limitation ( rule of 6% )

65 Lipid Lowering through Dual Inhibition of Both Cholesterol Production and Absorption HMG-CoA=3-hydroxy-3-methylglutaryl coenzyme A Adapted from Shepherd J Eur J Cardiol Suppl 2001:3(suppl E):E2–E5; Miettinen TA Int J Clin Pract 2001; 55:710–716. Production in liverAbsorption from intestine LDL-C VLDL Biliary cholesterol Chylomicrons Points of therapeutic intervention Cholesterol synthesis (HMG-CoA reductase) Bloodstream Dietary cholesterol Statin Ezetimibe

66 % of patients achieving target goal of LDL-C Statin + PLStatin + EZE N% to goalN DM * Non-DM * MetS * Non-MetS * * p < vs. Statin + Placebo Further reduction in LDL-C ranging from % across the 4 subgroups Ezetimibe Plus Statins in Patients with DM and Metabolic Syndrome Simons L et al Curr Med Res Opin 2004;20:

67 PI = Placebo; Rx = Treatment; SC = Structured Care; UC = Usual Care. Athyros VG et al. Curr Med Res Opin. 2002;18: Downs JR et al. JAMA. 1998;279: Heart Protection Study Collaborative Group. Lancet. 2002;360:7-22. The LIPID Study Group. N Engl J Med. 1998;339: S Study Group. Lancet. 1995;345: Sacks FM et al. N Engl J Med. 1996;335: Shepherd J et al. N Engl J Med. 1995;333: Relation Between CHD Events and LDL-C in Statin Trials AFCAPS-PI Mean LDL-C Level at Follow-up (mg/dL) % With CHD Event CARE-Rx LIPID-Rx 4S-Rx CARE-PI LIPID-PI 4S-PI SecondaryPrevention PrimaryPrevention WOSCOPS-PI WOSCOPS-Rx AFCAPS-Rx GREACE-UC GREACE-SCLIPS-PlLIPS-RX

68 Goals for Management of Hyperlipidemia in Patients With Diabetes LDL-C = low-density lipoprotein cholesterol; CVD = cardiovascular disease; ESC = European Society of Cardiology; EASD = European Association for the Study of Diabetes; ADA = American Diabetes Association; AHA = American Heart Association; ACC = American College of Cardiology; JBS2 = Second Joint British Societies; NCEP ATP III = National Cholesterol Education Program Adult Treatment Panel III a Optional/reasonable goals; b Or LDL-C reduction of 30% from baseline Rydén L, et al. Eur Heart J doi: /eurheartj/ehl261; American Diabetes Association. Diabetes Care. 2007;30(suppl 1):S4–S41; Smith SC, et al. Circulation. 2006;113:2363–2372; Buse JB, et al. Circulation. 2007;115:114–126; Joint British Societies 2. Heart. 2005; 91(suppl V):v1–v52; Grundy SM, et al. Circulation. 2004;110:227–239. Guidelines LDL-C Goal Diabetes With CVD a Diabetes Without CVD ESC/EASD 2007 <70 mg/dL (<1.8 mmol/L) <97 mg/dL (<2.5 mmol/L) ADA/AHA/ACC 2007 <70 mg/dL (<1.8 mmol/L) <100 mg/dL (<2.6 mmol/L) JBS <77 mg/dL b (<2.0 mmol/L) <77 mg/dL b (<2.0 mmol/L) NCEP ATP III 2004 <70 mg/dL (<1.8 mmol/L) <100 mg/dL (<2.6 mmol/L)

69 Upcoming 2009

70 Change Lifestyle is the Key Annu. Rev. Pharmacol. Toxicol. 2007;47:565–92

71 Acknowledgement ORC, SLRHC, NY, USA Xavier Pi-Sunyer Dympna Gallagher Jack Wang Stanley Heshka ZiMian Wang Richard N. Pierson,Jr Yiying Zhang Experts in ORC …… Kyoto University, Japan Kazuwa Nakao Yoshihiro Ogawa Inje University, Korea Jaeheon Kang NCKU, Taiwan Chih-Jen Chang Yi-Ching Yang Mi-Cha Ma Wei-Jen Yao Cho-Jeng Peng Shu-Hui Chen NTU, Taiwan Kuo-Chin Huang Keh-Song Tsai CMCU, Taiwan Wen-Yuan Lin WF Hospital, Taiwan Liu Tsan-Hung ChangHwa Christian H, Taiwan Shih-Te Tu VGH Taipei, Taiwan Low-Tone Ho Ching-Fai Kwok YangMing University, Taiwan Jin-Jong Chen Beijing Capital H, China Xiangyan Ruan Natl KS Normal Univ, Taiwan Ray-Tai Chang TSGH Taipei, Taiwan Shih Kwan-Jong Chu Nan-Fong

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