复旦大学：《循证医学》课程教学资源（预习资料）生命质量分析评价预习

Unt8:生命质量的分析评价 主讲教师:姜林娣助理教师:马莉莉 授课时间:2010年4月13日(1班);2010年4月16日(2班) 教学目的:掌握和熟悉生命质量评价的概念和方法 教学内容:1、掌握:生命质量分析评价的方法和原理;2、熟悉:生命质量 分析的应用,效用值临床意义,测定方法;3、了解:生命质量分析的常用量表 三、教学重点:生命质量分析评价的方法和原理 四、教学难点:1、生命质量分析评价方法的选择及对临床决策的作用。2、效用 值测定方法 五、课堂知识点 1.功能状况、健康和生命质量 2.健康相关生活质量包含内容 3.健康相关生活质量量表主要检验方面 4.效用值定义、表示方法和测定方法 六、中文和英文关键词 生命质量分析 quality of life analysis,质量调整生命年, quality- adjusted life year (QALY),费用-效果评价cost- effectiveness analysis 七、预习与思考: 1, The burden of osteoarthritis: clinical and quality-of-life issues. Moskowitz RW (1)关节有哪些损害 (2)我们如何评价它 (3)临床上还有那些实例:如肿瘤、心血管疾病 2、SF-36健康调査量表中文版的研制及其性能测试(李鲁) (1)熟悉量表检验包括几部分,几个方面如何将国外量表应用到我们的临床工作 中? (2)国外量表应用于临床的过程? 3. A Systematic Review of Health State Utility Values for Osteoporosis Related Conditions (J. E. Brazier) (1)效用值临床应用价值 (2)测定效用值方法 (3)测定效用值的人群 4、EQ-5D量表和HAQ量表 八、参考书及文献目录 1.《循证医学与临床实践》(第2版),王吉耀主编,科学出版社 2. The Lancet handbook of essential concepts in clinical research. Schulz KF, Grimes DA. Philadelphia, PA, USA: Elsevier, 2006 3. Measuring quality of life using quality of life measures in the clinical setting I Higginson et al. BMJ 2001; 322: 1297-1300 4.www.sf-36.org 第131页

Unit 8：生命质量的分析评价 主讲教师：姜林娣 助理教师：马莉莉 授课时间：2010 年 4 月 13 日（1 班）；2010 年 4 月 16 日（2 班） 一、教学目的：掌握和熟悉生命质量评价的概念和方法 二、教学内容：1、掌握：生命质量分析评价的方法和原理；2、熟悉：生命质量 分析的应用,效用值临床意义，测定方法；3、了解：生命质量分析的常用量表 三、教学重点：生命质量分析评价的方法和原理 四、教学难点：1、生命质量分析评价方法的选择及对临床决策的作用。2、效用 值测定方法 五、课堂知识点： 1． 功能状况、健康和生命质量 2． 健康相关生活质量包含内容 3． 健康相关生活质量量表主要检验方面 4． 效用值定义、表示方法和测定方法 六、中文和英文关键词 生命质量分析 quality of life analysis，质量调整生命年，quality-adjusted life year (QALY)，费用-效果评价 cost-effectiveness analysis 七、预习与思考： 1、The burden of osteoarthritis: clinical and quality-of-life issues.Moskowitz RW (1)关节有哪些损害 (2) 我们如何评价它 (3)临床上还有那些实例：如肿瘤、心血管疾病 2、SF-36 健康调查量表中文版的研制及其性能测试（李鲁） (1)熟悉量表检验包括几部分，几个方面如何将国外量表应用到我们的临床工作 中？ (2)国外量表应用于临床的过程？ 3、A Systematic Review of Health State Utility Values for Osteoporosis Related Conditions (J. E. Brazier1) (1)效用值临床应用价值 (2)测定效用值方法 (3)测定效用值的人群 4、EQ-5D 量表和 HAQ 量表 八、参考书及文献目录 1.《循证医学与临床实践》（第 2 版），王吉耀主编，科学出版社 2. The Lancet handbook of essential concepts in clinical research. Schulz KF, Grimes DA. Philadelphia, PA, USA: Elsevier, 2006. 3. Measuring quality of life using quality of life measures in the clinical setting. I.Higginson et al. BMJ 2001;322:1297-1300 . 4. www.sf-36.org 第 131 页

REPORT E The Burden of osteoarthritis: Clinical and Quality-of-Life Issues Roland W. Moskowitz. MD O steoarthritis (OA)is the most common form of arthritis, affecting 27 million adults in the United Abstract States. OA typically occurs in the hands, knees, steoarthritis (OA), the most common form rados y of jolesepine, and hips, although it may be seen in any of a f arthritis, is a potentially devastating joint mally supported through the use of laboratory studies. Although OA degenerative process accompanied by low- is often characterized as a degenerative disease grade inflammation, and, although there is gra a strong correlation between age and OA mation actually constitutes an important aspect of OA's pathologic risk, the abnormal changes that occur in the articular cartilage of people with OA differ OA is strongly correlated with aging: the risk of OAVincreases con notably from the typical changes associated siderably with each decade after the age of about 45 years. Nevertheless with joint aging in several important ways aging is not inevitably associated with OA. In fact, several pathophysi Risk factors for OA are multiple and span a variety of risk domains, such as lifestyle issues(eg, obesity and engagement in that associated with age-related changes in cartilage. That said,such manual labor), genetic predisposition, sex age-related changes do play an important role in OA pathogenesis and and ethnicity (risk is higher in women and predispose individuals to the d African Americans), and comorbidities. -Other th ber of risk factors for Clinical outcomes for people with Oa typi OA, including comorbidities both related and unrelated to musculo. cally involve pain, limitations of daily living skeletal conditions. ' The presence of other joint diseases is the most activities, and overall diminution of qual common Inuse k factor, whereas obesity ity of life (QoL). The need to evaluate the degree of this burden, as well as to deter on nonmusculoskeletal comorbidities associat mine treatment approaches and measure ed with OA. 7 Lifestyle variables, such as a history of manual labor and their success, requires instruments for mea- cigarette smoking, as well as sex-and phenotype-related conditions suring QOL. The 2 most commonly used such at menarche and joint hyperlaxity instruments to measure ooL in OA are the a role in conferring risk of oA. The genetic component of OA risk Western Ontario and McMaster Universities Osteoarthritis Index(WOMAC) and the while still being studied at present, has been partially elucidated in Medical Outcomes Study 36-Item Short de scan stud ed genetic vari Form Health Survey. Both provide useful nts' associated with OA. ommunications, global information to the clinician and Ultimately, it is the burden of suffering experienced by people researcher alike about pain and function in with Oa that is of primary concern, and that burden can be signifi patients with OA, although the WOMAC is more often used in the clinical setting as cant Pain and functional impairment are the key domains of that it is self-administered. A number of other burden,and taken together they often exert a significant reduction pain and function-specific measures are in quality of life(QOL). 0-13 The present review will briefly describe also available that may provide additiona the pathophysiology, prevalence, and typical outcomes of Oa before insight into patient status when used in addressing the issue of QoL in Oa and the best means in which to combination with global QoL instruments measure It Am J Manag Care. 2009: 15: S223-S229) For author information and disclosures. see end of text. Pathophysiology of OA Cartilage remodeling involves balanced interactions of synthesis VOL 15. NO. 8 THE AMERICAL第u13L

© Managed Care & Healthcare Communications, LLC VOL. 15, No. 8 n The American Journal of Managed Care n S223 Osteoarthritis (OA) is the most common form of arthritis, affecting 27 million adults in the United States.1 OA typically occurs in the hands, knees, spine, and hips, although it may be seen in any of a variety of joints.2 Clinical diagnosis is based on observed symptoms, radiographic changes, or both, whereas differential diagnosis is nor￾mally supported through the use of laboratory studies. Although OA is often characterized as a degenerative disease, low-grade inflam￾mation actually constitutes an important aspect of OA’s pathologic process.3,4 OA is strongly correlated with aging: the risk of OA increases con￾siderably with each decade after the age of about 45 years.1 Nevertheless, aging is not inevitably associated with OA. In fact, several pathophysi￾ologic changes that occur in osteoarthritic cartilage differ notably from that associated with age-related changes in cartilage.5 That said, such age-related changes do play an important role in OA pathogenesis and, at a minimum, predispose individuals to the disease.6 Other than increasing age, there are a number of risk factors for OA, including comorbidities both related and unrelated to musculo￾skeletal conditions.7 The presence of other joint diseases is the most common musculoskeletal comorbid risk factor, whereas obesity is among the most common nonmusculoskeletal comorbidities associat￾ed with OA.7 Lifestyle variables, such as a history of manual labor and cigarette smoking, as well as sex- and phenotype-related conditions— such as age at menarche and joint hyperlaxity in men—can also play a role in conferring risk of OA.8 The genetic component of OA risk, while still being studied at present, has been partially elucidated in recent years as genome-wide scan studies have identified genetic vari￾ants associated with OA.9 Ultimately, it is the burden of suffering experienced by people with OA that is of primary concern, and that burden can be signifi￾cant. Pain and functional impairment are the key domains of that burden, and taken together they often exert a significant reduction in quality of life (QOL).10-13 The present review will briefly describe the pathophysiology, prevalence, and typical outcomes of OA before addressing the issue of QOL in OA and the best means in which to measure it. Pathophysiology of OA Cartilage remodeling involves balanced interactions of synthesis The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues Roland W. Moskowitz, MD n report n Abstract Osteoarthritis (OA), the most common form of arthritis, is a potentially devastating joint disease, affecting 27 million US adults. Its pathophysiology is marked by a gradual degenerative process accompanied by low￾grade inflammation, and, although there is a strong correlation between age and OA risk, the abnormal changes that occur in the articular cartilage of people with OA differ notably from the typical changes associated with joint aging in several important ways. Risk factors for OA are multiple and span a variety of risk domains, such as lifestyle issues (eg, obesity and engagement in manual labor), genetic predisposition, sex and ethnicity (risk is higher in women and African Americans), and comorbidities. Clinical outcomes for people with OA typi￾cally involve pain, limitations of daily living activities, and overall diminution of qual￾ity of life (QOL). The need to evaluate the degree of this burden, as well as to deter￾mine treatment approaches and measure their success, requires instruments for mea￾suring QOL. The 2 most commonly used instruments to measure QOL in OA are the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC) and the Medical Outcomes Study 36-Item Short￾Form Health Survey. Both provide useful global information to the clinician and researcher alike about pain and function in patients with OA, although the WOMAC is more often used in the clinical setting as it is self-administered. A number of other pain and function-specific measures are also available that may provide additional insight into patient status when used in combination with global QOL instruments. (Am J Manag Care. 2009;15:S223-S229) For author information and disclosures, see end of text. 第 132 页

and degradation to achieve homeostasis of the ly doubled in patients aged 45 years or older extracellular matrix (ECM). 4 In Oa this pro- compared with those 26 years or older. The pro. cess becomes unbalanced, leading to pathologic portion of women with Oa also increases relative hanges in the affected joint. The articular carti- to men as age increases. Whereas the framingham lage cells, chrondocytes, are responsible for main- study found that 4.9% of women at least 26 years of taining homeostasis of the eCm by producing its age had knee Oa compared with 4.6% of men, the major components, collagen and proteoglycan, in gap increased to 7. 2% versus 5.9%, respectively, in response to deterioration. Changes in the chron- the 45 years or older group. This gap was replicated docytes are associated with abnormal anabolic and in the Johnston County study, although a highe catabolic activities as well as abnormal prolifera- rate of knee Oa for both men and women aged tion and apoptosis 45 years or older was observed. In that study, the In the early stages of OA, loosening of the col- rate of knee OA was 18.7% for women compared lagen network as well as proteoglycan loss occur with 13.5% for men. The Johnston County study in the upper cartilage zones and may still, at that further observed a higher rate of hip OA in women point, be reversible. 5 Over time, these changes 45 years or older(9.3%)compared with men in the occur within deeper cartilage zones, reducing the same age group(8.7%) lasticity of the cartilage and making a return The observation that the OA gap increases to homeostasis increasingly difficult to achieve. between men and women as they age is consis- Chrondocyte senescence--which is associated tent with incidence data from the framingham ith increasing age--also appears to play a part in Osteoarthritis Study focusing on individuals aged 63 a reduced capacity for cartilage repair and contrib- to 91 years(mean age, 70.8 years). 8 Among these utes to Oa progressed older subjects, the age-adjusted relative risk(rr)of Recent data support the notion that changes women experiencing radiographically determined in subchondral bone are also a factor in cartilage knee Oa compared with men was 1.79(95%con- degradation. The subchondral bone, which is in fidence interval [CIl, 1.08-2.94) s Symptomatic immediate proximity of cartilage, may contribute knee OA was almost twice as likely (rr, 1.96; to cytokines, growth factors, and prostaglandins 95% Cl, 1.01-3.82)for women compared with escalating-perhaps initiating-the degenerative men. 8 Estimates of the rate of increase for knee OA in women was approximately 2% per year fo radiographically determined disease s Prevalence Prevalence and Incidence of oa data regarding hand OA in more than 1000 study Collecting prevalence data from multiple subjects aged 71 to 100 years from the original sources, including the Third National Health and Framingham study (years analyzed: 1992-1993) Nutrition Examination Survey (NHANES Ill) n found a much higher rate of disease in women the Framingham Osteoarthritis Study, and the (26. 2%)compared with men(13.4%). The Figure Johnston County Osteoarthritis Project, the shows the distribution of Oa symptoms at various National Arthritis Data Workgroup arrived at joints in the hands for both men and women. 9 a prevalence figure for 2005 of 26.9 million Us Ethnicity also plays a role in OA risk. According adults(aged >25 years)with some form of OA. to prevalence data from NHANES III(1991-1994) This constitutes a growth of approximately 6 radiographic knee Oa was observed in 17.7% of nillion cases from 1995, more than a one-fourth African American participants aged 60 years or increase in just 10 years. This likely reflects, in part, older compared with 14.8% of Mexican American an aging of the US population, although increases and 11.9% of white participants in the same age in other related factors, such as obesity, as well group(both differences P <.01).20 Of note, the dual increases in methods of OA detection, may play a elevated risk of being both African American and role in this observed prevalence female was observed with a prevalence of radic Nevertheless, the prevalence ofoA does increase graphic knee OA of 60.2%(95%CL, 52.8-67.5).20 dramatically with age. Data from the Framingham Finally, with regard to the distribution of OA study showed that the prevalence of knee Oa across its 3 most common sites--hands, knees, and S224 w第4Rc SEPTEMBER 2009

Reports S224 n www.ajmc.com n september 2009 and degradation to achieve homeostasis of the extracellular matrix (ECM).14 In OA this pro￾cess becomes unbalanced, leading to pathologic changes in the affected joint.15 The articular carti￾lage cells, chrondocytes, are responsible for main￾taining homeostasis of the ECM by producing its major components, collagen and proteoglycan, in response to deterioration. Changes in the chron￾docytes are associated with abnormal anabolic and catabolic activities as well as abnormal prolifera￾tion and apoptosis. In the early stages of OA, loosening of the col￾lagen network as well as proteoglycan loss occur in the upper cartilage zones and may still, at that point, be reversible.15 Over time, these changes occur within deeper cartilage zones, reducing the elasticity of the cartilage and making a return to homeostasis increasingly difficult to achieve. Chrondocyte senescence—which is associated with increasing age—also appears to play a part in a reduced capacity for cartilage repair and contrib￾utes to OA progression.16 Recent data support the notion that changes in subchondral bone are also a factor in cartilage degradation.17 The subchondral bone, which is in immediate proximity of cartilage, may contribute to cytokines, growth factors, and prostaglandins escalating—perhaps initiating—the degenerative process. Prevalence and Incidence of OA Collecting prevalence data from multiple sources, including the Third National Health and Nutrition Examination Survey (NHANES III), the Framingham Osteoarthritis Study, and the Johnston County Osteoarthritis Project, the National Arthritis Data Workgroup arrived at a prevalence figure for 2005 of 26.9 million US adults (aged >25 years) with some form of OA.1 This constitutes a growth of approximately 6 million cases from 1995, more than a one-fourth increase in just 10 years. This likely reflects, in part, an aging of the US population, although increases in other related factors, such as obesity, as well as increases in methods of OA detection, may play a role in this observed prevalence. Nevertheless, the prevalence of OA does increase dramatically with age. Data from the Framingham study showed that the prevalence of knee OA nearly doubled in patients aged 45 years or older compared with those 26 years or older.1 The pro￾portion of women with OA also increases relative to men as age increases. Whereas the Framingham study found that 4.9% of women at least 26 years of age had knee OA compared with 4.6% of men, the gap increased to 7.2% versus 5.9%, respectively, in the 45 years or older group. This gap was replicated in the Johnston County study, although a higher rate of knee OA for both men and women aged 45 years or older was observed.1 In that study, the rate of knee OA was 18.7% for women compared with 13.5% for men. The Johnston County study further observed a higher rate of hip OA in women 45 years or older (9.3%) compared with men in the same age group (8.7%). The observation that the OA gap increases between men and women as they age is consis￾tent with incidence data from the Framingham Osteoarthritis Study focusing on individuals aged 63 to 91 years (mean age, 70.8 years).18 Among these older subjects, the age-adjusted relative risk (RR) of women experiencing radiographically determined knee OA compared with men was 1.79 (95% con￾fidence interval [CI], 1.08-2.94).18 Symptomatic knee OA was almost twice as likely (RR, 1.96; 95% CI, 1.01-3.82) for women compared with men.18 Estimates of the rate of increase for knee OA in women was approximately 2% per year for radiographically determined disease.18 Prevalence data regarding hand OA in more than 1000 study subjects aged 71 to 100 years from the original Framingham study (years analyzed: 1992-1993) again found a much higher rate of disease in women (26.2%) compared with men (13.4%). The Figure shows the distribution of OA symptoms at various joints in the hands for both men and women.19 Ethnicity also plays a role in OA risk. According to prevalence data from NHANES III (1991-1994), radiographic knee OA was observed in 17.7% of African American participants aged 60 years or older compared with 14.8% of Mexican American and 11.9% of white participants in the same age group (both differences P <.01).20 Of note, the dual elevated risk of being both African American and female was observed with a prevalence of radio￾graphic knee OA of 60.2% (95% CI, 52.8-67.5).20 Finally, with regard to the distribution of OA across its 3 most common sites—hands, knees, and 第 133 页

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues Figure. Prevalence of Symptomatic Hand Osteoarthritis Among People 271 Years of Age in the framingham Study 1992-1993 3rd 4th 2nd 2nd 4th Thumb R MCP MCP Thumb Thumb ase Right Men(n=369) a 2nd 4th 5th 0.60.90.8 MCP (/sMCP MCP humb Thumb 5. Left Women(n = 663) Right DIP indicates distal interphalangeal: MCP, metacarpophalangeal: PIP, proximal interphalange hips--incidence data from a large health mainte- the experience of pain, not to mention their con- nance organization database showed that for every siderable sequelae. An analysis of a compilation 100,000 person-years, the incidence of knee Oa of various surveys(including NHANES If), data occurred 240 times compared with 100 times for bases(including the National Hospital discharge hand Oa and 88 for hip OA.2 Database), disease registers, and epidemiologic stud ies found that Oa was the seventh leading cause of Clinical Outcomes in OA disability in women and the twelfth leading cause The burden that befalls people with OA is in men. Among people 65 to 74 years of age, OA enormous both in terms of reduced function and was found to be the fifth largest cause of disabilit VOL 15. NO. 8 THE AMERICAI箱u3头 L E MANAGED CARE S225

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues VOL. 15, No. 8 n The American Journal of Managed Care n S225 hips—incidence data from a large health mainte￾nance organization database showed that for every 100,000 person-years, the incidence of knee OA occurred 240 times compared with 100 times for hand OA and 88 for hip OA.21 Clinical Outcomes in OA The burden that befalls people with OA is enormous both in terms of reduced function and the experience of pain, not to mention their con￾siderable sequelae. An analysis of a compilation of various surveys (including NHANES III), data￾bases (including the National Hospital Discharge Database), disease registers, and epidemiologic stud￾ies found that OA was the seventh leading cause of disability in women and the twelfth leading cause in men.22 Among people 65 to 74 years of age, OA was found to be the fifth largest cause of disability, n Figure. Prevalence of Symptomatic Hand Osteoarthritis Among People >71 Years of Age in the Framingham Study 1992-1993 Left Right Left Right Men (n = 369) Women (n = 663) DIP DIP DIP DIP PIP PIP MCP MCP MCP MCP Thumb base Thumb base Thumb base Thumb base Thumb Thumb 2nd 2nd 3rd 3rd 4th 4th 5th 5th DIP DIP DIP DIP PIP PIP MCP MCP MCP MCP Thumb Thumb 2nd 2nd 3rd 3rd 4th 4th 5th 5th 8.8 7.3 9.3 0.6 0.9 7.3 9.9 10.4 7.4 0.8 7.4 1.5 5.0 7.1 0.3 2.5 1.6 3.0 0.0 0.3 3.6 3.8 4.1 3.0 0.0 4.4 3.3 2.7 2.7 2.7 0.0 0.0 0.3 2.2 2.5 2.2 2.5 4.1 0.5 2.7 11.9 11.9 8.9 8.5 1.1 0.3 0.5 1.7 5.1 6.5 8.0 6.0 9.6 1.1 7.5 1.9 0.0 3.0 2.8 0.0 DIP indicates distal interphalangeal; MCP, metacarpophalangeal; PIP, proximal interphalangeal. 第 134 页

ahead of dementia, diabetes, prostate cancer, and need to understand its impact on Oa patients in cancer ta are consistent with order to guide decision making-to determine how those from the framingham study, which found that and what interventions are appropriate--in the among older (mean age -74 years)study partici- management of the disease. Measuring QOL pants, knee OA, taken alone, represented I of the 4 ther allows clinicians the opportunity to determine rgest causes of disability along with heart disease, the efficacy of a given intervention. Numerous depression, and stroke. A significant proportion instruments are currently available for measuring of the patient population in the framingham study different aspects of QOL in the Oa patient, includ- with knee Oa were unable to perform a variety ing those that measure general QOL, functional of activities of daily living, such as heavy home capacities, the experience of pain, and psychologi- chores (34% disabled), walking 1 mile(31%), stair cal dimensions of QOL. The most commonly used ing(10%), and grocery shopping(10%). In instrument specific to OA is the Western Ontario fact, the ability to walk I mile or to undertake light and McMaster Universities Osteoarthritis Index housekeeping was notably more restricted among (WOMAC). WOMAC is a 24-item self-report those with knee OA compared with matched questionnaire that addresses joint pain, stiffness, patients with heart disease. 3 and loss of function related to oa of the knee and It is interesting to note that the burden of Oa in hip 24-26 Since its initial validation, WOMAC has terms of functional deficits can affect areas beyond been widely used in clinical trials, and has been the immediate OA loci. For example, an analysis of repeatedly shown to provide utility as a measure participants in the Johnston County Osteoarthritis of patient QOL, response to treatment, prediction Project with joint-specific hand symptoms found that of treatment outcomes, as well as sensitivity to not only did they experience significant deterioration minimal perceptible clinical improvement. 4. An in performance-based functional status overall--as electronic touch-screen version of the WOMAC might be expected-but that the disability extended (the e-WOMAC) has shown similar responsiveness beyond that which one would intuitively associate to the paper version in Oa patients. 1 with hand OA. People with hand Oa symptoms in The Medical Outcomes Study 36-Item Short this study experienced significant deterioration in Form Health Survey (SF-36)provides an 8-scale performing both upper- and lower-extremity tasks. evaluation of physical and mental QOL based on 36 These results were based on both a self-report instru- questions. Although the SF-36 is not specific to ment(the Health Assessment Questionnaire [HAQI OA, it is, like WOMAC, widely used to guide OA Disability Index)as well as performance-based func- treatment in clinical trials, being fairly sensitive to tional measures(timed 5 chair stands"and gait minimal perceptible clinical improvement. 24.27429 32A neasured over an 8-foot walking course ) I more OA-specific instrument, the SF-36 Arthritis- A separate analysis of participants in the Johnston Specific Health Index, was developed to better knee OA, and the severity of knee pain in particu- not been widely adopted. ation, but to date has County Osteoarthritis Project found that having target the Oa patient popul ar, was associated with a high degree of functional Although both the WoMAC and SF-36 instru- impairment. Even mild knee pain was strongly ments function relatively well in assessing various associated with disability in performing 16 of the QOL domains in OA, WOMAC may be more 20 upper- and lower-extremity tasks included in the responsive than the SF-36 instrument to detecting HaQ disability index. For those with moderate-to- changes in function. 4 In fact, the validity of both severe pain, significant disability was observed with instruments has been challenged. 5 Although it all 20 tasks in the HAQ index(all P<.001). 12 should be noted that WOMAC is widely accepted The common presence of comorbidities within for its ability to measure pain and functional deficits the Oa patient population exerts additional deleteri- in OA, Stratford et al have questioned its validity ous effects on both physical functioning and pain in measuring pain. According to their analysis, the factors that comprise pain evaluation are not Measuring QoL in OA alid, while they state that the pain scale as a whole The necessity of measuring QOL arises from a is not internally consistent. The authors suggest S226 w第4瓶5 SEPTEMBER 2009

Reports S226 n www.ajmc.com n september 2009 ahead of dementia, diabetes, prostate cancer, and breast cancer.22 These data are consistent with those from the Framingham study, which found that among older (mean age ~74 years) study partici￾pants, knee OA, taken alone, represented 1 of the 4 largest causes of disability along with heart disease, depression, and stroke.13 A significant proportion of the patient population in the Framingham study with knee OA were unable to perform a variety of activities of daily living, such as heavy home chores (34% disabled), walking 1 mile (31%), stair climbing (10%), and grocery shopping (10%).13 In fact, the ability to walk 1 mile or to undertake light housekeeping was notably more restricted among those with knee OA compared with matched patients with heart disease.13 It is interesting to note that the burden of OA in terms of functional deficits can affect areas beyond the immediate OA loci. For example, an analysis of participants in the Johnston County Osteoarthritis Project with joint-specific hand symptoms found that not only did they experience significant deterioration in performance-based functional status overall—as might be expected—but that the disability extended beyond that which one would intuitively associate with hand OA. People with hand OA symptoms in this study experienced significant deterioration in performing both upper- and lower-extremity tasks.11 These results were based on both a self-report instru￾ment (the Health Assessment Questionnaire [HAQ] Disability Index) as well as performance-based func￾tional measures (timed “5 chair stands” and gait measured over an 8-foot walking course).11 A separate analysis of participants in the Johnston County Osteoarthritis Project found that having knee OA, and the severity of knee pain in particu￾lar, was associated with a high degree of functional impairment.12 Even mild knee pain was strongly associated with disability in performing 16 of the 20 upper- and lower-extremity tasks included in the HAQ disability index.12 For those with moderate-to￾severe pain, significant disability was observed with all 20 tasks in the HAQ index (all P <.001).12 The common presence of comorbidities within the OA patient population exerts additional deleteri￾ous effects on both physical functioning and pain.10,23 Measuring QOL in OA The necessity of measuring QOL arises from a need to understand its impact on OA patients in order to guide decision making—to determine how and what interventions are appropriate—in the management of the disease. Measuring QOL fur￾ther allows clinicians the opportunity to determine the efficacy of a given intervention. Numerous instruments are currently available for measuring different aspects of QOL in the OA patient, includ￾ing those that measure general QOL, functional capacities, the experience of pain, and psychologi￾cal dimensions of QOL. The most commonly used instrument specific to OA is the Western Ontario and McMaster Universities Osteoarthritis Index (WOMAC). WOMAC is a 24-item self-report questionnaire that addresses joint pain, stiffness, and loss of function related to OA of the knee and hip.24-26 Since its initial validation, WOMAC has been widely used in clinical trials, and has been repeatedly shown to provide utility as a measure of patient QOL, response to treatment, prediction of treatment outcomes, as well as sensitivity to minimal perceptible clinical improvement.24,27-30 An electronic touch-screen version of the WOMAC (the e-WOMAC) has shown similar responsiveness to the paper version in OA patients.31 The Medical Outcomes Study 36-Item Short Form Health Survey (SF-36) provides an 8-scale evaluation of physical and mental QOL based on 36 questions. Although the SF-36 is not specific to OA, it is, like WOMAC, widely used to guide OA treatment in clinical trials, being fairly sensitive to minimal perceptible clinical improvement.24,27-29,32 A more OA-specific instrument, the SF-36 Arthritis￾Specific Health Index, was developed to better target the OA patient population, but to date has not been widely adopted.33,34 Although both the WOMAC and SF-36 instru￾ments function relatively well in assessing various QOL domains in OA, WOMAC may be more responsive than the SF-36 instrument to detecting changes in function.24 In fact, the validity of both instruments has been challenged.35 Although it should be noted that WOMAC is widely accepted for its ability to measure pain and functional deficits in OA, Stratford et al have questioned its validity in measuring pain.35 According to their analysis, the factors that comprise pain evaluation are not valid, while they state that the pain scale as a whole is not internally consistent.35 The authors suggest 第 135 页

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issue Table. Individual Functional Performance measures Timed"Up Go Patient is sitting in an armchair with his/her back up against to return to sitting the chair back. a piece of tape is placed 3 m from the chair. On the signal"go, the patient gets up, walks to the tape line tums around, walks back to the chair, and sits down again using a normal walking pace Six-Minute Walk Patient walks unaided and alone for a period of 6 minutes Distance walked in 6 minutes on a flat surface, not a bike or treadmill nor oval or circular track. Phrases used when speaking to patients should be standardized. Encouragement is allowed as long as it is ways the same from one patient to the next. Stair Measure On the signal"go, patient ascends and descends 9 stairs Time from"go"to return to initial step height 20 cm, at a comfortable pace position Fast self-Paced Walk Patient is instructed to walk a 20-m indoor course Time elapsed for two 20-m lengths hallway) as quickly as possible without overexertion. excluding the turn twice something other than pain is being measured by the the visual analog scale for pain is widely known pain"portion of WOMAC and used as are such functional measures as the he SF-36, apart from its lesser responsiveness Stair Measure, the Fast Self-Paced Walk Test, the to functional assessment, as already noted, has also Timed"Up Go"Test, the Six-Minute Walk been faulted as an inadequate instrument in the Test, range-of-motion tests, and the Knee Society rehabilitation setting. The primary complaint has clinical rating system 39(Table). These specific do with questions in the SF-36 that assume the testing modalities may provide useful additional subject is living in a fairly normal environment nformation in the clinical setting, particularly engaged in social and work activities as well as in combination with global instruments, to help housework--none of which may apply to patients physicians make treatment decisions. Some authors in a rehabilitation facility. s6 have suggested that clinical decision making should Similar to WOMAC, but unlike the SF-36, routinely utilize these specific functional tests, the Stanford HAQ is a self-report instrument; it observing that global QOL tests when used in isola was first developed in 1978 to measure disability tion are not sufficiently reliable indicators to guide in rheumatic diseases, and exists in a modified ver- treatment decision making, s40 sion(MSHAQ). Although it is still widely used In summary, a great deal is now known about in patients with musculoskeletal diseases, the HAq OA epidemiology and pathophysiology, as well rends to be applied more to rheumatoid arthritis than the anticipated disease course. Such information OA. The advantage of instruments such as WoMAc provides an opportunity to both target disease pre- and the HAQ, in the clinical setting, is that as self- vention as well as to define therapeutic approaches administered instruments, they are both simple to to decrease disease morbidity. Meaningful therapeu complete and require little time expenditure on the tic responses are more effectively delineated when part of the clinical staff. The SF-36, in contrast, based on reproducible functional QOL measures. requires administration by a clinician, which at least in clinical trials than in physicians'offices. 'used partly explains why the SF-36 is more frequently used Author Affiliation: From the Department of Medicine, Case Western Reserve University, Cleveland, OH WOMAC, the SF-36, and HAQ all represent by Endo Pharmaceuticals Funding Source: Financial support for this work was provided integrated instruments aimed at bringing together uthor Disclosure: The author(RWM)reports no relation- multiple QOL-related domains in order to arrive at ship or financial interest with any entity that would pose a con- a global view of patient status; however, there are flict of interest with the subject matter Authorship Information: Concept and design (RWM specific tests available that allow for more targeted drafting of the manuscript(RWM); and critical revision of the functional and pain measurement. For example anuscript for important intellectual content(RWM) VOL 15. NO. 8 THE AMERICAN第k36L MANAGED CARE■

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues VOL. 15, No. 8 n The American Journal of Managed Care n S227 something other than pain is being measured by the “pain” portion of WOMAC. The SF-36, apart from its lesser responsiveness to functional assessment, as already noted, has also been faulted as an inadequate instrument in the rehabilitation setting. The primary complaint has to do with questions in the SF-36 that assume the subject is living in a fairly normal environment— engaged in social and work activities as well as housework—none of which may apply to patients in a rehabilitation facility.36 Similar to WOMAC, but unlike the SF-36, the Stanford HAQ is a self-report instrument; it was first developed in 1978 to measure disability in rheumatic diseases, and exists in a modified ver￾sion (MSHAQ).37 Although it is still widely used in patients with musculoskeletal diseases, the HAQ tends to be applied more to rheumatoid arthritis than OA. The advantage of instruments such as WOMAC and the HAQ, in the clinical setting, is that as self￾administered instruments, they are both simple to complete and require little time expenditure on the part of the clinical staff. The SF-36, in contrast, requires administration by a clinician, which at least partly explains why the SF-36 is more frequently used in clinical trials than in physicians’ offices. WOMAC, the SF-36, and HAQ all represent integrated instruments aimed at bringing together multiple QOL-related domains in order to arrive at a global view of patient status; however, there are specific tests available that allow for more targeted functional and pain measurement. For example, the visual analog scale for pain is widely known and used, as are such functional measures as the Stair Measure, the Fast Self-Paced Walk Test, the Timed “Up & Go” Test, the Six-Minute Walk Test, range-of-motion tests, and the Knee Society clinical rating system38,39 (Table). These specific testing modalities may provide useful additional information in the clinical setting, particularly in combination with global instruments, to help physicians make treatment decisions. Some authors have suggested that clinical decision making should routinely utilize these specific functional tests, observing that global QOL tests when used in isola￾tion are not sufficiently reliable indicators to guide treatment decision making.38,40 In summary, a great deal is now known about OA epidemiology and pathophysiology, as well as the anticipated disease course. Such information provides an opportunity to both target disease pre￾vention as well as to define therapeutic approaches to decrease disease morbidity. Meaningful therapeu￾tic responses are more effectively delineated when based on reproducible functional QOL measures. Author Affiliation: From the Department of Medicine, Case Western Reserve University, Cleveland, OH. Funding Source: Financial support for this work was provided by Endo Pharmaceuticals. Author Disclosure: The author (RWM) reports no relation￾ship or financial interest with any entity that would pose a con￾flict of interest with the subject matter of this article. Authorship Information: Concept and design (RWM); drafting of the manuscript (RWM); and critical revision of the manuscript for important intellectual content (RWM). n Table. Individual Functional Performance Measures Test Instructions Measurement Timed “Up & Go” Patient is sitting in an armchair with his/her back up against the chair back. A piece of tape is placed 3 m from the chair. On the signal “go,” the patient gets up, walks to the tape line, turns around, walks back to the chair, and sits down again using a normal walking pace. Time from “go” to return to sitting position Six-Minute Walk Patient walks unaided and alone for a period of 6 minutes on a flat surface, not a bike or treadmill nor oval or circular track. Phrases used when speaking to patients should be standardized. Encouragement is allowed as long as it is always the same from one patient to the next. Distance walked in 6 minutes Stair Measure On the signal “go,” patient ascends and descends 9 stairs, step height 20 cm, at a comfortable pace. Time from “go” to return to initial position Fast Self-Paced Walk Patient is instructed to walk a 20-m indoor course (eg, hallway) as quickly as possible without overexertion, twice. Time elapsed for two 20-m lengths excluding the turn 第 136 页

to: Roland W. Moskowitz, MD, 15. Aigner T, Soeder S, Haag J IL-1beta and BMPs and. 11100 Euclid Ave. Cleveland OH 44106. E-mail: Roland. Moskowitz@UHHospitalsorg egeneration Eur Cell Mater. 2006: 12: 49-56 16. Martin JA, Buckwalter JA. The role of chondrocyte REFERENCES J Bone Joint Surg Am. 2003:85 alsup2):106-110 1. Lawrence RC, Felson DT, Helmick 17. Lajeunesse D, Massicotte F. pelletier J Subchondral bone ns in the United States. Part II tis: not just an innocent bysta e 2008:58(1)26-35. 2003;13:7-14. 2. Goldring SR, Goldring MB. Clinical aspects, pathology 18 Felson DT, Zhang Y, Hannan MT, et al. The incidence itis. J Musculoskelet nd natural history of knee osteoarthritis in the elder Neuronal Interact. 2006: 6(4): 376-378 y. The Framingham Osteoarthritis Study. Arthritis Rheum.1995:38(10):1500-1505 3. Pelletier JP, Martel-Pelletier J, Abramson SB M. Chaisson CE A Felson d gets. Arthritis Rheum. 2001: 44(6): 1237-1247 2002 y: the Framingham study. Am J Epidemiothe and its impact on fu increases in serum C-reactive protein are present in 0. Dillon CF, Rasch EK, Gu Q, Hirsch R. Prevalence disease. Arthritis Rheum. 1997: 40(45: 723-727ogresswv of knee osteoarthritis in the ited State si arthritis G, Schneiderman R, Mi A. Some biochemical and biophysical parameters for the study f the pathogenesis of osteoarthritis: a comparison 21 Oliveria SA. Felson DT, Reed Jl. Cirillo PA. Walker human hip cares of ageing and degenera- AM. Incidence of symptomatic hand, hip, and knee 199296 organization. Arthritis Rheum. 1995: 38(8): 1134-1141 6. Aigner T, Soder S, Gebhard PM, McAlinden A, 22 Michaud CM, McKenna MT, Begg s, et al. The burden Haag J Mechanisms of disease: role of chondrocytes in the pathogenesis of osteoarthritis-structure Health Metr. 2006: 4: 11 escence. Nat Clin Pract Rheumatol 20073(7):391-399. 23 Kadam UT, Croft PR Clinical comorbidity in osteo- rthritis: associations with physical function in older 7. Kadam UT, Jordan K, Croft PR. Clinical comorbidity atients in family practice. J Rheumatol 2007; 34(9) in patients with osteoarthritis: a case-control study of 24. Angst F, Aeschlimann A, Steiner W, Stucki G. eness of t 8. Hunter DJ, Zhang Y, Sokolove J, Niu J, Aliabadi P. vith th Felson DT. Trapeziometacarpal subluxation predispose to incident trapeziometacarpal osteoarthritis(OA): the amingham study Osteoarthritis Cartilage. 2005; 25. Sun Y, Sturmer T, Gunther KP, Brenner H Reliability and validity of clinical outcome measurements of Valdes AM KM, et al. Genome. w of the literature. Clin Rheumatol. 1997: 16(2): 185-198 Hum Genet ence with the womAc osteoarthritis index. Semin 200882(6):1231-1240 Arthritis Rheum. 1989; 18(4 suppl 2): 14-17 Dik GM, Veenhof C, Schellevis F, et al. 27 Desmeules F Dionne ce Belzile e. bourbonnais R dity, limitations in activities and pain in Its with osteoarthritis of the hip or knee. BMc factors associated with pain, stiffn Muscyloskelet disord. 2008: 9: 95. uality of life. BMC Musculoskelet 11. Elliott AL, Kraus VB, Fang F, et al. Joint-specific hand 28. Quintana JM, Escobar A, Aguirre U, Lafuente L, rs of health-related quality-of-life cans and caucasians: hange after total hip arthroplasty Clin Orthop rela the Johnston County Osteoarthritis Project. Ann es. 2009 May 2 [Epub ahead of print Rheum dis.2007:6612:16221626. 29. Escobar A, Quintana JM, Bilbao A, Arostegui l, 12.J A, Hochberg M, Fryer J Knee pain and knee osteoarthritis sever- important differences for the WOMAC and SF-36 ty in self-reported task specific disability: the fter total knee replacement. Osteoarthritis Cartil Johnston County Osteoarthritis Project. J Rheumatol. 2007:15{3)273-280. 199724(7):13441349 30. Ehrich EW, Davies GM, Watson DJ, Bolognese JA, 13. Guccione a son JJ, et al. The effects of specific medical conditions on the functional with the Western Ontario and mcmaster Public Health.199484(3):351-358. J Rheumatol.2000;2711):26352641 14. Lotz M, Blanco FJ, von Kempis J, et al. Cytokine reg- 31. Theiler R, Bischoff-Ferrari HA, Good M, Bellamy N. ulation of chondrocyte functions. J Rheumatol Suppl. ponsiveness of the electronic touch screen S228 w第证 SEPTEMBER 2009

Reports S228 n www.ajmc.com n september 2009 Address correspondence to: Roland W. Moskowitz, MD, University Hospitals/Cleveland, 11100 Euclid Ave, Cleveland, OH 44106. E-mail: Roland.Moskowitz@UHHospitals.org. References 1. Lawrence RC, Felson DT, Helmick CG, et al. Estimates of the prevalence of arthritis and other rheumatic con￾ditions in the United States. Part II. Arthritis Rheum. 2008;58(1):26-35. 2. Goldring SR, Goldring MB. Clinical aspects, pathology and pathophysiology of osteoarthritis. J Musculoskelet Neuronal Interact. 2006;6(4):376-378. 3. Pelletier JP, Martel-Pelletier J, Abramson SB. Osteoarthritis, an inflammatory disease: potential implication for the selection of new therapeutic tar￾gets. Arthritis Rheum. 2001;44(6):1237-1247. 4. Spector TD, Hart DJ, Nandra D, et al. Low-level increases in serum C-reactive protein are present in early osteoarthritis of the knee and predict progressive disease. Arthritis Rheum. 1997;40(4):723-727. 5. Grushko G, Schneiderman R, Maroudas A. Some biochemical and biophysical parameters for the study of the pathogenesis of osteoarthritis: a comparison between the processes of ageing and degenera￾tion in human hip cartilage. Connect Tissue Res. 1989;19(2-4):149-176. 6. Aigner T, Söder S, Gebhard PM, McAlinden A, Haag J. Mechanisms of disease: role of chondrocytes in the pathogenesis of osteoarthritis—structure, chaos and senescence. Nat Clin Pract Rheumatol. 2007;3(7):391-399. 7. Kadam UT, Jordan K, Croft PR. Clinical comorbidity in patients with osteoarthritis: a case-control study of general practice consulters in England and Wales. Ann Rheum Dis. 2004;63(4):408-414. 8. Hunter DJ, Zhang Y, Sokolove J, Niu J, Aliabadi P, Felson DT. Trapeziometacarpal subluxation predisposes to incident trapeziometacarpal osteoarthritis (OA): the Framingham study. Osteoarthritis Cartilage. 2005; 13(11):953-957. 9. Valdes AM, Loughlin J, Timms KM, et al. Genome￾wide association scan identifies a prostaglandin￾endoperoxide synthase 2 variant involved in risk of knee osteoarthritis. Am J Hum Genet. 2008;82(6):1231-1240. 10. van Dijk GM, Veenhof C, Schellevis F, et al. Comorbidity, limitations in activities and pain in patients with osteoarthritis of the hip or knee. BMC Musculoskelet Disord. 2008;9:95. 11. Elliott AL, Kraus VB, Fang F, et al. Joint-specific hand symptoms and self-reported and performance-based functional status in African Americans and Caucasians: the Johnston County Osteoarthritis Project. Ann Rheum Dis. 2007;66(12):1622-1626. 12. Jordan J, Luta G, Renner J, Dragomir A, Hochberg M, Fryer J. Knee pain and knee osteoarthritis sever￾ity in self-reported task specific disability: the Johnston County Osteoarthritis Project. J Rheumatol. 1997;24(7):1344-1349. 13. Guccione AA, Felson DT, Anderson JJ, et al. The effects of specific medical conditions on the functional limitations of elders in the Framingham study. Am J Public Health. 1994;84(3):351-358. 14. Lotz M, Blanco FJ, von Kempis J, et al. Cytokine reg￾ulation of chondrocyte functions. J Rheumatol Suppl. 1995;43:104-108. 15. Aigner T, Soeder S, Haag J. IL-1beta and BMPs— interactive players of cartilage matrix degradation and regeneration. Eur Cell Mater. 2006;12:49-56. 16. Martin JA, Buckwalter JA. The role of chondrocyte senescence in the pathogenesis of osteoarthritis and in limiting cartilage repair. J Bone Joint Surg Am. 2003;85-A(suppl 2):106-110. 17. Lajeunesse D, Massicotte F, Pelletier JP, Martel￾Pelletier J. Subchondral bone sclerosis in osteoarthri￾tis: not just an innocent bystander. Mod Rheumatol. 2003;13:7-14. 18. Felson DT, Zhang Y, Hannan MT, et al. The incidence and natural history of knee osteoarthritis in the elder￾ly. The Framingham Osteoarthritis Study. Arthritis Rheum. 1995;38(10):1500-1505. 19. Zhang Y, Niu J, Kelly-Hayes M, Chaisson CE, Aliabadi P, Felson DT. Prevalence of symptomatic hand osteoar￾thritis and its impact on functional status among the elderly: the Framingham study. Am J Epidemiol. 2002;156:1021-1027. 20. Dillon CF, Rasch EK, Gu Q, Hirsch R. Prevalence of knee osteoarthritis in the United States: arthritis data from the Third National Health and Nutrition Examination Survey 1991-1994. J Rheumatol. 2006;33:2271-2279. 21. Oliveria SA, Felson DT, Reed JI, Cirillo PA, Walker AM. Incidence of symptomatic hand, hip, and knee osteoarthritis among patients in a health maintenance organization. Arthritis Rheum. 1995;38(8):1134-1141. 22. Michaud CM, McKenna MT, Begg S, et al. The burden of disease and injury in the United States 1996. Popul Health Metr. 2006;4:11. 23. Kadam UT, Croft PR. Clinical comorbidity in osteo￾arthritis: associations with physical function in older patients in family practice. J Rheumatol. 2007;34(9): 1899-1904. 24. Angst F, Aeschlimann A, Steiner W, Stucki G. Responsiveness of the WOMAC osteoarthritis index as compared with the SF-36 in patients with osteoarthri￾tis of the legs undergoing a comprehensive rehabilita￾tion intervention. Ann Rheum Dis. 2001;60:834-840. 25. Sun Y, Stürmer T, Günther KP, Brenner H. Reliability and validity of clinical outcome measurements of osteoarthritis of the hip and knee—a review of the literature. Clin Rheumatol. 1997;16(2):185-198. 26. Bellamy N. Pain assessment in osteoarthritis: expe￾rience with the WOMAC osteoarthritis index. Semin Arthritis Rheum. 1989;18(4 suppl 2):14-17. 27. Desmeules F, Dionne CE, Belzile E, Bourbonnais R, Fremont P. Waiting for total knee replacement surgery: factors associated with pain, stiffness, function and quality of life. BMC Musculoskelet Disord. 2009;10:52. 28. Quintana JM, Escobar A, Aguirre U, Lafuente I, Arenaza JC. Predictors of health-related quality-of-life change after total hip arthroplasty. Clin Orthop Relat Res. 2009 May 2 [Epub ahead of print]. 29. Escobar A, Quintana JM, Bilbao A, Aróstegui I, Lafuente I, Vidaurreta I. Responsiveness and clinically important differences for the WOMAC and SF-36 after total knee replacement. Osteoarthritis Cartilage. 2007;15(3):273-280. 30. Ehrich EW, Davies GM, Watson DJ, Bolognese JA, Seidenberg BC, Bellamy N. Minimal perceptible clinical improvement with the Western Ontario and McMaster Universities osteoarthritis index questionnaire and global assessments in patients with osteoarthritis. J Rheumatol. 2000;27(11):2635-2641. 31. Theiler R, Bischoff-Ferrari HA, Good M, Bellamy N. Responsiveness of the electronic touch screen WOMAC 3.1 OA index in a short term clinical trial 第 137 页

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issue with rofecoxib. Osteoarthritis Cartilage. 2004: 12(11): 36. Jones JG, Leighton F. Comparison of WOMAC th SF-36 for OA of the knee or hip. Ann Rheum Dis. 32. Salaffi F Carotti M, Stancati A, Grassi W. ated quality of life in older adults with sy 37. Liang M, Schurman DJ, Fries J. A patient-admin essment. clir vith matched healthy controls. Aging Clin Exp Res 2005;17(4):255-263. Orthop Relat Res. 1978: 131: 123-129. 33. Keller SD, Ware JE Jr, Hatoum HT, Kong SX. The 8. Stratford PW, Kennedy DM. Performance mea- SF-36 Arthritis-Specific Health Index (ASHI): Il. Tests ures were necessary to obtain plete pic- of validity in four clinical trials. Med Care. 1999; 37(5 uppl): Ms51-MS60 2006:59(2):160-167 4. Ware JE Jr, Keller SD, Hatoum HT, Kong SX. 9. Insall JN. Dorr LD, Scott RD, Scott WN. Rationale of The SF-36 Arthritis-Specific Health Index(ASHI the Knee society clinical rating system. Clin Orthop Relat Res.1989248:13-14. 35. Stratford PW, Kennedy DM, Woodhouse LJ, Spadoni erformance measures provide assessments of pain GF Measurement properties of the WOMAC LK 3.1 ion in people with advanced osteoarthritis of pain scale. Osteoarthritis Cartilage. 2007: 15(3): 266-272. the hip or knee. Phys Ther. 2006: 86(11): 1489-1496. VOL 15. NO. 8 THE AMERICAMOUR&L F MANAGED CARE

The Burden of Osteoarthritis: Clinical and Quality-of-Life Issues VOL. 15, No. 8 n The American Journal of Managed Care n S229 with rofecoxib. Osteoarthritis Cartilage. 2004;12(11): 912-916. 32. Salaffi F, Carotti M, Stancati A, Grassi W. Health￾related quality of life in older adults with symp￾tomatic hip and knee osteoarthritis: a comparison with matched healthy controls. Aging Clin Exp Res. 2005;17(4):255-263. 33. Keller SD, Ware JE Jr, Hatoum HT, Kong SX. The SF-36 Arthritis-Specific Health Index (ASHI): II. Tests of validity in four clinical trials. Med Care. 1999;37(5 suppl):MS51-MS60. 34. Ware JE Jr, Keller SD, Hatoum HT, Kong SX. The SF-36 Arthritis-Specific Health Index (ASHI): I. Development and cross-validation of scoring algo￾rithms. Med Care. 1999;37(5 suppl):MS40-MS50. 35. Stratford PW, Kennedy DM, Woodhouse LJ, Spadoni GF. Measurement properties of the WOMAC LK 3.1 pain scale. Osteoarthritis Cartilage. 2007;15(3):266-272. 36. Jones JG, Leighton F. Comparison of WOMAC with SF-36 for OA of the knee or hip. Ann Rheum Dis. 2002;61(2):182-183. 37. Liang M, Schurman DJ, Fries J. A patient-admin￾istered questionnaire for arthritis assessment. Clin Orthop Relat Res. 1978;131:123-129. 38. Stratford PW, Kennedy DM. Performance mea￾sures were necessary to obtain a complete pic￾ture of osteoarthritic patients. J Clin Epidemiol. 2006;59(2):160-167. 39. Insall JN, Dorr LD, Scott RD, Scott WN. Rationale of the Knee Society clinical rating system. Clin Orthop Relat Res. 1989;248:13-14. 40. Stratford PW, Kennedy DM, Woodhouse LJ. Performance measures provide assessments of pain and function in people with advanced osteoarthritis of the hip or knee. Phys Ther. 2006;86(11):1489-1496. 第 138 页

预防医学杂志2002年3月第36卷第2期 hin J Prey Med,Marh2002,vd36,N.2 论著 SF-36健康调查量表中文版的研制 及其性能测试 李鲁王红妹沈毅 【摘要】目的研制SF-36健康调查量表中文版并验证量表维度建立及记分假设、信度和效度。 方法采用多阶段混合型等概率抽样法,用SF-36健康调查量表中文版对1000户家庭的居民进行自 评量表式调査:参照国际生命质量评价项目的标准程序,进行正式的心理测验学试验。结果在收回 的1985份问卷中,18岁以上的有效问卷1972份,其中应答者1688人(85.6%),1316人回答了所有 条目,372人有1个或以上的缺失答案,无应答者中文盲、半文盲占65.5%。等距假设在活力(VT)和 精神健康(MH)维度被打破了,按重编码后值计算维度分数:条目集群的分布接近源量表及其他2个 中文译本:除了生理功能(PF)躯体疼痛(BP)、社会功能(SF)维度,其余维度有相似的标准差:除了 SF、ⅥT维度,其余6个维度条目维度相关一致:除了SF维度,7个维度集合效度成功率范围为75% 100%,区分效度成功率范围为87.5%-100%。一致性信度系数除了sF、ⅥT维度,其余6维度变化范 围为0.72-0.88,满足群组比较的要求。两周重测信度变化范围为0.66-0.94。因子分析产生了2 个主成分,分别代表生理健康和心理健康,解释了56.3%的总方差。结论为SF-36健康调查量表适 用于中国提供了证据,已知群效度试验将为量表效度提供更有意义的证据。 【关键词】生活质量:心理学试验:SF-36量表 Development and psychometric tests of a Chinese version of the SF-36 Health Survey Scales L lu Hongmei, SHEN Yi. Department of Social Medicine, Zhejiang Unirersity School of Medicine, Hangzhou China [Abstract] Objective To develop and evaluate scaling and scoring assumptions, and the reliability and he validity of a Chinese version of the SF-36 scales. Methods A multi-stage mixed sampling procedure was used to select a representative sample of the general population. The sample size was 1 000 households. All family members of a selected household, aged 18 and older, completed a survey by self-administration. Formal psychometric methods for testing assumptions underlying item scoring and scale construction were used according to the standard procedure of the IQOLA Project. Results Of the 1 985 collected questionnaires, 1 972 were qualified. Of them, 1 688(85.6%)were respondents. I 316 respondents answered all 36 items, while the remaining(372 respondents) answered with one or several missing responses. Among the non-respondents, 65.5% illiteracy or quasi-illiteracy. The assumption of equal intervals was violated for the VT and MH scales. The recoded item values were used to calculate scale scores. The clustering and ordering of the item means were approximately the same as that of the source version and other two Chinese versions. The items in each scale had similar standard deviations except those in the PF, BP, SF scales. The correlations between an item and its pothesized scale were identical for all except the SF and VT scales. The scaling success rates of convergent alidity were 0% for the SF scale, 75% for the VT scale, and 100% for the other six scales. The scaling succ rates of discriminat validity ranged from 87.5% to 100% for all scales except for the SF scale. The Cronbach'a coefficients of internal consistency reliability ranged from 0. 72 to 0.88, which were satisfactory for group omparison except 0. 39 for the SF scale and 0. 66 for the VT scale. The two-weeks test-retest reliability coefficient ranged from 0. 66 to 0.94. Factor analysis identified two principal components: a physical factor and a mental factor. Taken together, these two factors could be used to explain 56.3% of the total variance. Conclusion The Chinese version of the SF-36 Health Survey Scale has achieved conceptual equivalence and satisfied the psychometric scaling assumptions well enough to warrant wide use in China. Known-groups validity will give more ngful evidences of the validity of the Chinese SF-36 scales I Key words] Quality of life: Psychological tests: SF-36 health surv 第139页 基金项目:浙江省科技计划项目资助(991104209) 作者单位:310031杭州,浙江大学医学院社会医学教研室(李鲁、王红妹),卫生统计学教研室(沈毅)

·论著· 基金项目：浙江省科技计划项目资助（991104209） 作者单位：310031 杭州，浙江大学医学院社会医学教研室（李鲁、王红妹），卫生统计学教研室（沈毅） SF-36 健康调查量表中文版的研制 及其性能测试 李鲁 王红妹 沈毅 【摘要】 目的 研制 SF-36 健康调查量表中文版并验证量表维度建立及记分假设、信度和效度。 方法 采用多阶段混合型等概率抽样法，用 SF-36 健康调查量表中文版对 1 000 户家庭的居民进行自 评量表式调查；参照国际生命质量评价项目的标准程序，进行正式的心理测验学试验。结果 在收回 的 1 985 份问卷中，18 岁以上的有效问卷 1 972 份，其中应答者 1 688 人（85.6%），1 316 人回答了所有 条目，372 人有 1 个或以上的缺失答案，无应答者中文盲、半文盲占 65.5%。等距假设在活力（VT）和 精神健康（MH）维度被打破了，按重编码后值计算维度分数；条目集群的分布接近源量表及其他 2 个 中文译本；除了生理功能（PF）、躯体疼痛（BP）、社会功能（SF）维度，其余维度有相似的标准差；除了 SF、VT 维度，其余 6 个维度条目维度相关一致；除了 SF 维度，7 个维度集合效度成功率范围为 75% ～ 100%，区分效度成功率范围为 87.5% ～ 100%。一致性信度系数除了 SF、VT 维度，其余 6 维度变化范 围为 0.72 ～ 0.88，满足群组比较的要求。两周重测信度变化范围为 0.66 ～ 0.94。因子分析产生了 2 个主成分，分别代表生理健康和心理健康，解释了 56.3%的总方差。结论 为 SF-36 健康调查量表适 用于中国提供了证据，已知群效度试验将为量表效度提供更有意义的证据。 【关键词】 生活质量； 心理学试验； SF-36 量表 Development and psychometric tests of a Chinese version of the SF-36 Health Survey Scales LI Lu*， WANG Hongmei，SHEN Yi .* Department of Social Medicine，Zhejiang University School of Medicine，Hangzhou 310031，China 【Abstract】 Objective To develop and evaluate scaling and scoring assumptions，and the reliability and the validity of a Chinese version of the SF-36 scales. Methods A multi-stage mixed sampling procedure was used to select a representative sample of the general population. The sample size was 1 000 households. All family members of a selected household，aged 18 and older，completed a survey by self-administration. Formal psychometric methods for testing assumptions underlying item scoring and scale construction were used according to the standard procedure of the IQOLA Project. Results Of the 1 985 collected questionnaires，1 972 were qualified. Of them，1 688（85.6%）were respondents. 1 316 respondents answered all 36 items，while the remaining（372 respondents）answered with one or several missing responses. Among the non-respondents，65.5% were illiteracy or quasi-illiteracy. The assumption of equal intervals was violated for the VT and MH scales. The recoded item values were used to calculate scale scores. The clustering and ordering of the item means were approximately the same as that of the source version and other two Chinese versions. The items in each scale had similar standard deviations except those in the PF，BP，SF scales. The correlations between an item and its hypothesized scale were identical for all except the SF and VT scales. The scaling success rates of convergent validity were 0% for the SF scale，75% for the VT scale，and 100% for the other six scales. The scaling success rates of discriminat validity ranged from 87.5% to 100% for all scales except for the SF scale. The Cronbach'α coefficients of internal consistency reliability ranged from 0.72 to 0.88，which were satisfactory for group comparison except 0.39 for the SF scale and 0.66 for the VT scale. The two-weeks test-retest reliability coefficient ranged from 0.66 to 0.94. Factor analysis identified two principal components：a“physical”factor and a“mental” factor. Taken together，these two factors could be used to explain 56.3% of the total variance.Conclusion The Chinese version of the SF-36 Health Survey Scale has achieved conceptual equivalence and satisfied the psychometric scaling assumptions well enough to warrant wide use in China. Known-groups validity will give more meaningful evidences of the validity of the Chinese SF-36 scales. 【Key words】 Quality of life； Psychological tests； SF-36 health survey 中华预防医学杂志 2002 年 3 月第 36 卷第 2 期 Chin J Prev Med，March 2002，Vol 36，No.2 · 109 · 第 139 页

中华预防医学杂志2002年3月第36卷第2期 Chin j Prev Med, March2002,Vd36,No.2 “健康相关生命质量”( health related quality of所有条目全部完成的比例;维度分数能被计算的比 if, HRQOL)的概念自70年代引入国外医学界以例。列联表卡方比较应答者与无应答者社会人口学 来,产生了许多生命质量测评量表。SF-36健康调查特征的差别, logistic回归分析诸因素对应答率的综 量表( the mos36- item Short Form Health Survey)成为合影响。 全球应用最广的生命质量测评工具。SF-36量表评 四、心理测验学试验 价 HRQOL的8个方面,即生理功能( physical 1.条目记分和维度建立的假设 functioning,PF)、生理职能( role-physical,P)、躯体疼 (1)是否为等距变量:选择项之间的距离应 痛( bodily pain,BP)、总体健康( general health,cCH)、活致。如果该假设被打破,应重编码。这一假设在含 力ⅶ itality,Vr)、社会功能( social functioning,sF)情2个以上条目且每一条目含2个以上水平的维度中 感职能( role-emotional,RE)、精神健康( mental health,得到检验——(H、FF、V、MH维度。我们对每一条 MH)。另外还有健康变化( health transition,H),用目每一水平,用所属维度其他条目分数和的平均值 于评价过去1年内健康改变。1991年,国际生命质来记分,然后分配经验分数:最低反应水平置为1, 量评价项目将SF36量表列为测评工具141。在此最高反应水平置为K(一共K个水平),中间值按平 介绍SF36量表中文版的研制过程,并用杭州市区均分的间距来置分2。 人群健康调查资料验证量表维度建立及记分假设 (2)每一维度各条目的方差是否一致。 信度和效度 (3)每一维度条目维度的相关是否一致。 资料与方法 (4)集合效度条目与所属维度显著相关(估计条 、SF-36健康调查量表的研制 目与所属维度其余条目总和的相关性r≥0.40)。 采用美国波士顿新英格兰医学中心健康研究所 (5)区分效度条目与所属维度的相关性高于与 的标准版SF-36健康调查量表1,由2名本专业研其他维度的相关性(2个标准差或以上,采用相关系 究生各完成一中译本,经比较讨论产生初稿。译员数的假设检验5]) 对问卷翻译有经验,但不熟悉SF-36量表。初稿经 2.信度和效度:本研究采用重测信度及内部 本校2名英语教师评价翻译质量,再经公共卫生、临致性信度( Cronbach'a)。 Cronbach'a≥0.7的信度系 床医疗、心理学8位对量表调查设计有经验的专业数用于群组比较令人满意[1。维度间相关系数应低 人员讨论,产生修改稿。在普通人群的方便样本中于 Cronbach'a信度系数。效度检验除了集合效度和 作预试,再作改动后产生终稿 区分效度,还采用因子分析法。考虑这样一种理论 二、研究背景 假设:量表测量2个概念,分别代表生理和心理健 采用多阶段混合型等概率抽样法,按街道、居民康。检查维度间相关以验证这种假设 区、户三级抽样。第1阶段分别从下城区(属中心城 样本资料使用SSS7.0 for windows软件进行分 区)和拱墅区(属次中心城区)抽3个街道,第2阶段析。 再从每个街道各抽取3个居民区。抽样方法采用等 距抽样法,最后阶段即户数的抽样数目,则根据每户 被抽中的概率P=n/N来确定(其中n为样本量 SF-36健康调查量表中文版 1000户,N为2区总户数173765户)。对抽中户进 中文版在尊重源量表概念的基础上对个别条目 行入户自评量表式调查。被调查者要求18岁以上,根据中国国情作了修正。在PF维度,推真空吸尘 有阅读能力。在第1天调查的居民中随机抽取57器,打保龄球、高尔夫球在中国不是一项普及的活 人,2周后重测 动。中国人很熟悉拖地板,打太极拳,但是否在各自 三、资料质量 文化中同属中等度活动无法确知,故都放在量表中 若一维度半数以上条目缺失,则维度分数置为以增加明晰度。1英里等于1609m,如果精确翻译, 缺失:半数或半数以下条目缺失,则用未缺失条目的并不表达源量表所希望表达的精确度,故译成1500 平均分代替缺失条目分数。计算 Mvers指数,该140在中国无街区(b)一词,用“路口”来代替。 数取值范围为0~99,若大于60,表明存在严重的年 在ⅥT、MH维度的翻译中,“ full of pep”," down in 龄堆积现象。计算每一条目的完成情况,每一维度 the dumps”,“ downhearted and blue”在中文中找不到

“健康相关生命质量”（health related quality of life，HRQoL）的概念自 70 年代引入国外医学界以 来，产生了许多生命质量测评量表。SF-36 健康调查 量表（the Mos 36-item Short Form Health Survey）成为 全球应用最广的生命质量测评工具。SF-36 量表评 价 HRQoL 的 8 个 方 面，即 生 理 功 能（ physical functioning，PF）、生理职能（role-physical，RP）、躯体疼 痛（bodily pain，BP）、总体健康（general health，GH）、活 力（vitality，VT）、社会功能（social functioning，SF）、情 感职能（role-emotional，RE）、精神健康（mental health， MH）。另外还有健康变化（health transition，HT），用 于评价过去 1 年内健康改变。1991 年，国际生命质 量评价项目将 SF-36 量表列为测评工具［1-4］。在此 介绍 SF-36 量表中文版的研制过程，并用杭州市区 人群健康调查资料验证量表维度建立及记分假设、 信度和效度。 资料与方法 一、SF-36 健康调查量表的研制 采用美国波士顿新英格兰医学中心健康研究所 的标准版 SF-36 健康调查量表［1］，由 2 名本专业研 究生各完成一中译本，经比较讨论产生初稿。译员 对问卷翻译有经验，但不熟悉 SF-36 量表。初稿经 本校 2 名英语教师评价翻译质量，再经公共卫生、临 床医疗、心理学 8 位对量表调查设计有经验的专业 人员讨论，产生修改稿。在普通人群的方便样本中 作预试，再作改动后产生终稿。 二、研究背景 采用多阶段混合型等概率抽样法，按街道、居民 区、户三级抽样。第 1 阶段分别从下城区（属中心城 区）和拱墅区（属次中心城区）抽 3 个街道，第 2 阶段 再从每个街道各抽取 3 个居民区。抽样方法采用等 距抽样法，最后阶段即户数的抽样数目，则根据每户 被抽中的概率 P = n / N 来确定（其中 n 为样本量 1 000户，N 为 2 区总户数 173 765 户）。对抽中户进 行入户自评量表式调查。被调查者要求 18 岁以上， 有阅读能力。在第 1 天调查的居民中随机抽取 57 人，2 周后重测。 三、资料质量 若一维度半数以上条目缺失，则维度分数置为 缺失；半数或半数以下条目缺失，则用未缺失条目的 平均分代替缺失条目分数。计算 Myer's 指数，该指 数取值范围为 0 ～ 99，若大于 60，表明存在严重的年 龄堆积现象。计算每一条目的完成情况，每一维度 所有条目全部完成的比例；维度分数能被计算的比 例。列联表卡方比较应答者与无应答者社会人口学 特征的差别，logistic 回归分析诸因素对应答率的综 合影响。 四、心理测验学试验 1. 条目记分和维度建立的假设： （1）是否为等距变量：选择项之间的距离应一 致。如果该假设被打破，应重编码。这一假设在含 2 个以上条目且每一条目含 2 个以上水平的维度中 得到检验———GH、PF、VT、MH 维度。我们对每一条 目每一水平，用所属维度其他条目分数和的平均值 来记分，然后分配经验分数：最低反应水平置为 1， 最高反应水平置为 K（一共 K 个水平），中间值按平 均分的间距来置分［2］。 （2）每一维度各条目的方差是否一致。 （3）每一维度条目维度的相关是否一致。 （4）集合效度条目与所属维度显著相关（估计条 目与所属维度其余条目总和的相关性 r≥0.40）。 （5）区分效度条目与所属维度的相关性高于与 其他维度的相关性（2 个标准差或以上，采用相关系 数的假设检验［5］）。 2.信度和效度：本研究采用重测信度及内部一 致性信度（Cronbach'α）。Cronbach'α≥0.7 的信度系 数用于群组比较令人满意［1］。维度间相关系数应低 于 Cronbach' α信度系数。效度检验除了集合效度和 区分效度，还采用因子分析法。考虑这样一种理论 假设：量表测量 2 个概念，分别代表生理和心理健 康。检查维度间相关以验证这种假设。 样本资料使用 SPSS 7.0 for Windows 软件进行分 析。 结 果 一、SF-36 健康调查量表中文版 中文版在尊重源量表概念的基础上对个别条目 根据中国国情作了修正。在 PF 维度，推真空吸尘 器，打保龄球、高尔夫球在中国不是一项普及的活 动。中国人很熟悉拖地板，打太极拳，但是否在各自 文化中同属中等度活动无法确知，故都放在量表中 以增加明晰度。1 英里等于 1 609 m，如果精确翻译， 并不表达源量表所希望表达的精确度，故译成 1 500 m。在中国无街区（block）一词，用“路口”来代替。 在 VT、MH 维度的翻译中，“full of pep”，“down in the dumps”，“downhearted and blue”在中文中找不到 · 110 · 中华预防医学杂志 2002 年 3 月第 36 卷第 2 期 Chin J Prev Med，March 2002，Vol 36，No.2 第 140 页