【VIP专享】2014年加拿大临床实践指南1

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2014年加拿大临床实践指引广泛性焦虑障碍

2014年加拿大临床实践指南（二）：广泛性焦虑障碍医脉通2014-08-20获加拿大卫生部批准的焦虑治疗药物一览流行病学广泛性焦虑障碍（GAD）的12个月患病率为1-4%，终生患病率接近6%。

与其他人种相比，GAD在白人中的发病率更高。

发病年龄呈双峰式分布，中位年龄为31岁，平均年龄为32.7岁。

GAD在儿童中的患病率约为3%，在成人中约为10.8%，儿童及青少年于10-14岁之间起病。

一些数据显示，女性罹患GAD的风险是男性的2-3倍，在老年人群中同样更为常见。

公众对GAD的识别存在不足，接受适宜治疗的患者不到全部患者的三分之一；由于先前儿童期过度焦虑（Overanxious Disorder of Childhood）的存在，以及成人及儿童GAD的潜在差异，这种识别不足的状况在儿童中尤为复杂。

GAD常与功能、职业及生活质量损害相关，同时也造成了沉重的社会负担。

另外，在初级医疗保健机构中，有60-94%的GAD患者报告存在疼痛性躯体症状；对于72%的GAD患者而言，他们就诊的初衷正是改善这些疼痛症状。

共病GAD共病其他精神障碍的比例很高，患者常共病其他类型的焦虑或相关障碍，以及重性抑郁（MDD）。

共病躯体疾病的风险同样较高，包括疼痛症状、高血压、心血管及胃部问题。

GAD所共病的抑郁增加了GAD的严重程度、功能损害及经济负担。

DSM-5诊断GAD以针对多种事件及活动的过度焦虑及担忧为特征，包括学业及工作困难。

上述症状出现于过去6个月内的大部分时间。

此外，GAD与不安、肌肉紧张、疲劳、注意困难、易激惹及睡眠问题相关。

与DSM-IV相比，DSM-5中的GAD诊断标准仅进行了一处小的修订：删除了心境障碍、精神病性障碍及弥漫性发育障碍的排除标准。

然而需要指出的是，以下大部分治疗相关内容均基于满足DSM-IV诊断标准（或更旧版本）的患者。

心理治疗Meta分析明确显示，认知行为疗法（CBT）可显著改善GAD症状，疗效远优于安慰剂或等候名单对照（1级证据）。

2014+SOGC临床实践指南：更年期骨质疏松症

SOGC CLINICAL PRACTICE GUIDELINEAbstractObjective: To provide guidelines for the health care provider on the prevention, diagnosis, and clinical management of postmenopausal osteoporosis.Outcomes: Strategies for identifying and evaluating high-risk individuals, the use of bone mineral density (BMD) and bone turnover markers in assessing diagnosis and response tomanagement, and recommendations regarding nutrition, physical activity, and the selection of pharmacologic therapy to prevent and manage osteoporosis.Evidence: Published literature was retrieved through searches of PubMed and The Cochrane Library on August 30 and September 18, 2012, respectively. The strategy included the use ofappropriate controlled vocabulary (e.g., oteoporosis, bone density, menopause) and key words (e.g., bone health, bone loss, BMD). Results were restricted to systematic reviews, practice guidelines, randomized and controlled clinical trials, and observational studies published in English or French. The search was limited to the publication years 2009 and following, and updates were incorporated into the guideline to March 2013. Grey (unpublished) literature was identified through searching the websites of health technology assessment and health technology assessment-related agencies, clinical practice guideline collections, clinical trial registries, and national and international medical specialty societies.Values: The quality of the evidence was rated using the criteriadescribed by the Canadian Task Force on Preventive Health Care (Table 1).Sponsors: The Society of Obstetricians and Gynaecologists of Canada.RECOMMENDATIONS For Postmenopausal Women1. Health care providers should be aware that the goals ofosteoporosis management include assess m ent of fracture risk and prevention of fracture. (I-A) 2. Health care providers should understand that a stable orincreasing bone mineral density reflects a response to therapy in the absence of low-trauma fracture or height loss due to vertebral-compression fracture. A pro g ressive decrease in bone mineral density, with the magnitude of bone loss being greater than the precision error of the density assessment, indicates a lack of response to current ther a py. Management should be reviewed and modified appropriately. (I-A)No. 312, September 2014 (Replaces No. 222, January 2009)Osteoporosis in MenopauseThis clinical practice guideline has been prepared by the Menopause and Osteoporosis Working Group, reviewed by the Clinical Practice Gynaecology and Family Physician Advisory Committees, and approved by the Executive and Council of the Society of Obstetricians and Gynaecologists of Canada.PRINCIPAL AUTHORS Aliya Khan, MD, Hamilton ON Michel Fortier, MD, Quebec QC MENOPAUSE AND OSTEOPOROSIS WORKING GROUPMichel Fortier, MD (Co-Chair), Quebec QC Robert Reid, MD (Co-Chair), Kingston ON Beth L. Abramson, MD, Toronto ON Jennifer Blake, MD, Toronto ON Sophie Desindes, MD, Sherbrooke QC Sylvie Dodin, MD, Quebec QC Lisa Graves, MD, Toronto ON Bing Guthrie, MD, Yellowknife NT Shawna Johnston, MD, Kingston ON Aliya Khan, MD, Hamilton ON Timothy Rowe, MB BS, Vancouver BC Namrita Sodhi, MD, Toronto ON Penny Wilks, ND, Dundas ON Wendy Wolfman, MD, Toronto ONDisclosure statements have been received from all contributors.The literature searches and bibliographic support for this guideline were undertaken by Becky Skidmore, MedicalResearch Analyst, Society of Obstetricians and Gynaecologists of Canada.Key Words : Osteoporosis, prevention, treatment, diagnosis, bone mineral density, dual energy x-ray absorptiometry, bone turnover markers, vertebral fractures, fragility fractures, antiresorptive, hormone therapy, selective estrogen-receptor modulator, bisphosphonates, calcitonin, anabolic, bone forming agentJ Obstet Gynaecol Can 2014;36(9 eSuppl C):S1–S15SOGC CLINICAL PRACTICE GUIDELINE3. Health care providers should identify the absolute fracture riskby integrating the key risk factors for fracture; namely, age,bone mineral density, prior fracture, and glucocorticoid use.These risk factors allow estimation of fracture risk using the tool of the Canadian Association of Radiologists and Osteoporosis Canada. (I-A)4. The Fracture Risk Assessment tool of the World HealthOrganization (FRAX) has now been validated in a Canadianpopulation and may also be used and incorporates additionalrisk factors; namely, low body mass index, parental history offracture, smoking status, alcohol intake, and the presence ofsecondary causes of osteoporosis. (I-A)5. Health care providers should be aware that a fragility fracturemarkedly increases the risk of a future fracture and confirms the diagnosis of osteo p orosis irrespective of the results of the bone density assessment, (I-A) and that the presence of a low-trauma fracture of a vertebra or hip or more than 1 fragility fractureconfirms a high fracture risk regardless of the bone mineraldensity. (I-A)6. Treatment should be initiated according to the results of the10-year absolute fracture risk assessment. (I-A)Calcium and Vitamin D7. Adequate calcium and vitamin D supplementation is keyto ensuring prevention of progressive bone loss. Forpostmenopausal women a total daily intake of 1200 mg ofelemental calcium from dietary and supplemental sourcesand daily supplementation with 800 to 2000 IU of vitamin Dare recommended. Calcium and vitamin D supplementationalone is insufficient to prevent fracture in those withosteoporosis; however, it is an important adjunct topharmacologic intervention with antiresorptive and anabolictherapy. (I-B)Hormone Therapy8. Hormone therapy should be prescribed for symptomaticpostmenopausal women as the most effective option formenopausal symptom relief. (I-A) It represents a reasonablechoice for the prevention of bone loss and fracture in this patient population. (I-A)9. Physicians may recommend low- and ultralow-dosage estrogentherapy to symptomatic women for relief of menopausalsymptoms (I-A) but should inform their patients that, despitethe fact that such therapy has demonstrated a beneficial effectin osteoporosis preven t ion, (I-A) no data are yet available onreduction of fracture risk.Bisphosphonates10. Alendronate, risedronate, and zoledronic acid are valuablefirst-line agents of choice in the treatment of postmenopausalosteoporosis and should be considered to decrease the risk ofvertebral, non-vertebral, and hip fractures. (I-A)11. Etidronate is a weak antiresorptive agent and is notrecommended as a first-line agent of choice for the treatmentof osteoporosis. (I-D)RANKL Inhibitor12. Denosumab is an effective antiresorptive agent, shown toreduce the risk of vertebral, non-vertebral, and hip fractures, (I-A) and should be considered as a first-line agent of choice in thetreatment of postmenopausal osteoporosis in women at a highfracture risk. (I-A)Table 1. Key to evidence statements and grading of recommendations, using the ranking of the Canadian Task Force on Preventive Health CareQuality of evidence assessment*Classification of recommendations†I: Evidence obtained from at least one properly randomizedcontrolled trialA. There is good evidence to recommend the clinical preventive actionII-1: Evidence from well-designed controlled trials withoutrandomizationB. There is fair evidence to recommend the clinical preventive actionII-2: Evidence from well-designed cohort (prospective or retrospective) or case–control studies, preferably from more than one centre or research group C. The existing evidence is conflicting and does not allow to make arecommendation for or against use of the clinical preventive action;however, other factors may influence decision-makingII-3: Evidence obtained from comparisons between times or places with or without the intervention. Dramatic results inuncontrolled experiments (such as the results of treatment with penicillin in the 1940s) could also be included in this category D. There is fair evidence to recommend against the clinical preventive actionE. There is good evidence to recommend against the clinical preventiveactionIII: Opinions of respected authorities, based on clinical experience, descriptive studies, or reports of expert committees L. There is insufficient evidence (in quantity or quality) to makea recommendation; however, other factors may influencedecision-making*The quality of evidence reported in these guidelines has been adapted from The Evaluation of Evidence criteria described in the Canadian Task Force on Preventive Health Care.89†Recommendations included in these guidelines have been adapted from the Classification of Recommendations criteria described in the Canadian Task Force on Preventive Health Care.89ABBREVIATIONSAFF atypical femoral fractureBMD bone mineral densityET estrogen therapyFIT Fracture Intervention TrialHR hazard ratioHT hormone therapyONJ osteonecrosis of the jawRANKL receptor activator of nuclear factor kappa-B ligandRCT randomized controlled trialSERM selective estrogen-receptor modulatorWHI Women’s Health InitiativeOsteoporosis in MenopauseSelective Estrogen-Receptor Modulators13. Treatment with raloxifene may be considered to decrease the riskof vertebral fractures, bearing in mind that this agent has not been shown to be effective in reducing the risk of non-vertebral or hipfractures. (I-A)Parathyroid Hormone14. Treatment with teriparatide should be considered to decrease therisk of vertebral and non-vertebral fractures in postmenopausalwomen with severe osteoporosis (I-A) and should also beconsidered in postmenopausal women experiencing bone loss ora new fracture despite antiresorptive therapy. (I-A) INTRODUCTIONO steoporosis is defined as an impairment in bone strength due to an abnormal quantity and/or quality of bone. Quantity is evaluated by measuring BMD. Quality is affected by many factors, including the degree of mineral i zation, the rate of bone remodelling, the connectivity of the bony trabeculae, the quality of the collagen fibres, and the health of the bone cells. The 3 types of bone cells are osteoblasts, osteoclasts, and osteocytes. The osteocytes function as “mechanostats”, sensing the degree of microdamage and triggering remodelling in areas of stress and strain, thus allowing continual renewal, repair, and replacement of bone. This process of remodelling maintains bone strength.Adequate calcium and vitamin D intake is necessary to attain and maintain normal bone quantity and quality and thus achieve optimal bone strength. Early assessment of skeletal health and then initiation of appropriate calcium and vitamin D supplementation and an exercise program are essential in the prevention and treatment of osteoporosis. Individuals at increased risk for fracture should also be offered pharmacologic therapy in order to reduce the fracture risk. Absolute frac t ure risk is identified by integrating age and BMD with other key risk factors for fracture including prior fracture history and use of glucocorticoid therapy. The decision to treat is based on the risk of fracture, and the quantification of absolute fracture risk enables targeting of treatment to those at greatest risk.RISK ASSESSMENT AND MANAGEMENTBone strength is determined by both bone quantity and bone quality. Bone densitometry provides information on BMD, which is a reflection of bone quantity. Bone quality is determined by a number of factors, including the rate of remodelling, bone mineralization, function of the bone cells, and quality of the collagen fibres. It is necessary to identify risk factors for fracture that may be present and the risk of falls. The timed “get up and go” test is valuable in assessing gait stability and is a reflection of fall risk. Risk factors for osteoporosis have been identi fi ed (Table 2),1 and the presence of risk factors in a postmenopausal woman justifies bone densitometry.2In 2005 Osteoporosis Canada recommended identifying absolute fracture risk by integrating the key risk factors for fracture; namely, age, BMD, prior fracture, and glucocorticoid use.3 The 10year risk of fragility fractures is thus determined (Figure)1and defined as high if it is greater than 20%, moderate if it is 10% to 20%, and low if it is less than 10%.4 The additional effect of a preexisting fragility fracture or glucocorticoid use moves the patient 1 risk category higher. These guidelines were based on Swedish data and have been recalibrated using Canadian hip fracture data. The version developed by the Canadian Association of Radiologists and Osteoporosis Canada4 has now been validated in 2 Canadian cohorts and has close to 90% agreement with the FRAX5 score (the FRAX tool can be downloaded from the Osteoporosis Canada website, http://www.osteoporosis.ca). The presence of a vertebral or hip fracture or more than 1 fragility fracture increases the fracture risk to high. Fracture risk is evaluated on the basis of femoral neck BMD and age and is modified by the presence of prior fragility fracture or the use of glucocorticoid therapy (7.5 mg for 3 months or longer); these modifiers increase the fracture risk to the next risk category.1 A BMD Tscore of −2.5 or less at either the lumbar spine or the femoral neck denotes at least a moderate risk of fracture.1 Height should be measured annually, and a decrease in measured height of more than 2 cm should be further evaluated by radiographs of the thoracic and lumbar spine with exclusion of vertebral fractures.6A more comprehensive calculation of the 10year absolute fracture risk, now available from the World Health Organization, incorporates additional risk factors: parental history of hip fracture, current tobacco smoking, rheumatoid arthritis or other secondary causes of bone loss, and alcohol intake of 3 or more units daily.5It is recommended that absolute fracture risk be calculated using the tool of either the Canadian Association of Radiologists and Osteoporosis Canada or FRAX and the decision to treat be based on the absolute fracture risk. Younger individuals at a low risk of fracture are appropriately managed with lifestyle changes and strategies designed to prevent bone loss.Osteoporosis is diagnosed in a postmenopausal woman on the basis of a BMD Tscore of less than −2.5 at theSOGC CLINICAL PRACTICE GUIDELINElumbar spine, hip (femoral neck or total hip), or radius (distal third). Clinically it is diagnosed in a postmenopausal woman in the presence of a lowtrauma fracture. In a premenopausal woman osteoporosis is diagnosed only in the presence of fragility fractures; BMD alone cannot be used for diagnosis.7In premenopausal women a normal BMD is defined as being within 2 standard deviations of the agematched reference mean. Comparison with the agematched reference range is represented by the Z score, and in premenopausal women Z scores should be used instead of T scores. Low bone density is defined as a BMD Z score 2 or more standard deviations below the mean agematched reference value.7Pharmacologic therapy is considered in postmenopausal women after exclusion of secondary causes of low bone density. If the 10year absolute fracture risk is greater than 20% (high), then drug therapy is advised. In those with a moderate risk (10% to 20%), management decisions are indi v idualized. Those with a low fracture risk (< 10%) can be treated conservatively after exclusion of secondary causes of bone loss with prevention strategies based on ensuring adequate calcium and vitamin D supplementation. It is also important to emphasize regular exercise and reduced con s umption of alcohol (fewer than 2 drinks/d) and coffee (fewer than 4 cups/d). Smoking cessation should also be strongly advised.Failure of therapy is confirmed by the development of a lowtrauma fracture or significant bone loss despite pharmacologic therapy for 2 years. In these individuals it is necessary to ensure that there are no secondary causes of bone loss. It is also important to ensure adequate adherence to therapy.8ADVANCES IN PHARMACOLOGIC THERAPYIn addition to adequate calcium, vitamin D, and exercise, options for the prevention and treatment of osteoporosis include antiresorptive and anabolic agents.9 Antiresorptive (anticatabolic) agents inhibit osteoclast activity and reduce bone turnover.9,10 The various agents have different mechanisms of action. Bisphosphonates reduce the rate of bone turnover, providing a longer time for bone to mineralize. Bisphosphonate therapy is thus associated with modest increases in BMD. Estrogen acts through the estrogen receptors on both osteoblasts and osteoclasts, suppressing receptor activator of nuclear factor κB ligand (RANKL)induced osteoclast differentiation and thereby decreasing bone remodeling.11 Raloxifene, a SERM, can bind to estrogen receptors, with tissuespecific agonist or antagonist effects. Raloxifene decreases bone remodelling in addition to its extraskeletal effects. Osteoclastic bone resorption is also inhibited by calcitonin acting on calcitonin receptors. Denosumab is a monoclonal antibodyTable 2. Risk factors for osteoporosis: indications for measuring BMDOlder adults (age ≥ 50 years)Younger adults (age < 50 years)Age ≥ 65 years (both women and men) Fragility fractureClinical risk factors for fracture(menopausal women and men age 50 to 64 years)Prolonged use of glucocorticoids* Fragility fracture after age 40 years Use of other high-risk medications†Prolonged use of glucocorticoids*Hypogonadism or premature menopause(age < 45 years)Use of other high-risk medications Malabsorption syndromeParental hip fracture Primary hyperparathyroidismVertebral fracture or osteopenia identified on radiography Other disorders strongly associated with rapid bone loss and/or fractureCurrent smokingHigh alcohol intakeLow body weight (< 60 kg) or major weight loss(> 10% of body weight at age 25 years)Rheumatoid arthritisOther disorders strongly associated withosteoporosis*At least 3 months’ cumulative therapy in the previous year at a prednisone-equivalent dose ≥ 7.5 mg daily.†For example, aromatase inhibitors or androgen deprivation therapy.Reproduced with permission of the Canadian Medical Association from Papaioannou A et al.1Osteoporosis in Menopauseto RANKL (receptor activator of nuclear factor κB) and binds to RANKL, lowering values to premenopausal levels. This results in a decrease in the formation, function, and survival of osteoclasts.Antiresorptive agents are effective in reducing frac t ure risk by approximately 30% to 68% in postmenopausal women. However, fractures may still occur, and anabolic therapy can complement antiresorptive therapy in the prevention of further fractures. Anabolic therapy can result in new bone formation, with increases in cortical thickness and trabecular connectivity, leading to major improvements in the quality and quantity of bone. Anabolic therapy can increase the production of new bone matrix by enhancing osteoblast function. Teriparatide (recombinant human parathyroid hormone, amino acid sequence 1 through 34) decreases the release of sclerostin from osteocytes. Sclerostin is a protein that decreases bone formation by inhibiting the Wnt signalling pathway in the osteoblast. With a decrease in this inhibitor of bone formation, there is an increase in new bone formation. Teriparatide, 20 μg daily, has been shown to reduce the risks of vertebral and nonvertebral fragility fractures by approximately 65% and 53%, respectively, over 18 months in postmenopausal women with osteoporosis.12 Teriparatide is the only anabolic agent available in Canada.CALCIUM AND VITAMIN D SUPPLEMENTATION The effectiveness of calcium and vitamin D supplementation in preventing hip fractures was evaluated in the WHI.13 The trial involved 36 282 postmenopausal women who daily received either 1000 mg of elemental cal c ium as calcium carbonate and 400 IU of vitamin D, or a placebo, for an average of7 years. Patients were allowed to take additional daily supplements of up to 1000 mg of cal c ium and 600 IU of vitamin D; approximately 38% of subjects took more than 1200 mg of elemental calcium daily. Personal use of bisphosphonates, calcitonin, SERMs, and ET was also permitted. The calcium and vita m in D study arm overlapped with the HT arm; thus, approximately 51% of women were receiving estrogen.Treatment compliance was poor: by the end of the study, only 59% of the women were taking 80% or more of their supplements. As compared with those taking placebo, the women taking 1000 mg of calcium and 400 IU of vitamin D daily showed a 1.06% increase in hip BMD (P < 0.01). In the treatmentcompliant group, the HR for hip fracture was 0.71 (95% CI 0.52 to 0.97), representing a statistically significant 29% reduction in hip fracture risk among the women taking 80% or more of their calcium and vitamin D supplements. Estrogen use was associated with a 42% Assessment of basal 10-year risk of fracture with the 2010 tool of the Canadian Association of Radiologist and Osteoporosis Canada.Reproduced with permission of the Canadian Medical Association from Papaioannou A et al.1The T-score for the femoral neck should be derived from the National Health and Nutrition Education Survey III reference database for white women. Fragility fracture after age 40 or recent prolonged use of systemic glucocorticoids increases the basal risk by one category (ie, from low to moderate or moderate to high). This model reflects the theoretical risk for a hypothetical patient who is treatment-naive; it cannot be used to determine risk reduction associated with therapy. Individuals with fragility fracture of a vertebra or hip and those with more than one fragility fracture are at high risk of an additional fracture.WomenLow risk (< 10%)High risk (> 20%)Moderate riskAge (year)T–score,femoralneck0.0–1.0–2.0–3.0–4.050 55 60 65 70 75 80 85MenLow risk (< 10%)High risk (> 20%)Moderate riskAge (year)T–score,femoralneck0.0–1.0–2.0–3.0–4.050 55 60 65 70 75 80 85SOGC CLINICAL PRACTICE GUIDELINEreduction in hip fracture risk. A small but significant 17% increase in the risk of renal stones was noted in the treatment group as compared with the placebo group: the HR was 1.17 (95% CI 1.02 to 1.34). Inadequate blood levels of vitamin D were also noted in the WHI study and may have contributed to the findings. In the nested case–control study, the mean serum 25hydroxy vitamin D level at baseline was 46.0 nmol/L in the women who had sustained hip fractures as compared with 48.4 nmol/L in their control subjects (P = 0.17). Vitamin D supplementation of more than 600 IU daily may have reduced the fracture risk, as has been demonstrated in other clinical trials.Calcium supplements have been linked to a possible increase in the risk of cardiovascular events.14 A recent 5year RCT of 1200 mg of elemental calcium carbonate daily versus placebo in 1460 postmenopausal women did not demonstrate any difference in rates of death or hospitalization due to coronary events.15 In the EPIC study of 23 980 people between the ages of 35 and 64 years followed for 11 years with questionnaires, those with a calciumenriched diet had a lower risk of myocardial infarction (HR 0.69; 95% CI 0.5 to 0.94), whereas those using a calcium supplement had a higher risk (HR 1.86; 95% CI 1.17 to 2.96).16Data from the WHI among those not using personal calcium or vitamin D supplements at baseline did not show an adverse effect of such supplementation on the risk of myocardial infarction, coronary heart disease, total heart disease, stroke, or overall cardiovascular disease.17 These RCT data are the best evidence currently available and do not support an increased risk of coronary events with calcium and vitamin D supplementation.It is recommended that the daily calcium requirement of 1200 mg be met ideally from dietary sources; if this is not possible, then supplements may be safely used. Calcium carbonate and calcium citrate are the supplements of choice.Ensuring adequate vitamin D supplementation is a key component of the prevention and treatment of osteoporosis. Although it might not be sufficient as the sole means of therapy for osteoporosis, routine supplementation with calcium (1000 mg/d) and vitamin D 3 (800 to 2000 IU/d) is still recommended as a mandatory adjunct to the main pharmacologic agents (antiresorptive and anabolic drugs). Vitamin D in doses of 800 IU daily has been shown to be effective in reducing the risk of falls by 49% over a 12week period of therapy.18 Vitamin D supplementation at a dose of 10 000 IU once weekly has been suggested for women unable to take daily supplements in areas wheresuch a preparation is available. Doses of 100 000 IU ofvitamin D 3 given orally every 4 months have been shownto be effective in reducing the risk of osteoporotic fractures.19Vitamin D levels depend on a number of factors, including dietary intake, sun exposure, skin pigmentation, body mass index, and smoking status.20 Extraskeletal benefits are currently being evaluated and may include a reduction in the risk of certain malignant diseases as well as autoimmune disorders.HORMONE THERAPYEstrogen has significant antiresorptive effects. Spe c ifically, it enhances the osteoblastic production of osteoprotegerin, which has antiosteoclastic properties because of its ability to bind to RANKL and subsequently to block the RANKL/RANK interaction required for osteoclast recruitment and activation.21,22 Estrogen also decreases RANKL expression from the osteoblast. In the WHI, a pri m ary prevention trial, the estrogenonly arm demonstrated a 30% to 39% reductionin fracture rates.23 This trial theref ore confirmed the antifracture effects of ET suggested by previous clinical trials.24,25The combined estrogen/progestogen arm of the WHI had similar results: an increase in total hip BMD, together with a 34% reduction in hip and vertebral fractures and a 24% reduction in total osteoporotic fractures.26 In earlypostmenopausal women, the combined therapy resulted in increases in BMD of 2% to 3% at the hip and spine over 2 years of therapy.24 A decline in the markers of bone turnover in response to HT was also seen in earlypostmenopausal women.25HT (with estrogen alone or combined with a progestogen) is still considered the most effective therapy for the medical management of meno p ausal symptoms. Bone protection with HT at a usual dosage is considered an added benefit. Recent studies designed to test various dosages of estrogen for bone pro t ection have shown a linear dose response of the skeleton from the lowest to the highest dosages tested.24,27,28 These RCTs have shown that lowdosage ET can prevent postmenopausal osteoporosis, and ultralowdosage ET has beneficial skeletal effects. However, no fracture trial has yet been carried out with low and ultralowdosage HT. A low dose is 0.3 mg of conjugated estrogen or its equivalent (e.g., 0.5 mg of micronized estradiol); half this amount is considered ultralow.29SERM THERAPYSERMs have demonstrated tissuespecific estrogenagonistic or estrogenantagonistic effects.30 In the Multiple。

[流程图]2014 RA临床实践指南：成人急性高钾血症的治疗

NO
□ Peaked T waa
Acute ECG changes present (tick if present)?
□ Absent or flattened P waves □ Sine wave □ VT
YES
Protect the Heart
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Glucose (25 g) over 15 min 50 ml 50% Glucose OR 125 ml 20% Glucose, WITH Soluble Insulin – 10 units Salbutamol Give 10 mg if history of IHD Avoid if tachyarrhythmia present Blood Monitoring: Baseline Glucose __.__ 15 min Glucose __.__ 30 min Glucose __.__ 60 min Glucose __.__ K+ ___.__ K+ ___.__
K+ ___.__ K+ ___.__ K+ ___.__ K+ ___.__
K+: potassium; Na+: sodium; Creat: creatinine; IV: intravenous; min: minutes; PR: per rectum; EWS: early warning score; IHD: Ischaemic Heart Disease; NSAIDS: non-steroidal anti-inflammatory drugs Publication date: 1.03.14 Review date: 1.03.16

临床实践指南的应用

临床实践指南的应用Moving from clinical practice guideline to action董碧蓉学习目的●了解临床实践指南中证据和推荐强度的分级●熟悉如何提出临床问题，如何根据临床问题检索临床实践指南●掌握评价临床实践指南质量的方法，以及如何运用临床实践指南解决具体临床问题定义临床指南(c1inical guidelines)，临床实践指南(clinical practice guidelines，CPG)：●“系统开发的多组临床指导意见（诊断治疗建议），以此来帮助医生和病人针对特定的临床问题做出恰当的处理，并选择、确定适宜的卫生保健服务”。

----美国医学研究所（IOM）●是以循证医学为基础，由官方政府机构或学术组织形成的医疗文件。

将规范化医疗与个体化医疗相结合，对提高医疗质量起重要的推动作用。

注意●其作为一种工具既不等于“食谱”，也不是教科书或必须遵守的指令与规则、普通常规和手册；●只是临床服务质量管理的有效手段之一，不能完全替代临床医生的临床思维和判断。

临床指南的制作方法（方法不同，质量迥异）●基于系统评价的制作方法●基于各方面专家一致性的意见●基于某方面专家一致性的意见优秀CPG的特点由于临床指南是具有权威性的医疗文件，因此制作质量非常重要。

好的临床指南应具有：●真实性（Validity）●可靠性（Reliability）●可重复性（Reproducibility）●实用性（Applicability）●灵活性（Flexibility）●表述清楚，简单明了（Clarity）●多学科参与（Multidisciplinary process)怎样解决临床问题？How to solve a Clinical problem?EBCP过程：4A●Ask clinical questions●Acquire the best evidence●Appraise the evidence●Apply evidence to patient care临床实践指南的循证应用步骤●提出需要解决的临床问题●获取证据●评价CPG的质量●指南是否回答了需要解决的问题？●应用证据●后效评价临床病例患者男性，65岁，哮喘病史40多年，近3天出现急性加重的呼吸困难，伴喘息和咳嗽。

NCCN临床实践指南：宫颈癌(2014.V1)

NCCN Guidelines Version 1.2014 Panel Members Cervical Cancer
* Wui-Jin Koh, MD/Co-Chair § Fred Hutchinson Cancer Research Center/Seattle Cancer Care Alliance * Benjamin E. Greer, MD/Co-Chair W Fred Hutchinson Cancer Research Center/Seattle Cancer Care Alliance * Nadeem R. Abu-Rustum, MD W Memorial Sloan-Kettering Cancer Center Sachin M. Apte, MD, MS W Moffitt Cancer Center Susana M. Campos, MD, MPH, MS † Dana-Farber/Brigham and Women’s Cancer Center Kathleen R. Cho, MD ¹ University of Michigan Comprehensive Cancer Center David Cohn, MD W The Ohio State University Comprehensive Cancer Center - James Cancer Hospital and Solove Research Institute Marta Ann Crispens, MD W Vanderbilt-Ingram Cancer Center Nefertiti DuPont, MD, MPH W Roswell Park Cancer Institute NCCN Lauren Gallagher, RPh, PhD Miranda Hughes, PhD Nicole McMillian, MS NCCN Guidelines Panel Disclosures Patricia J. Eifel, MD § The University of Texas MD Anderson Cancer Center Christine M. Fisher, MD, MPH § University of Colorado Cancer Center David K. Gaffney, MD, PhD § Huntsman Cancer Institute at the University of Utah Ernest Han, MD, PhD W City of Hope Comprehensive Cancer Center Warner K. Huh, MD W University of Alabama at Birmingham Comprehensive Cancer Center John R. Lurain, III, MD W Robert H. Lurie Comprehensive Cancer Center of Northwestern University Lainie Martin, MD † Fox Chase Cancer Center David Mutch, MD W Siteman Cancer Center at BarnesJewish Hospital and Washington University School of Medicine

循证医学复习重点

循证医学第一章1.循证医学（Evidence-Based Medicine, EBM）是指所有医疗卫生的决策都应当依据当前最佳的、可获得的研究证据。

P12.学习和实践循证医学对临床医务工作者提出的要求，具体体现在三个方面：①临床医生通过多年的临床实践熟悉并掌握临床专业技能，提高对疾病的判断能力并通过实践积累诊疗经验；②现代的临床医生应掌握如何鉴定和评估临床研究技能。

毕竟个人的临床经验往往是有限的，且不够全面；③临床医生应从患者的实际需求出发，结合具体患者的情况恰当地应用现有的研究证据，采用利大于弊的治疗措施。

P23.EBM的研究主要包括两个方面：①证据产出的研究；②传播和使用证据。

同时，这两方面的研究又有赖于方法学的研究。

P34.中医药学属于传统医学范畴，在西方国家被称之为补充与替代医学（complementary and alternative medicine, CAM）。

P55.（熟悉了解）循证医学方法在中医药应用的现状 P5：1传统的临床评价多为经验总结，缺乏严格设计的前瞻性对照试验研究，使得好的治疗方法得不到广泛的推广应用。

2.询证医学在中医理论的指导下对中医辩证和治疗在临床的应用加以验证，以确证其有效性和安全性。

6.实践循证医学的中医药可能面对的挑战包括：①中医师和研究人员的观念更新和转变，能够接受新的科学评价方法；②其次，需要对中医药从业人员和临床研究人员进行方法学的培训与教育；③培养循证实践的技能（提出正确的问题、查找文献与鉴定研究的能力、严格评价的技能、研究综合的能力、解释与使用证据的能力）；④此外，需要对现有研究方法学进行改进或创新，确定中医药临床研究的优先领域。

P7第二章1.描述性研究（descriptive study）：是利用已有的或专门调查的资料，按不同地区、时间或人群特征分类，将健康人群或患病人群的分布情况真实地展现出来的一类研究方法。

P102.现况研究（survey）：指通过普查或抽样调查等方法收集特定时点或时期内、特定范围人群中的有关变量（因素）、疾病或健康状况的资料，以描述目前疾病或健康状况的分布及某因素与疾病或健康的关联。

运用循证理论指导临床护理实践

循证护理的意义
20世纪90年代中期，循证医学(evidence based medicine，EBM)在发达国家得到了高度重视，并在医学领域得到了迅速发展。循证护理（ evidence based nursing，EBN）是伴随循证医学的发展而出现的护理概念。
期刊发表的研究
Dicenso A, Bayley L, Haynes RB. Accessing pre-appraised evidence: fine-tuning the 5S model into a 6S model. Evid Based Nurs. 2009 Oct;12(4):99-101
• 历史对照研究/不同期对照研究（Historically controlled study）
观察性研究论文
• 队列研究（cohort study）
• 病例对照研究（case-control study）
原始研究资源
• 非连续的时间序列研究（Interrupted-time-series study）
二、查询证据资源
先检索经过评鉴的证据资源：GL, SR, ES, BPIS, Care Bundle……
1. Cochrane：系统评价SR 2. OVID-JBI：SR、证据总结ES、RP、最佳证据总结BPIS 3. NICE（ UK National Institute for Health and Care Excellence)：指南GL 4. SIGN （Scottish intercollegiate guidelines network）：GL 5. RNAQ：50份护理指南 6. 专业协会网站：NCCN，AHA，INS… 7. CBM（中国生物医学文献数据库）：SR；必要时检索知网、万方新的文献 8. Medline/Embase/CINAL：SR、GL

2013加拿大糖尿病学会临床实践指南解读

加拿大，糖尿病是终末期肾脏疾病、非创伤性截肢、致盲的主要原因，糖尿病患者因终末期肾脏疾病而住院的人次比一般人群多１２倍。鉴于此，基于患者肾功能评估和调整降糖治疗对实现血糖安全达标并减少低血糖具有重要意义。而依照循证医学证据制定操作性强的指导意见则有助于在临床实践中
糖尿病临床２０１４年３月第８卷第３期ＤｉａｂｅｔｅｓＷｏｒｌｄ，Ｍａｒ２０１４，Ｖｏｌ８，Ｎｏ．３
ｌ２７
２型糖尿病管理要赢在起跑线
新诊断２型糖尿病患者的起始治疗方案与其预后密切相关，短期胰岛素强化治疗对于部分血糖较高（空腹血糖＞１１．１ｍｍｏｌ／Ｌ）的新诊断２型糖尿病患者有明显益处。虽然临床上仍需要更多的研究来了解不同治疗方案及疗程间是否有差异、影响患者缓解率的因素及如何预测哪些患者可能获得缓解等问题，但现在临床上已经在较广泛的开展，临床医生需要
作者单位：北京协和医院
能缺陷及胰岛素抵抗。针对这两项病理生理改变，
应用优化的血糖控制策略是改善糖尿病患者预后的
关键，否则，长期的高血糖状态可引起眼底、肾
脏、神经系统病变等微血管并发症，及心血管疾病
糖尿病ｌ临床２０１４年３ｇ第８卷第３期ＤｉａｂｅｔｅｓＷｏｌｄ，ｒＭａｒ２０１４，Ｖｏｌ８，Ｎｏ．３
诊断

2014年加拿大临床实践指南

2014年加拿大临床实践指南（四）：创伤后应激障碍医脉通2014-08-22发表评论分享获加拿大卫生部批准的焦虑治疗药物一览流行病学在加拿大，PTSD的终生患病率为9.2%，当前（1个月）患病率为2.4%。

超过76%的加拿大人报告称自己曾经历过严重的创伤性事件。

美国和欧洲的社区研究显示，PTSD的终生患病率为6.4-6.8%，12个月患病率为1.1-3.5%。

导致PTSD的最常见创伤形式包括亲人的意外去世、性攻击、亲人重伤或重病、生育罹患重病的子女及被配偶或照料者殴打。

PTSD常于25-30岁之间起病，女性患病率为男性的2倍。

PTSD与显著的生活质量及功能受损相关，这种损害随症状严重度的升高而加重。

另外，PTSD常伴有慢性疼痛、睡眠问题、性功能障碍、认知紊乱及述情障碍。

PTSD的存在可使个体尝试自杀的风险升高2-3倍。

在初级保健中，PTSD与更长的住院时间及更多的精神卫生医疗使用相关。

在加拿大军事人员中，精神卫生医疗服务的使用与累积创伤暴露、初始创伤类型、PTSD症状困扰、自杀意象、女性及共病重性抑郁（MDD）相关。

精神科共病大约75%的PTSD患者存在另一种精神障碍，尤其是焦虑及相关障碍、MDD、对立违抗性障碍（ODD）、注意缺陷多动障碍（ADHD）、物质使用障碍（SUDs）、酒精依赖及边缘型人格障碍（BPD）。

与仅患PTSD相比，共病惊恐或心境障碍与更严重的功能损害相关。

与仅患PTSD或BPD的患者相比，同时罹患两种疾病的个体生活质量更差，共患更多的精神科问题，一生中自杀未遂的风险也更高。

诊断根据定义，创伤暴露史为诊断PTSD的必备条件，包括事实发生的或威胁性的死亡、严重受伤或性暴力。

其特征为具有侵入性及痛苦的记忆或梦境、解离反应及与创伤事件相关的显著的心理或生理痛苦。

上述症状的持续时间应超过1个月；若持续时间＞3天但小于1个月，且满足急性应激障碍（ASD）的症状诊断标准，则可诊断为ASD。

加拿大安大略注册护士协会临床实践指南应用方法解析

他
中华护理教育２０１８年９月第ｌ５卷第９期
加拿大安大略注册护士协会临床实践指南应靖王晋芳赵俊强郝玉芳
［摘要］临床实践指南与临床实践之间的差距阻碍着最佳证据的有效实施。加拿大安大略注册护士协会发布的《工具书：如何实施最佳实践指南》一书，其以知识转化模型为框架，分别从确定问题、适应当地文化背景、评估知识使用过程中的促进和阻碍因素、选择和调整干预措施和策略、监测知识应用情况和评估实施结果以及知识的持续性应用等方面，为促进证据的临床转化提供了系统的策略指导。该文通过对书中以上６个方面进行解析，进一步介绍指南的应用方法，以促进我国对临床实践指南的高效运用。［关键词］临床护理研究；指南；加拿大［Ｋｅｙｗｏｒｄｓ］ＣｌｉｎｉｃａｌＮｕｒｓｉｎｇＲｅｓｅａｒｃｈ；Ｇｕｉｄｅｂｏｏｋｓ；Ｃａｎａｄａ
临床实践指南对提高医务人员医疗水平、规范医疗行为、提高服务质量、科学配置医药学资源和保障患者权益等方面起着重要作用。近年来，随着临『禾实践指南在临床实践、政策制订和管理决策等方面的广泛应用与发展．临床实践指南与临床实践之问的差距越加明显。研究表明，将最佳证据运用到临床实践，大约需要１０～２０年的时间，而以研究证据为依据的实践内容在美国临床上的使用率不到５０％，其他同家的研究［４均有类似报道，对指南的实践率均小高．这些差距导致最佳证据不能及时、合理有效地应用于临床，不仅浪费了研究资源．而且使患者不能享受到最佳的医疗服务。因此，如何高效、充分地将临床实践指南运用到临床实践完成知识转化成为嚼待解决的问题。加拿大安大略注册护士协会（ＲｅｇｉｓｔｅｒｅｄＮｕｒｓｅｓ’ＡｓｓｏｃｉａｔｉｏｎｏｆＯｎｔａｒｉｏ，ＲＮＡＯ）于２０１２年发布的《Ｔ具书：如何实施最佳实践指南》其以知识转化模型（ＫｎｏｗｌｅｄｇｅｔｏＡｃｔｉｏｎＦｒａｍｅ— Ｗｏｒｋ，ＫＴＡ）为框架 ’ Ｉ，从理论、研究和经验等方面进行分析，详细讲解了如何将最佳实践指南应用于临床实践，为指南实施者，包括护士和其他健康照护专家，尤其对那些在组织中应用最佳实践指南的队，提供＿ｒ合理使用指南的策略、１－具和方法，为临床实践指南推向临床应用搭建了桥梁，也为临床实践指

2014年加拿大临床实践指南1

2014年加拿大临床实践指南（一）：社交恐怖症医脉通2014-08-19发表评论(1人参与)分享获加拿大卫生部批准的焦虑治疗药物一览流行病学社交恐怖症（SAD）是最常见的焦虑障碍之一，终生患病率约为8-12%，女性较男性常见，发达国家发病率（6.1%）较发展中国家高（2.1%）。

SAD发病较早，多起病于青春期（平均12岁），常呈慢性迁延病程。

低教育成就、低社会经济地位、单身或与伴侣分离、共病重性抑郁（MDD）与SAD发病率的升高相关。

SAD常导致严重的功能损害，包括教育及职业表现、家庭功能及生活质量的总体下降。

该病同样对个体及社会造成沉重的经济负担。

罹患SAD的加拿大人在过去两周内报告至少一个残疾日（disability day）的可能性是其他人的2倍。

精神科共病SAD的精神科共病率很高，72%的SAD患者均满足另一种精神障碍的诊断标准。

最常见的共病为MDD及其他焦虑相关障碍，共病回避型人格障碍、躯体变形障碍、物质使用障碍、注意缺陷多动障碍（ADHD）及精神分裂症也较为常见。

DSM-5诊断标准DSM-IV-TR将与其他医学状况相关或继发于其他医学状况的社交恐怖及回避行为排除在外。

然而，DSM-5认识到，SAD完全可能继发于某种医学问题，如口吃、帕金森病导致的震颤、肥胖、烧伤或损伤所致毁容，这些个体同样可能因为社交恐怖导致功能受损。

另外，DSM-5移除了DSM-IV-TR中的“广泛型”社交恐怖症，同时添加了“仅限于表演”这一亚型。

原因在于，并无足够证据支持“广泛型”的诊断，同时有证据显示，SAD的严重度随恐怖症状数量的变化而处于谱系的不同位置中。

尽管以上呈现的是最新诊断标准，但需要指出的是，以下治疗相关内容均基于满足DSM-IV诊断标准的患者。

心理治疗认知行为治疗（CBT）是SAD非药物治疗的金标准。

针对SAD的CBT认知技术包括重构及挑战病态思维，而行为组分主要为暴露疗法。

很多随机对照研究（RCTs）及meta 分析均提示，CBT针对SAD的疗效优于安慰剂、常规治疗（TAU）或等候名单（wait-list）设置。

2014+低钠血症诊断和治疗临床实践指南

DOI: 10.1530/EJE-13-1020

Ñ 2014 European Society of Endocrinology, European Society of Intensive Care Medicine, European Renal Association-European Dialysis
However, the paucity of well-designed, prospective studies in the ﬁeld has limited the evidence-base to these approaches. Previous guidance has often been based on experience or practice, without a systematic approach to evaluation and lacking a clear, patientcentred focus. Clinicians using previous guidance may have noted a number of problems:
Goce Spasovski, Raymond Vanholder1, Bruno Allolio2, Djillali Annane3, Steve Ball4, Daniel Bichet5, Guy Decaux6, Wiebke Fenske2, Ewout Hoorn7, Carole Ichai8, Michael Joannidis9, Alain Soupart6, Robert Zietse7, Maria Haller10, Sabine van der Veer11, Wim Van Biesen1 and Evi Nagler1 on behalf of the Hyponatraemia Guideline

临床指南2014(1)

CPG——连接研究证据与临
床实践的桥梁
from clinical trial to practice
指南来自于临床试验的证据，又是临床实践的指南
2021/3/21
实用文档
28
二、制定方法和过程
1. 成立工作组
– 一般由10至20人组成
– 有多学科多领域能平衡各方利益的专家和代表组成
• 专业人员——应包括临床指南所涉及的各个领域的多学科的专家，常包括有专科医生、全科医生、公共卫生医生、心理医生、康复医师、护理人员、药剂师等
• Cost-effective – reducing the inappropriate use of resources.
• Representative/multidisciplinary – by involving key groups and their interests.
• Clinically applicable – patient populations affected should be unambiguously defined.
如比较和相关描述及病例分析 V级：病例报告和临床总结及专家意见
实用文档
推荐意见是根据证据的可信度决定的
- A级推荐意见由I级证据支持，准确而无偏倚，可直接用于患者
- B级由Ⅱ级证据支持，这些意见可能存在局限性，也可能在将来有更高质量的新研究出现时被取代
- C级意见常在Ⅲ～V级证据基础上，基于观察性研究有局限性，支持强度较弱，仅对诊断、预后等问题有指导意义
实用文档
以循证医学为基础的实践指南
定义：官方政府机构或学术组织形成的医疗文件目的：提高医疗质量和控制医疗费用的不断上涨检索：1993年年起在Index Medicus可用“实践指南”为关键词检索，

指南丨诊断急性主动脉综合征，加拿大指南建议两步走

指南丨诊断急性主动脉综合征，加拿大指南建议两步走急性主动脉综合征（AAS）是一类危及生命的急症，包括主动脉夹层、主动脉壁内血肿以及穿透性粥样硬化性主动脉溃疡等。

近日，加拿大更新了AAS诊断临床实践指南，在AAS危险因素、高危体检表现、诊断策略等方面给出了具体建议。

指南全文发表于《加拿大医学会杂志》（CMAJ）。

一评估验前概率指南建议对所有疑似AAS的患者进行常规评估，以确定疾病风险，并用于指导诊断的决策。

评估内容包括危险因素、高危疼痛特征以及体格检查。

1. 危险因素AAS的危险因素包括结缔组织疾病、主动脉瓣疾病、近期接受过主动脉手术、主动脉瘤（包括胸部或腹部主动脉瘤）以及AAS家族史。

2. 高危疼痛特征AAS的高危疼痛特征包括突发性疼痛或雷击样疼痛、剧烈或极严重的疼痛、撕裂样疼痛、迁移性疼痛或放射性疼痛。

3. 体格检查体格检查中，提示高危AAS的特征包括主动脉瓣关闭不全（听诊杂音或床旁超声心动图证实）、脉搏短绌、神经功能缺损、低血压或床旁超声心动图证实心包积液。

根据上述评估内容，计算得出评分，评分0分者，属AAS低风险概率（<0.5%）；评分1分者，属于AAS中等风险概率（0.5%~5%）；评分≥2分者，属于AAS高风险概率（>5%）。

二诊断策略（1）对于验前概率评估为AAS低风险概率（<0.5%）的人群，指南不建议进一步的评估和检测。

（2）验前概率评估为AAS中等风险概率（0.5%~5%）的人群，建议进行D-二聚体检查，以排除AAS。

D-二聚体阳性者，进行心电图门控CT检查。

如果无法进行D-二聚体检查，可单独进行心电图门控CT检查。

若D-二聚体检测阴性（<500 ng/ml），提示AAS的可能性较低，则无需进行其他检查。

（3）验前概率评估为AAS高风险概率（>5%）且怀疑AAS的人群，建议首先进行心电图门控CT检查，无需D-二聚体检查。

CT应进行心电图门控，以避免运动伪影，尤其是主动脉根部和升主动脉部位。

2014年加拿大整脊疗法治疗成人颈痛循证指南解读

2014年加拿大整脊疗法治疗成人颈痛循证指南解读魏戌;朱立国;李金学;高景华;王尚全;于杰;冯敏山【期刊名称】《中国医学前沿杂志（电子版）》【年(卷),期】2014(000)009【摘要】为提高非特异性颈痛（又称机械性颈痛）的治疗水平，加拿大颈痛指南形成委员会2014年更新了整脊疗法治疗成人颈痛循证指南（以下简称指南）。

指南所评价的治疗方法中不包括针灸、外科手术、侵入性镇痛治疗、注射剂、心理干预、药物治疗（处方药与非处方药）。

指南共纳入全世界发表的41篇随机对照试验，同时参照相关24篇系统综述，通过严格的偏倚风险评估与证据强度分级，对11种常见的治疗方法给出了推荐建议。

推荐强度分为：较强、中等、较弱、不推荐。

具体意见为：使用颈椎扳动手法、徒手治疗、功能锻炼联合其他疗法治疗慢性颈痛（较强推荐）；单独使用运动锻炼方法，包括伸展运动、肌力锻炼、耐力锻炼治疗慢性颈痛（较强推荐）；使用颈椎扳动手法、关节松动术联合其他形式治疗急性颈痛（中等推荐）；使用关节松动术、按摩联合其他形式治疗慢性颈痛（中等推荐）；单独使用功能锻炼治疗急性颈痛，单独使用颈椎扳动手法治疗慢性颈痛（较弱推荐）。

此外，胸椎手法、扳机点治疗不推荐作为急性颈痛的治疗方法；经皮神经电刺激、胸椎手法、激光疗法、颈椎牵引不推荐作为慢性颈痛的治疗方法。

指南委员会最后指出，临床实践表明综合疗法治疗颈痛能够获得更多效益。

【总页数】4页(P157-160)【作者】魏戌;朱立国;李金学;高景华;王尚全;于杰;冯敏山【作者单位】中国中医科学院望京医院科研处，北京 100102;中国中医科学院望京医院脊柱2科，北京 100102;中国中医科学院望京医院科研处，北京 100102;中国中医科学院望京医院脊柱2科，北京 100102;中国中医科学院望京医院骨伤综合科，北京 100102;中国中医科学院望京医院脊柱2科，北京 100102;中国中医科学院望京医院脊柱2科，北京 100102【正文语种】中文【相关文献】1.整脊疗法配合颈痛颗粒治疗神经根型颈椎病150例 [J], 石震;闫素敏;戈超;陈锋2.2012加拿大成人2型糖尿病筛查指南解读 [J], 王占辉;刘彦君3.成人峡部裂性腰椎滑脱症:NASS循证医学指南解读 [J], 梁龙;冯敏山;朱立国;于杰;魏戌;尹逊路4.2011年特发性肺纤维化诊断和治疗循证新指南解读 [J], 蔡后荣5.骨关节疼痛性疾患康复干预方法选择的循证临床实践指南(下) 四颈痛康复干预方法选择的循证临床实践指南 [J], 徐军因版权原因，仅展示原文概要，查看原文内容请购买。

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医脉通2014-08-19发表评论(1人参与)分享
获加拿大卫生部批准的焦虑治疗药物一览
流行病学
社交恐怖症（SAD）是最常见的焦虑障碍之一，终生患病率约为8-12%，女性较男性常见，发达国家发病率（6.1%）较发展中国家高（2.1%）。

SAD发病较早，多起病于青春期（平均12岁），常呈慢性迁延病程。

低教育成就、低社会经济地位、单身或与伴侣分离、共病重性抑郁（MDD）与SAD发病率的升高相关。

SAD常导致严重的功能损害，包括教育及职业表现、家庭功能及生活质量的总体下降。

该病同样对个体及社会造成沉重的经济负担。

罹患SAD的加拿大人在过去两周内报
告至少一个残疾日（disability day）的可能性是其他人的2倍。

精神科共病
SAD的精神科共病率很高，72%的SAD患者均满足另一种精神障碍的诊断标准。

最常见的共病为MDD及其他焦虑相关障碍，共病回避型人格障碍、躯体变形障碍、物质使
用障碍、注意缺陷多动障碍（ADHD）及精神分裂症也较为常见。

DSM-5诊断标准
DSM-IV-TR将与其他医学状况相关或继发于其他医学状况的社交恐怖及回避行为排
除在外。

然而，DSM-5认识到，SAD完全可能继发于某种医学问题，如口吃、帕金森病
导致的震颤、肥胖、烧伤或损伤所致毁容，这些个体同样可能因为社交恐怖导致功能受损。

另外，DSM-5移除了DSM-IV-TR中的“广泛型”社交恐怖症，同时添加了“仅限于表演”这一亚型。

原因在于，并无足够证据支持“广泛型”的诊断，同时有证据显示，SAD的严重度随恐怖症状数量的变化而处于谱系的不同位置中。

尽管以上呈现的是最新诊断标准，但需要指出的是，以下治疗相关内容均基于满足DSM-IV诊断标准的患者。

心理治疗
认知行为治疗（CBT）是SAD非药物治疗的金标准。

针对SAD的CBT认知技术包
括重构及挑战病态思维，而行为组分主要为暴露疗法。

很多随机对照研究（RCTs）及meta分析均提示，CBT针对SAD的疗效优于安慰剂、常规治疗（TAU）或等候名单（wait-list）设置。

尽管结果有所不同，但仍有多项研究提示，在治疗急性SAD方面，CBT与药物治疗疗效相仿。

还有研究显示，在治疗中断后，CBT疗效的持续时间较药物治疗更长。

针对SAD的CBT包括团体及个人形式。

尽管有研究显示，个人CBT的疗效优
于团体CBT，meta分析结果则显示，两者疗效并无显著差异。

既往研究同样检视了CBT中个别组分的疗效。

证据显示，单独的暴露疗法即具有一
定疗效。

然而，暴露疗法与CBT整体疗效的比较结果莫衷一是。

有研究对CBT中的若干变量进行了探讨。

例如证据显示，录像反馈技术并不能增强
暴露疗法的疗效。

然而，两项meta分析结果显示，CBT联合个体化虚拟现实暴露疗法（VRE）效果优于等候名单对照，与纳入拟放松及现场暴露法的CBT疗效相仿。

在改善社交焦虑方面，一种聚焦于人际间行为的CBT形式与CBT疗效相仿，同时可改善关系满意度及社交亲近行为。

人际疗法（IPT）针对SAD的疗效证据不一：有的研究结果为阴性，还有研究显示，IPT的疗效优于等候名单，劣于传统CBT。

与之类似，虽然疗效亦不如CBT，但正念疗法（MBT）同样可改善SAD症状。

另外，针对注意偏倚训练的小规模研究显示，该疗法有助于患者脱离负性社交线索，但结果同样
存在冲突。

整合认知行为治疗（ICBT）是一种相对较新的治疗形式，或有助于提高日后针对焦
虑及心境障碍的CBT的可获得性。

研究显示，ICBT在改善SAD症状方面显著优于等候
名单对照。

大部分ICBT项目中，治疗师与患者的接触程度均维持在最低限度，主要形式
为电子邮件或电话。

很多项目纳入了与其他参与者通过网络讨论小组互动的成分。

然而，治疗师成分是否必需目前尚不清楚，有无引导的ICBT疗效也难分优劣。

在一项RCT中，医师辅助的ICBT效果优于自我引导的ICBT，后者疗效不显著优于等候名单设置。

与之类似，一项有治疗师参与的ICBT自助项目疗效优于纯自助的治疗方案。

然而也有很多研究显示，两者疗效相仿。

一些ICBT项目纳入了面对面的现场暴露成分，但一项RCT显示，与单纯的自我引导相比，添加这一组分并未显著改善预后。

还有若干项研究显示，ICBT与面对面形式的CBT疗效相仿。

一些针对ICBT的研究纳入了与患者面对面或电话形式的初筛，以及治疗后的电话评估或患者自评措施。

这种设置与自行实施的治疗手段（ICBT或自助手册）相比疗效如何，目前仍所知甚少。

心理治疗联合药物治疗
一些研究显示，在心理治疗的基础上联合药物治疗的疗效并不优于心理治疗自身。

然而，一项研究显示，苯乙肼联合CBT疗效优于单用其中任一组分。

证据显示，暴露练习的过程中联用D-环丝氨酸可改善临床预后；另外，一项研究针对心理动力治疗的研究显示，联合氯硝西泮的疗效优于单用该药。

心理治疗的长期疗效
CBT的疗效可维持6-12个月；治疗5年后，患者仍有收益。

ICBT的疗效可维持1-5年。

治疗停止后，心理治疗疗效的维持时间长于药物治疗。

药物治疗
*：结果存在冲突；-ve：结果为阴性
药物维持治疗
一项纳入了4项预防复发研究、共760名个体的meta分析结果显示，与安慰剂相比，SSRIs可大幅降低3-6个月内的复发风险，相对危险度（RR）为0.39（95% CI 0.30-
0.49），需治数（NNT）为3.57（95%CI 2.94–4.76）。

抗惊厥药普瑞巴林也显示出降低
复发风险的作用。

相关阅读：
∙社交恐怖症：CBT和心理动力学疗法孰优孰劣？∙社交恐怖共病抑郁焦虑：CBT同样有效。