2016年ADA糖尿病诊疗指南解读
2016年ADA糖尿病诊疗标准解读
基础知识一．血糖控制标准1、A1C 目标：许多非妊娠成人合理的 A1C 目标是<7%。
·对于部分无明显低血糖或其他治疗副作用的患者，建议更严格的 A1C 目标（如<6.5%）或许也是合理的。
这些患者可能包括那些糖尿病病程较短、仅用生活方式或二甲双胍治疗的2 型糖尿病患者、预期寿命较长或无明显心血管疾病（CVD）的患者。
·对于有严重低血糖病史、预期寿命有限、有晚期微血管或大血管病并发症、有较多的伴发病，以及尽管实施了糖尿病自我管理教育、适当的血糖检测、应用了包括胰岛素在内的多种有效剂量的降糖药物，而仍难达标者的病程较长的糖尿病患者，较宽松的 A1C 目标（如<8%）或许是合理的。
2、低血糖·每次随访时应该询问有低血糖风险的患者症状性和无症状性低血糖。
·清醒的低血糖患者，虽可选用任何形式的含葡萄糖的碳水化合物，但葡萄糖（15～20 g）是治疗首选。
治疗 15 分钟后，如果 SMBG 显示为持续低血糖，应该重复治疗。
一旦 SMBG 血糖恢复正常，患者应进餐或小吃，以预防低血糖复发。
·所有具有严重低血糖风险的患者应处方胰高血糖素，指导照护者或家人如何使用胰高血糖素。
胰高血糖素给药不限于医护专业人员。
·对于无症状低血糖或一次或以上严重低血糖发作的糖尿病患者，应该重新评估其治疗方案。
·使用胰岛素治疗的患者如有无症状性低血糖或严重低血糖发作，建议放宽血糖控制目标，严格避免至少数周内再次发生低血糖，以部分逆转无症状性低血糖并减少以后发生低血糖的风险。
·如发现认知功能较低和 / 或认知功能下降，建议持续评估其认知功能，临床医生、患者和看护者应高度警惕低血糖。
3、院内糖尿病管理·持续高血糖患者，血糖不高于 180 mg/dL (10 mmol/L)，应该起始胰岛素治疗。
一旦开始胰岛素治疗，推荐将大多数危重患者 A 和非危重患者 C 血糖控制在 140–180 mg/dL (7.8–10 mmol/L) 之间。
2016指南：糖尿病血糖控制诊疗标准
ADA2016 指南：糖尿病血糖控制诊疗标准近日美国糖尿病学会（ADA）更新了2016 年糖尿病医学诊疗标准，于2015 年12 月22 日在线发表于2016 年1 月份增刊。
现将糖尿病血糖控制部分全文摘要如下：血糖控制的评估有两项措施可供医护人员和患者评估血糖控制的有效性：患者自我血糖监测（SMBG）、糖化血红蛋白（HbA1c）。
动态血糖监测（CGM）以及组织间隙葡萄糖测定可作为部分患者SMBG 的有益补充。
建议：1. 对于胰岛素注射次数较少或使用非胰岛素治疗的患者，SMBG 作为教育内容的一部分可能有助于指导治疗决策和/ 或患者自我管理。
2. 给予患者SMBG 处方后，应确保患者得到持续的SMB 技术指导、技术评估、结果评价及患者使用 SMBG 数据调整治疗的能力。
3. 大多数采用采用胰岛素强化治疗（每日多次胰岛素注射MDI 或胰岛素泵治疗）的患者应在餐前或加餐前行SMBG，偶尔在餐后、睡前、运动前、怀疑低血糖、低血糖治疗后直到血糖正常、在关键任务如驾驶操作前亦需行SMBG。
4. 对于部分成年（年龄≥ 25 岁）1 型糖尿病患者，正确使用CGM 并联合胰岛素强化治疗有助于降低HbA1c。
5. 虽然目前CGM 降低儿童、青少年及青年患者糖化血红蛋白的证据不足，但CGM 可能对这些人群有帮助，是否成功与坚持使用该装置的依从性相关。
6. CGM 可作为无症状低血糖和/ 或频发低血糖患者SMBG 的一个辅助方法。
7. 由于CGM 的依从性变异较大，给予患者CGM 处方前应评估患者持续使用GCM 的准备状态。
8. 给予患者CGM 处方时，应加强糖尿病教育、培训和支持，以获得最佳的CGM 实施方案和持续使用。
9. 成功使用CGM 的患者应该坚持使用到65 岁以后。
（译者注：此指南为2016 年新增）血糖监测MBGMBG 作为最基本的评价血糖控制水平的手段之一，可以反映实时血糖水平、评估餐前餐后血糖以及生活事件和降糖药物对血糖的影响、发现低血糖，有助于为患者制定个体化的治疗方案、提高治疗的有效性和安全性；同时SMBG 作为糖尿病自我管理的一部分，可使患者更好的了解自身疾病状态，使患者积极参与糖尿病管理、按需调整行为、及时向医务工作者咨询的手段，提高患者治疗的依从性。
刘佩文2016年ADA糖尿病医学诊疗标准解读
右图：利那鲁肽能使糖尿 病前期患者比例较基线值 明显下降，且优于减肥药 奥利司他
Arne Astrup. et al. Lancet 2009; 374: 1606–16
*p=0.007 vs placebo. †p=0.008 vs orlistat. ‡p≤0.0001 vs placebo or orlistat.
BMI≥35 kg/m2,需加用手术治疗
Diabetes Care. 2016 Jan;39 Suppl 1:S4-5.
肥胖管理 预防与筛查 诊断
关注心血管 特殊人群
关注降糖药对体重的影响，并给出减肥药物使用原则
关注降糖药对体重的影响
• 对超重、肥胖的T2DM患者，选择降糖药物时需考虑对体重的影响 E • 尽可能减少共病治疗药物导致的体重增加 E
New Section
11. Children and Adolescents
12. Management of Diabetes in Pregnancy
13. Diabetes Care in the Hospital
14. Diabetes Advocacy
肥胖管理 预防与筛查 诊断
推荐基于BMI水平的肥胖管理策略
Diabetes Care. 2016 Jan;39 Suppl 1:S4-5.
Standards of Medical Care in Diabetes—2016
1. Strategies for Improving Care 2. Classification and Diagnosis of Diabetes 3. Foundations of Care and Comprehensive Medical Evaluation 4. Prevention or Delay of Type 2 Diabetes 5. Glycemic Targets 6. Obesity Management for the Treatment of Type 2 Diabetes 7. Approaches to Glycemic Treatment 8. Cardiovascular Disease and Risk Management 9. Microvascular Complications and Foot Care 10. Older Adults 11. Children and Adolescents 12. Management of Diabetes in Pregnancy 13. Diabetes Care in the Hospital 14. Diabetes Advocacy
2016 AACE糖尿病管理最新指南
84 ENDOCRINE PRACTICE Vol 22 No. 1 January 2016AACE/ACE Consensus StatementCONSENSUS STATEMENT BY THE AMERICAN ASSOCIATION OF CLINICAL ENDOCRINOLOGISTS AND AMERICAN COLLEGE OF ENDOCRINOLOGY ON THE COMPREHENSIVE TYPE 2 DIABETES MANAGEMENT ALGORITHM – 2016 EXECUTIVE SUMMARYAlan J. Garber, MD, PhD, FACE 1; Martin J. Abrahamson, MD 2; Joshua I. Barzilay, MD, FACE 3; Lawrence Blonde, MD, FACP , FACE 4; Zachary T. Bloomgarden, MD, MACE 5; Michael A. Bush, MD 6;Samuel Dagogo-Jack, MD, DM, FRCP , FACE 7; Ralph A. DeFronzo, MD, BMS, MS, BS 8;Daniel Einhorn, MD, FACP , FACE 9; Vivian A. Fonseca, MD, FACE 10; Jeffrey R. Garber, MD, FACP , FACE 11; W. Timothy Garvey, MD, FACE 12;George Grunberger, MD, FACP , FACE 13; Yehuda Handelsman, MD, FACP , FNLA, FACE 14;Robert R. Henry, MD, FACE 15; Irl B. Hirsch, MD 16;Paul S. Jellinger, MD, MACE 17; Janet B. McGill, MD, FACE 18; Jeffrey I. Mechanick, MD, FACN, FACP , FACE, ECNU 19;Paul D. Rosenblit, MD, PhD, FNLA, FACE 20; Guillermo E. Umpierrez, MD, FACP , FACE 21From the 1Chair, Professor, Departments of Medicine, Biochemistry and Molecular Biology, and Molecular and Cellular Biology, Baylor College of Medicine, Houston, Texas, 2Beth Israel Deaconess Medical Center, Department of Medicine and Harvard Medical School, Boston, Massachusetts, 3Division of Endocrinology, Kaiser Permanente of Georgia and the Division of Endocrinology, Emory University School of Medicine, Atlanta, Georgia, 4Director, Ochsner Diabetes Clinical Research Unit, Department of Endocrinology, Diabetes and Metabolism, Ochsner Medical Center, New Orleans, Louisiana, 5Clinical Professor, Mount Sinai School of Medicine, Editor, Journal of Diabetes , New York, New York, 6Clinical Chief, Division of Endocrinology, Cedars-Sinai Medical Center, Associate Clinical Professor of Medicine, Geffen School of Medicine, UCLA, Los Angeles, California, 7A.C. Mullins Professor & Director, Division of Endocrinology, Diabetes and Metabolism, University of Tennessee Health Science Center, Memphis, Tennessee, 8Professor of Medicine, Chief, Diabetes Division, University of Texas Health Science Center at San Antonio, San Antonio, Texas, 9Immediate Past President, American College of Endocrinology, Past-President, American Association of Clinical Endocrinologists, Medical Director, Scripps Whittier Diabetes Institute, Clinical Professor of Medicine, UCSD, Associate Editor, Journal of Diabetes , Diabetes and Endocrine Associates, La Jolla, California, 10Professor of Medicine and Pharmacology, Tullis Tulane Alumni Chair in Diabetes, Chief, Section of Endocrinology, Tulane University Health Sciences Center, New Orleans, Louisiana, 11Endocrine Division, Harvard Vanguard Medical Associates, Boston, Massachusetts, Division of Endocrinology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, 12Professor and Chair, Department of Nutrition Sciences, University of Alabama at Birmingham, Director, UABThis document represents the official position of the American Association of Clinical Endocrinologists and American College of Endocrinology. Where there were no randomized controlled trials or specific U.S. FDA labeling for issues in clinical practice, the participating clinical experts utilized their judgment and experience. Every effort was made to achieve consensus among the committee members. Position statements are meant to provide guidance, but they are not to be consid -ered prescriptive for any individual patient and cannot replace the judgment of a clinician.Diabetes Research Center, Mountain Brook, Alabama, 13Grunberger Diabetes Institute, Clinical Professor, Internal Medicine and Molecular Medicine & Genetics, Wayne State University School of Medicine, Bloomfield Hills, Michigan, 14Medical Director & Principal Investigator, Metabolic Institute of America, President, American College of Endocrinology, Tarzana, California, 15Professor of Medicine, University of California San Diego, Chief, Section of Diabetes, Endocrinology & Metabolism, VA San Diego Healthcare System, San Diego, California, 16Professor of Medicine, University of Washington School of Medicine, Seattle, Washington, 17Professor of Clinical Medicine, University of Miami, Miller School of Medicine, Miami, Florida, The Center for Diabetes & Endocrine Care, Hollywood, Florida, 18Professor of Medicine, Division of Endocrinology, Metabolism & Lipid Research, Washington University, St. Louis, Missouri, 19Clinical Professor of Medicine, Director, Metabolic Support, Division of Endocrinology, Diabetes, and Bone Disease, Icahn School of Medicine at Mount Sinai, New York, New York, 20Clinical Professor, Medicine, Division of Endocrinology, Diabetes, Metabolism, University California Irvine School of Medicine, Irvine, California, Co-Director, Diabetes Out-Patient Clinic, UCI Medical Center, Orange, California, Director & Principal Investigator, Diabetes/Lipid Management & Research Center, Huntington Beach, California, and 21Professor of Medicine, Emory University School of Medicine, Director, Endocrinology Section, Grady Health System, Atlanta, Georgia.Address correspondence to American Association of ClinicalEndocrinologists, 245 Riverside Avenue, Suite 200, Jacksonville, FL 32202. E-mail: publications@. DOI: 10.4158/EP151126.CSTo purchase reprints of this article, please visit: /reprints.Copyright © 2016 AACE.85Abbreviations:A1C= hemoglobin A1C; AACE= American Association of Clinical Endocrinologists; ACCORD = Action to Control Cardiovascular Risk in Diabetes; ACCORD BP= Action to Control Cardiovascular Risk in Diabetes Blood Pressure; ACEI = angiotensin-converting enzyme inhibitor; AGI = alpha-glucosidase inhibitor; apo B = apolipoprotein B; ARB = angiotensin II receptor blocker; ASCVD= atherosclerotic cardio-vascular disease; BAS = bile acid sequestrant; BMI = body mass index; BP = blood pressure; CHD = coro-nary heart disease; CKD= chronic kidney disease; CVD = cardiovascular disease; DKA = diabetic ketoac-idosis; DPP-4 = dipeptidyl peptidase 4; EPA = eicosa-pentaenoic acid; FDA = Food and Drug Administration; GLP-1= glucagon-like peptide 1; HDL-C= high-density-lipoprotein cholesterol; LDL-C = low-density-lipoprotein cholesterol; LDL-P = low-density-lipopro-tein particle; Look AHEAD = Look Action for Health in Diabetes; NPH = neutral protamine Hagedorn; OSA = obstructive sleep apnea; SFU = sulfonylurea; SGLT-2 = sodium glucose cotransporter-2; SMBG = self-moni-toring of blood glucose; T2D = type 2 diabetes; TZD = thiazolidinedioneEXECUTIVE SUMMARYThis algorithm for the comprehensive management of persons with type 2 diabetes (T2D) was developed to provide clinicians with a practical guide that considers the whole patient, their spectrum of risks and complica-tions, and evidence-based approaches to treatment. It is now clear that the progressive pancreatic beta-cell defect that drives the deterioration of metabolic control over time begins early and may be present before the diagnosis of diabetes (1). In addition to advocating glycemic control to reduce microvascular complications, this document high-lights obesity and prediabetes as underlying risk factors for the development of T2D and associated macrovascular complications. In addition, the algorithm provides recom-mendations for blood pressure (BP) and lipid control, the two most important risk factors for cardiovascular disease (CVD).Since originally drafted in 2013, the algorithm has been updated as new therapies, management approach-es, and important clinical data have emerged. The 2016 edition includes a new section on lifestyle therapy as well as discussion of all classes of obesity, antihyperglycemic, lipid-lowering, and antihypertensive medications approved by the U.S. Food and Drug Administration (FDA) through December 2015.This algorithm supplements the American Association of Clinical Endocrinologists (AACE) and A merican College of Endocrinology (ACE) 2015 Clinical Practice Guidelines for Developing a Diabetes Mellitus Comprehensive Care Plan (2) and is organized into discrete sections that address the following topics: the founding principles of the algo-rithm, lifestyle therapy, obesity, prediabetes, glucose control with noninsulin antihyperglycemic agents and insulin, management of hypertension, and management of dyslipidemia. In the accompanying algorithm, a chart summarizing the attributes of each antihyperglycemic class and the principles of the algorithm appear at the end. (Endocr Pract. 2016;22:84-113)PrinciplesThe founding principles of the Comprehensive Type 2 Diabetes Management Algorithm are as follows (see Comprehensive Type 2 Diabetes Management Algorithm—Principles):1. Lifestyle optimization is essential for all patientswith diabetes. Lifestyle optimization is multifac-eted, ongoing, and should engage the entire diabe-tes team. However, such efforts should not delayneeded pharmacotherapy, which can be initiatedsimultaneously and adjusted based on patientresponse to lifestyle efforts. The need for medicaltherapy should not be interpreted as a failure oflifestyle management, but as an adjunct to it.2. The hemoglobin A1C (A1C) target should beindividualized based on numerous factors, such asage, life expectancy, comorbid conditions, dura-tion of diabetes, risk of hypoglycemia or adverseconsequences from hypoglycemia, patient moti-vation, and adherence. An A1C level of ≤6.5% isconsidered optimal if it can be achieved in a safeand affordable manner, but higher targets maybe appropriate for certain individuals and maychange for a given individual over time.3. Glycemic control targets include fasting and post-prandial glucose as determined by self-monitor-ing of blood glucose (SMBG).4. The choice of diabetes therapies must be individu-alized based on attributes specific to both patientsand the medications themselves. Medication attri-butes that affect this choice include antihyper-glycemic efficacy, mechanism of action, risk ofinducing hypoglycemia, risk of weight gain, otheradverse effects, tolerability, ease of use, likelyadherence, cost, and safety in heart, kidney, orliver disease.5. Minimizing risk of both severe and nonseverehypoglycemia is a priority. It is a matter of safety,adherence, and cost.6. Minimizing risk of weight gain is also a priority.It too is a matter of safety, adherence, and cost.7. The initial acquisition cost of medications is onlya part of the total cost of care, which includesmonitoring requirements and risks of hypoglyce-86mia and weight gain. Safety and efficacy shouldbe given higher priority than medication cost.8. This algorithm stratifies choice of therapies basedon initial A1C level. It provides guidance as towhat therapies to initiate and add but respectsindividual circumstances that could lead to differ-ent choices.9. Combination therapy is usually required andshould involve agents with complementary mech-anisms of action.10. Comprehensive management includes lipid andBP therapies and treatment of related comorbidi-ties.11. Therapy must be evaluated frequently (e.g., every3 months) until stable using multiple criteria,including A1C, SMBG records (fasting and post-prandial), documented and suspected hypoglyce-mia events, lipid and BP values, adverse events(weight gain, fluid retention, hepatic or renalimpairment, or CVD), comorbidities, other rele-vant laboratory data, concomitant drug adminis-tration, diabetic complications, and psychosocialfactors affecting patient care. Less frequent moni-toring is acceptable once targets are achieved.12. The therapeutic regimen should be as simple aspossible to optimize adherence.13. This algorithm includes every FDA-approved classof medications for T2D (as of December 2015).Lifestyle TherapyThe key components of lifestyle therapy include medical nutrition therapy, regular physical activity, suffi-cient amounts of sleep, behavioral support, and smok-ing cessation and avoidance of all tobacco products (see Comprehensive Type 2 Diabetes Management Algorithm—Lifestyle Therapy). In the algorithm, recommendations appearing on the left apply to all patients. Patients with increasing burden of obesity or related comorbidities may also require the additional interventions listed in the middle and right side of the figure.Lifestyle therapy begins with nutrition counseling and education. All patients should strive to attain and maintain an optimal weight through a primarily plant-based diet high in polyunsaturated and monounsaturated fatty acids, with limited intake of saturated fatty acids and avoidance of trans fats. Patients who are overweight (body mass index [BMI] of 25 to 29.9 kg/m2) or obese (BMI ≥30 kg/ m2) should also restrict their caloric intake with the goal of reducing body weight by at least 5 to 10%. As shown in the Look AHEAD (Action for Health in Diabetes) and Diabetes Prevention Program studies, lowering caloric intake is the main driver for weight loss (3-6). The clini-cian or a registered dietitian (or nutritionist) should discuss recommendations in plain language at the initial visit and periodically during follow-up office visits. Discussion should focus on foods that promote health versus those that promote metabolic disease or complications and should include information on specific foods, meal plan-ning, grocery shopping, and dining-out strategies. In addi-tion, education on medical nutrition therapy for patients with diabetes should also address the need for consisten-cy in day-to-day carbohydrate intake, limiting sucrose-containing or high-glycemic-index foods, and adjusting insulin doses to match carbohydrate intake (e.g., use of carbohydrate counting with glucose monitoring) (2,7). Structured counseling (e.g., weekly or monthly sessions with a specific weight-loss curriculum) and meal replace-ment programs have been shown to be more effective than standard in-office counseling (3,6,8-15). Additional nutri-tion recommendations can be found in the 2013 Clinical Practice Guidelines for Healthy Eating for the Prevention and Treatment of Metabolic and Endocrine Diseases in Adults from AACE/ACE and The Obesity Society (16).After nutrition, physical activity is the main compo-nent in weight loss and maintenance programs. Regular physical exercise—both aerobic exercise and strength training—improves glucose control, lipid levels, and BP; decreases the risk of falls and fractures; and improves functional capacity and sense of well-being (17-24). In Look AHEAD, which had a weekly goal of ≥175 minutes per week of moderately intense activity, minutes of physi-cal activity were significantly associated with weight loss, suggesting that those who were more active lost more weight (3). The physical activity regimen should involve at least 150 minutes per week of moderate-intensity exer-cise such as brisk walking (e.g., 15- to 20-minute mile) and strength training; patients should start any new activity slowly and increase intensity and duration gradually as they become accustomed to the exercise. Structured programs can help patients learn proper technique, establish goals, and stay motivated. Patients with diabetes and/or severe obesity or complications should be evaluated for contrain-dications and/or limitations to increased physical activity, and an exercise prescription should be developed for each patient according to both goals and limitations. More detail on the benefits and risks of physical activity and the practi-cal aspects of implementing a training program in people with T2D can be found in a joint position statement from the American College of Sports Medicine and American Diabetes Association (25).Adequate rest is important for maintaining energy levels and well-being, and all patients should be advised to sleep approximately 7 hours per night. Evidence supports an association of 6 to 9 hours of sleep per night with a reduction in cardiometabolic risk factors, whereas sleep deprivation aggravates insulin resistance, hypertension, hyperglycemia, and dyslipidemia and increases inflamma-tory cytokines (26-31). Daytime drowsiness—a frequent symptom of sleep disorders such as sleep apnea—is asso-ciated with increased risk of accidents, errors in judgment,87and diminished performance (32). The most common type of sleep apnea, obstructive sleep apnea (OSA), is caused by physical obstruction of the airway during sleep. The resulting lack of oxygen causes the patient to awaken and snore, snort, and grunt throughout the night. The awaken-ings may happen hundreds of times per night, often with-out the patient’s awareness. OSA is more common in men, the elderly, and persons with obesity (33,34). Individuals with suspected OSA should be referred to a sleep specialist for evaluation and treatment (2).Behavioral support for lifestyle therapy includes the structured weight loss and physical activity programs mentioned above as well as support from family and friends. Patients should be encouraged to join commu-nity groups dedicated to a healthy lifestyle for emotional support and motivation. In addition, obesity and diabetes are associated with high rates of anxiety and depression, which can adversely affect outcomes (35,36). Healthcare professionals should assess patients’ mood and psycho-logical well-being and refer patients with mood disorders to mental healthcare professionals. Cognitive behavior-al therapy may be beneficial. A recent meta-analysis of psychosocial interventions provides insight into successful approaches (37).Smoking cessation is the final component of lifestyle therapy and involves avoidance of all tobacco products. Structured programs should be recommended for patients unable to stop smoking on their own (2).ObesityObesity is a disease with genetic, environmental, and behavioral determinants that confers increased morbidity and mortality (38,39). An evidence-based approach to the treatment of obesity incorporates lifestyle, medical, and surgical options, balances risks and benefits, and empha-sizes medical outcomes that address the complications of obesity rather than cosmetic goals. Weight loss should be considered in all overweight and obese patients with prediabetes or T2D, given the known therapeutic effects of weight loss to lower glycemia, improve the lipid profile, reduce BP, and decrease mechanical strain on the lower extremities (hips and knees) (2,38).The AACE Obesity Treatment Algorithm emphasizes a complications-centric model as opposed to a BMI-centric approach for the treatment of patients who have obesity or are overweight (see Comprehensive Type 2 Diabetes Management Algorithm—Complications-Centric Model for Care of the Overweight/Obese Patient). The patients who will benefit most from medical and surgical interven-tion have obesity-related comorbidities that can be clas-sified into 2 general categories: insulin resistance/cardio-metabolic disease and biomechanical consequences of excess body weight (40). Clinicians should evaluate and stage patients for each category. The presence and severity of complications, regardless of patient BMI, should guide treatment planning and evaluation (41,42). Once these factors are assessed, clinicians can set therapeutic goals and select appropriate types and intensities of treatment that will help patients achieve their weight-loss goals. Patients should be periodically reassessed (ideally every 3 months) to determine if targets for improvement have been reached; if not, weight loss therapy should be changed or intensi-fied. Lifestyle therapy can be recommended for all patients with overweight or obesity, and more intensive options can be prescribed for patients with comorbidities. For exam-ple, weight-loss medications can be used in combination with lifestyle therapy for all patients with a BMI ≥27 kg/ m2 and comorbidities. As of 2015, the FDA has approved 8 drugs as adjuncts to lifestyle therapy in patients with over-weight or obesity. Diethylproprion, phendimetrazine, and phentermine are approved for short-term (a few weeks) use, whereas orlistat, phentermine/topiramate extended release (ER), lorcaserin, naltrexone/bupropion, and liraglutide 3 mg may be used for long-term weight-reduction therapy. In clinical trials, the 5 drugs approved for long-term use were associated with statistically significant weight loss (placebo-adjusted decreases ranged from 2.9% with orlistat to 9.7% with phentermine/topiramate ER) after 1 year of treatment. These agents improve BP and lipids, prevent progression to diabetes during trial periods, and improve glycemic control and lipids in patients with T2D (43-60). Bariatric surgery should be considered for adult patients with a BMI ≥35 kg/ m2 and comorbidities, especially if therapeutic goals have not been reached using other modalities (2,61).PrediabetesPrediabetes reflects failing pancreatic islet beta-cell compensation for an underlying state of insulin resistance, most commonly caused by excess body weight or obesity. Current criteria for the diagnosis of prediabetes include impaired glucose tolerance, impaired fasting glucose, or metabolic syndrome (see Comprehensive Type 2 Diabetes Management Algorithm—Prediabetes Algorithm). Any one of these factors is associated with a 5-fold increase in future T2D risk (62).The primary goal of prediabetes management is weight loss. Whether achieved through lifestyle therapy, pharma-cotherapy, surgery, or some combination thereof, weight loss reduces insulin resistance and can effectively prevent progression to diabetes as well as improve plasma lipid profile and BP (44,48,49,51,53,60,63). However, weight loss may not directly address the pathogenesis of declining beta-cell function. When indicated, bariatric surgery can be highly effective in preventing progression from prediabe-tes to T2D (62).No medications (either weight loss drugs or antihy-perglycemic agents) are approved by the FDA solely for the management of prediabetes and/or the prevention of T2D. However, antihyperglycemic medications such as metformin and acarbose reduce the risk of future diabetes88in prediabetic patients by 25 to 30%. Both medications are relatively well-tolerated and safe, and they may confer a cardiovascular risk benefit (63-66). In clinical trials, thia-zolidinediones (TZDs) prevented future development of diabetes in 60 to 75% of subjects with prediabetes, but this class of drugs has been associated with a number of adverse outcomes (67-69). Glucagon-like peptide 1 (GLP-1) receptor agonists may be equally effective, as demon-strated by the profound effect of liraglutide 3 mg in safely preventing diabetes and restoring normoglycemia in the vast majority of subjects with prediabetes (59,60,70,71). However, owing to the lack of long-term safety data on the GLP-1 receptor agonists and the known adverse effects of the TZDs, these agents should be considered only for patients at the greatest risk of developing future diabetes and those failing more conventional therapies.As with diabetes, prediabetes increases the risk for atherosclerotic cardiovascular disease (ASCVD). Patients with prediabetes should be offered lifestyle therapy and pharmacotherapy to achieve lipid and BP targets that will reduce ASCVD risk.T2D PharmacotherapyIn patients with T2D, achieving the glucose target and A1C goal requires a nuanced approach that balances age, comorbidities, and hypoglycemia risk (2). The AACE supports an A1C goal of ≤6.5% for most patients and a goal of >6.5% (up to 8%; see below) if the lower target cannot be achieved without adverse outcomes (see Comprehensive Type 2 Diabetes Management Algorithm—Goals for Glycemic Control). Significant reductions in the risk or progression of nephropathy were seen in the Action in Diabetes and Vascular Disease: Preterax and Diamicron MR Controlled Evaluation (ADV ANCE) study, which targeted an A1C <6.5% in the intensive therapy group versus standard approaches (72). In the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial, inten-sive glycemic control significantly reduced the risk and/ or progression of retinopathy, nephropathy, and neuropathy (73,74). However, in ACCORD, which involved older and middle-aged patients with longstanding T2D who were at high risk for or had established CVD and a baseline A1C >8.5%, patients randomized to intensive glucose-lowering therapy (A1C target of <6.0%) had increased mortality (75). The excess mortality occurred only in patients whose A1C remained >7% despite intensive therapy, whereas in the standard therapy group (A1C target 7 to 8%), mortality followed a U-shaped curve with increasing death rates at both low (<7%) and high (>8%) A1C levels (76). In contrast, in the Veterans Affairs Diabetes Trial (V ADT), which had a higher A1C target for intensively treated patients (1.5% lower than the standard treatment group), there were no between-group differences in CVD endpoints, cardiovas-cular death, or overall death during the 5.6-year study period (75,77). After approximately 10 years, however, V ADT patients participating in an observational follow-up study were 17% less likely to have a major cardiovascu-lar event if they received intensive therapy during the trial (P<.04; 8.6 fewer cardiovascular events per 1,000 person-years), whereas mortality risk remained the same between treatment groups (78). Severe hypoglycemia occurs more frequently with intensive glycemic control (72,75,77,79). In ACCORD, severe hypoglycemia may have account-ed for a substantial portion of excess mortality among patients receiving intensive therapy, although the hazard ratio for hypoglycemia-associated deaths was higher in the standard treatment group (80). Cardiovascular auto-nomic neuropathy may be another useful predictor of cardiovascular risk, and a combination of cardiovascular autonomic neuropathy (81) and symptoms of peripheral neuropathy increase the odds ratio to 4.55 for CVD and mortality (82).Taken together, this evidence supports individualization of glycemic goals (2). In adults with recent onset of T2D and no clinically significant CVD, an A1C between 6.0 and 6.5%, if achieved without substantial hypoglycemia or other unacceptable consequences, may reduce lifetime risk of microvascular and macrovascular complications. A broader A1C range may be suitable for older patients and those at risk for hypoglycemia. A less stringent A1C of 7.0 to 8.0% is appropriate for patients with history of severe hypoglycemia, limited life expectancy, advanced renal disease or macro-vascular complications, extensive comorbid conditions, or long-standing T2D in which the A1C goal has been diffi-cult to attain despite intensive efforts, so long as the patient remains free of polydipsia, polyuria, polyphagia, or other hyperglycemia-associated symptoms. Therefore, selection of glucose-lowering agents should consider a patient’s ther-apeutic goal, age, and other factors that impose limitations on treatment, as well as the attributes and adverse effects of each regimen. Regardless of the treatment selected, patients must be followed regularly and closely to ensure that glyce-mic goals are met and maintained.The order of agents in each column of the Glucose Control Algorithm suggests a hierarchy of recommended usage, and the length of each line reflects the strength of the expert consensus recommendation (see Comprehensive Type 2 Diabetes Management Algorithm—Glycemic Control Algorithm). Each medication’s properties should be considered when selecting a therapy for individual patients (see Comprehensive Type 2 Diabetes Management Algorithm—Profiles of Antidiabetic Medications), and healthcare professionals should consult the FDA prescrib-ing information for each agent.• Metformin has a low risk of hypoglycemia, can promote modest weight loss, and has good antihyper-glycemic efficacy at doses of 2,000 to 2,500 mg/day.Its effects are quite durable compared to sulfonylureas (SFUs), and it also has robust cardiovascular safety relative to SFUs (83-85). Owing to risk of lactic acido-。
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1．注射笔用针头应一次性使用[11,31,73,74,75,76,77,177]。 A2 2．应告知患者针头重复使用和脂肪增生之间及重复使用 与疼痛及出血之间的相关性。A2
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第三次全球胰岛素注射技术近况调查显示，由于经济条 件的限制和操作便利性的考虑[174]，重复使用针头不仅 是我国患者常见现象，也是全球糖尿病患者普遍存在的 问题，必须引起高度重视。 注射笔用针头重复使用后，针头中残留的药液会影响注 射剂量的准确性，使用后的针头内残留的胰岛素形成结 晶，会堵塞针头妨碍注射；此外，注射后的针头留在胰 岛素笔上，由于热胀冷缩的原因还会引起胰岛素注射剂 量的不准确。
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图6 正确（左）和错误（右）的捏皮方式
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1．所有患者在起始胰岛素治疗时就应掌握捏皮的正确方法。A3
2．应当分别检查每个注射部位，并结合所用的针头长度，以决定是 否需要捏皮。该建议应当以书面形式提供给患者并记录在他们的临 床病历中。A3 3．捏皮时力度不得过大导致皮肤发白或疼痛。A3 4．不能用整只手来提捏皮肤，以避免将肌肉及皮下组织一同提起； 最佳顺序应当是：（1）捏皮；（2）与皮肤表面成90°缓慢注射胰 岛素（图7）；（3）拇指按钮完全推下后（用胰岛素笔注射时）， 让针头在皮肤内停留10 s；（4）以刺入时的相同角度拔出针头； （5）松开捏皮；（6）安全处理用过的针头。A3
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胰岛素属于生长因子，有促合成作用，反复在同一部位 注射会导致该部位皮下脂肪增生而产生硬结，在该部位 注射胰岛素将导致药物吸收率下降，吸收时间延长，进 而导致血糖波动[158]。因此，在平时的注射中要注意注 射部位的轮换。医护人员可向患者提供皮肤标记笔，以 便其注射时在皮肤上画点标记并可作为下一次注射的参 考点，记号在5 d左右会完全洗脱褪色。使用正确轮换技 术的患者常血糖控制更好，HbA1c更低，脂肪增生更少， 不明原因低血糖的发生率更低，更少血糖波动和每日胰 岛素剂量。更多相关内容请参考ITQ部分。
2016版中国糖尿病药物注射技术指南解读
推荐；B推荐；C尚未解决的问题
目录
1
注射治疗的教育
2
注射药物及装置
大 价格较为昂贵；需24小时佩戴，时感不便；对使用者要求较高
无针注射器
药液分布广，扩散快，吸收快且均匀；消除针头引起的疼痛和恐
惧感
价格较高，拆洗安装过程较为复杂，瘦弱者常可造成皮肤青肿
胰岛素注射笔用针头
第三章
注射技术及常见注射并发症
胰岛素规范注射的方法
规范胰岛素注射标准9步骤*（以胰岛素注射笔为例）
皮下脂肪增生和其他并发症
皮下组织增生的表现：最初柔软、有弹性，之后变为质韧、橡皮状或缺乏弹性， AADE（美国糖尿病协会）推荐：注射部位轮换对于预防皮下脂肪增生至关重要
第四章
胰岛素注射相关问题
胰岛素注射相关问题
胰岛素的保存
• 胰岛素避免冷冻、阳光直射及反复震荡 ； 未开封的胰岛素贮存在冰箱的非冷 冻层。
4mm
5mm
8mm
12.7mm
1. 使用较短（4或5mm）的针头时，大部分患者无需提起皮肤，并可90°进针。 2. 使用较长（≥6mm）的针头时，需要捏皮和（或）45°进针以降低肌内注射风险。
针头留置时间
注射器材的规范废弃
胰岛素注射针头操作步骤
针头重复使用的危害
推荐： 1.注射笔用针头一次性使用
随身保温箱 胰岛素禁止托运
混悬型胰岛素的混匀法
• 水平滚动是指在手掌之间的水平旋转
美国糖尿病协会ADA糖尿病诊治指南解读 PPT课件
妊娠期糖尿病的筛查和诊断
● 在有危险因素的个体中，产前首次就诊 时用标准的诊断标准筛查未诊断的2型糖尿 病。（B） ● 在未知是否具有糖尿病的怀孕妇女中，在 妊娠24~28周用75g 2h OGTT筛查妊娠糖尿 病。（B） ● 妊娠糖尿病的妇女在产后6~12周筛查永 久性糖尿病。（E） ● 有妊娠糖尿病病史的妇女应至少每3年筛 查是否发展为糖尿病或糖尿病前期。（E）
免疫接种
年龄≥6个月的糖尿病患者每年都要接种 流感疫苗。（C）
所有2岁以上的糖尿病患者须接种肺炎 球菌疫苗。年龄>64岁者，如5年前接种过疫 苗需再接种一次。再接种指征还包括肾病综 合征、慢性肾病及其他免疫损害者如器官移 植后。（C）
高血压／血压控制
筛查和诊断 糖尿病患者每次随访时均应测量 血压。收缩压≥130mmHg或舒张压 ≥80mmHg的患者，应该改天重复测量。 再次测量仍收缩压≥130mmHg或舒张 压≥80mmHg，可确诊为高血压。（C）
低血糖
治疗症状性低血糖首选葡萄糖（15～20g），也可选用任 何含有葡萄糖的碳水化合物。如果治疗15分钟后SMBG依然 为低血糖，应该再次给药。一旦SMBG血糖正常后，患者应该 继续追加一次正常饮食或点心，以预防低血糖复发。（E） 所有严重低血糖高危的患者、照护者或家人均应给予胰高 血糖素，并教会如何用药。胰高血糖素不要求必须由专业人员 给予。（E） 对于无症状低血糖或出现过一次或多次严重低血糖的糖尿 病患者，应该降低血糖控制目标，以严格避免至少在近几周内 再次发生低血糖，还可以部分逆转无症状性低血糖并减少将来 发生低血糖的风险。（B）
在诊断或随访时，较重的高血压患者（收缩压≥140mmHg， 或者舒张压≥90mmHg），除了接受生活方式治疗外，还应接 受药物治疗。（A）
美国糖尿病学会2016年诊疗标准-精品医学课件
2型糖尿病的肥胖管理
根据患者基础体重，每日摄入的能量减少500-750 kcal或女性 摄入1200-1500 kcal，男性摄入1500-1800 kcal可使体重下降。
选择食物时，应考虑患者的健康状态及喜好，不同种类的食物 （即蛋白、脂肪、碳水化合物含量不同）只要提供相同热量， 其减重效果是相似的。
二甲双胍、α- 糖苷酶抑制剂、奥利司他和噻唑烷二酮类药物都 能不同程度地减少糖尿病的发生。二甲双胍作为治疗和预防糖尿 病的一线药物，在长期用药安全方面具有最强的循证依据支持， 而其他药物在价格、副作用、疗效的持久性等方面都有待考量。
DPP 和 DPPOS 长达 10 年的随访结果显示，虽然二甲双胍不如 改变生活方式带来的效果明显，但对于长期治疗，它却是患者节 约成本的好选择。
可以的话，尽可能减少引起体重增加的其他药物（E）
对于BMI>27kg/m2的T2DM患者而言，减肥药可以作为 饮食、运动、行为疗法等减肥方法的辅助途径。但同 时，需要对药物的潜在风险进行权衡。（A）
如果患者减重效果差（3个月内体重下降<5%），或出 现任何安全性、耐受性问题，应立即停药或换用其他 药物。 （A）
在用餐时间不规律或使用磺脲类药物出现延迟性餐后 低血糖的患者中，可用速效胰岛素促泌剂（格列奈类） 代替磺脲类药物。
未列出的其他药物（α- 葡萄糖苷酶抑制，考来维仑， 溴隐亭，普兰林肽）在合适的患者可以使用，但由于 其疗效有限、给药频繁和不良反应常不被采用。
当HbA1c>9% 时，初始治疗即可考虑联合用药使 HbA1c 在短期内迅速达标。
对于胰岛素注射次数少 B 或非胰岛素治疗的患者，自我血糖检测 （SMBG）作为教育内容的一部分或许有助于指导治疗和 / 或自我 管理。E
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1．餐时注射短效胰岛素等，最好选择腹部 [6,10,43,44,45,46,47]。A1 2．希望减缓胰岛素的吸收速度时，可选择臀部，臀部注 射可最大限度地降低注射至肌肉的风险[149,150]。A1 3．给儿童患者注射中效或者长效胰岛素时，最好选择臀 部或者大腿[104]。A1
在腹部捏皮相对比较容易（非常肥胖患者腹部皮肤紧绷 除外），可使皮肤到肌肉筋膜的距离几乎翻倍（增加 88%）。但在大腿部位，捏皮较为困难，平均增幅只有 20%左右。在偏瘦受试者中，在大腿处捏皮实际上缩短 了皮肤到肌肉筋膜的距离，和预期的恰好相反。臀部捏 皮难度更大（很少需要），并且在臀部几乎不可能进行 捏皮（自我注射患者）。选择上臂为注射部位时需捏皮 注射。捏皮的正确手法是用拇指、食指和中指提起皮肤。 如果用整只手来提捏皮肤，有可能将肌肉及皮下组织一 同捏起，导致肌内注射（图6）[111]。
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在中国4个大城市进行的类似观察性研究发现脂肪增生的 总体患病率为53%。约有95％的患者重复使用针头，相 比于无脂肪增生的患者，有脂肪增生的患者BMI更高，每 天注射次数更多，重复使用针头的次数也约为无脂肪增 生患者的2倍。回归分析发现，高BMI、针头重复使用次 数增加和针头无法报销与脂肪增生具有显著相关性。体 重调整后的胰岛素剂量与脂肪增生相关，最重要的危险 性因素是缺乏正确的注射部位轮换。以前发表的中国研 究也显示了类似的结果[176]。
a3在生产和工作岗位上从事各种劳动的职工围绕企业的经营战略方针目标和现场存在的问题以改进质量降低消耗提高人的素质和经济效益为目的组织起来捏皮注射时正确的注射角度左不捏皮的情况下以45注射右在生产和工作岗位上从事各种劳动的职工围绕企业的经营战略方针目标和现场存在的问题以改进质量降低消耗提高人的素质和经济效益为目的组织起来五进针角度为保证将胰岛素注射至皮下组织在不捏皮的情况下也可以45注射以增加皮下组织的厚度降低注射至肌肉的危险图7图8
2016年ADA糖尿病诊疗标准(中文版)
美国糖尿病协会制定（海南医学院附属医院内分泌科王新军王转锁译）美国糖尿病协会（ADA）制定了2016年糖尿病诊疗标准，诊疗标准更加强调个性化治疗，海南医学院附属医院内分泌科王新军、王转锁对相关内容进行了翻译，详情如下：改进治疗的策略●应该运用结合病人意愿、评估文化和计算力、处理文化障碍的以病人为中心的沟通方式。
B●治疗决策应及时并且应以循证指南为基础，并根据患者意愿、预后和伴发病调整。
B●治疗应与慢病管理模式的内容一致，以确保有准备的积极的医疗小组和受教育的主动的患者之间的有效互动。
A●如果可能，治疗体系应支持团队管理、社区参与、患者登记和决策支持工具，以满足患者需求。
B食品不安全供应商应评估食品高血糖和低血糖的风险并提出相应的解决方案。
A供应商应该认识到无家可归、识字能力差和计算能力低的糖尿病患者经常发生不安全问题，并为糖尿病患者提供合适的资源。
A认知功能障碍●不建议对认知功能较差的2型糖尿病患者进行强化血糖控制。
B●认知能力较差或有严重低血糖的患者，血糖治疗应该个体化，避免严重低血糖。
C●在心血管高危的糖尿病患者，他汀治疗的心血管获益超过认知功能障碍的风险。
A●如果处方第二代抗精神病药物，应该严密监测体重、血糖控制和胆固醇水平的变化，并应重新评估治疗方案。
CHIV糖尿病患者的诊治HIV患者在开始抗病毒治疗之前和治疗开始后3个月或治疗方案变化时应该用空腹血糖水平筛查糖尿病和糖尿病前期。
如果初始筛查结果正常，建议每年复查空腹血糖。
如果筛查结果是糖尿病前期，每3~6个月复查血糖水平，监测是否进展为糖尿病。
E糖尿病风险增加（糖尿病前期）的分类●超重或肥胖（BMI≥25kg/m2或亚裔美国人≥23kg/m2）且有一个或以上其他糖尿病危险因素的无症状的成人，不论年龄，进行检查以评估未来糖尿病的风险。
B●对所有病人，应从45岁开始应进行检查。
B●如果检查结果正常，至少每3年复查是合理的。
C●使用空腹血糖、75g OGTT 2h血糖或A1C筛查糖尿病前期都是合适的。
2016儿童及青少年糖尿病诊治指南
2016儿童及青少年糖尿病诊治指南近期，美国糖尿病学会（ADA）发布了 2016 年糖尿病医学诊疗标准，对之前的标准进行了更新。
该标准全文共分为 14 个章节，现就儿童及青少年糖尿病部分摘要如下（括号中标示内容为 ADA 证据等级分级标准）。
约四分之三的 1 型糖尿病患者年龄小于 18 岁，即 T1DM 的主要人群是儿童和青少年。
然而，儿童及青少年的糖尿病治疗需要考虑其特殊性，如身体发育、性成熟、自我管理能力、学校及托儿所的监管、易发生低血糖、高血糖及酮症酸中毒等。
因此，儿童青少年糖尿病的诊断和治疗应该联合糖尿病自我管理教育（DSME）和糖尿病自我管理支持（DSMS）、医学营养治疗（MNT）和社会心理支持，并注意成人监督和自我管理之间的平衡。
糖尿病自我管理教育和支持在糖尿病确诊及确诊后，T1DM 患儿（年龄＜18 岁）及其父母 / 监护人应根据所在国家的标准，进行兼有文化敏感性和发展适宜性的个体化糖尿病自我管理教育和支持。
（B）社会心理方面在诊断和常规随访治疗时，评估能影响糖尿病治疗依从性的心理问题和家庭压力，并适时转诊给心理医生，尤其是对儿童糖尿病有经验的专家。
（E）鼓励患儿家庭共同参与糖尿病管理中去，应认识到过早让儿童承担糖尿病管理会导致依从性下降和血糖控制恶化。
（B）将精神健康专家作为儿童糖尿病多学科团队的一员。
（E）血糖控制所有儿童年龄组均建议：HbA1c 控制目标＜7.5%。
（E）自身免疫性疾病在初诊或症状加重时，应评估是否存在其他自身免疫性疾病。
（E）甲状腺疾病1 型糖尿病确诊后即检查患儿的甲状腺过氧化物酶抗体和甲状腺球蛋白抗体。
(E)1 型糖尿病确诊后即测定患儿的 TSH 水平。
结果正常可 1-2 年复查一次，一旦出现甲状腺功能失调的症状、甲状腺肿、生长状态异常、血糖异常变化，应立即复查。
（E）乳糜泻1 型糖尿病确诊后应检查患儿组织型转谷氨酰胺酶水平和脱酰胺基麦胶蛋白抗体。
（E）具有乳糜泻阳性家族史或出现生长障碍、体重降低、体重不增、腹泻、腹胀、腹痛等症状及频繁发生不能解释的低血糖、血糖控制恶化的患儿，应进行筛查。
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HIV糖尿病患者的诊治
• HIV患者在开始抗病毒治疗之前和治疗开始 后3个月或治疗方案变化时应该用空腹血糖 水平筛查糖尿病和糖尿病前期。如果初始 筛查结果正常，建议每年复查空腹血糖。 如果筛查结果是糖尿病前期，每3~6个月复 查血糖水平，监测是否进展为糖尿病。(E)
糖尿病风险增加(糖尿病前期)的分 类
2型糖尿病
• 超重或肥胖(BMI≥25 kg/m2或亚裔美国人≥23 kg/m2)并 有一个或以上其他糖尿病危险因素的无症状的成人，不论 年龄，进行检查以筛查2型糖尿病。(B)
• 对所有病人，应从45岁开始筛查。(B) • 如果检查结果正常，至少每3年复查是合理的。(C) • 使用空腹血糖、75g OGTT 2h血糖或A1C筛查糖尿病均
• 技术辅助工具包括以互联网为基础的社会网络、 远程学习、DVD内容和移动APP对于有效的生活 方式干预预防糖尿病是有用的。(B)
血糖控制的评估
• 对于胰岛素注射次数少B或非胰岛素治疗的患者，SMBG 作为教育内容的一部分或许有助于指导治疗和/或自我管 理。(E)
• 处方SMBG后，应确保患者获得持续指导，定期评估 SMBG技术和SMBG结果以及他们用SMBG数据调整治疗 的能力。(E)
以达到个体化的血糖控制目标。(A) • 未确诊糖尿病的伴糖耐量异常的囊性纤维化患者，
应考虑餐前胰岛素治疗以维持体重。(B) • 诊断囊性纤维化相关糖尿病5年后开始，推荐每
年监测糖尿病并发症。(E)
糖尿病自我管理教育和支持
• 根据糖尿病自我管理教育(DSME)和糖尿病 自我管理支持(DSMS)的国家标准，糖尿病 患者在确诊后根据需要应接受DSME和 DSMS，以增加知识、特别是那些BMI>35kg/m2， 年龄<60岁和有GDM史的妇女，可以考虑使用二 甲双胍治疗来预防2型糖尿病。(A)
• 建议糖尿病前期患者至少每年进行监测是否进展 为糖尿病。(E)
• 建议筛查并治疗可改变的CVD危险因素(B)
• 糖尿病前期患者通过糖尿病自我管理(DSME)和支 持(DSMS)计划接受教育和支持，以形成和保持能 够预防或延缓糖尿病发生的行为。(B)
• 有效的自我管理、改善临床结局、健康状 态和生活质量是DSME和DSMS的主要目标， 作为管理的一部分应该进行判断和监测。 (C)
• DSME和DSMS应该以患者为中心，尊重患者的 喜好、需求和价值观，应该指导临床决策。(A)
• DSME和DSMS计划应该包括预防糖尿病的基 本课程。如果以预防糖尿病为目标，DSME和 DSMS应该专门为此制定相关内容。(B)
• 对于糖尿病前期的人群，评估并治疗其他 心血管疾病(CVD)危险因素。(B)
• 超重或肥胖且伴有2项或2项以上其他糖尿 病危险因素的儿童和青少年，进行检查以 筛查糖尿病前期。(E)
1型糖尿病
• 在有高血糖症状的个体应该用血糖而不 是A1C诊断急性起病的1型糖尿病。(E)
• 通知1型糖尿病患者的亲属筛查1型糖尿病 的风险，但仅限于临床研究机构。(E)
• 在轻度持续高血糖患者和多位家庭成员 患糖尿病者，如果不具备1型糖尿病或2型 糖尿病的特点，应该考虑青少年的成人起 病型糖尿病(MODY)。(E)
囊性纤维化相关糖尿病
• 无囊性纤维化相关糖尿病的囊性纤维化患者从10 岁开始应每年用OGTT筛查囊性纤维化相关糖尿 病。(B)
• 不推荐用A1C筛查囊性纤维化相关糖尿病。(B) • 囊性纤维化相关糖尿病患者应该用胰岛素治疗，
• 因DSME和DSMS可以节省花费和改善结局B， DSME和DSMS应由第三方支付者充分支付。(E)
营养治疗推荐
体力活动
• 应鼓励糖尿病或糖尿病前期的儿童每天参加至 少60分钟的体力活动。(B)
• 应劝告成年糖尿病患者每周至少进行150 分钟中 等强度有氧体力活动(最大心率的50～70%)，每 周至少3天，不能连续超过2天不运动。(A)
• 心理筛查和随访包括但不限于：对疾病的态度、对治疗和 预后的预期、情感/情绪、一般及与糖尿病相关的生活质 量、资源(经济、社会和情感方面)以及精神病史。(E)
• 常规筛查心理问题，如抑郁和糖尿病相关的苦恼、焦虑、 饮食障碍以及认知缺损。(B)
• 老年糖尿病患者(≥65岁)应优先考虑进行认知功能的评 估及抑郁症的筛查和治疗。(B)
预防或延缓2型糖尿病
• 糖尿病前期的患者，应转诊到强化饮食和体力活 动行为咨询计划单位，目标是减轻体重的7%，增 加中等强度的体力活动(如快步走)到每周至少150 分钟。(A)
• 应进行随访咨询和坚持计划以便长期成功预防糖 尿病。(B)
• 基于糖尿病预防的成本效益，这些计划的费用应 由第三方支付。(B)
免疫接种
• 和普通人群一样，应为儿童和成人糖尿病 患者提供常规接种疫苗。(C)
• 年龄在19岁至59岁的糖尿病患者如未曾接 种乙肝疫苗，应该接种。(C)
• 年龄≥60岁的糖尿病患者如未曾接种乙肝疫 苗，可以考虑接种。(C)
心理评估与治疗
• 患者心理和社会状态的评估是糖尿病持续治疗的一部分。 (B)
是合适的。(B) • 对于糖尿病患者，评估并治疗其他心血管疾病(CVD)危
险因素。(B) • 超重或肥胖且伴有2项或2项以上其他糖尿病危险因素的儿
童和青少年，进行检查以筛查2型糖尿病。(E)
妊娠糖尿病
• 伴有危险因素的孕妇，首次产前就诊时用非妊 娠的诊断标准筛查未诊断的2型糖尿病。(B)
• 无糖尿病史的孕妇，妊娠24~28周筛查妊娠糖 尿病(GDM)。(A)
2016年ADA糖尿病诊疗指南
歙县昌仁医院 胡吉亮
中国糖尿病流行病学形势更严峻
• 美国糖尿病学会(ADA)制定的《糖尿病医 学诊疗标准》(Standards of Medical Care in Diabetes)是指导糖尿病医生临床实践的 重要指南之一，每年ADA都会对该指南进 行更新和修改。近期，ADA发布了2016版 糖尿病医学诊疗指南。
• 虽然CGM在儿童、青少年和青年成年患者中降低 A1C的证据不强，但CGM或许有帮助。成功与这 种仪器持续使用的依从性相关。(B)
• 在无症状低血糖和/或频发低血糖的患者，CGM 可作为SMBG的一种补充工具。(C)
• 由于CGM的依从性变异较大，处方前应评估患 者持续应用CGM的准备状态。(E)
• 应用即时A1C检测有助于更及时调整治疗方 案。(E)
A1C目标
• 许多非妊娠成人合理的A1C目标是<7%(A)
• 对于部分无明显低血糖或其他治疗副作用的患者，建议更 严格的A1C目标(如<6.5%)或许也是合理的。这些患者可 能包括那些糖尿病病程较短、仅用生活方式或二甲双胍治 疗的2型糖尿病患者、预期寿命较长或无明显心血管疾病 (CVD)的患者。(C)
2型糖尿病患者的肥胖治疗
• 每次就诊时应该计算BMI并记录在病历中。 (B)
不怕饥饿： 就怕过饱
饮食、体力活动和行为治疗
• 准备减重的超重和肥胖的2型糖尿病患者， 应该处方饮食、体力活动和行为治疗，以 减轻体重的5%。(A)
• 这种干预措施应该是高强度的(6个月内≥16 次)，专注于饮食、体力活动和行为治疗， 以每天减少500~750千卡热量。(A)
• 妊娠糖尿病的妇女，产后6~12周用OGTT及非妊 娠的糖尿病诊断标准筛查永久性糖尿病。(E)
• 有妊娠糖尿病病史的妇女应至少每3年筛查是否发 展为糖尿病或糖尿病前期。(B)
• 有妊娠糖尿病病史的糖尿病前期妇女，应接受生 活方式干预或二甲双胍治疗以预防糖尿病。(A)
单基因糖尿病综合征
• 所有6个月以内诊断糖尿病的儿童应该进行 基因检测。(B)
认知功能障碍
• 不建议对认知功能较差的2型糖尿病患者进 行强化血糖控制。(B)
• 认知能力较差或有严重低血糖的患者，血 糖治疗应该个体化，避免严重低血糖。(C)
• 在心血管高危的糖尿病患者，他汀治疗的 心血管获益超过认知功能障碍的风险。(A)
• 如果处方第二代抗精神病药物，应该严密 监测体重、血糖控制和胆固醇水平的变化， 并应重新评估治疗方案。(C)
• 对于有严重低血糖病史、预期寿命有限、有晚期微血管或 大血管病并发症、有较多的伴发病，以及尽管实施了糖尿 病自我管理教育、适当的血糖检测、应用了包括胰岛素在 内的多种有效剂量的降糖药物，而仍难达标者的病程较长 的糖尿病患者，较宽松的A1C目标(如<8%)或许是合理的。 (B)
低血糖
• 每次随访时应该询问有低血糖风险的患者症状 性和无症状性低血糖。(C)
• 处方CGM时，需要加强糖尿病教育、培训和支持， 以获得最佳的CGM实施和持续使用。(E)
• 成功使用CGM的患者应该持续使用到65岁以后。 (E)
A1C检测
• 对于治疗达标(和血糖控制稳定)的患者， 每年应该检测A1C至少两次。(E)
• 对更改治疗方案或血糖控制未达标的患者， 每年检测A1C四次。(E)
• 对于无症状低血糖或一次或以上严重低血糖发作 的糖尿病患者，应该重新评估其治疗方案。(E)
• 使用胰岛素治疗的患者如有无症状性低血糖或 严重低血糖发作，建议放宽血糖控制目标，严格 避免至少数周内再次发生低血糖，以部分逆转无 症状性低血糖并减少以后发生低血糖的风险。(A)
• 如发现认知功能较低和/或认知功能下降，建议持 续评估其认知功能，临床医生、患者和看护者应 高度警惕低血糖。(B)
• 超重或肥胖(BMI≥25 kg/m2或亚裔美国人 ≥23 kg/m2)且有一个或以上其他糖尿病危 险因素的无症状的成人，不论年龄，进行 检查以评估未来糖尿病的风险。(B)
• 对所有病人，应从45岁开始应进行检查。 (B)
• 如果检查结果正常，至少每3年复查是合理 的。(C)
• 使用空腹血糖、75g OGTT 2h血糖或A1C 筛查糖尿病前期都是合适的。(B)