Standards of Medical Care in Diabetes 2015

January 2015 Volume 38, Supplement 1 Standards of Medial Care in Diabetes 2015 S1 S3 S4 S5 S8 Introdution Professional Pratie Committee Standards of Medial Care in Diabetes 2015: Summary of Revisions 1. Strategies for Improving Care Diabetes Care Conepts Care Delivery Systems When Treatment Goals Are Not Met 2. Classifiation and Diagnosis of Diabetes S49 S58 8. Cardiovasular Disease and Risk Management Hypertension/Blood Pressure Control Dyslipidemia/Lipid Management Antiplatelet Agents Coronary Heart Disease 9. Mirovasular Compliations and Foot Care Nephropathy Retinopathy Neuropathy Foot Care S17 S20 S31 S33 S41 Classifiation Diagnosti Tests for Diabetes Categories of Inreased Risk for Diabetes (Prediabetes) Type 1 Diabetes Type 2 Diabetes Gestational Diabetes Mellitus Monogeni Diabetes Syndromes Cysti Fibrosis Related Diabetes 3. Initial Evaluation and Diabetes Management Planning Medial Evaluation Management Plan Common Comorbid Conditions 4. Foundations of Care: Eduation, Nutrition, Physial Ativity, Smoking Cessation, Psyhosoial Care, and Immunization Diabetes Self-management Eduation and Support Medial Nutrition Therapy Physial Ativity Smoking Cessation Psyhosoial Assessment and Care Immunization 5. Prevention or Delay of Type 2 Diabetes Lifestyle Modifiations Pharmaologial Interventions Diabetes Self-management Eduation and Support 6. Glyemi Targets Assessment of Glyemi Control A1C Goals Hypoglyemia Interurrent Illness 7. Approahes to Glyemi Treatment Pharmaologial Therapy for Type 1 Diabetes Pharmaologial Therapy for Type 2 Diabetes Bariatri Surgery S67 S70 S77 S80 S86 S88 S90 10. Older Adults Treatment Goals Hypoglyemia Pharmaologial Therapy 11. Children and Adolesents Type 1 Diabetes Type 2 Diabetes Psyhosoial Issues 12. Management of Diabetes in Pregnany Diabetes in Pregnany Preoneption Counseling Glyemi Targets in Pregnany Pregnany and Antihypertensive Drugs Management of Gestational Diabetes Mellitus Management of Pregestational Type 1 Diabetes and Type 2 Diabetes in Pregnany Postpartum Care 13. Diabetes Care in the Hospital, Nursing Home, and Skilled Nursing Faility Hyperglyemia in the Hospital Glyemi Targets in Hospitalized Patients Antihyperglyemi Agents in Hospitalized Patients Preventing Hypoglyemia Diabetes Care Providers in the Hospital Self-management in the Hospital Medial Nutrition Therapy in the Hospital Bedside Blood Gluose Monitoring Disharge Planning Diabetes Self-management Eduation 14. Diabetes Advoay Advoay Position Statements Professional Pratie Committee for the Standards of Medial Care in Diabetes 2015 Index This issue is freely aessible online at are.diabetesjournals.org. Keep up with the latest information for Diabetes Care and other ADA titles via Faebook (/ADAJournals) and Twitter (@ADA_Journals).

Diabetes Care Volume 38, Supplement 1, January 2015 S1 Introdution Diabetes Care 2015;38(Suppl. 1):S1 S2 DOI: 10.2337/d15-S001 INTRODUCTION Diabetes is a omplex, hroni illness requiring ontinuous medial are with multifatorial risk-redution strategies beyond glyemi ontrol. Ongoing patient self-management eduation and support are ritial to preventing aute ompliations and reduing the risk of long-term ompliations. Signifiant evidene exists that supports a range of interventions to improve diabetes outomes. The Amerian Diabetes Assoiation s (ADA s) Standards of Medial Care in Diabetes is intended to provide liniians, patients, researhers, payers, and other interested individuals with the omponents of diabetes are, general treatment goals, and tools to evaluate the quality of are. The Standards of Care reommendations are not intended to prelude linial judgment and must be applied in the ontext of exellent linial are, with adjustments for individual preferenes, omorbidities, and other patient fators. For more detailed information about management of diabetes, please refer to Medial Management of Type 1 Diabetes (1) and Medial Management of Type 2 Diabetes (2). The reommendations inlude sreening, diagnosti, and therapeuti ations that are known or believed to favorably affet health outomes of patients with diabetes. Many of these interventionshavealsobeenshowntobeosteffetive (3). The ADA strives to improve and update the Standards of Care to ensure that liniians, health plans, and poliy makers an ontinue to rely on them as the most authoritative and urrent guidelines for diabetes are. ADA STANDARDS, STATEMENTS, AND REPORTS The ADA has been atively involved in the development and dissemination of diabetes are standards, guidelines, and related douments for over 20 years. ADA s linial pratie reommendations are viewed as important resoures for health are professionals who are for people with diabetes. ADA s Standards of Medial Care in Diabetes, position statements, and sientifi statements undergo a formal review proess by ADA s Professional Pratie Committee (PPC) and the Exeutive Committee of the Board of Diretors. The Standards and all ADA position statements, sientifi statements, and onsensus reports are available on the Assoiation s Web site at http://professional.diabetes.org/ adastatements. Standards of Medial Care in Diabetes Standards of Care: ADA position statement that provides key linial pratie reommendations. The PPC performs an extensive literature searh and updates the Standards annually based on the quality of new evidene. ADA Position Statement A position statement is an offiial ADA point of view or belief that ontains linial or researh reommendations. Position statements are issued on sientifi or medial issues related to diabetes. They are published in ADA journals and other sientifi/medial publiations. ADA position statements are typially based on a systemati review or other review of published literature. Position statements undergo a formal review proess. They are updated annually or as needed. ADA Sientifi Statement A sientifi statement is an offiial ADA point of view or belief that may or may not ontain linial or researh reommendations. Sientifi statements ontain sholarly synopsis of a topi related to diabetes. Workgroup reports fall into this ategory. Sientifi statements are published in the ADA journals and other sientifi/medial publiations, as appropriate. Sientifi statements also undergo a formal review proess. Consensus Report A onsensus report ontains a omprehensive examination by an expert panel (i.e., onsensus panel) of a sientifi or medial issue related to diabetes. A onsensus report is not an ADA position and represents expert opinion only. The ategory may also inlude task fore and expert ommittee reports. The need for a onsensus report arises when liniians or sientists desire guidane on a subjet for whih the evidene is ontraditory or inomplete. A onsensus report is typially developed immediately following a onsensus onferene where the ontroversial issue is extensively disussed. The report represents the panel s olletive analysis, evaluation, and opinion at that point in time based in part on the onferene proeedings. A onsensus report does not undergo a formal ADA review proess. GRADING OF SCIENTIFIC EVIDENCE Sine the ADA first began publishing pratie guidelines, there has been onsiderable evolution in the evaluation of sientifi evidene and in the development of evidene-based guidelines. In 2002, we developed a lassifiation Standards of Medial Care in Diabetes was originally approved in 1988. Most reent review/revision: Otober 2014. 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

S2 Introdution Diabetes Care Volume 38, Supplement 1, January 2015 Table 1 ADA evidene-grading system for Standards of Medial Care in Diabetes Level of evidene Desription A Clear evidene from well-onduted, generalizable randomized ontrolled trials that are adequately powered, inluding Evidene from a well-onduted multienter trial Evidene from a meta-analysis that inorporated quality ratings in the analysis Compelling nonexperimental evidene; i.e., all or none rule developed by the Centre for Evidene-Based Mediine at the University of Oxford Supportive evidene from well-onduted randomized ontrolled trials that are adequately powered, inluding Evidene from a well-onduted trial at one or more institutions Evidene from a meta-analysis that inorporated quality ratings in the analysis B Supportive evidene from well-onduted ohort studies Evidene from a well-onduted prospetive ohort study or registry Evidene from a well-onduted meta-analysis of ohort studies Supportive evidene from a well-onduted ase-ontrol study C Supportive evidene from poorly ontrolled or unontrolled studies Evidene from randomized linial trials with one or more major or three or more minor methodologial flaws that ould invalidate the results Evidene from observational studies with high potential for bias (suh as ase series with omparison with historial ontrols) Evidene from ase series or ase reports Confliting evidene with the weight of evidene supporting the reommendation E Expert onsensus or linial experiene reommendations have the best hane of improving outomes when applied to the population to whih they are appropriate. Reommendations with lower levels of evidene may be equally important but are not as well supported. Of ourse, evidene is only one omponent of linial deision making. Cliniians are for patients, not populations; guidelines must always be interpreted with the individual patient in mind. Individual irumstanes, suh as omorbid and oexisting diseases, age, eduation, disability, and, above all, patients values and preferenes, must be onsidered and may lead to different treatment targets and strategies. Also, onventional evidene hierarhies, suh as the one adapted by the ADA, may miss nuanes important in diabetes are. For example, although there is exellent evidene from linial trials supporting the importane of ahieving multiple risk fator ontrol, the optimal way to ahieve this result is less lear. It is diffiult to assess eah omponent of suh a omplex intervention. system to grade the quality of sientifi evidene supporting ADA reommendations for all new and revised ADA position statements. A reent analysis of the evidene ited in the Standards of Care found steady improvement in quality over the past 10 years, with last year s Standards for the first time having the majority of bulleted reommendations supported by A- orb-level evidene (4). A grading system (Table 1) developed by ADA and modeled after existing methods was used to larify and odify the evidene that forms the basis for the reommendations. ADA reommendations are assigned ratings of A, B, orc, depending on the quality of evidene. Expert opinion E is a separate ategory for reommendations in whih there is no evidene from linial trials, in whih linial trials may be impratial, or in whih there is onfliting evidene. Reommendations with an A rating are based on large well-designed linial trials or welldone meta-analyses. Generally, these Referenes 1. Kaufman FR (Ed.). Medial Management of Type 1 Diabetes, 6th ed. Alexandria, VA, Amerian Diabetes Assoiation, 2012 2. Burant CF (Ed.). Medial Management of Type 2 Diabetes, 7th ed. Alexandria, VA, Amerian Diabetes Assoiation, 2012 3. Li R, Zhang P, Barker LE, Chowdhury FM, Zhang X. Cost-effetiveness of interventions to prevent and ontrol diabetes mellitus: a systemati review. Diabetes Care 2010;33:1872 1894 4. Grant RW, Kirkman MS. Trends in the evidene level for the Amerian Diabetes Assoiation s Standards of Medial Care in Diabetes from 2005 to 2014. Diabetes Care 2015;38:6 8

Diabetes Care Volume 38, Supplement 1, January 2015 Professional Pratie Committee Diabetes Care 2015;38(Suppl. 1):S3 DOI: 10.2337/d15-S002 The Professional Pratie Committee (PPC) of the Amerian Diabetes Assoiation (ADA) is responsible for the Standards of Medial Care in Diabetes position statement, referred to as the Standards of Care. The PPC is a multidisiplinary expert ommittee omprised of physiians, diabetes eduators, registered dietitians, and others who have expertise in a range of areas, inluding adult and pediatri endorinology, epidemiology, publi health, lipid researh, hypertension, and preoneption and pregnany are. Appointment to the PPC is based on exellene in linial pratie and/or researh. While the primary role of the PPC is to review and update the Standards of Care, it is also responsible for overseeing the review and revisions of ADA s position statements and sientifistatements. All members of the PPC are required to dislose potential onflitsofinterest with industry and/or other relevant organizations. These dislosures are disussed at the onset of eah Standards of Care revision meeting. Members of the ommittee, their employer, and their dislosed onflits of interest are listed in the Professional Pratie Committee for the Standards of Medial Care in Diabetesd2015 table (see p. S88). For the urrent revision, PPC members systematially searhed MEDLINE for human studies related to eah setion and published sine 1 January 2014. Reommendations were revised based on new evidene or, in some ases, to larify the prior reommendation or math the strength of the wording to the strength of the evidene. A table linking the hanges in reommendations to new evidene an be reviewed at http:// professional.diabetes.org/soc. As for all position statements, the Standards of Care position statement was reviewed andapprovedbytheexeutivecommittee of ADA s Board of Diretors, whih inludes health are professionals, sientists, and lay people. Feedbak from the larger linial ommunity was valuable for the 2015 revision of the Standards of Care. Readers who wish to omment on the Standards of Medial Care in Diabetesd2015 are invited to do so at http://professional.diabetes.org/soc. The ADA funds development of the Standards of Care and all ADA position statements out of its general revenues and does not use industry support for these purposes. The PPC would like to thank the following individuals who provided their expertise in reviewing and/or onsulting with the ommittee: Donald R. Coustan, MD; Stephanie Dunbar, MPH, RD; Robert H. Ekel, MD; Henry N. Ginsberg, MD; Edward W. Gregg, PhD; Silvio E. Inzuhi, MD; Mark E. Molith, MD; John M. Morton, MD; Robert E. Ratner, MD; Linda M. Siminerio, RN, PhD, CDE; and Katherine R. Tuttle, MD. Members of the PPC Rihard W. Grant, MD, MPH (Chair)* Thomas W. Donner, MD Judith E. Fradkin, MD Charlotte Hayes, MMS, MS, RD, CDE, ACSM CES William H. Herman, MD, MPH William C. Hsu, MD Eileen Kim, MD Lori Laffel, MD, MPH Rodia Pop-Busui, MD, PhD Neda Rasouli, MD* Desmond Shatz, MD Joseph A. Stankaitis, MD, MPH* Traey H. Taveira, PharmD, CDOE, CVDOE Deborah J. Wexler, MD* *Subgroup leaders ADA Staff Jane L. Chiang, MD Erika Gebel Berg, PhD S3 PROFESSIONAL PRACTICE COMMITTEE 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

S4 Diabetes Care Volume 38, Supplement 1, January 2015 SUMMARY OF REVISIONS Standards of Medial Care in Diabetesd2015: Summary of Revisions Diabetes Care 2015;38(Suppl. 1):S4 DOI: 10.2337/d15-S003 GENERAL CHANGES Diabetes Care Supplement 1 was previously alled Clinial Pratie Reommendations and inluded the Standards of Medial Care in Diabetes and key Amerian Diabetes Assoiation (ADA) position statements. The supplement has been renamed Standards of Medial Care in Diabetes ( Standards ) and ontains a single ADA position statement that provides evidene-based linial pratie reommendations for diabetes are. Whereas the Standards of Medial Care in Diabetesd2015 should still be viewed as a single doument, it has been divided into 14 setions, eah individually referened, to highlight important topi areas and to failitate navigation. The supplement now inludes an index to help readers find information on partiular topis. SECTION CHANGES Although the levels of evidene for several reommendations have been updated, these hanges are not inluded below as the linial reommendations have remained the same. Changes in evidene level from, for example, C to E are not noted below. The Standards of Medial Care in Diabetesd2015 ontains, in addition to many minor hanges that larify reommendations or reflet new evidene, the following more substantive revisions. Setion 2. Classifiation and Diagnosis of Diabetes The BMI ut point for sreening overweight or obese Asian Amerians for prediabetes and type 2 diabetes was hanged to 23 kg/m 2 (vs. 25 kg/m 2 )toreflet the evidene that this population is at an inreased risk for diabetes at lower BMI levels relative to the general population. Setion 4. Foundations of Care: Eduation, Nutrition, Physial Ativity, Smoking Cessation, Psyhosoial Care, and Immunization The physial ativity setion was revised to reflet evidene that all individuals, inluding those with diabetes, should be enouraged to limit the amount of time they spend being sedentary by breaking up extended amounts of time (.90 min) spent sitting. Due to the inreasing use of e-igarettes, the Standards were updated to make lear that e-igarettes are not supported as an alternative to smoking or to failitate smoking essation. Immunization reommendations were revised to reflet reent Centers for Disease Control and Prevention guidelines regarding PCV13 and PPSV23 vainations in older adults. Setion 6. Glyemi Targets The ADA now reommends a premeal blood gluose target of 80 130 mg/dl, rather than 70 130 mg/dl, to better reflet new data omparing atual average gluose levels with A1C targets. To provide additional guidane on the suessful implementation of ontinuous gluose monitoring (CGM), the Standards inlude new reommendations on assessing apatient s readiness for CGM and on providing ongoing CGM support. Setion 7. Approahes to Glyemi Treatment The type 2 diabetes management algorithm was updated to reflet all of the urrently available therapies for diabetes management. Setion 8. Cardiovasular Disease and Risk Management The reommended goal for diastoli blood pressure was hanged from 80 mmhg to 90 mmhg for most people with diabetes and hypertension to better reflet evidene from randomized linial trials. Lower diastoli targets may still be appropriate for ertain individuals. Reommendations for statin treatment and lipid monitoring were revised after onsideration of 2013 Amerian College of Cardiology/Amerian Heart Assoiation guidelines on the treatment of blood holesterol. Treatment initiation (and initial statin dose) is now driven primarily by risk status rather than LDL holesterol level. With onsideration for the new statin treatment reommendations, the Standards now provide the following lipid monitoring guidane: a sreening lipid profile is reasonable at diabetes diagnosis, at an initial medial evaluation and/or at age 40 years, and periodially thereafter. Setion 9. Mirovasular Compliations and Foot Care To better target those at high risk for foot ompliations, the Standards emphasize that all patients with insensate feet, foot deformities, or a history of foot ulers have their feet examined at every visit. Setion 11. Children and Adolesents To reflet new evidene regarding the risks and benefits of tight glyemi ontrol in hildren and adolesents with diabetes, the Standards now reommend a target A1C of,7.5% for all pediatri age-groups; however, individualization is still enouraged. Setion 12. Management of Diabetes in Pregnany This new setion was added to the Standards to provide reommendations related to pregnany and diabetes, inluding reommendations regarding preoneption ounseling, mediations, blood gluose targets, and monitoring. 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

Diabetes Care Volume 38, Supplement 1, January 2015 S5 1. Strategies for Improving Care Diabetes Care 2015;38(Suppl. 1):S5 S7 DOI: 10.2337/d15-S004 Amerian Diabetes Assoiation Reommendations A patient-entered ommuniation style that inorporates patient preferenes, assesses literay and numeray, and addresses ultural barriers to are should be used. B Treatment deisions should be timely and founded on evidene-based guidelines that are tailored to individual patient preferenes, prognoses, and omorbidities. B Care should be aligned with omponents of the Chroni Care Model (CCM) to ensure produtive interations between a prepared proative pratie team and an informed ativated patient. A When feasible, are systems should support team-based are, ommunity involvement, patient registries, and deision support tools to meet patient needs. B DIABETES CARE CONCEPTS In the following setions, different omponents of the linial management of patients with (or at risk for) diabetes are reviewed. We highlight the following three themes that are woven throughout these setions that liniians, poliymakers, and advoates should keep in mind: POSITION STATEMENT 1. Patient-Centeredness: Pratie reommendations, whether based on evidene or expert opinion, are intended to guide an overall approah to are. The siene and art of mediine ome together when the liniian is faed with making treatment reommendations for a patient who would not have met eligibility riteria for the studies on whih guidelines were based. Reognizing that one size does not fit all, these Standards provide guidane for when and how to adapt reommendations (e.g., see Setion 10. Older Adults and Fig. 6.1. Approah to the Management of Hyperglyemia). Beause patients with diabetes are also at greatly inreased risk of ardiovasular disease, a patient-entered approah should inlude a omprehensive plan to redue ardiovasular risk by addressing blood pressure and lipid ontrol, smoking essation, weight management, and healthy lifestyle hanges that inlude adequate physial ativity. 2. Diabetes Aross the Life Span: An inreasing proportion of patients with type 1 diabetes are adults. Conversely, and for less salutary reasons, the inidene of type 2 diabetes is inreasing in hildren and young adults. Finally, patients both with type 1 diabetes and with type 2 diabetes are living well into older age, a stage of life for whih there is little evidene from linial trials to guide therapy. All these demographi hanges highlight another hallenge to high-quality diabetes are, whih is the need to improve oordination between linial teams as patients pass through different stages of the life span or the stages of pregnany (preoneption, pregnany, and postpartum). 3. Advoay for Patients With Diabetes: Advoay an be defined as ative support and engagement to advane a ause or poliy. Advoay in the ause of improving the lives of patients with (or at risk for) diabetes is an ongoing need. Given the tremendous toll that lifestyle fators suh as obesity, physial inativity, and smoking have on the health of patients with diabetes, ongoing and energeti efforts are needed to address and hange the soietal determinants at the root of these problems. Within the more narrow domain of linial pratie guidelines, the appliation of evidene level grading to pratie reommendations an help identify areas that require more researh investment (1). This topi is explored in more depth in Setion 14. Diabetes Advoay. Suggested itation: Amerian Diabetes Assoiation. Strategies for improving are. Se. 1. In Standards of Medial Care in Diabetesd2015. Diabetes Care 2015;38(Suppl. 1):S5 S7 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

S6 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 CARE DELIVERY SYSTEMS There has been steady improvement in the proportion of diabeti patients ahieving reommended levels of A1C, blood pressure, and LDL holesterol in the last 10 years (2). The mean A1C nationally has delined from 7.6% in 1999 2002 to 7.2% in 2007 2010 based on the National Health and Nutrition Examination Survey (NHANES) data (E.W. Gregg, Centers for Disease Control and Prevention, personal ommuniation). This has been aompanied by improvements in lipids and blood pressure ontrol and has led to substantial redutions in end-stage mirovasular ompliations in patients with diabetes. Nevertheless, between 33 and 49% of patients still do not meet targets for glyemi, blood pressure, or holesterol ontrol, and only 14% meet targets for all three measures and nonsmoking status (2). Evidene also suggests that progress in ardiovasular risk fator ontrol (partiularly tobao use) may be slowing (2,3). Certain patient groups, suh as young adults and patients with omplex omorbidities, finanial or other soial hardships, and/or limited English profiieny, may present partiular hallenges to goal-based are (4 6). Persistent variation in quality of diabetes are aross providers and aross pratie settings even after adjusting for patient fators indiates that there remains potential for substantial systemlevelimprovementsindiabetesare. Chroni Care Model Although numerous interventions to improve adherene to the reommended standards have been implemented, a major barrier to optimal are is a delivery system that too often is fragmented, laks linial information apabilities, dupliates servies, and is poorly designed for the oordinated delivery of hroni are. The CCM has been shown to be an effetive framework for improving the quality of diabetes are (7). The CCM inludes six ore elements for the provision of optimal are of patients with hroni disease: 1) delivery system design (moving from a reative to a proative are delivery system where planned visits are oordinated through a team-based approah, 2) self-management support, 3) deision support (basing are on evidene-based, effetive are guidelines), 4) linial information systems (using registries that an provide patientspeifi and population-based support to the are team), 5) ommunity resoures and poliies (identifying or developing resoures to support healthy lifestyles), and 6)healthsystems(toreateaqualityoriented ulture). Redefining the roles of the lini staff and promoting selfmanagement on the part of the patient are fundamental to the suessful implementation of the CCM (8). Collaborative, multidisiplinary teams are best suited to provide are for people with hroni onditions suh as diabetes and to failitate patients self-management (9 12). Key Objetives The National Diabetes Eduation Program (NDEP) maintains an online resoure (www.betterdiabetesare.nih.gov) to help health are professionals design and implement more effetive health are delivery systems for those with diabetes. Three speifi objetives, with referenes to literature that outlines pratial strategies to ahieve eah, are delineated below. Objetive 1: Optimize Provider and Team Behavior The are team should prioritize timely and appropriate intensifiation of lifestyle and/ or pharmaeutial therapy for patients who have not ahieved benefiial levels of blood pressure, lipid, or gluose ontrol (13). Strategies suh as expliit goal setting with patients (14); identifying and addressing language, numeray, or ultural barriers to are (15 18); integrating evidene-based guidelines and linial information tools into the proess of are (19 21); and inorporating are management teams inluding nurses, pharmaists, and other providers (22 24) have eah been shown to optimize provider and team behavior and thereby atalyze redutions in A1C, blood pressure, and LDL holesterol. Objetive 2: Support Patient Behavior Change Suessful diabetes are requires a systemati approah to supporting patients behavior hange efforts, inluding 1) healthy lifestyle hanges (physial ativity, healthy eating, tobao essation, weight management, and effetive oping), 2) disease self-management (taking and managing mediation and, when linially appropriate, self-monitoring of gluose and blood pressure), and 3) prevention of diabetes ompliations (self-monitoring of foot health; ative partiipation in sreening for eye, foot, and renal ompliations; and immunizations). High-quality diabetes self-management eduation (DSME) has been shown to improve patient self-management, satisfation, and gluose ontrol (25,26), as has delivery of ongoing diabetes self-management support (DSMS), so that gains ahieved during DSME are sustained (27 29). National DSME standards all for an integrated approah that inludes linial ontent and skills, behavioral strategies (goal setting, problem solving), and engagement with emotional onerns in eah needed urriulum ontent area. Objetive 3: Change the Care System An institutional priority in most suessful are systems is providing a high quality of are (30). Changes that have been shown to inrease quality of diabetes are inlude basing are on evidene-based guidelines (19); expanding the role of teams and staff and implementing more intensive disease management strategies (6,22,31); redesigning the are proess (32); implementing eletroni health reord tools (33,34); ativating and eduating patients (35,36); removing finanial barriers and reduing patient out-ofpoket osts for diabetes eduation, eye exams, self-monitoring of blood gluose, and neessary mediations (6); and identifying/developing/engaging ommunity resoures and publi poliy that support healthy lifestyles (37). Reent initiatives suh as the Patient-Centered Medial Home show promise for improving outomes through oordinated primary are and offer new opportunities for teambased hroni disease are (38). Additional strategies to improve diabetes are inlude reimbursement strutures that, in ontrast to visit-based billing, reward the provision of appropriate and high-quality are (39), and inentives that aommodate personalized are goals (6,40). It is lear that optimal diabetes management requires an organized, systemati approah and the involvement of a oordinated team of dediated health are professionals workinginanenvironment where patient-entered highquality are is a priority (6). WHEN TREATMENT GOALS ARE NOT MET Some patients and their health are providers may not ahieve the desired treatment goals. Reassessing the treatment regimen may require evaluation of

are.diabetesjournals.org Position Statement S7 barriers suh as inome, health literay, diabetes-related distress, depression, poverty, and ompeting demands, inluding those related to family responsibilities and dynamis. Other strategies may inlude ulturally appropriate and enhaned DSME and DSMS, omanagement with a diabetes team, referral to a medial soial worker for assistane with insurane overage, mediationtaking behavior assessment, or hange in pharmaologial therapy. Initiation of or inrease in self-monitoring of blood gluose, ontinuous gluose monitoring, frequent patient ontat, or referral to a mental health professional or physiian with speial expertise in diabetes may be useful. Referenes 1. Grant RW, Kirkman MS. Trends in the evidene level for the Amerian Diabetes Assoiation s Standards of Medial Care in Diabetes from 2005 to 2014. Diabetes Care 2015;38:6 8 2. Ali MK, Bullard KM, Saaddine JB, Cowie CC, Imperatore G, Gregg EW. Ahievement of goals in U.S. diabetes are, 1999-2010. N Engl J Med 2013;368:1613 1624 3. Wang J, Geiss LS, Cheng YJ, et al. Long-term and reent progress in blood pressure levels among U.S. adults with diagnosed diabetes, 1988-2008. Diabetes Care 2011;34:1579 1581 4. Kerr EA, Heisler M, Krein SL, et al. Beyond omorbidity ounts: how do omorbidity type and severity influene diabetes patients treatment priorities and self-management? J Gen Intern Med 2007;22:1635 1640 5. Fernandez A, Shillinger D, Warton EM, et al. Language barriers, physiian-patient language onordane, and glyemi ontrol among insured Latinos with diabetes: the Diabetes Study of Northern California (DISTANCE). J Gen Intern Med 2011;26:170 176 6. TRIAD Study Group. Health systems, patients fators, and quality of are for diabetes: a synthesis of findings from the TRIAD study. Diabetes Care 2010;33:940 947 7. Stellefson M, Dipnarine K, Stopka C. The hroni are model and diabetes management in US primary are settings: a systemati review. Prev Chroni Dis 2013;10:E26 8. Coleman K, Austin BT, Brah C, Wagner EH. Evidene on the Chroni Care Model in the new millennium. Health Aff (Millwood) 2009;28:75 85 9. Piatt GA, Anderson RM, Brooks MM, et al. 3- year follow-up of linial and behavioral improvements following a multifaeted diabetes are intervention: results of a randomized ontrolled trial. Diabetes Edu 2010;36:301 309 10. Renders CM, Valk GD, Griffin SJ, Wagner EH, Eijk Van JT, Assendelft WJ. Interventions to improve the management of diabetes in primary are, outpatient, and ommunity settings: a systemati review. Diabetes Care 2001;24: 1821 1833 11. Katon WJ, Lin EHB, Von Korff M, et al. Collaborative are for patients with depression and hroni illnesses. N Engl J Med 2010;363:2611 2620 12. Parhman ML, Zeber JE, Romero RR, Pugh JA. Risk of oronary artery disease in type 2 diabetes and the delivery of are onsistent with the hroni are model in primary are settings: a STARNet study. Med Care 2007;45:1129 1134 13. Davidson MB. How our urrent medial are system fails people with diabetes: lak of timely, appropriate linial deisions. Diabetes Care 2009;32:370 372 14. Grant RW, Pabon-Nau L, Ross KM, Youatt EJ, Pandisio JC, Park ER. Diabetes oral mediation initiation and intensifiation: patient views ompared with urrent treatment guidelines. Diabetes Edu 2011;37:78 84 15. Shillinger D, Piette J, Grumbah K, et al. Closing the loop: physiian ommuniation with diabeti patients who have low health literay. Arh Intern Med 2003;163:83 90 16. Rosal MC, Okene IS, Restrepo A, et al. Randomized trial of a literay-sensitive, ulturally tailored diabetes self-management intervention for low-inome Latinos: Latinos en Control. Diabetes Care 2011;34:838 844 17. Osborn CY, Cavanaugh K, Wallston KA, et al. Health literay explains raial disparities in diabetes mediation adherene. J Health Commun 2011;16(Suppl. 3):268 278 18. Rothman R, Malone R, Bryant B, Horlen C, DeWalt D, Pignone M. The relationship between literay and glyemi ontrol in a diabetes disease-management program. Diabetes Edu 2004;30:263 273 19. O Connor PJ, Bodkin NL, Fradkin J, et al. Diabetes performane measures: urrent status and future diretions. Diabetes Care 2011;34: 1651 1659 20. Garg AX, Adhikari NK, MDonald H, et al. Effets of omputerized linial deision support systems on pratitioner performane and patient outomes: a systemati review. JAMA 2005;293:1223 1238 21. Smith SA, Shah ND, Bryant SC, et al.; Evidens Researh Group. Chroni are model and shared are in diabetes: randomized trial of an eletroni deision support system. Mayo Clin Pro 2008;83:747 757 22. Jaffe MG, Lee GA, Young JD, Sidney S, Go AS. Improved blood pressure ontrol assoiated with a large-sale hypertension program. JAMA 2013;310:699 705 23. Davidson MB, Ansari A, Karlan VJ. Effet of a nurse-direted diabetes disease management program on urgent are/emergeny room visits and hospitalizations in a minority population. Diabetes Care 2007;30:224 227 24. Stone RA, Rao RH, Sevik MA, et al. Ative are management supported by home telemonitoring in veterans with type 2 diabetes: the DiaTel randomized ontrolled trial. Diabetes Care 2010;33:478 484 25. Dunan I, Birkmeyer C, Coughlin S, Li QE, Sherr D, Boren S. Assessing the value of diabetes eduation. Diabetes Edu 2009;35:752 760 26. Berikai P, Meyer PM, Kazlauskaite R, Savoy B, Kozik K, Fogelfeld L. Gain in patients knowledge of diabetes management targets is assoiated with better glyemi ontrol. Diabetes Care 2007;30:1587 1589 27. Funnell MM, Brown TL, Childs BP, et al. National standards for diabetes self-management eduation. Diabetes Care 2007;30:1630 1637 28. Klein S, Sheard NF, Pi-Sunyer X, et al. Weight management through lifestyle modifiation for the prevention and management of type 2 diabetes: rationale and strategies: a statement of the Amerian Diabetes Assoiation, the North Amerian Assoiation for the Study of Obesity, and the Amerian Soiety for Clinial Nutrition. Diabetes Care 2004;27:2067 2073 29. Norris SL, Zhang X, Avenell A, et al. Effiay of pharmaotherapy for weight loss in adults with type 2 diabetes mellitus: a meta-analysis. Arh Intern Med 2004;164:1395 1404 30. Trio AC, Ivers NM, Grimshaw JM, et al. Effetiveness of quality improvement strategies on the management of diabetes: a systemati review and meta-analysis. Lanet 2012;379: 2252 2261 31. Peikes D, Chen A, Shore J, Brown R. Effets of are oordination on hospitalization, quality of are, and health are expenditures among Mediare benefiiaries: 15 randomized trials. JAMA 2009;301:603 618 32. Feifer C, Nemeth L, Nietert PJ, et al. Different paths to high-quality are: three arhetypes of top-performing pratie sites. Ann Fam Med 2007;5:233 241 33. Reed M, Huang J, Graetz I, et al. Outpatient eletroni health reords and the linial are and outomes of patients with diabetes mellitus. Ann Intern Med 2012;157:482 489 34. Cebul RD, Love TE, Jain AK, Hebert CJ. Eletroni health reords and quality of diabetes are. N Engl J Med 2011;365:825 833 35. Battersby M, Von Korff M, Shaefer J, et al. Twelve evidene-based priniples for implementing self-management support in primary are. Jt Comm J Qual Patient Saf 2010;36:561 570 36. Grant RW, Wald JS, Shnipper JL, et al. Pratie-linked online personal health reords for type 2 diabetes mellitus: a randomized ontrolledtrial.arhinternmed2008;168:1776 1782 37. Pullen-Smith B, Carter-Edwards L, Leathers KH. Community health ambassadors: a model for engaging ommunity leaders to promote better health in North Carolina. J Publi Health Manag Prat 2008;14(Suppl.): S73 S81 38. Bojadzievski T, Gabbay RA. Patient-entered medial home and diabetes. Diabetes Care 2011; 34:1047 1053 39. Rosenthal MB, Cutler DM, Feder J. The ACO rulesdstriking the balane between partiipation and transformative potential. N Engl J Med 2011;365:e6 40. Washington AE, Lipstein SH. The Patient- Centered Outomes Researh Instituted promoting better information, deisions, and health. N Engl J Med 2011;365:e31

S8 Diabetes Care Volume 38, Supplement 1, January 2015 2. Classifiation and Diagnosis of Diabetes Amerian Diabetes Assoiation Diabetes Care 2015;38(Suppl. 1):S8 S16 DOI: 10.2337/d15-S005 CLASSIFICATION Diabetes an be lassified into the following general ategories: POSITION STATEMENT 1. Type 1 diabetes (due to b-ell destrution, usually leading to absolute insulin defiieny) 2. Type 2 diabetes (due to a progressive insulin seretory defet on the bakground of insulin resistane) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the seond or third trimester of pregnany that is not learly overt diabetes) 4. Speifi types of diabetes due to other auses, e.g., monogeni diabetes syndromes (suh as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exorine panreas (suh as ysti fibrosis), and drug- or hemial-indued diabetes (suh as in the treatment of HIV/AIDS or after organ transplantation) This setion reviews most ommon forms of diabetes but is not omprehensive. For additional information, see the Amerian Diabetes Assoiation (ADA) position statement Diagnosis and Classifiation of Diabetes Mellitus (1). Assigning a type of diabetes to an individual often depends on the irumstanes present at the time of diagnosis, with individuals not neessarily fitting learly into a single ategory. For example, some patients annot be learly lassified as having type 1 or type 2 diabetes. Clinial presentation and disease progression may vary onsiderably in both types of diabetes. The traditional paradigms of type 2 diabetes ourring only in adults and type 1 diabetes only in hildren are no longer aurate, as both diseases our in both ohorts. Oasionally, patients with type 2 diabetes may present with diabeti ketoaidosis (DKA). Children with type 1 diabetes typially present with the hallmark symptoms of polyuria/polydipsia and oasionally with DKA. The onset of type 1 diabetes may be variable in adults and may not present with the lassi symptoms seen in hildren. However, diffiulties in diagnosis may our in hildren, adolesents, and adults, with the true diagnosis beoming more obvious over time. DIAGNOSTIC TESTS FOR DIABETES Diabetes may be diagnosed based on A1C riteria or plasma gluose riteria, either the fasting plasma gluose (FPG) or the 2-h plasma gluose (2-h PG) value after a 75-g oral gluose tolerane test (OGTT) (1,2) (Table 2.1). The same tests are used to both sreen for and diagnose diabetes. Diabetes may be identified anywhere along the spetrum of linial senarios: in seemingly lowrisk individuals who happen to have gluose testing, in symptomati patients, and in higher-risk individuals whom the provider tests beause of a suspiion of diabetes. The same tests will also detet individuals with prediabetes. A1C The A1C test should be performed using a method that is ertified by the NGSP and standardized or traeable to the Diabetes Control and Compliations Trial (DCCT) referene assay. Although point-of-are (POC) A1C assays may be NGSP ertified, profiieny testing is not mandated for performing the test, so use of POC assays for diagnosti purposes may be problemati and is not reommended. The A1C has several advantages to the FPG and OGTT, inluding greater onveniene (fasting not required), greater preanalytial stability, and less day-to-day perturbations during stress and illness. These advantages must be balaned by Suggested itation: Amerian Diabetes Assoiation. Classifiation and diagnosis of diabetes. Se. 2. In Standards of Medial Care in Diabetesd2015. Diabetes Care 2015;38(Suppl. 1):S8 S16 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

are.diabetesjournals.org Position Statement S9 Table 2.1 Criteria for the diagnosis of diabetes A1C $6.5%. The test should be performed in a laboratory using a method that is NGSP ertified and standardized to the DCCT assay.* OR FPG $126 mg/dl (7.0 mmol/l). Fasting is defined as no alori intake for at least 8h.* OR 2-h PG $200 mg/dl (11.1 mmol/l) during an OGTT. The test should be performed as desribed by the WHO, using a gluose load ontaining the equivalent of 75 g anhydrous gluose dissolved in water.* OR In a patient with lassi symptoms of hyperglyemia or hyperglyemi risis, a random plasma gluose $200 mg/dl (11.1 mmol/l). *In the absene of unequivoal hyperglyemia, results should be onfirmed by repeat testing. greater ost, the limited availability of A1C testing in ertain regions of the developing world, and the inomplete orrelation between A1C and average gluose in ertain individuals. It is important to take age, rae/ ethniity, and anemia/hemoglobinopathies into onsideration when using the A1C to diagnose diabetes. Age The epidemiologial studies that formed the framework for reommending A1C to diagnose diabetes only inluded adult populations. Therefore, it remains unlear if A1C and the same A1C ut point should be used to diagnose diabetes in hildren and adolesents (3 5). Rae/Ethniity A1C levels may vary with patients rae/ ethniity (6,7). For example, Afrian Amerians may have higher A1C levels than non-hispani whites despite similar fasting and postgluose load gluose levels. A reent epidemiologial study found that, when mathed for FPG, Afrian Amerians (with and without diabetes) had higher A1C levels than non- Hispani whites, but also had higher levels of frutosamine and glyated albumin and lower levels of 1,5-anhydrogluitol, suggesting that their glyemi burden (partiularly postprandially) may be higher (8). Hemoglobinopathies/Anemias Interpreting A1C levels in the presene of ertain hemoglobinopathies and anemia may be problemati. For patients with an abnormal hemoglobin but normal red ell turnover, suh as those with the sikle ell trait, an A1C assay without interferene from abnormal hemoglobins should be used. An updated list of interferenes is available at www.ngsp.org/interf.asp. In onditions assoiated with inreased red ell turnover, suh as pregnany (seond and third trimesters), reent blood loss or transfusion, erythropoietin therapy, or hemolysis, only blood gluose riteria should be used to diagnose diabetes. Fasting and 2-Hour Plasma Gluose In addition to the A1C test, the FPG and 2-h PG may also be used to diagnose diabetes (Table 2.1). The onordane between the FPG and 2-h PG tests is imperfet, as is the onordane between A1C and either gluose-based test. National Health and Nutrition Examination Survey (NHANES) data indiate that an A1C ut point of $6.5% identifies one-third fewer ases of undiagnosed diabetes than a fasting gluose ut point of $126 mg/dl (7.0 mmol/l) (9). Numerous studies have onfirmed that, ompared with these A1C and FPG ut points, the 2-h PG value diagnoses more people with diabetes. Of note, the lower sensitivity of A1C at the designated ut point may be offset by the test s ease of use and failitation of more widespread testing. Unless there is a lear linial diagnosis (e.g., a patient in a hyperglyemi risis or with lassi symptoms of hyperglyemia and a random plasma gluose $200 mg/dl), it is reommended that the same test be repeated immediately using a new blood sample for onfirmation beause there will be a greater likelihood of onurrene. For example, if the A1C is 7.0% and a repeat result is 6.8%, the diagnosis of diabetes is onfirmed. If two different tests (suh as A1C and FPG) are both above the diagnosti threshold, this also onfirms the diagnosis. On the other hand, if a patient has disordant results from two different tests, then the test result that is above the diagnosti ut point should be repeated. The diagnosis is made on the basis of the onfirmed test. For example, if a patient meets the diabetes riterion of the A1C (two results $6.5%), but not FPG (,126 mg/dl [7.0 mmol/l]), that person should nevertheless be onsidered to have diabetes. Sine all the tests have preanalyti and analyti variability, it is possible that an abnormal result (i.e., above the diagnosti threshold), when repeated, will produe a value below the diagnosti ut point. This senario is least likely for A1C, more likely for FPG, and most likely for the 2-h PG, espeially if the gluose samples are olleted at room temperature and not entrifuged promptly. Barring laboratory error, suh patients will likely have test results near the margins of the diagnosti threshold. The health are professional should follow the patient losely and repeat the test in 3 6 months. CATEGORIES OF INCREASED RISK FOR DIABETES (PREDIABETES) Reommendations Testing to assess risk for future diabetes in asymptomati people should be onsidered in adults of any age who are overweight or obese (BMI $25 kg/m 2 or $23 kg/m 2 in Asian Amerians) and who have one or more additional risk fators for diabetes. For all patients, partiularly those who are overweight or obese, testing should begin at age 45 years. B If tests are normal, repeat testing arried out at a minimum of 3- year intervals is reasonable. C To test for prediabetes, the A1C, FPG, and 2-h PG after 75-g OGTT are appropriate. B In patients with prediabetes, identify and, if appropriate, treat other ardiovasular disease (CVD) risk fators. B Testing to detet prediabetes should be onsidered in hildren and adolesents who are overweight or obese and who have two or more additional risk fators for diabetes. E Desription In 1997 and 2003, the Expert CommitteeonDiagnosisandClassifiation of Diabetes Mellitus (10,11) reognized a group of individuals whose gluose levels did not meet the riteria for diabetes but were too high to be onsidered

S10 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 Table 2.2 Criteria for testing for diabetes or prediabetes in asymptomati adults 1. Testing should be onsidered in all adults who are overweight (BMI $25 kg/m 2 or $23 kg/m 2 in Asian Amerians) and have additional risk fators: physial inativity first-degree relative with diabetes high-risk rae/ethniity (e.g., Afrian Amerian, Latino, Native Amerian, Asian Amerian, Paifi Islander) women who delivered a baby weighing.9 lb or were diagnosed with GDM hypertension ($140/90 mmhg or on therapy for hypertension) HDL holesterol level,35 mg/dl (0.90 mmol/l) and/or a triglyeride level.250 mg/dl (2.82 mmol/l) women with polyysti ovary syndrome A1C $5.7%, IGT, or IFG on previous testing other linial onditions assoiated with insulin resistane (e.g., severe obesity, aanthosis nigrians) history of CVD 2. For all patients, partiularly those who are overweight or obese, testing should begin at age 45 years. 3. If results are normal, testing should be repeated at a minimum of 3-year intervals, with onsideration of more frequent testing depending on initial results (e.g., those with prediabetes should be tested yearly) and risk status. normal. Prediabetes is the term used for individuals with impaired fasting gluose (IFG) and/or impaired gluose tolerane (IGT) and indiates an inreased risk for the future development of diabetes. IFG and IGT should not be viewed as linial entities in their own right but rather risk fators for diabetes (Table 2.2) andcvd.ifg and IGT are assoiated with obesity (espeially abdominal or viseral obesity), dyslipidemia with high triglyerides and/or low HDL holesterol, and hypertension. Diagnosis In 1997 and 2003, the Expert Committee on Diagnosis and Classifiation of Diabetes Mellitus (10,11) defined IFG as FPG levels 100 125 mg/dl (5.6 6.9 mmol/l) and IGT as 2-h PG after 75-g OGTT levels 140 199 mg/dl (7.8 11.0 mmol/l). It should be noted that the WorldHealthOrganization(WHO)and numerous diabetes organizations define the IFG utoff at 110 mg/dl (6.1 mmol/l). As with the gluose measures, several prospetive studies that used A1C to predit the progression to diabetes demonstrated a strong, ontinuous assoiation between A1C and subsequent diabetes. In a systemati review of 44,203 individuals from 16 ohort studies with a follow-up interval averaging 5.6 years (range 2.8 12 years), those with an A1C between 5.5 6.0% had a substantially inreased risk of diabetes (5-year inidene from 9to25%).AnA1Crangeof6.0 6.5% had a 5-year risk of developing diabetes between 25 50% and a relative risk 20 times higher ompared with an A1C of 5.0% (12). In a ommunity-based study of Afrian Amerian and non- Hispani white adults without diabetes, baseline A1C was a stronger preditor of subsequent diabetes and ardiovasular events than fasting gluose (13). Other analyses suggest that an A1C of 5.7% is assoiated with a diabetes risk similar to that of the high-risk partiipants in the Diabetes Prevention Program (DPP) (14). Hene, it is reasonable to onsider an A1C range of 5.7 6.4% as identifying individuals with prediabetes. As with those with IFG and/or IGT, individuals with an A1C of 5.7 6.4% should be informed of their inreased risk for diabetes and CVD and ounseled about effetive strategies to lower their risks (see Setion 5. Prevention or Delay of Type 2 Diabetes). Similar to gluose measurements, the ontinuum of risk is urvilinear, so as A1C rises, the diabetes risk rises disproportionately (12). Aggressive interventions and vigilant follow-up should be pursued for those onsidered at very high risk (e.g., those with A1C.6.0%). Table 2.3 summarizes the ategories of prediabetes. For reommendations regarding risk fators and sreening for prediabetes, see p. S12 ( Testing for Type 2 Diabetes and Prediabetes in Asymptomati Adults and Testing for Type 2 Diabetes and Prediabetes in Children and Adolesents ). TYPE 1 DIABETES Reommendation Inform the relatives of patients with type 1 diabetes of the opportunity to be tested for type 1 diabetes risk, but only in the setting of a linial researh study. E Immune-Mediated Diabetes This form, previously alled insulindependent diabetes or juvenile-onset diabetes, aounts for 5 10% of diabetes and is due to ellular-mediated autoimmune destrution of the panreati b-ells. Autoimmune markers inlude islet ell autoantibodies, autoantibodies to insulin, autoantibodies to GAD (GAD65), autoantibodies to the tyrosine phosphatases IA-2 and IA-2b, and autoantibodies to zin transporter 8 (ZnT8). Type 1 diabetes is defined by the presene of one or more of these autoimmune markers. The disease has strong HLA assoiations, with linkage to the DQA and DQB genes. These HLA-DR/DQ alleles an be either predisposing or protetive. Therateofb-ell destrution is quite variable, being rapid in some individuals (mainly infants and hildren) and slow in others (mainly adults). Children and adolesents may present with ketoaidosis as the first manifestation of the disease. Others have modest fasting hyperglyemia that an rapidly hange to severe hyperglyemia and/or ketoaidosis with infetion or other stress. Adults may retain suffiient b-ell funtion to prevent ketoaidosis for many years; suh individuals eventually beome dependent on insulin for survival and are at risk for ketoaidosis. At this latter stage of the disease, there is little or no insulin seretion, as manifested by low or undetetable levels of plasma C-peptide. Immune-mediated diabetes Table 2.3 Categories of inreased risk for diabetes (prediabetes)* FPG 100 mg/dl (5.6 mmol/l) to 125 mg/dl (6.9 mmol/l) (IFG) OR 2-h PG in the 75-g OGTT 140 mg/dl (7.8 mmol/l) to 199 mg/dl (11.0 mmol/l) (IGT) OR A1C 5.7 6.4% *For all three tests, risk is ontinuous, extending below the lower limit of the range and beoming disproportionately greater at higher ends of the range.

are.diabetesjournals.org Position Statement S11 ommonly ours in hildhood and adolesene, but it an our at any age, even in the 8th and 9th deades of life. Autoimmune destrution of b-ells has multiple geneti predispositions and is also related to environmental fators that are still poorly defined. Although patients are not typially obese when they present with type 1 diabetes, obesity should not prelude the diagnosis. These patients are also prone to other autoimmune disorders suh as Graves disease, Hashimoto s thyroiditis, Addison s disease, vitiligo, elia disease, autoimmune hepatitis, myasthenia gravis, and perniious anemia. Idiopathi Diabetes Some forms of type 1 diabetes have no known etiologies. These patients have permanent insulinopenia and are prone to ketoaidosis, but have no evidene of autoimmunity. Although only a minority of patients with type 1 diabetes fall into this ategory, of those who do, most are of Afrian or Asian anestry. Individuals with this form of diabetes suffer from episodi ketoaidosis and exhibit varying degrees of insulin defiieny between episodes. This form of diabetes is strongly inherited, laks immunologial evidene for b-ell autoimmunity, and is not HLA assoiated. An absolute requirement for insulin replaement therapy in affeted patients may ome and go. Testing for Type 1 Diabetes The inidene and prevalene of type 1 diabetes is inreasing (15). Type 1 diabeti patients often present with aute symptoms of diabetes and markedly elevated blood gluose levels, and some are diagnosedwithlife-threateningketoaidosis. Several studies suggest that measuring islet autoantibodies in relatives of those with type 1 diabetes may identify individuals who are at risk for developing type 1 diabetes. Suh testing, oupled with eduation about diabetes symptoms and lose follow-up in an observational linial study, may enable earlier identifiation of type 1 diabetes onset. There is evidene to suggest that early diagnosis may limit aute ompliations (16) and extend long-term endogenous insulin prodution (17). A reent study reported the risk of progression to type 1 diabetes from the time of seroonversion to autoantibody positivity in three pediatri ohorts from Finland, Germany, and the U.S. Of the 585 hildren who developed more than two autoantibodies, nearly 70% developed type 1 diabetes within 10 years and 84% within 15 years (16,18). These findings are highly signifiant beause, while the German group was reruited from offspring of parents with type 1 diabetes, the Finnish and Amerian groups were reruited from the general population. Remarkably, the findings in all three groups were the same, suggesting that the same sequene of events led to linial disease in both sporadi and geneti ases of type 1 diabetes. While there is urrently a lak of aepted sreening programs, one should onsider referring relatives of those with type 1 diabetes for antibody testing for risk assessment in the setting of a linial researh study (http://www2.diabetestrialnet.org). Widespread linial testing of asymptomati low-risk individuals is not urrently reommended due to lak of approved therapeuti interventions. Higher-risk individuals may be tested, but only in the ontext of a linial researh setting. Individuals who test positive will be ounseled about the risk of developing diabetes, diabetes symptoms, and DKA prevention. Numerous linial studies are being onduted to test various methods of preventing type 1 diabetes in those with evidene of autoimmunity (www.linialtrials.gov). TYPE 2 DIABETES Reommendations Testing to detet type 2 diabetes in asymptomati people should be onsidered in adults of any age who are overweight or obese (BMI $25 kg/m 2 or $23 kg/m 2 in Asian Amerians) and who have one or more additional risk fators for diabetes. For all patients, partiularly those who are overweight or obese, testing should begin at age 45 years. B If tests are normal, repeat testing arried out at a minimum of 3-year intervals is reasonable. C To test for diabetes, the A1C, FPG, and 2-h PG after 75-g OGTT are appropriate. B In patients with diabetes, identify and, if appropriate, treat other CVD risk fators. B Testing to detet type 2 diabetes should be onsidered in hildren andadolesentswhoareoverweight or obese and who have two or more additional risk fators for diabetes. E Desription This form, previously referred to as noninsulin-dependent diabetes or adultonset diabetes, aounts for ;90 95% of all diabetes. Type 2 diabetes enompasses individuals who have insulin resistane and usually relative (rather than absolute) insulin defiieny. At least initially, and often throughout their lifetime, these individuals may not need insulin treatment to survive. There are various auses of type 2 diabetes. Although the speifi etiologies are not known, autoimmune destrution of b-ells does not our, and patients do not have any of the other known auses of diabetes. Most, but not all, patients with type 2 diabetes are obese. Obesity itself auses some degree of insulin resistane. Patients who are not obese by traditional weight riteria may have an inreased perentage of body fat distributed predominantly in the abdominal region. Ketoaidosis seldom ours spontaneously in type 2 diabetes; when seen, it usually arises in assoiation with the stress of another illness suh as infetion. Type 2 diabetes frequently goes undiagnosed for many years beause hyperglyemia develops gradually and at earlier stages is often not severe enough for the patient to notie the lassi diabetes symptoms. Nevertheless, suh patients are at an inreased risk of developing marovasular and mirovasular ompliations. Whereaspatientswithtype2diabetes may have insulin levels that appear normal or elevated, the higher blood gluose levels in these patients would be expeted to result in even higher insulin values had their b-ell funtion been normal. Thus, insulin seretion is defetive in these patients and insuffiient to ompensate for insulin resistane. Insulin resistane may improve with weight redution and/or pharmaologial treatment of hyperglyemia but is seldom restored to normal. The risk of developing type 2 diabetes inreases with age, obesity, and lak of physial ativity. It ours more frequently

S12 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 in women with prior GDM, in those with hypertension or dyslipidemia, and in ertain raial/ethni subgroups (Afrian Amerian, Amerian Indian, Hispani/ Latino, and Asian Amerian). It is often assoiated with a strong geneti predisposition, more so than type 1 diabetes. However, the genetis of type 2 diabetes is poorly understood. Testing for Type 2 Diabetes and Prediabetes in Asymptomati Adults Prediabetes and diabetes meet riteria for onditions in whih early detetion is appropriate. Both onditions are ommon and impose signifiant linial and publi health burdens. There is often a long presymptomati phase before the diagnosis of type 2 diabetes. Simple tests to detet prelinial disease are readily available. The duration of glyemi burden is a strong preditor of adverse outomes. There are effetive interventions that prevent progression from prediabetes to diabetes (see Setion 5. Prevention or Delay of Type 2 Diabetes) and redue the risk of diabetes ompliations (see Setion 8. Cardiovasular Disease and Risk Management and Setion 9. Mirovasular Compliations and Foot Care). Approximately one-quarter of people with diabetes in the U.S. are undiagnosed. Although sreening of asymptomati individuals to identify those with prediabetes or diabetes might seem reasonable, rigorous linial trials to prove the effetiveness of suh sreening have not been onduted and are unlikely to our. A large European randomized ontrolled trial ompared the impat of sreening for diabetes and intensive multifatorial intervention with that of sreening and routine are (19). General pratie patients between the ages of 40 69 years were sreened for diabetes and randomized by pratie to intensive treatment of multiple risk fators or routine diabetes are. After 5.3 years of follow-up, CVD risk fators were modestly but signifiantly improved with intensive treatment ompared with routine are, but the inidene of first CVD events or mortality was not signifiantly different between the groups (19). The exellent are provided to patients in the routine are group and the lak of an unsreened ontrol arm limit our ability to prove that sreening and early intensive treatment impat outomes. Mathematial modeling studies suggest that sreening, beginning at age 30 or 45 years and independent of risk fators, may be ost-effetive (,$11,000 per qualityadjusted life-year gained) (20). Additional onsiderations regarding testing for type 2 diabetes and prediabetes in asymptomati patients inlude the following: Age Testing reommendations for diabetes in asymptomati adults are listed in Table 2.2. Age is a major risk fator for diabetes. Testing should begin at age 45 years for all patients, partiularly those who are overweight or obese. BMI and Ethniity Testingshouldbeonsideredinadults of any age with BMI $25 kg/m 2 and one or more additional risk fators for diabetes. However, reent data (21) and evidene from the ADA position statement BMI Cut Points to Identify At-Risk Asian Amerians for Type 2 Diabetes Sreening (22)suggestthattheBMI ut point should be lower for the Asian Amerian population. For diabetes sreening purposes, the BMI ut points fall onsistently between 23 24 kg/m 2 (sensitivity of 80%) for nearly all Asian Amerian subgroups (with levels slightly lower for Japanese Amerians). This makes a rounded ut point of 23 kg/m 2 pratial. In determining a single BMI ut point, it is important to balane sensitivity and speifiity so as to provide a valuable sreening tool without numerous false positives. An argument an be made to push the BMI ut point to lower than 23 kg/m 2 in favor of inreased sensitivity; however, this would lead to an unaeptably low speifiity (13.1%). Data from the WHO also suggest that a BMI $23 kg/m 2 should be used to define inreased risk in Asian Amerians (23). Evidene also suggests that other populations may benefit fromlower BMI ut points. For example, in a large multiethni ohort study, for an equivalent inidene rate of diabetes, a BMI of 30 kg/m 2 in non-hispani whites was equivalent to a BMI of 26 kg/m 2 in Afrian Amerians (24). Mediations Certain mediations, suh as gluoortioids, thiazide diuretis, and atypial antipsyhotis (25), are known to inrease the risk of diabetes and should be onsidered when asertaining a diagnosis. Diagnosti Tests The A1C, FPG, and 2-h PG after 75-g OGTT are appropriate for testing. It should be noted that the tests do not neessarily detet diabetes in the same individuals. The effiay of interventions for primary prevention of type 2 diabetes (26 32) has primarily been demonstrated among individuals with IGT, not for individuals with isolated IFG or for those with prediabetes defined by A1C riteria. Testing Interval The appropriate interval between tests is not known (33). The rationale for the 3-year interval is that with this interval, the number of false-positive tests that require onfirmatory testing will be redued and individuals with false-negative tests will be retested before substantial time elapses and ompliations develop (33). Community Sreening Ideally, testing should be arried out within a health are setting beause of the need for follow-up and treatment. Community testing outside a health are setting is not reommended beause people with positive tests may not seek, or have aess to, appropriate follow-up testing and are. Community testing may also be poorly targeted; i.e., it may fail to reah the groups most at risk and inappropriately test those at very low risk or even those who have already been diagnosed. Testing for Type 2 Diabetes and Prediabetes in Children and Adolesents In the last deade, the inidene and prevalene of type 2 diabetes in adolesents has inreased dramatially, espeially in ethni populations (15). Reent studies question the validity of A1C in the pediatri population, espeially among ertain ethniities, and suggest OGTT or FPG as more suitable diagnosti tests (34). However, many of these studies do not reognize that diabetes diagnosti riteria are based on longterm health outomes, and validations are not urrently available in the pediatri population (35). The ADA aknowledges the limited data supporting A1C for diagnosing diabetes in hildren and adolesents. However, aside from rare instanes, suh as ysti fibrosis and hemoglobinopathies, the ADA ontinues to reommend A1C in this ohort (36,37). The modified reommendations of the ADA onsensus report Type 2 Diabetes in Children and Adolesents are summarized in Table 2.4.

are.diabetesjournals.org Position Statement S13 Table 2.4 Testing for type 2 diabetes or prediabetes in asymptomati hildren* Criteria Overweight (BMI.85th perentile for age and sex, weight for height.85th perentile, or weight.120% of ideal for height) Plus any two of the following risk fators: Family history of type 2 diabetes in first- or seond-degree relative Rae/ethniity (Native Amerian, Afrian Amerian, Latino, Asian Amerian, Paifi Islander) Signs of insulin resistane or onditions assoiated with insulin resistane (aanthosis nigrians, hypertension, dyslipidemia, polyysti ovary syndrome, or smallfor-gestational-age birth weight) Maternal history of diabetes or GDM during the hild s gestation Age of initiation: age 10 years or at onset of puberty, if puberty ours at a younger age Frequeny: every 3 years *Persons aged #18 years. GESTATIONAL DIABETES MELLITUS Reommendations Test for undiagnosed type 2 diabetes at the first prenatal visit in those with risk fators, using standard diagnosti riteria. B Test for GDM at 24 28 weeks of gestation in pregnant women not previously known to have diabetes. A Sreen women with GDM for persistent diabetes at 6 12 weeks postpartum, using the OGTT and linially appropriate nonpregnany diagnosti riteria. E WomenwithahistoryofGDM should have lifelong sreening for the development of diabetes or prediabetes at least every 3 years. B WomenwithahistoryofGDM found to have prediabetes should reeive lifestyle interventions or metformin to prevent diabetes. A Definition For many years, GDM was defined as any degree of gluose intolerane that was first reognized during pregnany (10), regardless of whether the ondition may have predated the pregnany or persisted after the pregnany. This definition failitated a uniform strategy for detetion and lassifiation of GDM, but it was limited by impreision. The ongoing epidemi of obesity and diabetes has led to more type 2 diabetes in women of hildbearing age, resulting in an inrease in the number of pregnant women with undiagnosed type 2 diabetes (38). Beause of the number of pregnant women with undiagnosed type 2 diabetes, it is reasonable to test women with risk fators for type 2 diabetes (Table 2.2) at their initial prenatal visit, using standard diagnosti riteria (Table 2.1). Women with diabetes in the first trimester would be lassified as having type 2 diabetes. GDM is diabetes diagnosed in the seond or third trimester of pregnany that is not learly overt diabetes. Diagnosis GDM arries risks for the mother and neonate. Not all adverse outomes are of equal linial importane. The Hyperglyemia and Adverse Pregnany Outome (HAPO) study (39), a large-sale (;25,000 pregnant women) multinational ohort study, demonstrated that risk of adverse maternal, fetal, and neonatal outomes ontinuously inreased as a funtion of maternal glyemia at 24 28 weeks, even within ranges previously onsidered normal for pregnany. For most ompliations, there was no threshold for risk. These results have led to areful reonsideration of the diagnosti riteria for GDM. GDM diagnosis (Table 2.5) an be aomplished with either of two strategies: 1. One-step 75-g OGTT or 2. Two-step approah with a 50-g (nonfasting) sreen followed by a 100-g OGTT for those who sreen positive Different diagnosti riteria will identify different degrees of maternal hyperglyemia and maternal/fetal risk, leading some experts to debate, and disagree on, optimal strategies for the diagnosis of GDM. One-Step Strategy In the 2011 Standards of Care (40), the ADA for the first time reommended that all pregnant women not known to have prior diabetes undergo a 75-g OGTT at 24 28 weeks of gestation, basedonareommendationoftheinternational Assoiation of the Diabetes and Pregnany Study Groups (IADPSG) (41). The IADPSG defined diagnosti ut points for GDM as the average gluose values (fasting, 1-h, and 2-h PG) in the HAPO study at whih odds for adverse outomes reahed 1.75 times the estimated odds of these outomes at the mean gluose levels of the study population. This one-step strategy was antiipated to signifiantly inrease the inidene of GDM (from 5 6% to ;15 20%), primarily beause only one abnormal value, not two, beame suffiient to make the diagnosis. The ADA reognized that the antiipated inrease in the inidene of GDM would have signifiant impat on the osts, medial infrastruture apaity, and potential for inreased medialization of pregnanies previously ategorized as normal, but reommended these diagnosti riteria hanges in the ontext of worrisome worldwide inreases in obesity and diabetes rates with the intent of optimizing gestational outomes for women and their offspring. The expeted benefits to these pregnanies and offspring are inferred from intervention trials that foused on women with lower levels of hyperglyemia than identified using older GDM diagnosti riteria and that found modest benefits inluding redued rates of largefor-gestational-age births and preelampsia (42,43). It is important to note that 80 90% of women being treated for mild GDM in two randomized ontrolled trials (whose gluose values overlapped with the thresholds reommended by the IADPSG) ould be managed with lifestyle therapy alone. Data are laking on how the treatment of lower levels of hyperglyemia affets a mother s risk for the development of type 2 diabetes in the future and her offspring s riskfor obesity, diabetes, and other metaboli dysfuntion. Additional well-designed linial studies are needed to determine the optimal intensity of monitoring and treatment of women with GDM diagnosed by the one-step strategy. Two-Step Strategy In 2013, the National Institutes of Health (NIH) onvened a onsensus development onferene on diagnosing GDM. The 15-member panel had representatives from obstetris/gyneology, maternalfetal mediine, pediatris, diabetes researh, biostatistis, and other related fields to onsider diagnosti riteria (44). The panel reommended the two-step approah of sreening with a 1-h 50-g

S14 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 Table 2.5 Sreening for and diagnosis of GDM One-step strategy Perform a 75-g OGTT, with plasma gluose measurement when patient is fasting and at 1 and 2h,at24 28 weeks of gestation in women not previously diagnosed with overt diabetes. The OGTT should be performed in the morning after an overnight fast of at least 8 h. The diagnosis of GDM is made when any of the following plasma gluose values are met or exeeded: Fasting: 92 mg/dl (5.1 mmol/l) 1 h: 180 mg/dl (10.0 mmol/l) 2 h: 153 mg/dl (8.5 mmol/l) Two-step strategy Step 1: Perform a 50-g GLT (nonfasting), with plasma gluose measurement at 1 h, at 24 28 weeks of gestation in women not previously diagnosed with overt diabetes. If the plasma gluose level measured 1 h after the load is $140 mg/dl* (7.8 mmol/l), proeed to a 100-g OGTT. Step 2: The 100-g OGTT should be performed when the patient is fasting. The diagnosis of GDM is made if at least two of the following four plasma gluose levels (measured fasting and 1 h, 2 h, 3 h after the OGTT) are met or exeeded: Carpenter/Coustan (56) or NDDG (57) Fasting 95 mg/dl (5.3 mmol/l) 105 mg/dl (5.8 mmol/l) 1 h 180 mg/dl (10.0 mmol/l) 190 mg/dl (10.6 mmol/l) 2 h 155 mg/dl (8.6 mmol/l) 165 mg/dl (9.2 mmol/l) 3 h 140 mg/dl (7.8 mmol/l) 145 mg/dl (8.0 mmol/l) NDDG, National Diabetes Data Group. *The ACOG reommends a lower threshold of 135 mg/dl (7.5 mmol/l) in high-risk ethni populations with higher prevalene of GDM; some experts also reommend 130 mg/dl (7.2 mmol/l). gluose load test (GLT) followed by a 3-h 100-g OGTT for those who sreen positive, a strategy ommonly used in the U.S. Key fators reported in the NIH panel s deision-making proess were the lak of linial trial interventions demonstrating the benefits of the one-step strategy and the potential negative onsequenes of identifying a large new group of women with GDM, inluding medialization of pregnany with inreased interventions and osts. Moreover, sreening with a 50-g GLT does not require fasting and is therefore easier to aomplish for many women. Treatment of higher threshold maternal hyperglyemia, as identified by the two-step approah, redues rates of neonatal marosomia, large-for-gestational-age births, and shoulder dystoia, without inreasing small-for-gestational-age births (45). The Amerian College of Obstetriians and Gyneologists (ACOG) updated its guidelines in 2013 and supported the two-step approah (46). Future Considerations The onfliting reommendations from expert groups undersore the fat that there are data to support eah strategy. The deision of whih strategy to implement must therefore be made based on the relative values plaed on fators thathaveyettobemeasured(e.g.,ostbenefit estimation, willingness to hange pratie based on orrelation studies rather than linial intervention trial results, relative role of ost onsiderations, and available infrastruture loally, nationally, and internationally). As the IADPSG riteria have been adopted internationally, further evidene has emerged to support improved pregnany outomes with ost savings (47) and may be the preferred approah. In addition, pregnanies ompliated by GDM per IADPSG riteria, but not reognized as suh, have omparable outomes to pregnanies diagnosed as GDM by the more stringent two-step riteria (48). There remains strong onsensus that establishing a uniform approah to diagnosing GDM will benefit patients, aregivers, and poliymakers. Longer-term outome studies are urrently underway. MONOGENIC DIABETES SYNDROMES Monogeni defets that ause b-ell dysfuntion, suh as neonatal diabetes and MODY, represent a small fration of patients with diabetes (,5%). These forms of diabetes are frequently haraterized by onset of hyperglyemia at an early age (generally before age 25 years). Neonatal Diabetes Diabetes diagnosed in the first 6 months of life has been shown not to be typial autoimmune type 1 diabetes. This so-alled neonatal diabetes an either be transient or permanent. The most ommon geneti defet ausing transient disease is a defet on ZAC/HYAMI imprinting, whereas permanent neonatal diabetes is most ommonly a defet in the gene enoding the Kir6.2 subunit of the b-ell K ATP hannel. Diagnosing the latter has impliations, sine suh hildren an be well managed with sulfonylureas. Maturity-Onset Diabetes of the Young MODY is haraterized by impaired insulin seretion with minimal or no defets in insulin ation. It is inherited in an autosomal dominant pattern. Abnormalities at six geneti loi on different hromosomes have been identified to date. The most ommon form is assoiated with mutations on hromosome 12 in a hepati transription fator referred to as hepatoyte nulear fator (HNF)-1a. A seond form is assoiated with mutations in the gluokinase gene on hromosome 7p and results in a defetive gluokinase moleule. Gluokinase onverts gluose to gluose-6-phosphate, the metabolism of whih, in turn, stimulates insulin seretion by the b-ell. The less ommon forms of MODY result from mutations in other transription fators, inluding HNF-4a,HNF-1b, insulin promoter fator (IPF)-1, and NeuroD1. Diagnosis Readily available ommerial geneti testing now enables a true geneti diagnosis. It is important to orretly diagnose one of the monogeni forms of diabetes beause these hildren may be inorretly diagnosed with type 1 or type 2 diabetes, leading to suboptimal treatment regimens and delays in diagnosing other family members (49). The diagnosis of monogeni diabetes should be onsidered in hildren with the following findings: Diabetes diagnosed within the first 6 months of life Strong family history of diabetes but without typial features of type 2 diabetes (nonobese, low-risk ethni group)

are.diabetesjournals.org Position Statement S15 Mild fasting hyperglyemia (100 150 mg/dl [5.5 8.5 mmol/l]), espeially if young and nonobese Diabetes with negative autoantibodies and without signs of obesity or insulin resistane CYSTIC FIBROSIS RELATED DIABETES Reommendations Annual sreening for ysti fibrosis related diabetes (CFRD) with OGTT should begin by age 10 years in all patients with ysti fibrosis who do not have CFRD. B A1C as a sreening test for CFRD is not reommended. B Patients with CFRD should be treated with insulin to attain individualized glyemi goals. A In patients with ysti fibrosis and IGT without onfirmed diabetes, prandial insulin therapy should be onsidered to maintain weight. B Annual monitoring for ompliations of diabetes is reommended, beginning 5 years after the diagnosis of CFRD. E CFRD is the most ommon omorbidity in people with ysti fibrosis, ourring in about 20% of adolesents and 40 50% of adults. Diabetes in this population is assoiated with worse nutritional status, more severe inflammatory lung disease, and greater mortality from respiratory failure. Insulin insuffiieny related to partial fibroti destrution of the islet mass is the primary defet in CFRD. Genetially determined funtion of the remaining b-ells and insulin resistane assoiated with infetion and inflammation may also play a role. While sreening for diabetes before the age of 10 years an identify risk for progression to CFRD in those with abnormal gluose tolerane, there appears to be no benefit withrespet to weight, height, BMI, or lung funtion ompared with those with normal gluose tolerane,10 years of age. The use of ontinuous gluose monitoring may be more sensitive than OGTT to detet risk for progression to CFRD, but this likely needs more evidene. Enouraging data suggest that improved sreening (50,51) and aggressive insulin therapy have narrowed the gap in mortality between ysti fibrosis patients with and without diabetes and have eliminatedthesexdiffereneinmortality(52). Reent trials omparing insulin with oral repaglinide showed no signifiant differene between the groups. However, another study ompared three different groups: premeal insulin aspart, repaglinide, or oral plaebo in ysti fibrosis patients with abnormal gluose tolerane. Patients all had weight loss; however, in the insulin-treated group, this pattern was reversed, and they gained 0.39 (6 0.21) BMI units (P 5 0.02). Patients in the repaglinide-treated group had initial weight gain, but this was not sustained by 6 months. The plaebo group ontinued to lose weight (53). Insulin remains the most widely used therapy for CFRD (54). Reommendations for the linial management of CFRD an be found in the ADA position statement Clinial Care Guidelines for Cysti Fibrosis Related Diabetes: A Position Statement of the Amerian Diabetes Assoiation and a Clinial Pratie Guideline of the Cysti Fibrosis Foundation, Endorsed by the Pediatri Endorine Soiety (55). Referenes 1. Amerian Diabetes Assoiation. Diagnosis and lassifiation of diabetes mellitus. Diabetes Care 2014;37(Suppl. 1):S81 S90 2. The International Expert Committee. International Expert Committee report on the role of the A1C assay in the diagnosis of diabetes. Diabetes Care 2009;32:1327 1334 3. Nowika P, Santoro N, Liu H, et al. Utility of hemoglobin A 1 for diagnosing prediabetes and diabetes in obese hildren and adolesents. Diabetes Care 2011;34:1306 1311 4. Garía de Guadiana Romualdo L, González Morales M, Albaladejo Otón MD, et al. 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S16 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 assessing diabetes risk. Diabetes Care 2011;34: 1741 1748 25. Erikson SC, Le L, Zakharyan A, et al. Newonset treatment-dependent diabetes mellitus and hyperlipidemia assoiated with atypial antipsyhoti use in older adults without shizophrenia or bipolar disorder. J Am Geriatr So 2012;60:474 479 26. Knowler WC, Barrett-Connor E, Fowler SE, et al.; Diabetes Prevention Program Researh Group. Redution in the inidene of type 2 diabetes with lifestyle intervention or metformin. N Engl J Med 2002;346:393 403 27. Tuomilehto J, Lindström J, Eriksson JG, et al.; Finnish Diabetes Prevention Study Group. Prevention of type 2 diabetes mellitus by hanges in lifestyle among subjets with impaired gluose tolerane. N Engl J Med 2001; 344:1343 1350 28. Pan X-R, Li G-W, Hu Y-H, et al. Effets of diet and exerise in preventing NIDDM in people with impaired gluose tolerane: the Da Qing IGT and Diabetes Study. Diabetes Care 1997;20:537 544 29. Buhanan TA, Xiang AH, Peters RK, et al. Preservation of panreati b-ell funtion and prevention of type 2 diabetes by pharmaologial treatment of insulin resistane in high-risk Hispani women. Diabetes 2002;51:2796 2803 30. Chiasson J-L, Josse RG, Gomis R, Hanefeld M, Karasik A, Laakso M; STOP-NIDDM Trial Researh Group. Aarbose for prevention of type 2 diabetes mellitus: the STOP-NIDDM randomised trial. Lanet 2002;359:2072 2077 31. Gerstein HC, Yusuf S, Bosh J, et al.; DREAM (Diabetes REdution Assessment with ramipril and rosiglitazone Mediation) Trial Investigators. Effet of rosiglitazone on the frequeny of diabetes in patients with impaired gluose tolerane or impaired fasting gluose: a randomised ontrolled trial. Lanet 2006;368:1096 1105 32. Ramahandran A, Snehalatha C, Mary S, Mukesh B, Bhaskar AD, Vijay V; Indian Diabetes Prevention Programme (IDPP). 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J Adoles Health 2012;50:321 323 37. Wu E-L, Kazzi NG, Lee JM. Cost-effetiveness of sreening strategies for identifying pediatri diabetes mellitus and dysglyemia. JAMA Pediatr 2013;167:32 39 38. Lawrene JM, Contreras R, Chen W, Saks DA. Trends in the prevalene of preexisting diabetes and gestational diabetes mellitus among a raially/ethnially diverse population of pregnant women, 1999-2005. Diabetes Care 2008;31:899 904 39. Metzger BE, Lowe LP, Dyer AR, et al.; HAPO Study Cooperative Researh Group. Hyperglyemia and adverse pregnany outomes. N Engl J Med 2008;358:1991 2002 40. Amerian Diabetes Assoiation. Standards of medial are in diabetes 2011. Diabetes Care 2011;34(Suppl. 1):S11 S61 41. Metzger BE, Gabbe SG, Persson B, et al.; International Assoiation of Diabetes and Pregnany Study Groups Consensus Panel. International Assoiation of Diabetes and Pregnany Study Groups reommendations on the diagnosis and lassifiation of hyperglyemia in pregnany. Diabetes Care 2010;33:676 682 42. Landon MB, Spong CY, Thom E, et al.; Eunie Kennedy Shriver National Institute of Child Health and Human Development Maternal-Fetal Mediine Units Network. A multienter, randomized trial of treatment for mild gestational diabetes. N Engl J Med 2009;361: 1339 1348 43. Crowther CA, Hiller JE, Moss JR, MPhee AJ, Jeffries WS, Robinson JS; Australian Carbohydrate Intolerane Study in Pregnant Women (ACHOIS) Trial Group. Effet of treatment of gestational diabetes mellitus on pregnany outomes. N Engl J Med 2005;352: 2477 2486 44. Vandorsten JP, Dodson WC, Espeland MA, et al. NIH onsensus development onferene: diagnosing gestational diabetes mellitus. NIH Consens State Si Statements 2013;29:1 31 45. Horvath K, Koh K, Jeitler K, et al. Effets of treatment in women with gestational diabetes mellitus: systemati review and meta-analysis. BMJ 2010;340:1395 46. Committee on Pratie Bulletins Obstetris. Pratie Bulletin No. 137: gestational diabetes mellitus. Obstet Gyneol 2013;122:406 416 47. Duran A, Sáenz S, Torrejón MJ, et al. Introdution of IADPSG riteria for the sreening and diagnosis of gestational diabetes mellitus results in improved pregnany outomes at a lower ost in a large ohort of pregnant women: the St. Carlos Gestational Diabetes Study. Diabetes Care 2014;37: 2442 2450 48. Ethridge JK Jr, Catalano PM, Waters TP. Perinatal outomes assoiated with the diagnosis of gestational diabetes made by the International Assoiation of the Diabetes and Pregnany Study Groups riteria. Obstet Gyneol 2014;124:571 578 49. Hattersley A, Bruining J, Shield J, Njolstad P, Donaghue KC. The diagnosis and management of monogeni diabetes in hildren and adolesents. Pediatr Diabetes 2009;10(Suppl. 12):33 42 50. Kern AS, Prestridge AL. Improving sreening for ysti fibrosis-related diabetes at a pediatri ysti fibrosis program. Pediatris 2013;132: e512 e518 51. Waugh N, Royle P, Craigie I, et al. Sreening for ysti fibrosis-related diabetes: a systemati review. Health Tehnol Assess 2012; 16:iii iv, 1 179 52. Moran A, Dunitz J, Nathan B, Saeed A, Holme B, Thomas W. Cysti fibrosis-related diabetes: urrent trends in prevalene, inidene, and mortality. Diabetes Care 2009;32:1626 1631 53. MoranA,PekowP,GroverP,etal.;Cysti Fibrosis Related Diabetes Therapy Study Group. Insulin therapy to improve BMI in ysti fibrosisrelated diabetes without fasting hyperglyemia: results of the ysti fibrosis related diabetes therapy trial. Diabetes Care 2009;32:1783 1788 54. Onady GM, Stolfi A. Insulin and oral agents for managing ysti fibrosis-related diabetes. Cohrane Database Syst Rev 2013;7: CD004730 55. Moran A, Brunzell C, Cohen RC, et al.; CFRD Guidelines Committee. Clinial are guidelines for ysti fibrosis-related diabetes: a position statement of the Amerian Diabetes Assoiation and a linial pratie guideline of the Cysti Fibrosis Foundation, endorsed by the Pediatri Endorine Soiety. Diabetes Care 2010;33: 2697 2708 56. Carpenter MW, Coustan DR. 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Diabetes Care Volume 38, Supplement 1, January 2015 S17 3. Initial Evaluation and Diabetes Management Planning Amerian Diabetes Assoiation Diabetes Care 2015;38(Suppl. 1):S17 S19 DOI: 10.2337/d15-S006 MEDICAL EVALUATION Reommendation Consider sreening those with type 1 diabetes for autoimmune diseases (e.g., thyroid dysfuntion, elia disease) as appropriate. E A omplete medial evaluation should be performed at the initial visit to 1. Classify diabetes 2. Detet diabetes ompliations 3. Review previous treatment and risk fator ontrol in patients with established diabetes 4. Assist in formulating a management plan 5. Provide a basis for ontinuing are Laboratory tests appropriate to the evaluation of eah patient s medial ondition should be ompleted. A fous on the omponents of omprehensive are (Table 3.1) will enable the health are team to optimally manage the patient with diabetes. Adults who develop type 1 diabetes an develop additional autoimmune disorders, although their risk is lower than that in hildren and adolesents with type 1 diabetes. For additional details on autoimmune onditions, see Setion 11. Children and Adolesents. POSITION STATEMENT MANAGEMENT PLAN People with diabetes should reeive medial are from a ollaborative, integrated team with expertise in diabetes. This team may inlude physiians, nurse pratitioners, physiian s assistants, nurses, dietitians, pharmaists, and mental health professionals. Individuals with diabetes must also assume an ative role in their are. The management plan should be written with input from the patient and family, the physiian, and other members of the health are team. Diabetes self-management eduation (DSME) and ongoing diabetes support should be integral omponents of the management plan. Various strategies and tehniques should be used to enable patients to self-manage diabetes, inluding providing eduation on problem-solving skills for all aspets of diabetes management. Treatment goals and plans should be individualized and take patient preferenes into aount. In developing the plan, onsideration should be given to the patient s age, shool/work shedule and onditions, physial ativity, eating patterns, soial situation, ultural fators, presene of diabetes ompliations, health priorities, and other medial onditions. COMMON COMORBID CONDITIONS Reommendation Consider assessing for and addressing ommon omorbid onditions (e.g., depression, obstrutive sleep apnea) that may ompliate diabetes management. B Improved disease prevention and treatment effiay means that patients with diabetes are living longer, often with multiple omorbidities requiring ompliated medial regimens (1). Obesity, hypertension, and dyslipidemia are the most ommonly appreiated omorbidities. However, onurrent onditions, suh as heart Suggested itation: Amerian Diabetes Assoiation. Initial evaluation and diabetes management planning. Se. 3. In Standards of Medial Care in Diabetesd2015. Diabetes Care 2015;38 (Suppl. 1):S17 S19 2015 by the Amerian Diabetes Assoiation. Readers may use this artile as long as the work is properly ited, the use is eduational and not for profit, and the work is not altered.

S18 Position Statement Diabetes Care Volume 38, Supplement 1, January 2015 Table 3.1 Components of the omprehensive diabetes evaluation Medial history Age and harateristis of onset of diabetes (e.g., DKA, asymptomati laboratory finding) Eating patterns, physial ativity habits, nutritional status, and weight history; growth and development in hildren and adolesents Presene of ommon omorbidities, psyhosoial problems, and dental disease Diabetes eduation history Review of previous treatment regimens and response to therapy (A1C reords) Current treatment of diabetes, inluding mediations, mediation adherene and barriers thereto, meal plan, physial ativity patterns, and readiness for behavior hange Results of gluose monitoring and patient s use of data DKA frequeny, severity, and ause Hypoglyemi episodes Hypoglyemia awareness Any severe hypoglyemia: frequeny and ause History of diabetes-related ompliations Mirovasular: retinopathy, nephropathy, neuropathy (sensory, inluding history of foot lesions; autonomi, inluding sexual dysfuntion and gastroparesis) Marovasular: oronary heart disease, erebrovasular disease, and peripheral arterial disease Physial examination Height, weight, BMI Blood pressure determination, inluding orthostati measurements when indiated Fundosopi examination Thyroid palpation Skin examination (for aanthosis nigrians and insulin injetion sites) Comprehensive foot examination Inspetion Palpation of dorsalis pedis and posterior tibial pulses Presene/absene of patellar and Ahilles reflexes Determination of proprioeption, vibration, and monofilament sensation Laboratory evaluation A1C, if results not available within past 3 months If not performed/available within past year Fasting lipid profile, inluding total, LDL, and HDL holesterol and triglyerides, as needed Liver funtion tests Test for urine albumin exretion with spot urine albumin-to-reatinine ratio Serum reatinine and alulated glomerular filtration rate TSH in type 1 diabetes, dyslipidemia, or women over age 50 years Referrals Eye are professional for annual dilated eye exam Family planning for women of reprodutive age Registered dietitian for medial nutrition therapy DSME/DSMS Dentist for omprehensive periodontal examination Mental health professional, if needed DKA, diabeti ketoaidosis; DSMS, diabetes self-management support; TSH, thyroid-stimulating hormone. failure, depression, anxiety, and arthritis, are found at higher rates in people with diabetes than in age-mathed people without diabetes and often ompliate diabetes management. These onurrent onditions present linial hallenges relatedtopolypharmay,prevalent symptoms, and omplexity of are (2 5). Depression As disussed in Setion 4. Foundations of Care, depression, anxiety, and other mental health symptoms are highly prevalent in people with diabetes and are assoiated with worse outomes. Obstrutive Sleep Apnea Age-adjusted rates of obstrutive sleep apnea, a risk fator for ardiovasular disease, are signifiantly higher (4- to 10-fold) with obesity, espeially with entral obesity, in men and women (6). The prevalene in general populations with type 2 diabetes may be up to 23% (7) and in obese partiipants enrolled in the Look AHEAD trial exeeded 80% (8). Treatment of sleep apnea signifiantly improves quality of life and blood pressure ontrol. The evidene for a treatment effet on glyemi ontrol is mixed (9). Fatty Liver Disease Unexplained elevations of hepati transaminase onentrations are signifiantly assoiated with higher BMI, waist irumferene, triglyerides, and fasting insulin and with lower HDL holesterol. In a prospetive analysis, diabetes was signifiantly assoiated with inident nonaloholi hroni liver disease and with hepatoellular arinoma (10). Interventions that improve metaboli abnormalities in patients with diabetes (weight loss, glyemi ontrol, and treatment with speifi drugs for hyperglyemia or dyslipidemia) are also benefiial for fatty liver disease (11). Caner Diabetes (possibly only type 2 diabetes) is assoiated with inreased risk of aners of the liver, panreas, endometrium, olon/retum, breast, and bladder (12). The assoiation may result from shared risk fators between type 2 diabetes and aner (obesity, older age, and physial inativity), but may also be due to hyperinsulinemia or hyperglyemia (13). Patients with diabetes should be enouraged to undergo reommended age- and sex-appropriate aner sreenings and to redue their modifiable aner risk fators (obesity, smoking, and physial inativity). Fratures Age-mathed hip frature risk is signifiantlyinreasedinbothtype1(summary relative risk [RR] 6.3) and type 2 diabetes (summary RR 1.7) in both sexes (14). Type 1 diabetes is assoiated with osteoporosis, but in type 2 diabetes an inreased risk of hip frature is seen despite higher bone mineral density (BMD) (15). In three large observational studies of older adults, femoral nek BMD T sore and the WHO Frature Risk Algorithm (FRAX) sore were assoiated with hip and nonspine frature, although frature risk was higher in partiipants with diabetes ompared with those without diabetes for a given T sore and age or for a given FRAX sore (16). It is appropriate to assess frature history and risk fators in older patients with diabetes and reommend BMD testing if appropriate for the patient s age and sex. Prevention strategies are the same as for the general population. For type 2 diabeti patients with frature risk fators, avoiding thiazolidinediones is warranted.

are.diabetesjournals.org Position Statement S19 Cognitive Impairment Diabetes is assoiated with a signifiantly inreased risk, and rate, of ognitive deline and with inreased risk of dementia (17,18). In a 15-year prospetive study of ommunity-dwelling people over the age of 60 years, the presene of diabetes at baseline signifiantly inreased the age- and sexadjusted inidene of all-ause dementia, Alzheimer disease, and vasular dementiaomparedwithratesinthosewith normal gluose tolerane (19). In a substudy of the Ation to Control Cardiovasular Risk in Diabetes (ACCORD) linial trial, there were no differenes in ognitive outomes between intensive and standard glyemi ontrol, although there was signifiantly less of a derement in total brain volume, as measured by MRI, in partiipants in the intensive arm (20). The effets of hyperglyemia and insulin on the brain are areas of intense researh interest. Low Testosterone in Men Mean levels of testosterone are lower in menwithdiabetesomparedwithagemathed men without diabetes, but obesity is a major onfounder (21). Treatment in asymptomati men is ontroversial. The evidene that testosterone replaement affets outomes is mixed, and reent guidelines suggest that testing and treating men without symptoms are not reommended (22). Periodontal Disease Periodontal disease is more severe, but not neessarily more prevalent, in patients with diabetes than in those without (23). Current evidene suggests that periodontal disease adversely affets diabetes outomes, although evidene for treatment benefits remains ontroversial (5). Hearing Impairment Hearing impairment, both in high frequeny and low/mid frequeny ranges, is more ommon in people with diabetes than in those without, perhaps due to neuropathy and/or vasular disease. In a National Health and Nutrition Examination Survey (NHANES) analysis, hearing impairment was about twie as prevalent in people with diabetes ompared with those without, after adjusting for age and other risk fators for hearing impairment (24). Referenes 1. Selvin E, Coresh J, Branati FL. The burden and treatment of diabetes in elderly individuals in the U.S. Diabetes Care 2006;29:2415 2419 2. Grant RW, Ashburner JM, Hong CS, Chang Y, Barry MJ, Atlas SJ. Defining patient omplexity from the primary are physiian s perspetive: a ohort study. Ann Intern Med 2011;155: 797 804 3. Tinetti ME, Fried TR, Boyd CM. Designing health are for the most ommon hroni onditiondmultimorbidity. JAMA 2012;307: 2493 2494 4. Sudore RL, Karter AJ, Huang ES, et al. Symptom burden of adults with type 2 diabetes aross the disease ourse: Diabetes & Aging Study. J Gen Intern Med 2012;27:1674 1681 5. Borgnakke WS, Ylöstalo PV, Taylor GW, Geno RJ. Effet of periodontal disease on diabetes: systemati review of epidemiologi observational evidene. J Periodontol 2013; 84(Suppl.):S135 S152 6. Li C, Ford ES, Zhao G, Croft JB, Balluz LS, Mokdad AH. Prevalene of self-reported linially diagnosed sleep apnea aording to obesity status in men and women: National Health and Nutrition Examination Survey, 2005-2006. Prev Med 2010;51:18 23 7. West SD, Nioll DJ, Stradling JR. Prevalene of obstrutive sleep apnoea in men with type 2 diabetes. Thorax 2006;61:945 950 8. Foster GD, Sanders MH, Millman R, et al.; Sleep AHEAD Researh Group. Obstrutive sleep apnea among obese patients with type 2 diabetes. Diabetes Care 2009;32:1017 1019 9. Shaw JE, Punjabi NM, Wilding JP, Alberti KGMM, Zimmet PZ; International Diabetes Federation Taskfore on Epidemiology and Prevention. Sleep-disordered breathing and type 2 diabetes: a report from the International Diabetes Federation Taskfore on Epidemiology and Prevention. Diabetes Res Clin Prat 2008;81:2 12 10. El-Serag HB, Tran T, Everhart JE. Diabetes inreases the risk of hroni liver disease and hepatoellular arinoma. Gastroenterology 2004;126:460 468 11. Amerian Gastroenterologial Assoiation. Amerian Gastroenterologial Assoiation medial position statement: nonaloholi fatty liver disease. Gastroenterology 2002;123:1702 1704 12. Suh S, Kim KW. Diabetes and aner: is diabetes ausally related to aner? Diabetes Metab J 2011;35:193 198 13. Giovannui E, Harlan DM, Arher MC, et al. Diabetes and aner: a onsensus report. Diabetes Care 2010;33:1674 1685 14. Janghorbani M, Van Dam RM, Willett WC, Hu FB. Systemati review of type 1 and type 2 diabetes mellitus and risk of frature. Am J Epidemiol 2007;166:495 505 15. Vestergaard P. Disrepanies in bone mineral density and frature risk in patients with type 1 and type 2 diabetesda meta-analysis. Osteoporos Int 2007;18:427 444 16. Shwartz AV, Vittinghoff E, Bauer DC, et al.; Study of Osteoporoti Fratures (SOF) Researh Group; Osteoporoti Fratures in Men (MrOS) Researh Group; Health, Aging, and Body Composition (Health ABC) Researh Group. Assoiation of BMD and FRAX sore with risk of frature in older adults with type 2 diabetes. JAMA 2011;305:2184 2192 17. Cukierman T, Gerstein HC, Williamson JD. Cognitive deline and dementia in diabetesd systemati overview of prospetive observational studies. Diabetologia 2005;48:2460 2469 18. Biessels GJ, Staekenborg S, Brunner E, Brayne C, Sheltens P. Risk of dementia in diabetes mellitus: a systemati review. Lanet Neurol 2006;5:64 74 19. Ohara T, Doi Y, Ninomiya T, et al. Gluose tolerane status and risk of dementia in the ommunity: the Hisayama study. Neurology 2011;77:1126 1134 20. Launer LJ, Miller ME, Williamson JD, et al.; ACCORD MIND investigators. Effets of intensive gluose lowering on brain struture and funtion in people with type 2 diabetes (ACCORD MIND): a randomised open-label substudy. Lanet Neurol 2011;10:969 977 21. Dhindsa S, Miller MG, MWhirter CL, et al. Testosterone onentrations in diabeti and nondiabeti obese men. Diabetes Care 2010; 33:1186 1192 22. Bhasin S, Cunningham GR, Hayes FJ, et al. Testosterone therapy in men with androgen defiieny syndromes: an Endorine Soiety linial pratie guideline. J Clin Endorinol Metab 2010;95:2536 2559 23. Khader YS, Dauod AS, El-Qaderi SS, Alkafajei A, Batayha WQ. Periodontal status of diabetis ompared with nondiabetis: a metaanalysis. J Diabetes Compliations 2006;20: 59 68 24. Bainbridge KE, Hoffman HJ, Cowie CC. Diabetes and hearing impairment in the United States: audiometri evidene from the National Health and Nutrition Examination Survey, 1999 to 2004. Ann Intern Med 2008;149:1 10