4. Comprehensive MedicalEvaluation and Assessment ofComorbidities: Standards ofMedical Care in Diabetesd2020Diabetes Care 2020;43(Suppl. 1):S37–S47 | https://doi.org/10.2337/dc20-S004

The American Diabetes Association (ADA) “Standards of Medical Care in Diabetes”includes the ADA’s current clinical practice recommendations and is intended to providethe components of diabetes care, general treatment goals and guidelines, and tools toevaluate quality of care. Members of the ADA Professional Practice Committee, amultidisciplinaryexpertcommittee(https://doi.org/10.2337/dc20-SPPC),areresponsiblefor updating the Standards of Care annually, or more frequently as warranted. For adetailed description of ADA standards, statements, and reports, as well as the evidence-grading system for ADA’s clinical practice recommendations, please refer to the StandardsofCareIntroduction(https://doi.org/10.2337/dc20-SINT).Readerswhowishtocommenton the Standards of Care are invited to do so at professional.diabetes.org/SOC.

PATIENT-CENTERED COLLABORATIVE CARE

Recommendations

4.1 A patient-centered communication style that uses person-centered andstrength-based language and active listening; elicits patient preferencesand beliefs; and assesses literacy, numeracy, and potential barriers tocare should be used to optimize patient health outcomes and health-relatedquality of life. B

4.2 Diabetes care should be managed by a multidisciplinary team that may drawfrom primary care physicians, subspecialty physicians, nurse practitioners,physician assistants, nurses, dietitians, exercise specialists, pharmacists,dentists, podiatrists, and mental health professionals. E

A successful medical evaluation depends on beneficial interactions between thepatient and the care team. The Chronic Care Model (1–3) (see Section 1 “ImprovingCare and Promoting Health in Populations,” https://doi.org/10.2337/dc20-S001)is a patient-centered approach to care that requires a close working relationshipbetween the patient and clinicians involved in treatment planning. People withdiabetes should receive health care from an interdisciplinary team that may includephysicians, nurse practitioners, physician assistants, nurses, dietitians, exercise special-ists, pharmacists, dentists, podiatrists, andmental healthprofessionals. Individualswithdiabetesmust assumean active role in their care. Thepatient, family or support people,physicians, and health care team should together formulate the management plan,which includes lifestyle management (see Section 5 “Facilitating Behavior Change andWell-being to Improve Health Outcomes,” https://doi.org/10.2337/dc20-S005).The goals of treatment for diabetes are to prevent or delay complications andoptimize

quality of life (Fig. 4.1). Treatment goals and plans should be created with patients based

Suggested citation: American Diabetes Associa-tion. 4. Comprehensive medical evaluation andassessment of comorbidities: Standards of Med-ical Care in Diabetesd2020. Diabetes Care2020;43(Suppl. 1):S37–S47

© 2020 by the American Diabetes Association.Readersmayuse this article as longas thework isproperly cited, the use is educational and not forprofit, and the work is not altered. More infor-mation is available at http://www.diabetesjournals.org/content/license.

American Diabetes Association

Diabetes Care Volume 43, Supplement 1, January 2020 S37

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on their individual preferences, values, andgoals. The management plan should takeinto account the patient’s age, cognitiveabilities, school/work schedule and con-ditions, health beliefs, support systems,eating patterns, physical activity, socialsituation, financial concerns, cultural fac-tors, literacy and numeracy (mathematicalliteracy), diabetes complications and du-ration of disease, comorbidities, healthpriorities, other medical conditions, pref-erences for care, and life expectancy. Var-ious strategies and techniques should beused to supportpatients’ self-managementefforts, including providing educationon problem-solving skills for all aspectsof diabetes management.Provider communication with patients

and families should acknowledge thatmultiple factors impact glycemic manage-ment but also emphasize that collabo-ratively developed treatment plans anda healthy lifestyle can significantly im-prove disease outcomes and well-being(4–7). Thus, the goal of provider-patientcommunication is to establish a collaborativerelationship and to assess and addressself-management barriers without blam-ing patients for “noncompliance” or

“nonadherence” when the outcomesof self-management are not optimal (8).The familiar terms “noncompliance” and“nonadherence” denote a passive, obe-dient role for a person with diabetes in“following doctor’s orders” that is at oddswith the active role people with diabetestake in directing the day-to-day decision-making, planning,monitoring, evaluation,andproblem-solving involved in diabetesself-management.Usinganonjudgmentalapproach that normalizes periodic lapsesin self-management may help minimizepatients’ resistance to reportingproblemswith self-management. Empathizing andusing active listening techniques, such asopen-ended questions, reflective state-ments, and summarizing what the patientsaid, can help facilitate communication.Patients’ perceptions about their ownability, or self-efficacy, to self-managediabetes are one important psychosocialfactor related to improved diabetes self-management and treatment outcomes indiabetes (9–13) and should be a target ofongoing assessment, patient education,and treatment planning.

Language has a strong impact on percep-tions and behavior. The use of empowering

language in diabetes care and educationcan help to inform and motivate people,yet language that shames and judgesmayundermine this effort. The American Diabe-tes Association (ADA) and the AmericanAssociation of Diabetes Educators consen-sus report, “TheUseof Language inDiabetesCare and Education,” provides the authors’expertopinionregarding theuseof languageby health care professionals when speakingor writing about diabetes for people withdiabetes or for professional audiences (14).Although further research is needed to ad-dress the impact of language on diabetesoutcomes, the report includes five keyconsensus recommendations for lan-guage use:

c Use language that is neutral, nonjudg-mental, and based on facts, actions, orphysiology/biology.

c Use language free from stigma.c Use languagethat is strengthbased, respect-

ful, and inclusive and that imparts hope.c Use language that fosters collabora-

tion between patients and providers.c Use language that is person centered

(e.g., “person with diabetes” is pre-ferred over “diabetic”).

Figure 4.1—Decision cycle for patient-centered glycemic management in type 2 diabetes. Reprinted from Davies et al. (99).

S38 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 43, Supplement 1, January 2020

COMPREHENSIVE MEDICALEVALUATION

Recommendations

4.3 A complete medical evaluationshould be performed at the initialvisit to:

c Confirm thediagnosis and classifydiabetes. B

c Evaluate for diabetes complica-tions and potential comorbidconditions. B

c Review previous treatment andrisk factor control in patientswithestablished diabetes. B

c Begin patient engagement in theformulation of a care manage-ment plan. B

c Developaplan for continuingcare.B4.4 A follow-up visit should include

most components of the initialcomprehensive medical evalua-tion, including intervalmedical his-tory, assessment of medication-taking behavior and intolerance/side effects, physical examination,laboratory evaluation as appro-priate to assess attainment ofA1C and metabolic targets, andassessment of risk for complica-tions, diabetes self-managementbehaviors, nutrition, psychosocialhealth, and the need for referrals,immunizations, or other routinehealth maintenance screening. B

4.5 Ongoing management shouldbe guided by the assessmentof diabetes complications andshared decision-making to settherapeutic goals. B

4.6 The 10-year risk of a first atheroscle-rotic cardiovascular disease eventshould be assessed using the race-andsex-specificPooledCohortEqua-tionstobetterstratifyatheroscleroticcardiovascular disease risk. B

The comprehensive medical evalua-tion includes the initial and follow-upevaluations, assessment of complica-tions, psychosocial assessment, manage-ment of comorbid conditions, andengagement of the patient throughouttheprocess.Whilea comprehensive list isprovided in Table 4.1, in clinical practicethe provider may need to prioritize thecomponents of the medical evaluationgiven the available resources and time.The goal is to provide the health careteam information so it can optimally

support a patient. In addition to themedical history, physical examination,and laboratory tests, providers shouldassess diabetes self-management behav-iors, nutrition, and psychosocial health (seeSection5 “FacilitatingBehavior Change andWell-beingtoImproveHealthOutcomes,”https://doi.org/10.2337/dc20-S005) andgiveguidanceon routine immunizations.The assessment of sleep pattern andduration should be considered; a recentmeta-analysis found that poor sleepquality, short sleep, and long sleepwere associated with higher A1C inpeople with type 2 diabetes (15). In-terval follow-up visits should occur atleast every 3–6 months, individualizedto the patient, and then annually.

Lifestyle management and psychoso-cial care are the cornerstones of diabetesmanagement. Patients should be re-ferred for diabetes self-management ed-ucation and support, medical nutritiontherapy, and assessment of psychosocial/emotional health concerns if indicated.Patients should receive recommendedpreventive care services (e.g., immuniza-tions, cancer screening, etc.); smokingcessation counseling; and ophthalmolog-ical, dental, and podiatric referrals.

The assessment of risk of acute andchronic diabetes complications and treat-ment planning are key components ofinitial and follow-upvisits (Table4.2). Therisk of atherosclerotic cardiovasculardisease and heart failure (Section 10“Cardiovascular Disease and Risk Man-agement,”https://doi.org/10.2337/dc20-S010), chronic kidney disease staging(Section 11 “Microvascular Complica-tions and Foot Care,” https://doi.org/10.2337/dc20-S011), and risk of treatment-associated hypoglycemia (Table 4.3)should be used to individualize targetsforglycemia(Section6“GlycemicTargets,”https://doi.org/10.2337/dc20-S006), bloodpressure, and lipids and to select specificglucose-lowering medication (Section9 “PharmacologicApproachestoGlycemicTreatment,” https://doi.org/10.2337/dc20-S009), antihypertension medication, andstatin treatment intensity.

Additional referrals should be arrangedas necessary (Table 4.4). Clinicians shouldensure that individuals with diabetes areappropriately screened for complicationsand comorbidities. Discussing and imple-menting an approach to glycemic controlwith thepatient is apart,not the sole goal,of the patient encounter.

Immunizations

Recommendations

4.7 Provide routinely recommen-ded vaccinations for childrenand adults with diabetes as in-dicated by age. C

4.8 Annual vaccination against in-fluenza is recommended for allpeople $6 months of age, es-pecially those with diabetes. C

4.9 Vaccination against pneumo-coccal disease, including pneu-mococcal pneumonia, with13-valent pneumococcal conju-gate vaccine (PCV13) is recom-mended for children before age2 years. People with diabetesages 2 through 64 years shouldalso receive 23-valent pneumo-coccal polysaccharide vaccine(PPSV23). At age $65 years,regardless of vaccination his-tory, additional PPSV23 vacci-nation is necessary. C

4.10 Administer a 2- or 3-dose seriesof hepatitis B vaccine, depend-ing on the vaccine, to unvacci-nated adults with diabetes ages18 through 59 years. C

4.11 Consider administering a3-doseseries of hepatitis B vaccine tounvaccinated adults withdiabetes $60 years of age. C

Children and adults with diabetes shouldreceive vaccinations according to age-appropriate recommendations (16,17). TheCenters for Disease Control and Prevention(CDC) provides vaccination schedulesspecifically for children, adolescents, andadults with diabetes at cdc.gov/vaccines/schedules/.

People with diabetes are at higher riskfor hepatitis B infection and are morelikely to develop complications from in-fluenza and pneumococcal disease. TheCDCAdvisoryCommitteeon ImmunizationPractices (ACIP) recommends influenza,pneumococcal, and hepatitis B vaccina-tions specifically for people with diabetes.Vaccinations against tetanus-diphtheria-pertussis, measles-mumps-rubella, humanpapillomavirus, and shingles are also im-portantforadultswithdiabetes,as theyarefor the general population.

Influenza

Influenza is a common, preventable in-fectious disease associated with high

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Continued on p. S41

S40 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 43, Supplement 1, January 2020

mortality and morbidity in vulnerablepopulations, including youth, olderadults, and people with chronic dis-eases. Influenza vaccination in peoplewith diabetes has been found to sig-nificantly reduce influenza and diabe-tes-related hospital admissions (18).

Pneumococcal Pneumonia

Like influenza, pneumococcal pneumo-nia is a common, preventable disease.Peoplewith diabetes are at increased riskfor the bacteremic form of pneumococ-cal infection and have been reported tohaveahigh riskofnosocomialbacteremia,

with a mortality rate as high as 50% (19).The ADA endorses recommendations fromthe CDC ACIP that adults age $65 years,who are at higher risk for pneumococcaldisease, receive an additional 23-valentpneumococcal polysaccharide vaccine(PPSV23), regardlessofpriorpneumococcalvaccination history. See detailed recom-mendations atwww.cdc.gov/vaccines/hcp/acip-recs/vacc-specific/pneumo.html.

Hepatitis B

Compared with the general population,people with type 1 or type 2 diabeteshave higher rates of hepatitis B. This may

be due to contact with infected blood orthrough improper equipment use (glucosemonitoring devices or infected needles).Because of the higher likelihood of trans-mission, hepatitis B vaccine is recommen-ded for adultswith diabetes age,60 years.Foradultsage$60years,hepatitisBvaccinemaybeadministeredat thediscretionof thetreating clinician based on the patient’slikelihood of acquiring hepatitis B infection.

ASSESSMENT OF COMORBIDITIES

Besides assessing diabetes-related com-plications, clinicians and their patients

care.diabetesjournals.org Comprehensive Medical Evaluation and Assessment of Comorbidities S41

need to be aware of common comorbid-ities that affect people with diabetes andmay complicate management (20–24).Diabetes comorbidities are conditionsthat affect people with diabetes moreoften than age-matched people withoutdiabetes. This section discusses many ofthe common comorbidities observed inpatients with diabetes but is not neces-sarily inclusive of all the conditions thathave been reported.

Autoimmune Diseases

Recommendations

4.12 Patients with type 1 diabetesshould be screened for autoim-mune thyroid disease soon af-ter diagnosis and periodicallythereafter. B

4.13 Adult patients with type 1 di-abetes should be screened forceliac disease in the presence ofgastrointestinal symptoms, signs,or laboratorymanifestations sug-gestive of celiac disease. B

People with type 1 diabetes are at in-creased risk for other autoimmune

diseases, with thyroid disease, celiac dis-ease, and pernicious anemia (vitamin B12deficiency) being among themost common(25). Other associated conditions includeautoimmune hepatitis, primary adrenal in-sufficiency (Addisondisease), dermatomyo-sitis, andmyasthenia gravis (26–29). Type 1diabetes may also occur with other auto-immune diseases in the context of specificgenetic disorders or polyglandular autoim-mune syndromes (30). Given the high prev-alence, nonspecific symptoms, andinsidious onset of primary hypothyroidism,routine screening for thyroid dysfunction isrecommended for all patients with type 1diabetes.Screeningforceliacdiseaseshouldbe considered in adult patients with sug-gestive symptoms (e.g., diarrhea, malab-sorption, abdominal pain) or signs (e.g.,osteoporosis, vitamin deficiencies, iron de-ficiency anemia) (31,32). Measurement ofvitamin B12 levels should be considered forpatientswithtype1diabetesandperipheralneuropathy or unexplained anemia.

CancerDiabetes is associated with increasedrisk of cancers of the liver, pancreas,

endometrium, colon/rectum, breast,and bladder (33). The association mayresult from shared risk factors betweentype 2 diabetes and cancer (older age,obesity, and physical inactivity) but mayalso be due to diabetes-related factors(34), such as underlying disease physiol-ogy or diabetes treatments, althoughevidence for these links is scarce.Patientswith diabetes should be encouraged toundergo recommended age- and sex-appropriate cancer screenings and toreduce their modifiable cancer risk fac-tors (obesity, physical inactivity, andsmoking). New onset of atypical diabetes(lean body habitus, negative family his-tory) in a middle-aged or older patientmay precede the diagnosis of pancreaticadenocarcinoma (35). However, in theabsence of other symptoms (e.g., weightloss, abdominal pain), routine screen-ing of all such patients is not currentlyrecommended.

Cognitive Impairment/Dementia

Recommendation

4.14 In the presence of cognitive im-pairment, diabetes treatment regi-mensshouldbesimplifiedasmuchas possible and tailored to min-imize the risk of hypoglycemia.B

Diabetes is associated with a signifi-cantly increased risk and rate of cogni-tive decline and an increased risk ofdementia (36,37). A recent meta-analysisof prospective observational studies inpeople with diabetes showed 73% in-creased risk of all types of dementia,56% increased risk of Alzheimer demen-tia, and 127% increased risk of vasculardementia compared with individualswithout diabetes (38). The reverse isalso true: people with Alzheimer de-mentia are more likely to develop di-abetes than people without Alzheimerdementia. In a 15-year prospectivestudy of community-dwelling people.60 years of age, the presence of di-abetes at baseline significantly increasedthe age- and sex-adjusted incidence ofall-cause dementia, Alzheimer dementia,and vascular dementia compared withrates in those with normal glucose tol-erance (39).

Hyperglycemia

In those with type 2 diabetes, the de-gree and duration of hyperglycemia are

Table 4.2—Assessment and treatment plan*

Assessing risk of diabetes complicationsc ASCVD and heart failure historyc ASCVD risk factors and 10-year ASCVD risk assessmentc Staging of chronic kidney disease (see Table 11.1)c Hypoglycemia risk (Table 4.3)

Goal settingc Set A1C/blood glucose targetc If hypertension is present, establish blood pressure targetc Diabetes self-management goals

Therapeutic treatment plansc Lifestyle managementc Pharmacologic therapy: glucose loweringc Pharmacologic therapy: cardiovascular disease risk factors and renalc Use of glucose monitoring and insulin delivery devicesc Referral to diabetes education and medical specialists (as needed)

ASCVD, atherosclerotic cardiovascular disease. *Assessment and treatment planning are essentialcomponents of initial and all follow-up visits.

Table 4.3—Assessment of hypoglycemia riskFactors that increase risk of treatment-associated hypoglycemia

c Use of insulin or insulin secretagogues (i.e., sulfonylureas, meglitinides)c Impaired kidney or hepatic functionc Longer duration of diabetesc Frailty and older agec Cognitive impairmentc Impaired counterregulatory response, hypoglycemia unawarenessc Physical or intellectual disability that may impair behavioral response to hypoglycemiac Alcohol usec Polypharmacy (especially ACE inhibitors, angiotensin receptor blockers, nonselective b-blockers)

See references 100–104.

S42 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 43, Supplement 1, January 2020

related to dementia. More rapid cog-nitive decline is associated with bothincreased A1C and longer duration ofdiabetes (38). The Action to ControlCardiovascular Risk in Diabetes (ACCORD)study found that each 1% higher A1Clevel was associated with lower cog-nitive function in individuals withtype 2 diabetes (40). However, theACCORD study found no differencein cognitive outcomes in participantsrandomly assigned to intensive andstandard glycemic control, supportingthe recommendation that intensiveglucose control should not be advisedfor the improvement of cognitive func-tion in individuals with type 2 diabetes(41).

Hypoglycemia

In type 2 diabetes, severe hypoglycemiais associated with reduced cognitivefunction, and those with poor cognitivefunction have more severe hypoglyce-mia. In a long-term study of older pa-tients with type 2 diabetes, individualswith one or more recorded episodes ofsevere hypoglycemia had a stepwise in-crease in risk of dementia (42). Likewise,the ACCORD trial found that as cognitivefunction decreased, the risk of severehypoglycemia increased (43). Tailoringglycemic therapy may help to preventhypoglycemia in individuals with cogni-tive dysfunction.

Nutrition

In one study, adherence to the Mediter-ranean diet correlated with improvedcognitive function (44). However, a re-cent Cochrane review found insufficientevidence to recommend any dietarychange for the prevention or treatmentof cognitive dysfunction (45).

Statins

A systematic review has reported that datado not support an adverse effect of statinson cognition (46). TheU.S. FoodandDrugAdministration postmarketing surveil-lance databases have also revealed a

low reporting rate for cognitive-relatedadverse events, including cognitive dys-function or dementia, with statin ther-apy, similar to rates seen with othercommonly prescribed cardiovascularmedications (46). Therefore, fear ofcognitive decline should not be a bar-rier to statin use in individuals withdiabetes and a high risk for cardiovas-cular disease.

Nonalcoholic Fatty Liver Disease

Recommendation

4.15 Patients with type 2 diabetes orprediabetes and elevated liverenzymes (ALT) or fatty liver onultrasound should be evaluatedfor presence of nonalcoholic stea-tohepatitis and liver fibrosis. C

Diabetes is associated with the develop-ment of nonalcoholic fatty liver disease,including its more severe manifesta-tions of nonalcoholic steatohepatitis,liver fibrosis, cirrhosis, and hepatocel-lular carcinoma (47). Elevations of he-patic transaminase concentrations areassociated with higher BMI, waist cir-cumference, and triglyceride levels andlower HDL cholesterol levels. Noninva-sive tests, such as elastography or fibrosisbiomarkers, may be used to assess risk offibrosis, but referral to a liver specialistand liver biopsy may be required fordefinitive diagnosis (48). Interventionsthat improve metabolic abnormalitiesin patients with diabetes (weight loss,glycemic control, and treatment withspecific drugs for hyperglycemia or dyslip-idemia) are also beneficial for fatty liverdisease(49,50).PioglitazoneandvitaminEtreatment of biopsy-proven nonalcoholicsteatohepatitis have been shown to im-prove liver histology, but effects on longer-term clinical outcomes are not known(51,52). Treatment with liraglutide andwith sodium–glucose cotransporter 2 in-hibitors (dapagliflozin and empagliflozin)has also shown some promise in prelim-inary studies, although benefits may be

mediated, at least in part, by weight loss(53–55).

Hepatitis C InfectionInfection with hepatitis C virus (HCV) isassociated with a higher prevalence oftype 2 diabetes, which is present in up toone-third of individuals with chronic HCVinfection. HCV may impair glucose me-tabolism by several mechanisms, in-cluding directly via viral proteins andindirectly by altering proinflammatorycytokine levels (56). The use of newerdirect-acting antiviral drugs produces asustained virological response (cure) innearly all cases and has been reportedto improve glucose metabolism in in-dividuals with diabetes (57). A meta-analysis of mostly observational stud-ies found a mean reduction in A1Clevels of 0.45% (95% CI 20.60 to20.30) and reduced requirement forglucose-lowering medication use fol-lowing successful eradication of HCVinfection (58).

Pancreatitis

Recommendation

4.16 Islet autotransplantation shouldbe considered for patients re-quiring total pancreatectomyfor medically refractory chronicpancreatitis to prevent postsur-gical diabetes. C

Diabetes is linked to diseases of theexocrine pancreas such as pancreatitis,which may disrupt the global architec-ture or physiology of the pancreas, oftenresulting in both exocrine and endocrinedysfunction. Up to half of patients withdiabetes may have some degree of im-paired exocrine pancreas function (59).People with diabetes are at an approx-imately twofold higher risk of developingacute pancreatitis (60).

Conversely, prediabetes and/or diabe-tes has been found to develop in approx-imately one-third of patients after anepisode of acute pancreatitis (61); thus,the relationship is likely bidirectional.Postpancreatitis diabetes may includeeither new-onset disease or previouslyunrecognized diabetes (62). Studies ofpatients treated with incretin-based ther-apies for diabetes have also reported thatpancreatitis may occur more frequentlywith these medications, but results havebeen mixed (63,64).

Table 4.4—Referrals for initial care managementc Eye care professional for annual dilated eye exam

c Family planning for women of reproductive age

c Registered dietitian nutritionist for medical nutrition therapy

c Diabetes self-management education and support

c Dentist for comprehensive dental and periodontal examination

c Mental health professional, if indicated

care.diabetesjournals.org Comprehensive Medical Evaluation and Assessment of Comorbidities S43

Islet autotransplantation should beconsidered for patients requiring totalpancreatectomy for medically refractorychronic pancreatitis to prevent postsur-gical diabetes. Approximately one-thirdof patients undergoing total pancreatec-tomy with islet autotransplantation areinsulin free 1 year postoperatively, andobservational studies fromdifferent cen-ters have demonstrated islet graft func-tion up to a decade after the surgery insome patients (65–69). Both patient anddisease factors should be carefully con-sidered when deciding the indicationsand timing of this surgery. Surgeriesshould be performed in skilled facilitiesthat have demonstrated expertise in isletautotransplantation.

FracturesAge-specific hip fracture risk is signifi-cantly increased in both people withtype 1 diabetes (relative risk 6.3) andthose with type 2 diabetes (relative risk1.7) in both sexes (70). Type 1 diabetes isassociated with osteoporosis, but in type 2diabetes, an increased risk of hip fractureis seen despite higher bone mineral den-sity (BMD) (71). In three large observa-tional studies of older adults, femoral neckBMD T score and the World HealthOrganization Fracture Risk AssessmentTool (FRAX) score were associated withhip and nonspine fractures. Fracturerisk was higher in participants withdiabetes compared with those withoutdiabetes for a given T score and age orfor a given FRAX score (72). Providersshould assess fracture history and riskfactors in older patients with diabetesand recommend measurement of BMDif appropriate for the patient’s age andsex. Fracture prevention strategies forpeople with diabetes are the sameas for the general population and in-clude vitamin D supplementation. Forpatients with type 2 diabetes with fracturerisk factors, thiazolidinediones (73) andsodium–glucose cotransporter 2 inhibi-tors (74) should be used with caution.

Sensory ImpairmentHearing impairment, both in high-frequencyand low- to mid-frequency ranges, is morecommon in people with diabetes than inthose without, perhaps due to neuropathyand/or vascular disease. In aNational HealthandNutrition Examination Survey (NHANES)analysis, hearing impairment was about

twice as prevalent in people with diabetescompared with those without, afteradjusting for age and other risk factorsfor hearing impairment (75). Low HDL,coronary heart disease, peripheral neu-ropathy, and general poor health havebeen reported as risk factors for hearingimpairment for people with diabetes,but an association of hearing loss withblood glucose levels has not beenconsistently observed (76). In the Di-abetes Control and Complications Trial/Epidemiology of Diabetes Interventionsand Complications (DCCT/EDIC) cohort,time-weighted mean A1C was associatedwith increased risk of hearing impairmentwhen tested after long-term (.20 years)follow-up (77). Impairment in smell, butnot taste, has also been reported in in-dividuals with diabetes (78).

HIV

Recommendation

4.17 Patients with HIV should bescreened for diabetes and pre-diabetes with a fasting glucosetestbeforestartingantiretroviraltherapy, at the time of switchingantiretroviral therapy, and 3–6months after starting or switch-ing antiretroviral therapy. If ini-tial screening results are normal,fasting glucose should be checkedannually. E

Diabetes risk is increased with certainprotease inhibitors (PIs) and nucleosidereverse transcriptase inhibitors (NRTIs).New-onset diabetes is estimated tooccur in more than 5% of patientsinfected with HIV on PIs, whereasmore than 15% may have prediabetes(79). PIs are associated with insulinresistance and may also lead to apo-ptosis of pancreatic b-cells. NRTIs alsoaffect fat distribution (both lipohyper-trophy and lipoatrophy), which is asso-ciated with insulin resistance.

Individuals with HIV are at higher riskfor developing prediabetes and diabeteson antiretroviral (ARV) therapies, so ascreening protocol is recommended (80).The A1C test may underestimate glyce-mia in people with HIV; it is not recom-mended for diagnosis and may presentchallenges for monitoring (81). In thosewith prediabetes, weight loss throughhealthy nutrition and physical activitymay reduce the progression toward

diabetes. Among patients with HIVand diabetes, preventive health careusing an approach similar to that usedin patients without HIV is critical toreduce the risks of microvascular andmacrovascular complications.

ForpatientswithHIVandARV-associatedhyperglycemia, it may be appropriate toconsider discontinuing the problematicARV agents if safe and effective alter-natives are available (82). BeforemakingARV substitutions, carefully considerthe possible effect on HIV virologicalcontrol and the potential adverse ef-fects of new ARV agents. In some cases,antihyperglycemic agents may still benecessary.

Low Testosterone in Men

Recommendation

4.18 In men with diabetes who havesymptoms or signs of hypogo-nadism, such as decreased sex-ual desire (libido) or activity, orerectile dysfunction, considerscreening with a morning se-rum testosterone level. B

Mean levels of testosterone are lowerinmenwithdiabetes comparedwith age-matched men without diabetes, butobesity is a major confounder (83,84).Treatment in asymptomatic men is con-troversial. Testosterone replacement inmen with symptomatic hypogonadismmay have benefits including improvedsexual function, well-being, muscle massand strength, and bone density (85). Inmen with diabetes who have symp-toms or signs of low testosterone(hypogonadism), a morning total testos-terone level should be measured usingan accurate and reliable assay. In menwho have total testosterone levels closeto the lower limit, it is reasonable to checksex hormone–binding globulin, as it isoften low in diabetes andassociatedwithlower testosterone levels. Further test-ing (such as luteinizing hormone andfollicle-stimulating hormone levels) maybe needed to determine if the patienthas hypogonadism. Testosterone re-placement inoldermenwithhypogonad-ism has been associated with increasedcoronary artery plaque volume and, insome studies, an increase in cardiovas-cular events, which should be consideredwhen assessing the risks and benefits oftreatment (86,87).

S44 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 43, Supplement 1, January 2020

Obstructive Sleep ApneaAge-adjusted rates of obstructive sleepapnea, a risk factor for cardiovasculardisease, are significantly higher (4- to10-fold) with obesity, especially withcentral obesity (88). The prevalence ofobstructive sleep apnea in the popula-tion with type 2 diabetes may be as highas 23%, and the prevalence of any sleep-disordered breathing may be as high as58% (89,90). In obese participants en-rolled in theAction for Health in Diabetes(Look AHEAD) trial, it exceeded 80% (91).Patients with symptoms suggestive ofobstructive sleep apnea (e.g., excessivedaytime sleepiness, snoring, witnessedapnea) should be considered for screen-ing (92). Sleep apnea treatment (lifestylemodification, continuous positive airwaypressure, oral appliances, and surgery)significantly improves quality of life andblood pressure control. The evidencefor a treatment effect on glycemic con-trol is mixed (93).

Periodontal DiseasePeriodontal disease is more severe, andmay be more prevalent, in patients withdiabetes than in those without and hasbeen associated with higher A1C levels(94–96). Longitudinal studies suggestthat people with periodontal diseasehave higher rates of incident diabetes.Current evidence suggests that peri-odontal disease adversely affects diabe-tes outcomes, although evidence fortreatmentbenefits remains controversial(24,97). In a randomized clinical trial,intensive periodontal treatment wasassociated with better glycemic control(A1C 8.3% vs. 7.8% in control subjectsand the intensive-treatment group, re-spectively) and reduction in inflam-matory markers after 12 months offollow-up (98).

References1. Stellefson M, Dipnarine K, Stopka C. Thechronic care model and diabetes managementin US primary care settings: a systematic review.Prev Chronic Dis 2013;10:E262. Coleman K, Austin BT, Brach C, Wagner EH.Evidence on the Chronic Care Model in the newmillennium. Health Aff (Millwood) 2009;28:75–853. GabbayRA,BailitMH,MaugerDT,WagnerEH,Siminerio L. Multipayer patient-centered med-ical home implementation guided by the chroniccare model. Jt Comm J Qual Patient Saf 2011;37:265–2734. UKProspectiveDiabetesStudy (UKPDS)Group.Intensive blood-glucose control with sulphonylur-eas or insulin compared with conventional

treatment and risk of complications in patientswith type 2 diabetes (UKPDS 33). Lancet 1998;352:837–8535. NathanDM,GenuthS, Lachin J, etal.;DiabetesControl and Complications Trial Research Group.The effect of intensive treatment of diabetes onthe development and progression of long-termcomplications in insulin-dependent diabetesmellitus. N Engl J Med 1993;329:977–9866. Lachin JM, Genuth S, Nathan DM, Zinman B,Rutledge BN; DCCT/EDIC Research Group. Effectof glycemic exposure on the risk ofmicrovascularcomplications in the Diabetes Control and Com-plications Trialdrevisited. Diabetes 2008;57:995–10017. White NH, Cleary PA, Dahms W, Goldstein D,Malone J, TamborlaneWV; Diabetes Control andComplications Trial (DCCT)/Epidemiology of Di-abetes Interventions and Complications (EDIC)Research Group. Beneficial effects of intensivetherapy of diabetes during adolescence: out-comes after the conclusion of the DiabetesControl and Complications Trial (DCCT). J Pediatr2001;139:804–8128. Anderson RM, Funnell MM. Compliance andadherence are dysfunctional concepts in diabe-tes care. Diabetes Educ 2000;26:597–6049. Sarkar U, Fisher L, Schillinger D. Is self-efficacyassociated with diabetes self-managementacross race/ethnicity and health literacy? Dia-betes Care 2006;29:823–82910. King DK, Glasgow RE, Toobert DJ, et al. Self-efficacy,problemsolving, andsocial-environmentalsupport are associated with diabetes self-management behaviors. Diabetes Care 2010;33:751–75311. Nouwen A, Urquhart Law G, Hussain S,McGovern S, Napier H. Comparison of therole of self-efficacy and illness representationsin relation to dietary self-care and diabetesdistress in adolescents with type 1 diabetes.Psychol Health 2009;24:1071–108412. Beckerle CM, Lavin MA. Association of self-efficacy and self-care with glycemic control indiabetes. Diabetes Spectr 2013;26:172–17813. Iannotti RJ, SchneiderS,Nansel TR, et al. Self-efficacy, outcome expectations, and diabetesself-management in adolescents with type 1diabetes. J Dev Behav Pediatr 2006;27:98–10514. Dickinson JK,GuzmanSJ,MaryniukMD,et al.The use of language in diabetes care and edu-cation. Diabetes Care 2017;40:1790–179915. Lee SWH, Ng KY, Chin WK. The impact ofsleep amount and sleep quality on glycemiccontrol in type 2 diabetes: a systematic reviewand meta-analysis. Sleep Med Rev 2017;31:91–10116. RobinsonCL, Romero JR, KempeA, PellegriniC; Advisory Committee on Immunization Prac-tices (ACIP) Child/Adolescent ImmunizationWork Group. Advisory Committee on Immuni-zation Practices recommended immunizationschedule for children and adolescents aged18 years or younger – United States, 2017.MMWR Morb Mortal Wkly Rep 2017;66:134–13517. Kim DK, Riley LE, Harriman KH, Hunter P,Bridges CB. Advisory Committee on Immuniza-tion Practices recommended immunizationschedule for adults aged 19 years or older –United States, 2017. MMWR Morb Mortal WklyRep 2017;66:136–138

18. GoeijenbierM, van Sloten TT, Slobbe L, et al.Benefits of flu vaccination for persons with di-abetes mellitus: a review. Vaccine 2017;35:5095–510119. Smith SA, Poland GA. Use of influenza andpneumococcal vaccines in people with diabetes.Diabetes Care 2000;23:95–10820. Selvin E, Coresh J, Brancati FL. The burdenand treatment of diabetes in elderly individualsin the U.S. Diabetes Care 2006;29:2415–241921. Grant RW, Ashburner JM, Hong CS, Chang Y,Barry MJ, Atlas SJ. Defining patient complexityfrom the primary care physician’s perspective:a cohort study [published correction appears inAnn Intern Med 2012;157:152]. Ann Intern Med2011;155:797–80422. Tinetti ME, Fried TR, Boyd CM. Designinghealth care for the most common chronic con-ditiondmultimorbidity. JAMA 2012;307:2493–249423. Sudore RL, Karter AJ, Huang ES, et al. Symp-tomburden of adults with type 2 diabetes acrossthe disease course: diabetes & aging study.J Gen Intern Med 2012;27:1674–168124. Borgnakke WS, Ylostalo PV, Taylor GW,Genco RJ. Effect of periodontal disease on di-abetes: systematic review of epidemiologicobservational evidence. J Periodontol 2013;84(Suppl.):S135–S15225. Nederstigt C, Uitbeijerse BS, Janssen LGM,Corssmit EPM, de Koning EJP, Dekkers OM.Associated auto-immune disease in type 1 di-abetes patients: a systematic review and meta-analysis. Eur J Endocrinol 2019;180:135–14426. De Block CE, De Leeuw IH, Van Gaal LF. Highprevalence of manifestations of gastric autoim-munity in parietal cell antibody-positive type 1(insulin-dependent) diabetic patients. The Bel-gian Diabetes Registry. J Clin Endocrinol Metab1999;84:4062–406727. Triolo TM, Armstrong TK, McFann K, et al.Additional autoimmune disease found in 33% ofpatients at type 1 diabetes onset. Diabetes Care2011;34:1211–121328. Hughes JW, Riddlesworth TD, DiMeglio LA,Miller KM, Rickels MR, McGill JB; T1D ExchangeClinicNetwork. Autoimmunediseases in childrenand adults with type 1 diabetes from the T1DExchange Clinic Registry. J Clin EndocrinolMetab2016;101:4931–493729. Kahaly GJ, Hansen MP. Type 1 diabetesassociated autoimmunity. Autoimmun Rev 2016;15:644–64830. Eisenbarth GS, Gottlieb PA. Autoimmunepolyendocrine syndromes. N Engl J Med 2004;350:2068–207931. Rubio-Tapia A, Hill ID, Kelly CP, CalderwoodAH, Murray JA; American College of Gastroen-terology. ACG clinical guidelines: diagnosis andmanagement of celiac disease. Am J Gastro-enterol 2013;108:656–676; quiz 67732. Husby S, Murray JA, Katzka DA. AGA clinicalpractice update on diagnosis and monitoring ofceliac diseasedchanging utility of serology andhistologic measures: expert review. Gastroen-terology 2019;156:885–88933. Suh S, Kim K-W. Diabetes and cancer: isdiabetes causally related to cancer? DiabetesMetab J 2011;35:193–19834. Giovannucci E, Harlan DM, Archer MC, et al.Diabetes and cancer: a consensus report. CACancer J Clin 2010;60:207–221

care.diabetesjournals.org Comprehensive Medical Evaluation and Assessment of Comorbidities S45

35. Aggarwal G, Kamada P, Chari ST. Prevalenceof diabetes mellitus in pancreatic cancer com-pared to common cancers. Pancreas 2013;42:198–20136. Cukierman T, Gerstein HC, Williamson JD.Cognitive decline and dementia in diabetesdsystematic overview of prospective observa-tional studies. Diabetologia 2005;48:2460–246937. BiesselsGJ,StaekenborgS,BrunnerE,BrayneC,Scheltens P. Risk of dementia in diabetes mellitus:a systematic review. Lancet Neurol 2006;5:64–7438. Gudala K, Bansal D, Schifano F, Bhansali A.Diabetes mellitus and risk of dementia: a meta-analysis of prospective observational studies. JDiabetes Investig 2013;4:640–65039. Ohara T, Doi Y, Ninomiya T, et al. Glucosetolerance status and risk of dementia in thecommunity: the Hisayama study. Neurology2011;77:1126–113440. Cukierman-Yaffe T, Gerstein HC, WilliamsonJD, et al.; Action to Control Cardiovascular Risk inDiabetes-Memory in Diabetes (ACCORD-MIND)Investigators. Relationship between baselineglycemic control and cognitive function in indi-viduals with type 2 diabetes and other cardio-vascular risk factors: the Action to ControlCardiovascular Risk in Diabetes-Memory in Di-abetes (ACCORD-MIND) trial. Diabetes Care2009;32:221–22641. Launer LJ, Miller ME, Williamson JD, et al.;ACCORDMIND investigators. Effects of intensiveglucose lowering on brain structure and functionin people with type 2 diabetes (ACCORD MIND):a randomised open-label substudy. Lancet Neu-rol 2011;10:969–97742. Whitmer RA, Karter AJ, Yaffe K, QuesenberryCP Jr, Selby JV. Hypoglycemic episodes and risk ofdementia in older patients with type 2 diabetesmellitus. JAMA 2009;301:1565–157243. Punthakee Z, Miller ME, Launer LJ, et al.;ACCORD Group of Investigators; ACCORD-MINDInvestigators. Poor cognitive function and risk ofsevere hypoglycemia in type 2 diabetes: post hocepidemiologic analysis of the ACCORD trial. Di-abetes Care 2012;35:787–79344. Scarmeas N, Stern Y, Mayeux R, Manly JJ,Schupf N, Luchsinger JA.Mediterranean diet andmild cognitive impairment. ArchNeurol 2009;66:216–22545. Ooi CP, Loke SC, Yassin Z, Hamid T-A. Car-bohydrates for improving the cognitive perfor-mance of independent-living older adults withnormal cognition or mild cognitive impairment.Cochrane Database Syst Rev 2011;4:CD00722046. Richardson K, Schoen M, French B, et al.Statins and cognitive function: a systematic re-view. Ann Intern Med 2013;159:688–69747. El-Serag HB, Tran T, Everhart JE. Diabetesincreases the risk of chronic liver disease andhepatocellular carcinoma. Gastroenterology 2004;126:460–46848. Chalasani N, Younossi Z, Lavine JE, et al. Thediagnosis andmanagement of nonalcoholic fattyliver disease: practice guidance from the Amer-ican Association for the Study of Liver Diseases.Hepatology 2018;67:328–35749. American Gastroenterological Association.American Gastroenterological Association medicalposition statement: nonalcoholic fatty liver disease.Gastroenterology 2002;123:1702–170450. Cusi K, Orsak B, Bril F, et al. Long-term pio-glitazone treatment for patients with nonalcoholic

steatohepatitis and prediabetes or type 2 diabetesmellitus: a randomized trial. Ann Intern Med 2016;165:305–31551. Belfort R, Harrison SA, Brown K, et al. Aplacebo-controlled trial of pioglitazone in sub-jects with nonalcoholic steatohepatitis. N Engl JMed 2006;355:2297–230752. Sanyal AJ, Chalasani N, Kowdley KV, et al.;NASHCRN.Pioglitazone, vitaminE, or placebo fornonalcoholic steatohepatitis. N Engl J Med 2010;362:1675–168553. Armstrong MJ, Gaunt P, Aithal GP, et al.;LEAN trial team. Liraglutide safety and efficacy inpatients with non-alcoholic steatohepatitis(LEAN): amulticentre,double-blind, randomised,placebo-controlled phase 2 study. Lancet 2016;387:679–69054. ShimizuM, Suzuki K, Kato K, et al. Evaluationof the effects of dapagliflozin, a sodium-glucoseco-transporter-2 inhibitor, on hepatic steatosisand fibrosis using transient elastography in pa-tients with type 2 diabetes and non-alcoholicfatty liver disease. Diabetes Obes Metab 2019;21:285–29255. Sattar N, Fitchett D, Hantel S, George JT,ZinmanB. Empagliflozin is associatedwith improve-ments in liver enzymes potentially consistent withreductions in liver fat: results from randomisedtrials including the EMPA-REGOUTCOME� trial.Diabetologia 2018;61:2155–216356. Lecube A, Hernandez C, Genesca J, Simo R.Proinflammatory cytokines, insulin resistance,and insulin secretion in chronic hepatitis Cpatients: a case-control study. Diabetes Care2006;29:1096–110157. Hum J, Jou JH, Green PK, et al. Improvementin glycemic control of type 2 diabetes aftersuccessful treatment of hepatitis C virus. Di-abetes Care 2017;40:1173–118058. Carnovale C, Pozzi M, Dassano A, et al. Theimpact of a successful treatment of hepatitis Cvirus on glyco-metabolic control in diabeticpatients: a systematic review and meta-analysis.Acta Diabetol 2019;56:341–35459. Piciucchi M, Capurso G, Archibugi L, DelleFave MM, Capasso M, Delle Fave G. Exocrinepancreatic insufficiency in diabetic patients:prevalence, mechanisms, and treatment. Int JEndocrinol 2015;2015:59564960. Lee Y-K, Huang M-Y, Hsu C-Y, Su Y-C. Bidirec-tional relationship between diabetes and acutepancreatitis: a population-based cohort study inTaiwan. Medicine (Baltimore) 2016;95:e244861. Das SLM, Singh PP, Phillips ARJ, Murphy R,Windsor JA, PetrovMS.Newlydiagnoseddiabetesmellitus after acute pancreatitis: a systematicreview and meta-analysis. Gut 2014;63:818–83162. Petrov MS. Diabetes of the exocrine pan-creas: American Diabetes Association-compliantlexicon. Pancreatology 2017;17:523–52663. Thomsen RW, Pedersen L, Møller N, KahlertJ, Beck-Nielsen H, Sørensen HT. Incretin-basedtherapy and risk of acute pancreatitis: a nation-wide population-based case-control study. Di-abetes Care 2015;38:1089–109864. Tkac I, Raz I. Combined analysis of threelarge interventional trials with gliptins indicatesincreased incidence of acute pancreatitis inpatients with type 2 diabetes. Diabetes Care2017;40:284–28665. BellinMD,GelrudA,Arreaza-RubinG,etal.Totalpancreatectomy with islet autotransplantation:

summary of an NIDDK workshop. Ann Surg2015;261:21–2966. Sutherland DER, Radosevich DM, Bellin MD,et al. Total pancreatectomy and islet autotrans-plantation for chronic pancreatitis. J AmColl Surg2012;214:409–424; discussion 424–42667. QuartuccioM, Hall E, Singh V, et al. Glycemicpredictors of insulin independence after totalpancreatectomy with islet autotransplantation.J Clin Endocrinol Metab 2017;102:801–80968. Webb MA, Illouz SC, Pollard CA, et al. Isletauto transplantation following total pancreatec-tomy: a long-term assessment of graft function.Pancreas 2008;37:282–28769. Wu Q, Zhang M, Qin Y, et al. Systematicreview and meta-analysis of islet autotransplan-tation after total pancreatectomy in chronicpancreatitis patients. Endocr J 2015;62:227–23470. JanghorbaniM,VanDamRM,WillettWC,HuFB. Systematic review of type 1 and type 2diabetes mellitus and risk of fracture. Am JEpidemiol 2007;166:495–50571. Vestergaard P. Discrepancies in bone min-eral density and fracture risk in patients withtype 1 and type 2 diabetesda meta-analysis.Osteoporos Int 2007;18:427–44472. Schwartz AV, Vittinghoff E, Bauer DC, et al.;Study of Osteoporotic Fractures (SOF) ResearchGroup; Osteoporotic Fractures in Men (MrOS)Research Group; Health, Aging, and Body Com-position (Health ABC) Research Group. Associ-ation of BMD and FRAX score with risk of fracturein older adults with type 2 diabetes. JAMA 2011;305:2184–219273. KahnSE, ZinmanB, Lachin JM,etal.;DiabetesOutcomeProgressionTrial (ADOPT)StudyGroup.Rosiglitazone-associated fractures in type 2 di-abetes: an analysis from A Diabetes OutcomeProgressionTrial (ADOPT).Diabetes Care 2008;31:845–85174. Taylor SI, Blau JE, Rother KI. Possible adverseeffects of SGLT2 inhibitors on bone. Lancet Di-abetes Endocrinol 2015;3:8–1075. Bainbridge KE, Hoffman HJ, Cowie CC. Di-abetes and hearing impairment in the UnitedStates: audiometric evidence from the NationalHealth and Nutrition Examination Survey,1999 to 2004. Ann Intern Med 2008;149:1–1076. Bainbridge KE, Hoffman HJ, Cowie CC. Riskfactors forhearing impairmentamongU.S.adultswith diabetes: National Health and NutritionExamination Survey 1999-2004. Diabetes Care2011;34:1540–154577. Schade DS, Lorenzi GM, Braffett BH, et al.;DCCT/EDIC ResearchGroup.Hearing impairmentand type 1 diabetes in the Diabetes Control andComplications Trial/Epidemiology of DiabetesInterventions and Complications (DCCT/EDIC)cohort. Diabetes Care 2018;41:2495–250178. Rasmussen VF, Vestergaard ET, Hejlesen O,Andersson CUN, Cichosz SL. Prevalence of tasteand smell impairment in adults with diabetes:a cross-sectional analysis of data from the Na-tional Health and Nutrition Examination Survey(NHANES). Prim Care Diabetes 2018;12:453–45979. Monroe AK, Glesby MJ, Brown TT. Diagnos-ing and managing diabetes in HIV-infected pa-tients: current concepts. Clin Infect Dis 2015;60:453–46280. Schambelan M, Benson CA, Carr A, et al.;International AIDS Society-USA. Managementof metabolic complications associated with

S46 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 43, Supplement 1, January 2020

antiretroviral therapy for HIV-1 infection: rec-ommendations of an International AIDS Society-USApanel. J Acquir ImmuneDefic Syndr 2002;31:257–27581. Kim PS, Woods C, Georgoff P, et al. A1Cunderestimates glycemia in HIV infection. Di-abetes Care 2009;32:1591–159382. Wohl DA, McComsey G, Tebas P, et al.Current concepts in the diagnosis and manage-ment of metabolic complications of HIV infec-tion and its therapy. Clin Infect Dis 2006;43:645–65383. Dhindsa S, Miller MG, McWhirter CL, et al.Testosteroneconcentrations indiabeticandnon-diabetic obese men. Diabetes Care 2010;33:1186–119284. Grossmann M. Low testosterone in menwith type 2 diabetes: significance and treatment.J Clin Endocrinol Metab 2011;96:2341–235385. Bhasin S, Cunningham GR, Hayes FJ, et al.;Task Force, Endocrine Society. Testosteronetherapy in men with androgen deficiency syn-dromes: an Endocrine Society clinical practiceguideline. J Clin Endocrinol Metab 2010;95:2536–255986. Budoff MJ, Ellenberg SS, Lewis CE, et al.Testosterone treatment and coronary arteryplaque volume in older men with low testoster-one. JAMA 2017;317:708–71687. Kloner RA, Carson C III, Dobs A, Kopecky S,Mohler ER III. Testosterone and cardiovasculardisease. J Am Coll Cardiol 2016;67:545–55788. Li C, Ford ES, Zhao G, Croft JB, Balluz LS,Mokdad AH. Prevalence of self-reported clini-cally diagnosed sleep apnea according to obesitystatus in men and women: National Health and

Nutrition Examination Survey, 2005-2006. PrevMed 2010;51:18–2389. West SD, Nicoll DJ, Stradling JR. Prevalenceof obstructive sleep apnoea in men with type 2diabetes. Thorax 2006;61:945–95090. Resnick HE, Redline S, Shahar E, et al.; SleepHeart Health Study. Diabetes and sleep distur-bances: findings from the Sleep Heart HealthStudy. Diabetes Care 2003;26:702–70991. Foster GD, Sanders MH, Millman R, et al.;Sleep AHEAD Research Group. Obstructive sleepapnea among obese patients with type 2 di-abetes. Diabetes Care 2009;32:1017–101992. Bibbins-Domingo K, Grossman DC, Curry SJ,et al.;USPreventiveServicesTaskForce.Screeningfor obstructive sleep apnea in adults: US Pre-ventive Services Task Force recommendationstatement. JAMA 2017;317:407–41493. Shaw JE, Punjabi NM, Wilding JP, AlbertiKGMM, Zimmet PZ; International Diabetes Fed-eration Taskforce on Epidemiology and Preven-tion. Sleep-disordered breathing and type 2diabetes: a report from the International DiabetesFederation Taskforce on Epidemiology and Pre-vention. Diabetes Res Clin Pract 2008;81:2–1294. Khader YS, Dauod AS, El-Qaderi SS, AlkafajeiA, Batayha WQ. Periodontal status of diabeticscompared with nondiabetics: a meta-analysis. JDiabetes Complications 2006;20:59–6895. Casanova L, Hughes FJ, Preshaw PM. Di-abetes and periodontal disease: a two-way re-lationship. Br Dent J 2014;217:433–43796. Eke PI, Thornton-Evans GO,Wei L, BorgnakkeWS, Dye BA, Genco RJ. Periodontitis in US adults:National Health andNutrition Examination Survey2009-2014. J Am Dent Assoc 2018;149:576–588.e6

97. Simpson TC, Weldon JC, Worthington HV,et al. Treatment of periodontal disease forglycaemic control in people with diabetes melli-tus. Cochrane Database Syst Rev 2015 11:CD00471498. D’Aiuto F, Gkranias N, Bhowruth D, et al.;TASTEGroup. Systemic effects of periodontitis treat-ment in patients with type 2 diabetes: a 12 month,single-centre, investigator-masked, randomised trial.Lancet Diabetes Endocrinol 2018;6:954–96599. Davies MJ, D’Alessio DA, Fradkin J, et al.Management of hyperglycemia in type 2 diabe-tes, 2018. A consensus report by the AmericanDiabetes Association (ADA) and the EuropeanAssociation for the Study of Diabetes (EASD).Diabetes Care 2018;41:2669–2701100. Lipska KJ, Ross JS, Wang Y, et al. Nationaltrends in US hospital admissions for hypergly-cemia and hypoglycemia among Medicare ben-eficiaries, 1999 to 2011. JAMA Intern Med 2014;174:1116–1124101. Shorr RI, Ray WA, Daugherty JR, Griffin MR.Incidence and risk factors for serious hypoglyce-mia inolderpersonsusing insulin or sulfonylureas.Arch Intern Med 1997;157:1681–1686102. Abdelhafiz AH, Rodrıguez-Ma~nas L, MorleyJE, Sinclair AJ. Hypoglycemia in older people - aless well recognized risk factor for frailty. AgingDis 2015;6:156–167103. Yun J-S, Ko S-H, Ko S-H, et al. Presence ofmacroalbuminuria predicts severe hypoglycemiainpatientswith type2diabetes: a10-year follow-upstudy. Diabetes Care 2013;36:1283–1289104. ChelliahA,BurgeMR.Hypoglycaemiainelderlypatientswithdiabetesmellitus: causesandstrategiesfor prevention. Drugs Aging 2004;21:511–530

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