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strong genetic predisposition or family his-\ntory in first-degree relatives (more so thantype 1 diabetes). However, the genetics oftype 2 diabetes are poorly understood and\nunder intense investigation in this era ofprecision medicine (52). In adults without\ntraditional risk factors for type 2 diabetes | [
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traditional risk factors for type 2 diabetes\nand/or of younger age, consider islet auto-antibody testing (e.g., GAD autoantibod-\nies) to exclude the diagnosis of type 1\ndiabetes (36) ( Fig. 2.1 ).\nScreening and Testing for\nPrediabetes and Type 2 Diabetes inAsymptomatic Adults\nScreening for prediabetes and type 2 ... | [
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Screening for prediabetes and type 2 dia-\nbetes risk through a targeted assessmentof risk factors ( Table 2.4 )o rw i t ha n\nassessment tool, such as the ADA risk\ntest ( Fig. 2.2 ) (online at diabetes.org/\nsocrisktest), is recommended to guide\nhealth care professionals on whether\nperforming a diagnostic test ( Ta... | [
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performing a diagnostic test ( Table 2.1 )\nis appropriate. Prediabetes and type 2\ndiabetes meet criteria for conditions inwhich early detection via screening is ap-\npropriate. Both conditions are common\nand impose signi ficant clinical and public\nhealth burdens. There is often a long pre-\nsymptomatic phase before ... | [
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symptomatic phase before the diagnosis\nof type 2 diabetes. Simple tests to detectpreclinical disease are readily available\n(95). The duration of glycemic burden is\na strong predictor of adverse outcomes.There are effective interventions that pre-vent progression from prediabetes to dia-\nbetes. It is important to in... | [
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betes. It is important to individualize\nrisk-to-bene fit ratio of formal intervention\nfor people with prediabetes and consider\nperson-centered goals. Risk models have\nexplored the bene fit, in general finding\nhigher bene fit of intervention in those at\nhighest risk (96) (see Section 3, “Prevention | [
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highest risk (96) (see Section 3, “Prevention\nor Delay of Diabetes and AssociatedComorbidities ”) and reduce the risk of dia-\nbetes complications (97) (see Section 10,\n“Cardiovascular Disease and Risk Man-\nagement, ”Section 11, “Chronic Kidney\nDisease and Risk Management, ”and Sec-\ntion 12, “Retinopathy, Neuropat... | [
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tion 12, “Retinopathy, Neuropathy, and\nFoot Care ”). In the most recent National In-\nstitutes of Health (NIH) Diabetes Preven-\ntion Program Outcomes Study (DPPOS)\nreport, prevention of progression from pre-\ndiabetes to diabetes (98) resulted in lowerrates of developing retinopathy and ne-\nphropathy (99). Similar ... | [
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phropathy (99). Similar impact on diabe-\ntes complications was reported withscreening, diagnosis, and comprehensiverisk factor management in the U.K. Clini-\ncal Practice Research Datalink database | [
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cal Practice Research Datalink database\n( 9 7 ) .I nt h a tr e p o r t ,p r o g r e s s i o nf r o mS28 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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prediabetes to diabetes augmented risk\nof complications.\nDespite the numerous bene fits of screen-\ning and early diagnosis for prediabetes ordiabetes, unfortunately many people in theU.S. and globally either remain undiagnosedor are diagnosed late, when complicationshave already arisen.Additional considerations regar... | [
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testing for type 2 diabetes and prediabe-tes in asymptomatic individuals are de-scribed below.®American \nDiabetesAssociation\n®\nAre you at risk for type 2 diabetes?Connected for Life\nDiabetes Risk Test:\n1. How old are you? ...................................................\n2. Are you a man or a woman? .............. | [
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2. Are you a man or a woman? .................................\n3. If you are a woman, have you ever been \n diagnosed with gestational diabetes?..................Less than 40 years (0 points)\n40–49 years (1 point)\n50–59 years (2 points)\n60 years or older (3 points) | [
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50–59 years (2 points)\n60 years or older (3 points)\n4. Do you have a mother, father, sister or brother with diabetes? ........................................................\n5. Have you ever been diagnosed with high \n blood pressure? ..................................................... | [
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6. Are you physically active? ....................................\n7. What is your weight category? .............................\nSee chart at right.\nYou are at increased risk for having type 2 diabetes. \nHowever, only your doctor can tell for sure if you do \nhave type 2 diabetes or prediabetes, a condition in | [
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have type 2 diabetes or prediabetes, a condition in \nwhich blood glucose levels are higher than normal \nbut not yet high enough to be diagnosed as diabetes. \nTalk to your doctor to see if additional testing is needed.\nType 2 diabetes is more common in African Americans, \nHispanics/Latinos, Native Americans, Asian ... | [
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Hispanics/Latinos, Native Americans, Asian Americans, \nand Native Hawaiians and Pacific Islanders.\nHigher body weight increases diabetes risk for everyone. \nAsian Americans are at increased diabetes risk at lower body weight than the rest of the general public (about 15 pounds lower).If you scored 5 or higher:\nLowe... | [
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Lower Your Risk\nThe good news is you can manage your risk for type 2 diabetes. Small steps make a big difference in helping you live a longer, \nhealthier life.\nIf you are at high risk, your first step is to \nvisit your doctor to see if additional testing is needed.\nVisit diabetes.org or call 1-800-DIABETES | [
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Visit diabetes.org or call 1-800-DIABETES \n(800-342-2383) for information, tips on getting started, and ideas for simple, small \nsteps you can take to help lower your risk.Adapted from Bang et al., Ann Intern Med151:775–783, 2009 \x81 Original algorithm was validated \nwithout gestational diabetes as part of the m... | [
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Yes(1 point) No(0 points)\nYes(1 point) No(0 points)\nYes(1 point) No(0 points)\nYes(0 points) No(1 point)\nLearn more at diabetes.org/risktest | 1-800-DIABETES (800-342-2383)\nDiabetes Risk Test |American Diabetes Association ®If you weigh less than the amount inthe left column: 0 points4’ 10”\n4’ 11”\n5’ 0”5’ 1”\n5’ ... | [
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4’ 11”\n5’ 0”5’ 1”\n5’ 2”\n5’ 3”\n5’ 4”\n5’ 5”\n5’ 6”\n5’ 7”\n5’ 8”\n5’ 9”\n5’ 10”\n5’ 11”\n6’ 0”\n6’ 1”\n6’ 2”\n6’ 3”6’ 4”119–142 143–190 191+124–147 148–197 198+128–152 153–203 204+\n132–157 158–210 211+136–163 164–217 218+\n141–168 169–224 225+\n145–173 174–231 232+\n150–179 180–239 240+\n155–185 186–246 247+\n159–1... | [
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155–185 186–246 247+\n159–190 191–254 255+\n164–196 197–261 262+\n169–202 203–269 270+\n174–208 209–277 278+\n179–214 215–285 286+\n184–220 221–293 294+\n189–226 227–301 302+\n194–232 233–310 311+\n200–239 240–318 319+205–245 246–327 328+WRITE YOUR SCORE\nIN THE BOX.\nADD UP\nYOUR SCORE.Height Weight (lbs.)\n1 point 2 ... | [
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ADD UP\nYOUR SCORE.Height Weight (lbs.)\n1 point 2 points 3 points\nFigure 2.2 —ADA risk test (diabetes.org/socrisktest).diabetesjournals.org/care Diagnosis and Classification of Diabetes S29\n©AmericanDiabetesAssociation | [
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Age\nAge is a major risk factor for diabetes.\nTesting should begin at no later than age35 years for all people (100). Screeningshould be considered in adults of anyage with overweight or obesity and one\nor more risk factors for diabetes.\nMedications\nCertain medications, such as glucocorti- | [
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Medications\nCertain medications, such as glucocorti-\ncoids, statins (101), proprotein convertasesubtilisin/kexin type 9 (PCSK9) inhibitors,thiazide diuretics, some HIV medications\n(19), and second-generation antipsychotic | [
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(19), and second-generation antipsychotic\nmedications (102), should be consideredwhen deciding whether to screen for pre-diabetes or diabetes, as these medica-tions are known to increase the risks ofthese conditions.\nFor example, people taking second- | [
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generation antipsychotic medications,such as olanzapine, require greater mon-itoring because of an increase in risk oftype 2 diabetes associated with thismedication (102). There is a range of ef-fects on metabolic parameters (e.g., glu-cose concentration, hyperglycemia, andweight gain) across second-generationantipsych... | [
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andweight gain) across second-generationantipsychotic medications; aripiprazoleand ziprasidone tend to have fewer met- | [
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abolic effects, and haloperidol, cloza-\npine, quetiapine, and risperidone tendto have more metabolic effects. Peopletreated with these agents should bescreened for prediabetes or diabetes atbaseline, rescreened 12 –16 weeks after\nmedication initiation, and screened an-nually thereafter (102).\nPeople With HIV | [
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People with HIV are at higher risk for de-veloping prediabetes and diabetes onantiretroviral (ARV) therapies; a screen-ing protocol is therefore recommended(103). The A1C test may underestimateglycemia in people with HIV; it is not rec-ommended for diagnosis and may presentchallenges for monitoring (20). In thosewith p... | [
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for monitoring (20). In thosewith prediabetes, weight loss throughhealthy nutrition and physical activity mayreduce the progression toward diabetes. | [
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Among people with HIV and diabetes, pre- | [
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ventive health care using an approachused in people without HIV is critical to re-duce the risks of microvascular and macro-vascular complications. Diabetes risk isincreased with certain protease inhibitors(PIs) and nucleoside/nucleotide reversetranscriptase inhibitors (NRTIs). New-onsetdiabetes is estimated to occur i... | [
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New-onsetdiabetes is estimated to occur in morethan 5% of individuals infected with HIV | [
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on PIs, whereas more than 15% may haveprediabetes (104).\nPIs are associated with insulin resis-\ntance and may also lead to apoptosis of\npancreatic b-cells. NRTIs also affect fat\ndistribution (both lipohypertrophy and\nlipoatrophy), which is associated with in-sulin resistance. For people with HIV and\nARV-associate... | [
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ARV-associated hyperglycemia, it may be\nappropriate to consider discontinuingthe problematic ARV agents if safe andeffective alternatives are available (105).\nBefore making ARV substitutions, care-\nfully consider the possible effect on HIVvirological control and the potential ad-verse effects of new ARV agents. In s... | [
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cases, antihyperglycemic agents may still\nbe necessary.\nTesting Interval\nThe appropriate interval between screen-ing tests is not known (106). The rationale\nfor the 3-year interval is that with this inter-\nval, the number of false-positive tests thatrequire con firmatory testing will be re- | [
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0... |
duced, and individuals with false-negativetests will be retested before substantialtime elapses and complications develop(106). In especially high-risk individuals,\nparticularly with weight gain, shorter\nintervals between screenings may beuseful.\nCommunity Screening\nIdeally, screening should be carried out\nwithin ... | [
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within a health care setting because of\nthe need for follow-up and treatment.Community screening outside a healthcare setting is generally not recom-\nmended because people with positive\ntests may not seek, or have access to,appropriate follow-up testing and care.However, in speci fic situations where an | [
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adequate referral system is establishedbeforehand for positive tests, commu-nity screening may be considered. Com-munity screening may also be poorly\ntargeted; i.e., it may fail to reach the\ngroups most at risk and inappropriatelytest those at very low risk or even thosewho have already been diagnosed\n(107).\nScreen... | [
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0... |
(107).\nScreening in Dental Practices\nBecause periodontal disease is associ-\nated with diabetes, the utility of screen-ing in a dental setting and referral to\nprimary care as a means to improve the\ndiagnosis of prediabetes and diabetesh a sb e e ne x p l o r e d( 1 0 8 –110), with one | [
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study estimating that 30% of individuals$30 years of age seen in general dentalpractices (including people with and with-out periodontal disease) had newly diag-nosed dysglycemia (110). A similar studyin 1,150 dental patients >40 years old in\nIndia reported 20.7% and 14.6% meetingcriteria for prediabetes and diabetes,... | [
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spectively, using random blood glucose\n(111). Further research is needed to dem-onstrate the feasibility, effectiveness,and cost-effectiveness of screening inthis setting.\nScreening and Testing for\nPrediabetes and Type 2 Diabetes in\nChildren and Adolescents\nThe epidemiologic studies that formed | [
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0.0578... |
Children and Adolescents\nThe epidemiologic studies that formed\nthe basis for recommending A1C to diag-nose diabetes included only adult popula-tions (112). However, recent ADA clinical\nguidance concluded that A1C, FPG, or 2-h\nPG could be used to test for prediabetesor type 2 diabetes in children and adoles-cents (1... | [
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0.... |
In the last decade, the incidence and\nprevalence of type 2 diabetes in childrenand adolescents has increased dramati-cally, especially in racial and ethnic mi-nority populations (114). See Table 2.5 | [
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0.08717591315507889,
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0.017728134989738464,
0.0575285367667675,
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0.054259... |
for recommendations on risk-basedscreening for type 2 diabetes or predia-betes in asymptomatic children andadolescents in a clinical setting (113).SeeTable 2.1 andTable 2.2 for the cri-\nteria for the diagnosis of diabetes andprediabetes, respectively, that apply tochildren, adolescents, and adults. SeeSection 14, “Chi... | [
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0.020235775038599968,
-0.06422426551580429,
0.044819... |
for additional information on type 2 diabetes\nin children and adolescents.\nPANCREATIC DIABETES OR\nDIABETES IN THE CONTEXT OFDISEASE OF THE EXOCRINE\nPANCREAS\nRecommendation\n2.17 Screen people for diabetes within\n3–6 months following an episode of\nacute pancreatitis and annually there- | [
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0.007222594693303108,
-0.11472147703170776,
0.01837... |
acute pancreatitis and annually there-\nafter. Screening for diabetes is recom-mended annually for people withchronic pancreatitis. E | [
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0.0349348783493042,
0.04174115136265755,
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0.02349977008998394,
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0.027... |
Pancreatic diabetes (also termed pancrea-t o g e n i cd i a b e t e so rt y p e3 cd i a b e t e s )i n -cludes both structural and functional lossof glucose-normalizing insulin secretion inS30 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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the context of exocrine pancreatic dysfunc-\ntion and is commonly misdiagnosed astype 2 diabetes. The diverse set of etiolo-\ngies includes pancreatitis (acute and\nchronic), trauma or pancreatectomy, neo-\nplasia, cystic fibrosis (addressed later in this\nsection), hemochromatosis, fibrocalculous\npancreatopathy, rare g... | [
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pancreatopathy, rare genetic disorders,\nand idiopathic forms (2); as such, pancre-atic diabetes is the preferred umbrella\nterm (115).\nPancreatitis, even a single bout, can lead\nto postpancreatitis diabetes mellitus. Bothacute and chronic pancreatitis can lead to\npostpancreatitis diabetes mellitus, and the | [
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0... |
postpancreatitis diabetes mellitus, and the\nrisk is highest with recurrent bouts. A dis-\ntinguishing feature is concurrent pancreatic\nexocrine insuf ficiency (consider screening\nindividuals with acute and chronic pancrea-\ntitis for exocrine pancreatic insuf ficiency\nby measuring fecal elastase), pathologicalpancrea... | [
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0.0881495550274849,
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0.0307961106300354,
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0.068... |
MRI, and computed tomography), and\nabsence of type 1 diabetes –associated\nautoimmunity (116 –120). There is loss\nof both insulin and glucagon secretion\nand often higher-than-expected insulin re-\nquirements. Risk for microvascular compli-c a t i o n sa p p e a r st ob es i m i l a rt ot h a to f\nother forms of dia... | [
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0.08375173062086105,
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0.0692887082695961,
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other forms of diabetes.\nFor people with pancreatitis and dia-\nbetes, therapy should be advanced ifA1C goals are not met. Glucose-lowering\ntherapies associated with increased risk\nof pancreatitis (i.e., incretin-based thera-\npies) should be avoided. Early initiation of\ninsulin therapy should be considered. In | [
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0.03297371044754982,
0.05773361772298813,
0.08473090082406998,
0.0023065300192683935,
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-0.056456420570611954,
0.08654842525720596,
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0.0... |
insulin therapy should be considered. In\nthe context of pancreatectomy, islet auto-transplantation can be considered for se-\nlected individuals with medically refractory\nchronic pancreatitis in specialized centers\nto preserve endogenous islet function and\ninsulin secretion (121,122). In some cases,\nautotransplant... | [
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0.008899814449250698,
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0.10755617916584015,
0.05368572846055031,
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0.08033765107393265,
-0.06745065003633499,
0.02542... |
autotransplant can lead to insulin indepen-\ndence. In others, it may decrease insulinrequirements (123).\nCystic Fibrosis –Related Diabetes\nRecommendations\n2.18 Annual screening for cystic\nfibrosis –related diabetes (CFRD) with\nan OGTT should begin by age 10 years\nin all people with cystic fibrosis not\npreviously ... | [
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0.034303028136491776,
0.04850199818611145,
-0.04076069965958595,
0.04421646... |
previously diagnosed with CFRD. B\n2.19 A 1 Ci sn o tr e c o m m e n d e da sa\nscreening test for CFRD due to low sensi-tivity. However, a value of $6.5%\n($48 mmol/mol) is consistent with a di-\nagnosis of CFRD. B2.20 Beginning 5 years after the diag-\nnosis of CFRD, annual monitoring for\ncomplications of diabetes i... | [
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0.03151443228125572,
0.13242487609386444,
0.024228805676102638,
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0.... |
complications of diabetes is recom-mended. E\nCystic fibrosis is a multisystem condition\narising from recessive mutations in the\ngene encoding the cystic fibrosis trans-\nmembrane conductance regulator (CFTR)protein. Pancreatic exocrine damage ulti-\nmately manifests as pancreatic exocrineinsufficiency that begins as ea... | [
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0.13070400059223175,
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0.006353016011416912,
0.014087336137890816,
-0.049467574805021286,
0.0... |
fancy (124). Cystic fibrosis –related diabetes\n(CFRD) is the most common comorbidity inpeople with cystic fibrosis, occurring in\nabout 20% of adolescents and 40 –50% of\nadults (125). The relevance of CFRD ishighlighted by its association with increased\nmorbidity, mortality, and patient burden. | [
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0.0500183030962944,
0.10968635976314545,
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-0.06950025260448456,
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0.051940370351076126,
0.01139023620635271,
0.0584516... |
morbidity, mortality, and patient burden.\nDiabetes in this population, compared withindividuals with type 1 or type 2 diabetes, is\nassociated with worse nutritional status,\nmore severe in flammatory lung disease,\nand greater mortality. Insulin insuf ficiency is\nthe primary defect in CFRD. Geneticallydetermined b-cel... | [
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0.08364083617925644,
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0.024832988157868385,
0.11741174012422562,
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0.04444589465856552,
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-0.0090... |
sistance associated with infection and in-fla m m a t i o nm a ya l s oc o n t r i b u t et ot h e\ndevelopment of CFRD. Milder abnormali-\nties of glucose tolerance are even more\ncommon and occur at earlier ages thanCFRD. Whether individuals with IGT should\nbe treated with insulin replacement has | [
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0.014250018633902073,
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0.06157729774713516,
0.1321016103029251,
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0.004962222650647163,
0.06978678703308105,
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0.0... |
be treated with insulin replacement has\nnot currently been determined. Althoughscreening for diabetes before the age of\n10 years can identify risk for progression\nto CFRD in those with abnormal glucosetolerance, no bene fit has been established\nwith respect to weight, height, BMI, orlung function. OGTT is the recomm... | [
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0.012573556043207645,
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0.04969337210059166,
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screening test for CFRD. Not unexpectedly,\nannual OGTTs are perceived as burden-some, and adherence to current CFRD\nscreening guidelines is poor, with only\n30% of adults with cystic fibrosis having\nannual OGTTs (126). A1C is not recom-\nmended for screening due to low sensitivity;\nhowever, a value $6.5% ( $48 mmol/... | [
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0... |
however, a value $6.5% ( $48 mmol/mol)\nis consistent with a diagnosis of CFRD and\nreduces patient screening burden (127 –\n129). Regardless of age, weight loss or fail-\nure of expected weight gain is a risk for\nCFRD and should prompt screening\n(127,128). The Cystic Fibrosis Foundation Pa-\ntient Registry (130) eva... | [
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0.04475879296660423,
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0.022091038525104523,
0.022526... |
tient Registry (130) evaluated 3,553 people\nwith cystic fibrosis and diagnosed 445\n(13%) with CFRD. Early diagnosis and treat-\nment of CFRD was associated with preserva-\ntion of lung function. The European CysticFibrosis Society Patient Registry reported an\nincrease in CFRD with age (10% increase\nper decade), geno... | [
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-0.014853999018669128,
0.011954501271247864,
0.0627... |
per decade), genotype, decreased lung\nfunction, and female sex (131,132). CGM or\nHOMA of b-cell function (133) may be\nmore sensitive than OGTT to detect riskfor progression to CFRD; however, evi-\ndence linking these results to long-term\noutcomes is lacking, and these tests are\nnot recommended for screening outsid... | [
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not recommended for screening outside\nthe research setting (134).\nCFRD mortality has signi ficantly de-\ncreased over time, and the gap in mor-tality between people with cystic fibrosis\nwith and without diabetes has consider-ably narrowed (135). There are limited\nclinical trial data on therapy for CFRD. | [
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clinical trial data on therapy for CFRD.\nPeople with CFRD should be treated withinsulin to attain individualized glycemic\ngoals.\nAdditional resources for the clinical\nmanagement of CFRD can be found inthe position statement “Clinical Care\nGuidelines for Cystic Fibrosis –Related Di-\nabetes ”(136) and in the Intern... | [
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abetes ”(136) and in the International Soci-\nety for Pediatric and Adolescent Diabetes2018 clinical practice consensus guidelines\n(125).\nPOSTTRANSPLANTATION\nDIABETES MELLITUS\nRecommendations\n2.21 After organ transplantation, screen-\ning for hyperglycemia should be done. A\nformal diagnosis of posttransplantation | [
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0.0... |
formal diagnosis of posttransplantation\ndiabetes mellitus (PTDM) is best made\nonce the individual is stable on an immu-\nnosuppressive plan and in the absence\nof an acute infection. B\n2.22 The OGTT is the preferred test\nto make a diagnosis of PTDM. B\n2.23 Immunosuppressive plans shown | [
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0.0359940379858017,
0.01825878955423832,
-0.05934688821434975,
0.067993819... |
to make a diagnosis of PTDM. B\n2.23 Immunosuppressive plans shown\nto provide the best outcomes for indi-viduals and graft survival should be\nused, irrespective of PTDM risk. E\nSeveral terms are used in the literature to\ndescribe the presence of diabetes follow-\ning organ transplantation (137). New-\nonset diabete... | [
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0.0115744... |
onset diabetes after transplantation\n(NODAT) is one such designation that de-\nscribes individuals who develop new-onset\ndiabetes following transplant. NODAT ex-\ncludes people with pretransplant diabetes\nthat was undiagnosed as well as posttrans-\nplant hyperglycemia that resolves by the\ntime of discharge (138). A... | [
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time of discharge (138). Another term,\nposttransplantation diabetes me llitusdiabetesjournals.org/care Diagnosis and Classification of Diabetes S31\n©AmericanDiabetesAssociation | [
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(PTDM) (138,139), describes the pres-\nence of diabetes in the posttransplant\nsetting irrespective of the timing of diabe-\ntes onset (140). The clinical importance of\nPTDM lies in its unquestionable impact asas i g n i ficant risk factor for cardiovascular\ndisease and chronic kidney disease insolid-organ transplanta... | [
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Hyperglycemia is very common during\nthe early posttransplant period, with/C2490% of kidney allograft recipients exhib-\niting hyperglycemia in the first few weeks\nfollowing transplant (138,139,141,142).In most cases, such stress- or steroid-\ninduced hyperglycemia resolves by the\ntime of discharge (142,143). Although... | [
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time of discharge (142,143). Although the\nuse of immunosuppressive therapies is a\nmajor contributor to the development ofPTDM, the risks of transplant rejection\noutweigh the risks of PTDM, and the role\nof the diabetes health care professional isto treat hyperglycemia appropriately re-\ngardless of the type of immun... | [
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gardless of the type of immunosuppres-\nsion (138). Risk factors for PTDM include\nboth general diabetes risks (such as age,\nfamily history of diabetes, obesity, etc.)and transplant-speci ficf a c t o r s ,s u c ha su s e\nof immunosuppressant agents (144 –146).\nWhereas posttransplantation hyperglyce-mia is an importa... | [
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quent PTDM, a formal diagnosis of PTDM\nis optimally made once the individual isstable on maintenance immunosuppres-\nsion (usually at least 45 days after trans-\nplantation) and in the absence of acute\ninfection (138,142– 144,147).\nThe OGTT is considered the gold-\nstandard test for the diagnosis of PTDM\n(1 year po... | [
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(1 year posttransplant) (138,139,148,149).\nPretransplant elevation in hs-CRP was as-\nsociated with PTDM in the setting of renaltransplant (150,151). However, screening\npeople with FPG and/or A1C can identify\nhigh-risk individuals who require furtherassessment and may reduce the number\nof overall OGTTs required.\nF... | [
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of overall OGTTs required.\nFew randomized controlled studies\nhave reported on the short- and long-\nterm use of antihyperglycemic agents in\nthe setting of PTDM (144,152,153). Most\nstudies have reported that transplant pa-\ntients with hyperglycemia and PTDM after\ntransplantation have higher rates of rejec-tion, in... | [
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144,154). Insulin therapy is the agent of\nchoice for the management of hyperglyce-mia, PTDM, preexisting diabetes, and dia-\nbetes in the hospital setting and can be\ncontinued postdischarge. No studies todate have firmly established which nonin-\nsulin agents are safest or most ef ficacious\nin PTDM. The choice of agen... | [
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in PTDM. The choice of agent is usually\nmade based on the side effect pro file of the\nmedication, possible interactions with the in-\ndividual ’s immunosuppression plan, and po-\ntential cardiovascular and renal bene fits in\nindividuals with PTDM (144). Well-designed\nintervention trials examining the ef ficacy\nand sa... | [
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and safety of these and other antihyper-\nglycemic agents in people with PTDM areneeded.\nMONOGENIC DIABETES\nSYNDROMES\nRecommendations\n2.24a Regardless of current age, all\npeople diagnosed with diabetes in the\nfirst 6 months of life should have im-\nmediate genetic testing for neonataldiabetes. A\n2.24b Children an... | [
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0.037292756140232086,
0.08290238678455353,
0.11367705464363098,
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0.04724769666790962,
0.03492549806833267,
0.06348656117916107,
-0.08833447843790054,
0.011738... |
2.24b Children and young adults who\ndo not have typical characteristics oftype 1 or type 2 diabetes and who of-\nten have a family history of diabetes in\nsuccessive generations (suggestive of an\nautosomal dominant pattern of inheri-\ntance) should have genetic testing formaturity-onset diabetes of the young\n(MODY).... | [
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0.04378011077642441,
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0.052440859377384186,
0.04278283566236496,
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0.043235693126916885,
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0.01926... |
(MODY). A\n2.24c In both instances, consultation\nwith a center specializing in diabetesgenetics is recommended to under-\nstand the signi ficance of genetic muta-\ntions and how best to approachfurther evaluation, treatment, and ge-\nnetic counseling. E\nMonogenic defects that cause b-cell dys-\nfunction, such as neona... | [
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0.0361... |
function, such as neonatal diabetes and\nMODY, are present in a small fraction of\npeople with diabetes ( <5%) (155). Table 2.6\ndescribes the most common causes of\nmonogenic diabetes. For a comprehen-sive list of causes, see “Genetic Diagnosis\nof Endocrine Disorders ”(156).\nNeonatal Diabetes\nDiabetes occurring und... | [
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Neonatal Diabetes\nDiabetes occurring under 6 months of\nage is termed neonatal or congenital dia-betes, and about 80 –85% of cases can be\nfound to have an underlying monogenic\ncause (36,157– 160). Neonatal diabetes\noccurs much less often after 6 months of\nage, whereas autoimmune type 1 diabe-\ntes rarely occurs be... | [
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... |
tes rarely occurs before 6 months of age.\nNeonatal diabetes can either be transientor permanent. Transient diabetes is mostoften due to overexpression of genes on\nchromosome 6q24, is recurrent in abouthalf of cases, and may be treatable with\nmedications other than insulin. Permanent\nneonatal diabetes is most common... | [
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neonatal diabetes is most commonly due\nto autosomal dominant mutations in\nthe genes encoding the Kir6.2 subunit(KCNJ11 ) and SUR1 subunit ( ABCC8 )o ft h e\nb-cell K\nATPchannel. A recent report details\nad en o v om u t a t i o ni n EIF2B1 affecting\neIF2 signaling associated with permanent\nneonatal diabetes and he... | [
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0.01724211312830448,
0.03566868603229523,
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0.0008385138353332877,
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neonatal diabetes and hepatic dysfunc-\ntion, similar to Wolcott-Rallison syndrome\nbut with few severe comorbidities (161).\nThe recent ADA-European Association forthe Study of Diabetes type 1 diabetes con-\nsensus report recommends that regardless\nof current age, individuals diagnosed un-\nder 6 months of age should... | [
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0.09682517498731613,
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0.006... |
der 6 months of age should have genetic\ntesting (36). Correct diagnosis has criticalimplications, because 30 –50% of people\nwith K\nATP-related neonatal diabetes will ex-\nhibit improved blood glucose levels when\ntreated with high-dose oral sulfonylureas\ninstead of insulin. Insulin gene ( INS)m u -\ntations are the... | [
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0.001... |
tations are the second most common\ncause of permanent neonatal diabetes,\nand while intensive insulin management\nis currently the preferred treatment\nstrategy, there are important geneticcounseling considerations, as most of\nthe mutations that cause diabetes are\ndominantly inherited.\nMaturity-Onset Diabetes of th... | [
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0.0036603319458663464,
0.07436228543519974,
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0.00... |
dominantly inherited.\nMaturity-Onset Diabetes of the\nYoung\nMODY is frequently characterized by onset\nof hyperglycemia at an early age (classically\nbefore age 25 years, although diagnosis\nmay occur at older ages). MODY is charac-\nt e r i z e db yi m p a i r e di n s u l i ns e c r e t i o nw i t h | [
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0.07584988325834274,
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0.05808491259813309,
0.06187250465154648,
-0.012231150642037392,
0.013... |
t e r i z e db yi m p a i r e di n s u l i ns e c r e t i o nw i t h\nminimal or no defects in insulin action (inthe absence of coexistent obesity). It is in-\nherited in an autosomal dominant pattern\nw i t ha b n o r m a l i t i e si na tl e a s t1 3g e n e so n\ndifferent chromosomes identi fied to date\n(162). The m... | [
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0.005383908282965422,
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0.053781989961862564,
0.042837340384721756,
0.047994937747716904,
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0.027618998661637306,
0.033192772418260574,
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0.002... |
(162). The most commonly reported forms\nare GCK-MODY (MODY2), HNF1A-MODY\n(MODY3), and HNF4A-MODY (MODY1).\nFor individuals with MODY, the treatment\nimplications are considerable and warrantgenetic testing (163,164). Clinically, people\nwith GCK-MODY exhibit mild, stable fastinghyperglycemia and do not require antihy... | [
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perglycemic therapy, although it is com-\nmonly needed during pregnancy. Individu-\nals with HNF1A-MODY or HNF4A-MODY\nusually respond well to low doses of sulfo-nylureas, which are considered first-line\ntherapy; in some instances, insulin willS32 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supple... | [
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©AmericanDiabetesAssociation | [
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0.0067015099339187145,
0.0... |
be required over time. Mutations or dele-\ntions in HNF1B are associated with renal\ncysts and uterine malformations (renalcysts and diabetes [RCAD] syndrome).Other extremely rare forms of MODYhave been reported to involve other tran-scription factor genes, including PDX1\n(IPF1)a n d NEUROD1 .\nDiagnosis of Monogenic ... | [
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(IPF1)a n d NEUROD1 .\nDiagnosis of Monogenic Diabetes\nA diagnosis of one of the three most com-\nmon forms of MODY, including HNF1A-\nMODY, GCK-MODY, and HNF4A-MODY, al-lows for more cost-effective personalizedtherapy (i.e., no therapy for GCK-MODYand sulfonylureas as first-line therapy for\nHNF1A-MODY and HNF4A-MODY)... | [
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HNF1A-MODY and HNF4A-MODY). Addi-\ntionally, diagnosis can lead to identifi ca-\ntion of other affected family members\nand can indicate potential extrapancreaticcomplications in affected individuals. Ge-netic screening (i.e., next-generation se-\nquencing) is increasingly available and\ncost-effective (161,163).\nA dia... | [
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... |
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