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2.7 Having multiple con firmed islet\nautoantibodies is a risk factor for clini-cal diabetes. Testing for dysglycemiamay be used to further forecast near-\nterm risk. When multiple islet autoanti-\nbodies are identi fied, referral to a spe-\ncialized center for further evaluationand/or consideration of a clinical trial | [
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or approved therapy to potentially de-\nlay development of clinical diabetes\nshould be considered. B\n2.8 Standardized islet autoantibody\ntests are recommended for classi fica-\ntion of diabetes in adults who havephenotypic risk factors that overlap\nwith those for type 1 diabetes (e.g.,\nyounger age at diagnosis, uni... | [
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younger age at diagnosis, unintentional\nweight loss, ketoacidosis, or short time\nto insulin treatment). E\nImmune-Mediated Diabetes\nAutoimmune type 1 diabetes accounts for\n5–10% of diabetes and is caused by auto-\nimmune destruction of the pancreatic\nb-cells. Autoimmune markers include islet\ncell autoantibodies a... | [
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cell autoantibodies and autoantibodies to\nglutamic acid decarboxylase (GAD) (suchas GAD65), insulin, the tyrosine phospha-tases islet antigen 2 (IA-2) and IA-2 b,a n d\nzinc transporter 8 (ZnT8). Numerous clini-\ncal studies are being conducted to test | [
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cal studies are being conducted to test\nvarious methods of preventing or delayingtype 1 diabetes in those with evidence ofislet autoimmunity (trialnet.org/our-research/prevention-studies) (42 –44,49,55,56). The\ndisease has strong HLA associations, with\nlinkage to the DQB1 and DRB1 haplo- | [
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linkage to the DQB1 and DRB1 haplo-\ntypes, and genetic screening has beenused in some research studies to identifyhigh-risk populations. Speci fic alleles in\nthese genes can be either predisposing(e.g., DRB1*0301-DQB1*0201 [DR3-DQ2]and DRB1*0401-DQB1*0302 [DR4-DQ8])or protective (e.g., DRB1*1501 and DQA1*\n0102-DQB1*0... | [
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0102-DQB1*0602). Stage 1 of type 1 diabe-\ntes is de fined by the presence of two or\nmore of these autoantibodies and normo-glycemia. At stage 1, the 5-year risk of de-veloping symptomatic type 1 diabetes is/C2444% overall but varies considerably\nbased on number, titer, and speci ficity of | [
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based on number, titer, and speci ficity of\nautoantibodies as well as age of seroconver-sion and genetic risk (47). Stage 2 includesindividuals with multiple islet autoantibod-ies and dysglycemia. At stage 2 of the dis-ease, there is /C2460% risk by 2 years and\n/C2475% risk within 5 years of developing\nsymptomatic ty... | [
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symptomatic type 1 diabetes (57,58).\nThe rate of b-cell destruction is quite\nvariable, being rapid in some individuals(particularly but not exclusively in infantsand children) and slow in others (mainlybut not exclusively adults) (46,59). Childrenand adolescents often present with DKAas the first manifestation of the ... | [
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and rates in the U.S. have increased dra-\nmatically over the past 20 years (30 –32).\nOthers have modest fasting hyperglycemia\nthat can rapidly change to severe hypergly-cemia and/or DKA with infection or otherstress. Adults may retain suf ficient b-cell\nfunction to prevent DKA for many years;such individuals may hav... | [
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decreased insulin needs for months or\nyears, eventually become dependent oninsulin for survival, and are at risk for DKA(33–35,60,61). At this later stage of thed i s e a s e ,t h e r ei sl i t t l eo rn oi n s u l i ns e c r e -tion, as manifested by low or undetectablelevels of plasma C-peptide. Immune-mediated diab... | [
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mon form of diabetes in childhood and\nadolescence, but it can occur at anyage.\nAutoimmune destruction of b-cells has\nmultiple genetic factors and is also re-lated to environmental factors that arestill poorly defi ned. Although individuals | [
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do not typically have obesity when theypresent with type 1 diabetes, obesity isincreasingly common in the general pop-ulation; as such, obesity should not pre-\nclude testing for type 1 diabetes. People | [
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clude testing for type 1 diabetes. People\nwith type 1 diabetes are also prone toother autoimmune disorders, such asHashimoto thyroiditis, Graves disease, ce-liac disease, Addison disease, vitiligo, au-toimmune hepatitis, myasthenia gravis,and pernicious anemia (see Section 4,“Comprehensive Medical Evaluation and | [
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Assessment of Comorbidities” ). Type 1 di-\nabetes can be associated with monogenic\npolyglandular autoimmune syndromes, | [
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polyglandular autoimmune syndromes,\nincluding immune dysregulation, polyen-docrinopathy, enteropathy, and X-linked(IPEX) syndrome, which is an early-onsetsystemic autoimmune, genetic disordercaused by mutation of the forkhead boxprotein 3 (FOXP3 ) gene, and another dis-\norder caused by the autoimmune regula-tor (AIRE... | [
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Introduction of immunotherapy, specif-\nically checkpoint inhibitors, for cancer\ntreatment has led to unexpected adverse | [
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treatment has led to unexpected adverse\nevents, including immune system activa-tion precipitating autoimmune disease.Fulminant onset of type 1 diabetes canoccur, with DKA and low or undetectablelevels of C-peptide as a marker of endoge-nousb-cell function (64 –66). Fewer thanTable 2.3 —Staging of type 1 diabetes\nStag... | [
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Stage 1 Stage 2 Stage 3\nCharacteristics /C15Autoimmunity /C15Autoimmunity /C15Autoimmunity\n/C15Normoglycemia /C15Dysglycemia /C15Overt hyperglycemia\n/C15Presymptomatic /C15Presymptomatic /C15Symptomatic\nDiagnostic criteria /C15Multiple islet\nautoantibodies\n/C15No IGT or IFG/C15Islet autoantibodies (usually multip... | [
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/C15Dysglycemia: IFG and/or IGT\n/C15FPG 100 –125 mg/dL (5.6 –6.9 mmol/L)\n/C152-h PG 140 –199 mg/dL (7.8 –11.0 mmol/L)\n/C15A1C 5.7 –6.4% (39 –47 mmol/mol) or $10%\nincrease in A1C/C15Autoantibodies may become absent\n/C15Diabetes by standard criteria | [
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/C15Diabetes by standard criteria\nAdapted from Skyler et al. (40). FPG, fasting plasma glucose; IFG, impaired fasting glucose; IGT, impaired glucose tolerance; 2-h PG, 2-h plasmaglucose. Alternative additional stage 2 diagnostic criteria of 30-, 60-, or 90-min plasma glucose on oral glucose tolerance test $200 mg/dL | [
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($11.1 mmol/L) and con firmatory testing in those aged $18 years have been used in clinical trials (79).S24 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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Type 1 \ndiabetesIndeterminate9\nConsider repeat \nC-peptide at >5 yearsType 2 \ndiabetesGenetic testing for \nmonogenic diabetes \nwhere available6Are there features of \ntype 2 diabetes?5 Test C-peptide4Are there features of monogenic diabetes?3Islet autoantibody negative\n(5-10% of adult-onset type 1 diabetes)Islet ... | [
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(5-10% of adult-onset type 1 diabetes)Islet autoantibody positive\nType 1 diabetes Age\nUnclear classification7\nMake clinical decision as to \nhow person with diabetes \nshould be treated\nTrial of noninsulin therapy may \n8\nConsider C-peptide4 test after \n>3 years duration>35 years\nYes No | [
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8\nConsider C-peptide4 test after \n>3 years duration>35 years\nYes No\n<200 pmol/L 200-600 pmol/L >600 pmol/L <200 pmol/L >200 pmol/L NoTest islet autoantibodies2\n<35 years\nYesAdult with suspected type 1 diabetes1Flow chart for investigation of suspected type 1 diabetes in newly \ndiagnosed adults, based on data fro... | [
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diagnosed adults, based on data from White European populations\nFigure 2.1 —Flowchart for investigation of suspected type 1 diabetes in newly diagnosed adults, based on data from White European populations.1No sin- | [
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gle clinical feature con firms type 1 diabetes in isolation.2Glutamic acid decarboxylase (GAD) should be the primary antibody measured and, if negative,\nshould be followed by islet tyrosine phosphatase 2 (IA-2) and/or zinc transporter 8 (ZnT8) where these tests are available. In individuals who have no t | [
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been treated with insulin, antibodies against insulin may also be useful. In those diagnosed at <3 5y e a r so fa g ew h oh a v en oc l i n i c a lf e a t u r e so ft y p e2d i a -\nbetes or monogenic diabetes, a negative result does not change the diagnosis of type 1 diabetes, since 5 –10% of people with type 1 diabet... | [
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antibodies.3Monogenic diabetes is suggested by the presence of one or more of the following features: A1C <58 mmol/mol ( <7.5%) at diagnosis, one\nparent with diabetes, features of a speci fic monogenic cause (e.g., renal cysts, partial lipodystrophy, maternally inherited deafness, and severe insulin resis- | [
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tance in the absence of obesity), and monogenic diabetes prediction model probability >5% (diabetesgenes.org/exeter-diabetes-app/ModyCalculator).\n4A C-peptide test is only indicated in people receiving insulin treatment. A random sample (with concurrent glucose) within 5 h of eating can replace a f or- | [
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mal C-peptide stimulation test in the context of classi fication. If the result is $600 pmol/L ( $1.8 ng/mL), the circumstances of testing do not matter. If\nthe result is <600 pmol/L ( <1.8 ng/mL) and the concurrent glucose is <4m m o l / L( <70 mg/dL) or the person may have been fasting, consider repeating | [
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the test. Results showing very low levels (e.g., <80 pmol/L [ <0.24 ng/mL]) do not need to be repeated. Where a person is insulin treated, C-peptide\nmust be measured prior to insulin discontinuation to exclude severe insulin defi ciency. Do not test C-peptide within 2 weeks of a hyperglycemic emer- | [
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gency.5Features of type 2 diabetes include increased BMI ( $25 kg/m2), absence of weight loss, absence of ketoacidosis, and less marked hyperglycemia.\nLess discriminatory features include non-White ethnicity, family history, longer duration and milder severity of symptoms prior to presentation, features | [
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of the metabolic syndrome, and absence of a family history of autoimmunity.6If genetic testing does not confi rm monogenic diabetes, the classi fication\nis unclear and a clinical decision should be made about treatment.7Type 2 diabetes should be strongly considered in older individuals. In some cases, in- | [
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vestigation for pancreatic or other types of diabetes may be appropriate.8A person with possible type 1 diabetes who is not treated with insulin will re-\nquire careful monitoring and education so that insulin can be rapidly initiated in the event of glycemic deterioration.9C-peptide values 200 –600 pmol/L | [
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(0.6–1.8 ng/mL) are usually consistent with type 1 diabetes or maturity-onset diabetes of the young but may occur in insulin-treated type 2 diabetes, par-\nticularly in people with normal or low BMI or after long duration. Reprinted and adapted from Holt et al. (36).diabetesjournals.org/care Diagnosis and Classificatio... | [
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©AmericanDiabetesAssociation | [
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half of these individuals have autoanti-\nbodies that are seen in type 1 diabetes,\nsupporting alternate pathobiology. Thisimmune-related adverse event occurs injust under 1% of checkpoint inhibitor – | [
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treated individuals but most commonlyoccurs with agents that block the pro-grammed cell death protein 1/programmedcell death ligand 1 pathway alone or in com-bination with other checkpoint inhibitors\n(67). To date, the majority of immune\ncheckpoint inhibitor –related cases of type 1 | [
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checkpoint inhibitor –related cases of type 1\ndiabetes occur in people with high-riskHLA-DR4 (present in 76% of individuals),whereas other high-risk HLA alleles are notmore common than those in the generalpopulation (67). To date, risk cannot be pre-dicted by family history or autoantibodies,so all health care profess... | [
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these medications or caring for people who\nhave a history of current or past exposure tothese agents should be mindful of this ad-verse effect and educate and monitor indi-viduals appropriately.\nA number of viruses have been associated | [
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A number of viruses have been associated\nwith type 1 diabetes, including enterovirusessuch as Coxsackievirus B. During the corona-virus disease 2019 (COVID-19) pandemic,c a s e so fh y p e r g l y c e m i a ,D K A ,a n dn e wdiabetes increased, suggesting that severe\nacute respiratory syndrome coronavirus 2 | [
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acute respiratory syndrome coronavirus 2\n(SARS-CoV-2) is a trigger for or can unmasktype 1 diabetes (68). Possible mechanismsofb-cell damage include virus-triggered\nb-cell death, immune-mediated loss of\npancreatic b-cells, and damage to b-cells | [
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pancreatic b-cells, and damage to b-cells\nbecause of infection of surrounding exo-crine cells. The cytokine storm associatedwith COVID-19 infection is a highly in flam-\nmatory state that could also contribute. Tobetter characterize and understand thepathogenesis of new-onset COVID-19 –re- | [
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lated diabetes, a global registry, CoviDIAB,has been established (69).\nIdiopathic Type 1 Diabetes\nSome forms of type 1 diabetes have noknown etiologies. Individuals have per-manent insulinopenia and are prone toDKA but have no evidence of b-cell auto-\nimmunity. However, only a minority ofpeople with type 1 diabetes ... | [
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category.\nIndividuals with autoantibody-negative\ndiabetes of African or Asian ancestry may\nsuffer from episodic DKA and exhibit vary-ing degrees of insulin de ficiency between\nepisodes (70). This form of diabetes isusually considered a form of type 2diabetes (ketosis-prone type 2 diabetes),\nis strongly inherited, a... | [
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is strongly inherited, and is not HLA asso-\nciated. An absolute requirement for insu-lin replacement therapy in affectedindividuals may be intermittent. Futureresearch is needed to determine thecause of b-cell dysfunction/destruction in\nthis rare clinical scenario.\nScreening for Type 1 Diabetes Risk | [
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this rare clinical scenario.\nScreening for Type 1 Diabetes Risk\nT h ei n c i d e n c ea n dp r e v a l e n c eo ft y p e1d i -abetes are increasing (71). People withtype 1 diabetes often present with acute\nsymptoms of diabetes and markedly ele-\nvated blood glucose levels, and 25 –50%\nare diagnosed with life-threat... | [
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are diagnosed with life-threatening DKA\n(30–32). Multiple studies indicate that\nmeasuring islet autoantibodies in relativesof those with type 1 diabetes (47) or in\nchildren from the general population\n(72,73) can effectively identify those who\nwill develop type 1 diabetes. A study re-ported the risk of progression... | [
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abetes from the time of seroconversion to\nautoantibody positivity in three pediatric\ncohorts from Finland, Germany, and the\nU.S. Of the 585 children who developed\nmore than two autoantibodies, nearly\n70% developed type 1 diabetes within\n10 years and 84% within 15 years (42).\nThese findings are highly signifi cant,... | [
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These findings are highly signifi cant, be-\ncause while the German group was re-cruited from offspring of parents withtype 1 diabetes, the Finnish and American\ngroups were recruited from the general\npopulation. Remarkably, the findings in all\nthree groups were the same, suggestingthat the same sequence of events led t... | [
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clinical disease in both “sporadic ”and fa-\nmilial cases of type 1 diabetes. Indeed,the risk of type 1 diabetes increases as\nthe number of relevant autoantibodies\ndetected increases (55,74,75). In The\nEnvironmental Determinants of Diabetes\nin the Young (TEDDY) study, type 1 diabe- | [
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in the Young (TEDDY) study, type 1 diabe-\ntes developed in 21% of 363 subjectswith at least one autoantibody at 3 years\nof age (76). Such testing, coupled with\neducation about diabetes symptoms and\nclose follow-up, has been shown to en-\nable earlier diagnosis and to prevent\nDKA (77,78).\nSeveral screening program... | [
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DKA (77,78).\nSeveral screening programs are available\nin Europe (e.g., Fr1da and gppad.org) and\nthe U.S. (e.g., trialnet.org, askhealth.org,and cascadekids.org). Family history ofautoimmune diabetes and personal or\nfamily history of allergic diseases or otherautoimmune diseases increases the risk of\nautoimmune dia... | [
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autoimmune diabetes compared with the\ngeneral population (78,79). Individualswho test autoantibody positive should be\nprovided with or referred for counseling\nabout the risk of developing diabetes, dia-\nbetes symptoms, and DKA prevention and\nshould be given consideration for addi-tional testing as applicable to he... | [
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mine if they meet criteria for intervention\naimed at delaying progression.\nPREDIABETES AND TYPE 2\nDIABETES\nRecommendations\n2.9 Screening for prediabetes and\ntype 2 diabetes with an assessment\nof risk factors or validated risk calcula-tor should be done in asymptomatic\nadults. B\n2.10a Testing for prediabetes or... | [
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0.0... |
adults. B\n2.10a Testing for prediabetes or type 2\ndiabetes in asymptomatic people should\nbe considered in adults of any age with\noverweight or obesity who have one\nor more risk factors ( Table 2.4 ).B\n2.10b For all other people, screening\nshould begin at age 35 years. B\n2.11 If tests are normal, repeat screen- | [
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2.11 If tests are normal, repeat screen-\ning recommended at a minimum of3-year intervals is reasonable, sooner\nwith symptoms or change in risk (e.g.,\nweight gain). C\n2.12 To screen for prediabetes and\ntype 2 diabetes, FPG, 2-h PG during\n75-g OGTT, and A1C are each appro-\npriate ( Table 2.1 andTable 2.2 ).B\n2.13... | [
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2.13 When using OGTT as a screen for\nprediabetes or diabetes, adequate car-bohydrate intake (at least 150 g/day)should be assured for 3 days prior to\ntesting. A\n2.14 Risk-based screening for predia-\nbetes or type 2 diabetes should be con-\nsidered after the onset of puberty or\nafter 10 years of age, whichever occu... | [
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after 10 years of age, whichever occurs\nearlier, in children and adolescents\nwith overweight (BMI $85th percen-\ntile) or obesity (BMI $95th percentile)\nand who have one or more risk factors\nfor diabetes. (See Table 2.5 for evi-\ndence grading of risk factors.) B\n2.15a Consider screening people for | [
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dence grading of risk factors.) B\n2.15a Consider screening people for\nprediabetes or diabetes if on certainmedications, such as glucocorticoids,statins, thiazide diuretics, some HIVS26 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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medications, and second-generation\nantipsychotic medications, as theseagents are known to increase the riskof these conditions. E\n2.15b In people who are prescribed\nsecond-generation antipsychotic medi-cations, screen for prediabetes anddiabetes at baseline and repeat 12 –16 | [
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weeks after medication initiation or soon-er, if clinically indicated, and annually. B\n2.16 People with HIV should be\nscreened for diabetes and prediabeteswith an FPG test before starting antire-troviral therapy, at the time of switchingantiretroviral therapy, and 3 –6m o n t h s\nafter starting or switching antiretr... | [
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0.0371750... |
after starting or switching antiretroviral\ntherapy. If initial screening results are\nnormal, FPG should be checked annu-ally.E\nPrediabetes\nPrediabetes is the term used for individ-\nuals whose glucose or A1C levels do not | [
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uals whose glucose or A1C levels do not\nmeet the criteria for diabetes yet haveabnormal carbohydrate metabolism thatresults in elevated glucose levels (dysgly-cemia) intermediate between normogly-cemia and diabetes (28,80). People withprediabetes are defi ned by the presence\nof IFG and/or IGT and/or A1C 5.7 –6.4% | [
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of IFG and/or IGT and/or A1C 5.7 –6.4%\n(39–47 mmol/mol) ( Table 2.2 ). As predi-\nabetes is an intermediate state betweennormoglycemia and diabetes, it is clearlyas i g n i ficant risk factor for progression todiabetes as well as cardiovascular disease | [
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and several other cardiometabolic out-comes. Criteria for screening for diabetesor prediabetes in asymptomatic adults areoutlined in Table 2.4 . Prediabetes is asso- | [
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ciated with obesity (especially abdominalor visceral obesity), dyslipidemia with hightriglycerides and/or low HDL cholesterol,and hypertension. The presence of predi-abetes should prompt comprehensivescreening for cardiovascular risk factors.\nDiagnosis of Prediabetes\nIFG is de fined as FPG levels from 100 to | [
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-0.... |
Diagnosis of Prediabetes\nIFG is de fined as FPG levels from 100 to\n125 mg/dL (from 5.6 to 6.9 mmol/L)(78,79) and IGT as 2-h PG levels during75-g OGTT from 140 to 199 mg/dL (from7.8 to 11.0 mmol/L) (10). It should benoted that the World Health Organization\nand a number of diabetes organizationsdefine the IFG lower limi... | [
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0.021175608038902283,
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0.0... |
(6.1 mmol/L). The ADA also initially endorsedthis IFG lower limit in 1997 (10). However, in\n2003 the ADA adopted the new range of\n100– 125 mg/dL (5.6– 6.9 mmol/L) to better\ndefine IFG so that the population risk of de-\nveloping diabetes with IFG would be similar\nto that with IGT (11).\nAs with the glucose measures,... | [
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to that with IGT (11).\nAs with the glucose measures, several\nprospective studies that used A1C to pre-\ndict the progression to diabetes as de fined\nby A1C criteria demonstrated a strong,\ncontinuous association between A1C and\nsubsequent diabetes. In a systematic re-view of 44,203 individuals from 16 cohortstudies ... | [
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0.04946999251842499,
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0.0028822962194681168,
0.0006244084215722978,
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5.6 years (range 2.8 –12 years), those with\nA1C between 5.5% and 6.0% (between 37\nand 42 mmol/mol) had a substantially in-creased risk of diabetes (5-year incidence\nfrom 9% to 25%). Those with an A1C range\nof 6.0 –6.5% (42– 48 mmol/mol) had a\n5-year risk of developing diabetes be-t w e e n2 5 %a n d5 0 %a n dar e ... | [
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0.06698838621377945,
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0.14264188706874847,
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20 times higher than that with A1C of\n5.0% (31 mmol/mol) (81). In a commu-nity-based study of African Americanand non-Hispanic White adults withoutdiabetes, baseline A1C was a stronger\npredictor of subsequent diabetes and\ncardiovascular events than fasting glu-cose (82). Other analyses suggest thatA1C of 5.7% (39 mm... | [
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-0.05544034019112587,
0.07584044337272644,
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-0.02857299894094467,
0.020321860909461975,
0.08343392610549927,
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-0.0604766383767128,
-0.010223370045423508,
0.02918272279202938,
-0.07509131729602814,
-0.0... |
associated with a diabetes risk similar\nto that of the high-risk participants in theDiabetes Prevention Program (DPP) (83),and A1C at baseline was a strong pre-\ndictor of the development of glucose-\ndefined diabetes during the DPP and\nits follow-up (7).Table 2.4 —Criteria for screening for diabetes or prediabetes in... | [
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0.0367424339056015,
0.01943066157400608,
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0.040129102766513824,
0.11306639760732651,
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adults\n1. Testing should be considered in adults with overweight or obesity (BMI $25 kg/m2or$23 kg/m2\nin Asian American individuals) who have one or more of the following risk factors:\n/C15First-degree relative with diabetes\n/C15High-risk race and ethnicity (e.g., African American, Latino, Native American, Asian\nA... | [
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0.09904100000858307,
-0.04350903630256653,
0.034482356160879135,
-0.014255539514124393,
-0.022953609004616737,
0.0322284996509552,
0.00448269909247756,
-0.03960752859711647,
-0.004829382058233023,
0.011455281637609005,
-0.08218532055616379,
-0.08554918318986893,
-0.00... |
American, Paci fic Islander)\n/C15History of cardiovascular disease\n/C15Hypertension ( $130/80 mmHg or on therapy for hypertension)\n/C15HDL cholesterol level <35 mg/dL ( <0.9 mmol/L) and/or a triglyceride level >250 mg/dL\n(>2.8 mmol/L)\n/C15Individuals with polycystic ovary syndrome\n/C15Physical inactivity | [
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0.0796385332942009,
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-0.06443610787391663,
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0.06695589423179626,
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-0.0... |
/C15Physical inactivity\n/C15Other clinical conditions associated with insulin resistance (e.g., severe obesity,acanthosis nigricans)\n2. People with prediabetes (A1C $5.7% [$39 mmol/mol], IGT, or IFG) should be tested yearly.\n3. People who were diagnosed with GDM should have lifelong testing at least every 3 years. | [
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0.034649092704057693,
0.016783885657787323,
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0.031190011650323868,
0.10174145549535751,
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0.033077433705329895,
-0.006313483230769634,
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... |
4. For all other people, testing should begin at age 35 years.\n5. If results are normal, testing should be repeated at a minimum of 3-year intervals, with\nconsideration of more frequent testing depending on initial results and risk status.\n6. People with HIV, exposure to high-risk medicines, history of pancreatitis | [
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0.045234695076942444,
-0.0009183171787299216,
0.06117180362343788,
-0.07607457041740417,
0.03603873774409294,
0.05956881865859032,
0.016208196058869362,
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0... |
GDM, gestational diabetes mellitus; IFG, impaired fasting glucose; IGT, impaired glucose tolerance.\nTable 2.5 —Risk-based screening for type 2 diabetes or prediabetes in\nasymptomatic children and adolescents in a clinical setting\nScreening should be considered in youth* who have overweight ( $85th percentile) or | [
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0.011758660897612572,
-0.04056573286652565,
0.051479801535606384,
0.006000159308314323,
0.08585013449192047,
0.10763590037822723,
-0.09910412132740021,
0.028316225856542587,
0.018023187294602394,
0.01713332161307335,
-0.11983316391706467,
0.01121... |
obesity ( $95th percentile) Aand who have one or more additional risk factors based\non the strength of their association with diabetes:\n/C15Maternal history of diabetes or GDM during the child ’s gestation A\n/C15Family history of type 2 diabetes in first- or second-degree relative A | [
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0.05252862721681595,
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0.06597089767456055,
0.03410540893673897,
0.03721332922577858,
0.052262190729379654,
0.058271437883377075,
-0.07495798915624619,
0.027120929211378098,
0.02510063908994198,
-0.036675531417131424,
-0.08288563787937164,
-0.04269... |
/C15Race and ethnicity (e.g., Native American, African American, Latino, Asian American,\nPacific Islander) A\n/C15Signs of insulin resistance or conditions associated with insulin resistance (acanthosis\nnigricans, hypertension, dyslipidemia, polycystic ovary syndrome, or small-for-gestational-\nage birth weight) B | [
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0.03997368738055229,
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0.05212550237774849,
0.024986278265714645,
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0.034044552594423294,
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-0.08380035310983658,
-0.0... |
age birth weight) B\nGDM, gestational diabetes mellitus. *After the onset of puberty or after 10 years of age, which-ever occurs earlier. If tests are normal, repeat testing at a minimum of 3-year intervals (or more\nfrequently if BMI is increasing or risk factor pro file is deteriorating) is recommended. Reports of | [
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0.032036688178777695,
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0.05... |
type 2 diabetes before age 10 years exist, and this can be considered with numerous risk factors.diabetesjournals.org/care Diagnosis and Classification of Diabetes S27\n©AmericanDiabetesAssociation | [
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0.03... |
An A1C range of 5.7– 6.4% (39–\n47 mmol/mol) identi fies a group of indi-\nviduals at high risk for diabetes and car-\ndiovascular outcomes. Similar to thosewith IFG and/or IGT, individuals with A1Cof 5.7 –6.4% (39– 47 mmol/mol) should be | [
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0... |
informed of their increased risk for diabe-tes and cardiovascular disease and coun-seled about effective strategies to lowertheir risks (see Section 3, “Prevention\nor Delay of Diabetes and AssociatedComorbidities ”). Similar to glucose meas- | [
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0.04853126406669617,
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0.01762612722814083,
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0.02146686241030693,
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urements, the continuum of risk is contin-uous: as A1C rises, the diabetes risk risesdisproportionately (81). Aggressive inter-ventions and vigilant follow-up shouldbe pursued for those considered at veryhigh risk (e.g., those with A1C >6.0%\n[>42 mmol/mol] and individuals with\nboth IFG and IGT).\nTable 2.4 outlines t... | [
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0.05492110550403595,
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0.06894979625940323,
0.04896649345755577,
0.12735386192798615,
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0.02219030074775219,
-0.014685271307826042,
-0.0003071215469390154,
-0.06378220021724701,
-... |
both IFG and IGT).\nTable 2.4 outlines the criteria for\nscreening for prediabetes. The ADA risktest is an additional option for assess-ment to determine the appropriatenessof screening for diabetes or prediabetesin asymptomatic adults ( Fig. 2.2)( o n l i n e | [
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0.021435387432575226,
0.08534181118011475,
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0.10988274216651917,
0.11004289239645004,
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0.013018126599490643,
-0.01814623922109604,
-0.01082422025501728,
-0.10980857163667679,
0.02329... |
at diabetes.org/socrisktest). For additionalbackground regarding risk factors andscreening for prediabetes, see\nSCREENING\nAND TESTING FOR PREDIABETES AND TYPE 2DIABETES IN\nASYMPTOMATIC ADULTS and SCREENING AND TESTING\nFOR PREDIABETES AND TYPE 2DIABETES IN CHILDREN\nAND ADOLESCENTS , below. For details regard- | [
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-0.0120621332898736,
0.012645463459193707,
0.02218872867524624,
0.041452351957559586,
0.08459644764661789,
-0.03579717501997948,
0.03527156263589859,
-0.0003692144528031349,
0.05665447935461998,
-0.12626726925373077,
0.041837... |
AND ADOLESCENTS , below. For details regard-\ning individuals with prediabetes mostlikely to bene fit from a formal behavioral\nor lifestyle intervention, see Section 3,“Prevention or Delay of Diabetes and\nAssociated Comorbidities. ”\nType 2 Diabetes\nType 2 diabetes accounts for 90 –95% of | [
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0.008265... |
Type 2 Diabetes\nType 2 diabetes accounts for 90 –95% of\nall diabetes. This form encompasses indi-viduals who generally have relative (rather\nthan absolute) insulin de ficiency and have\nperipheral insulin resistance (i.e., decreased\nbiological response to insulin).\nThere are various causes of type 2 dia-\nbetes. Al... | [
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0.000... |
betes. Although the speci fic etiologies\nare not known, autoimmune destructionofb-cells does not occur, and individuals\ndo not have any of the other knowncauses of diabetes. Most, but not all,people with type 2 diabetes have over-\nweight or obesity. Excess weight itself | [
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weight or obesity. Excess weight itself\ncauses some degree of insulin resistance.Individuals who do not have obesity oroverweight by traditional weight criteriamay have an increased percentage ofbody fat distributed predominantly inthe abdominal region, including sites in- | [
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volved in nonalcoholic fatty liver disease(also known as metabolic dysfunction-associated steatotic liver disease) and/orectopic sites (e.g., skeletal muscle).\nDKA seldom occurs spontaneously in\ntype 2 diabetes; when seen, it usuallyarises in individuals already treated with in-sulin (e.g., missed or inadequate doses... | [
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0.08409306406974792,
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0.06636396795511246,
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0.02079... |
people with ketosis-prone type 2 diabetes,\nin association with the stress of another ill-ness such as infection (e.g., COVID-19) ormyocardial infarction, or in association withillicit drug use (e.g., cocaine) or with the use\nof certain medications such as glucocorti- | [
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of certain medications such as glucocorti-\ncoids, second-generation antipsychotics, orsodium –glucose cotransporter 2 inhibitors\n(84,85). Type 2 diabetes frequently goes un-\ndiagnosed for many years, because hyper-\nglycemia develops gradually and, at earlierstages, is often not severe enough for theindividual to no... | [
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0... |
symptoms caused by hyperglycemia, such\nas dehydration or unintentional weightloss. Nevertheless, even undiagnosed peo-ple with diabetes are at increased risk of\ndeveloping macrovascular and microvascu-\nlar complications.\nPeople with type 2 diabetes early in\nthe disease course may have insulin levelsthat appear nor... | [
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... |
failure to normalize blood glucose re flects\na relative defect in glucose-stimulated\ninsulin secretion that is insuf ficient to\ncompensate for insulin resistance. Insu-lin resistance may improve with weight\nreduction, physical activity, and/or phar- | [
-0.05235041305422783,
0.027207346633076668,
-0.04811517894268036,
0.056256625801324844,
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0.009899533353745937,
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-0.... |
reduction, physical activity, and/or phar-\nmacologic treatment of hyperglycemiabut is seldom restored to normal. Recentinterventions with intensive diet and exer-\ncise, newer pharmacological agents (e.g.,\nglucagon-like peptide 1 receptor agonists),or surgical weight loss have led to diabe-tes remission (86 –92) (see... | [
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0.02479475736618042,
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-0... |
“Obesity and Weight Management for\nthe Prevention and Treatment of Type 2Diabetes ”).\nThe risk of developing type 2 diabetes\nincreases with age, obesity, and lack of\nphysical activity (93,94). It occurs more\nfrequently in individuals with prediabetes,prior gestational diabetes mellitus, or poly-cystic ovary syndro... | [
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-0.049806... |
mon in people with hypertension or\ndyslipidemia and in certain racial and eth-nic subgroups (e.g., African American, Na-tive American, Hispanic/Latino, and AsianAmerican). It is often associated with a\nstrong genetic predisposition or family his- | [
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0.06920135766267776,
-0.09757737070322037,
0.07975799590349197,
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0.039056237787008286,
-0.09976709634065628,
-0.014751083217561245,
-0.0303... |
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