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cost-effective (161,163).\nA diagnosis of MODY should be consid-\nered in individuals who have atypical dia-betes and multiple family members withdiabetes not characteristic of type 1 or\ntype 2 diabetes, although admittedly,\natypical diabetes is becoming increasingly\ndifficult to precisely de fine in the absence | [
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difficult to precisely de fine in the absence\nof a defi nitive set of tests for either type\nof diabetes (158 –160,163 –169) ( Fig. 2.1 ).\nIn most cases, the presence of autoanti-bodies for type 1 diabetes precludes fur-\nther testing for monogenic diabetes, but | [
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ther testing for monogenic diabetes, but\nthe presence of autoantibodies in peoplewith monogenic diabetes has been re-ported (170). Individuals in whom mono-genic diabetes is suspected should be\nreferred to a specialist for further evalua- | [
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referred to a specialist for further evalua-\ntion. Readily available commercial genetictesting following the criteria listed belownow enables a cost-effective (170), oftencost-saving, genetic diagnosis that is in-\ncreasingly supported by health insurance. A | [
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creasingly supported by health insurance. A\nbiomarker screening pathway, such as thecombination of urinary C-peptide/creatinineratio and antibody screening, may aid in de-termining who should get genetic testing\nfor MODY (171). It is critical to correctly di- | [
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agnose one of the monogenic forms of dia-betes, because these individuals may be in-correctly diagnosed with type 1 or type 2diabetes, leading to suboptimal, even po-tentially harmful, treatment plans and de-lays in diagnosing other family members(172). The correct diagnosis is especiallycritical for those with GCK-MOD... | [
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especiallycritical for those with GCK-MODY muta-tions, where multiple studies have shown | [
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that no complications ensue in the absence\nof glucose-lowering therapy (173). It hasbeen reported that low hs-CRP can beused in identifying those more likely tohave HNF1A-MODY as opposed to otherforms of diabetes, supporting genetic test-ing in such individuals (174). The risks ofmicrovascular and macrovascular compli... | [
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cations with HNF1A-MODY and HNF4A-\nMODY are similar to those observed inpeople with type 1 and type 2 diabetes(175,176). Genetic counseling is recom-mended to ensure that affected individu-als understand the patterns of inheritanceand the importance of a correct diagnosisand to address comprehensive cardiovas-cular ri... | [
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The diagnosis of monogenic diabetes\nshould be considered in children andadults diagnosed with diabetes in earlyadulthood with the following findings:Table 2.6 —Most common causes of monogenic diabetes\nGene Inheritance Clinical features\nMODY HNF1A AD HNF1A-MODY: progressive insulin secretory defect with presentation i... | [
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or early adulthood; lowered renal threshold for glucosuria; large rise in 2-h PG\nlevel on OGTT ( >90 mg/dL [ >5 mmol/L]); sensitive to sulfonylureas\nHNF4A AD HNF4A-MODY: progressive insulin secretory defect with presentation in | [
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adolescence or early adulthood; may have large birth weight andtransient neonatal hypoglycemia; sensitive to sulfonylureas\nHNF1B AD HNF1B-MODY: developmental renal disease (typically cystic); genitourinary\nabnormalities; atrophy of the pancreas; hyperuricemia; gout | [
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abnormalities; atrophy of the pancreas; hyperuricemia; gout\nGCK AD GCK-MODY: higher glucose threshold (set point) for glucose-stimulated insulin\nsecretion, causing stable, nonprogressive elevated fasting blood glucose;\ntypically does not require treatment; microvascular complications are rare; | [
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-... |
small rise in 2-h PG level on OGTT ( <54 mg/dL [ <3 mmol/L])\nNeonatal diabetes KCNJ11 AD Permanent or transient: IUGR; possible developmental delay and seizures;\nresponsive to sulfonylureas\nINS AD Permanent: IUGR; insulin requiring\nABCC8 AD Permanent or transient: IUGR; rarely developmental delay; responsive to\nsu... | [
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sulfonylureas\n6q24 ( PLAGL1 ,\nHYMA1 )AD for paternal\nduplicationsTransient: IUGR; macroglossia; umbilical hernia; mechanisms include\nUPD6, paternal duplication, or maternal methylation defect; may betreatable with medications other than insulin\nGATA6 AD Permanent: pancreatic hypoplasia; cardiac malformations; panc... | [
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exocrine insuf ficiency; insulin requiring\nEIF2AK3 AR Permanent: Wolcott-Rallison syndrome: epiphyseal dysplasia; pancreatic\nexocrine insuf ficiency; insulin requiring\nEIF2B1 AD Permanent diabetes: can be associated with fluctuating liver function (157)\nFOXP3 X-linked Permanent: immunodysregulation, polyendocrinopathy... | [
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X-linked (IPEX) syndrome: autoimmune diabetes, autoimmune thyroiddisease, exfoliative dermatitis; insulin requiring\nAdapted from Carmody et al. (156). AD, autosomal dominant; AR, autosomal recessive; IUGR, intrauterine growth restriction; OGTT, oral glu- | [
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cose tolerance test; UPD6, uniparental disomy of chromosome 6; 2-h PG, 2-h plasma glucose.diabetesjournals.org/care Diagnosis and Classification of Diabetes S33\n©AmericanDiabetesAssociation | [
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\x81Diabetes diagnosed within the first\n6 months of life (with occasional cases\npresenting later, mostly INSandABCC8\nmutations) (157,177)\n\x81Diabetes without typical features oftype 1 or type 2 diabetes (negative di-abetes-associated autoantibodies, noobesity, and lacking other metabolicfeatures, especially with st... | [
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\x81Stable, mild fasting hyperglycemia\n(100– 150 mg/dL [5.6 –8.5 mmol/L]),\nstable A1C between 5.6% and 7.6%\n(between 38 and 60 mmol/mol), es-pecially if no obesity\nGESTATIONAL DIABETES MELLITUS\nRecommendations\n2.25 In individuals who are planning\npregnancy, screen those with risk fac-\ntors ( Table 2.4 )Band con... | [
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tors ( Table 2.4 )Band consider testing\nall individuals of childbearing potentialfor undiagnosed prediabetes or diabe-tes.E\n2.26a Before 15 weeks of gestation,\ntest individuals with risk factors\n(Table 2.4 )Band consider testing all\nindividuals Efor undiagnosed diabetes\nat the first prenatal visit using standard\n... | [
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diagnostic criteria if not screened\npreconception.2.26b Before 15 weeks of gestation,\nscreen for abnormal glucose metab-olism to identify individuals who areat higher risk of adverse pregnancy\nand neonatal outcomes, are more\nlikely to need insulin, and are at highrisk of a later gestational diabetes\nmellitus (GDM)... | [
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mellitus (GDM) diagnosis. BEarly\ntreatment for individuals with abnor-\nmal glucose metabolism may pro-\nvide some bene fit.E\n2.26c Screen for early abnormal glu-\ncose metabolism with dysglycemia us-ing FPG of 110– 125 mg/dL (6.1– 6.9\nmmol/L) or A1C 5.9 –6.4% (41– 47\nmmol/mol). B\n2.27 Screen for GDM at 24 –28 week... | [
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mmol/mol). B\n2.27 Screen for GDM at 24 –28 weeks\nof gestation in pregnant individuals\nnot previously found to have diabe-tes or high-risk abnormal glucose\nmetabolism detected earlier in the\ncurrent pregnancy. A\n2.28 Screen individuals with GDM for\nprediabetes or diabetes at 4 –12 weeks | [
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prediabetes or diabetes at 4 –12 weeks\npostpartum, using the 75-g OGTT andclinically appropriate nonpregnancy\ndiagnostic criteria. A2.29 Individuals with a history of\nGDM should have lifelong screening\nfor the development of prediabetesor diabetes at least every 3 years. B\nDefinition\nFor many years, gestational di... | [
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Definition\nFor many years, gestational diabetes melli-\nt u s( G D M )w a sd e fined as any degree of\nglucose intolerance that was first recog-\nnized during pregnancy (81), regardless oft h ed e g r e eo fh y p e r g l y c e m i a .T h i sd e fini-\ntion facilitated a uniform strategy for detec-tion and classi fication o... | [
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definition has serious limitations (178).\nFirst, the best available evidence revealsthat many cases of GDM represent pre-\nexisting hyperglycemia that is detected\nby routine screening in pregnancy, as rou-\ntine screening is not widely performed in\nnonpregnant individuals of reproductive\nage. It is the severity of h... | [
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age. It is the severity of hyperglycemia\nthat is clinically important regarding bothshort- and long-term maternal and fetal\nrisks.\nThe ongoing epidemic of obesity and\ndiabetes has led to more type 2 diabetes\nin people of reproductive age, with an in-crease in the number of pregnant individ-uals with undiagnosed ty... | [
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early pregnancy (179 –181). Ideally, un-\ndiagnosed diabetes should be identi fied\npreconception in individuals with risk fac-\ntors or in high-risk populations (182 –187),\nas the preconception care of people with\npreexisting diabetes results in lower A1C | [
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preexisting diabetes results in lower A1C\nand reduced risk of birth defects, pretermdelivery, perinatal mortality, small-for-gestational-age birth weight, and neona-tal intensive care unit admission (188). If\nindividuals are not screened prior to\npregnancy, universal early screening at<15 weeks of gestation for undi... | [
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diabetes may be considered over selec-tive screening ( Table 2.4 ), particularly in\npopulations with high prevalence of riskfactors and undiagnosed diabetes inpeople of childbearing age. Strong racialand ethnic disparities exist in the preva-lence of undiagnosed diabetes. There-\nfore, early screening provides an init... | [
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fore, early screening provides an initial\nstep to identify these health disparitiesso that they can begin to be addressed(184–187). Standard diagnostic criteria\nfor identifying undiagnosed diabetes in\nearly pregnancy are the same as those | [
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early pregnancy are the same as those\nused in the nonpregnant population(Table 2.1 ). Individuals found to havediabetes by the standard diagnostic criteria\nused outside of pregnancy should be classi-fied as having diabetes complicating preg-\nnancy (most often type 2 diabetes, rarelytype 1 diabetes or monogenic diabet... | [
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managed accordingly.\nEarly abnormal glucose metabolism,\ndefined as a fasting glucose threshold\nof 110 mg/dL (6.1 mmol/L) or an A1C\nof 5.9% (41 mmol/mol), may identify\nindividuals who are at higher risk of\nadverse pregnancy and neonatal out-comes (preeclampsia, macrosomia, shoul-der dystocia, and perinatal death), ... | [
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more likely to need insulin treatment,\nand are at high risk of a later GDM diag-nosis (189 –194). An A1C threshold of\n5.7% has not been shown to be associ-\nated with adverse perinatal outcomes\n(195,196).\nIf early screening is negative, individuals\nshould be rescreened for GDM between 24and 28 weeks of gestation (... | [
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“Management of Diabetes in Pregnancy ”).\nThe International Association of the\nDiabetes and Pregnancy Study Groups(IADPSG) GDM diagnostic criteria for the75-g OGTT, as well as the GDM screening\nand diagnostic criteria used in the\ntwo-step approach, were not derivedfrom data in the first half of pregnancy\nand should ... | [
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and should not be used for early screen-\ning (197). To date, most randomized con-\ntrolled trials of treatment of earlyabnormal glucose metabolism have beenunderpowered for outcomes. A recent ran-\ndomized controlled trial performed at | [
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domized controlled trial performed at\n17 centers administered early screening(mean 15.6 ± 2.5 weeks) for GDM with a75-g OGTT. Individuals who met WorldHealth Organization criteria for GDM were\nrandomized to receive early treatment or a\nrepeat OGTT at 24 –28 weeks (with de-\nferred treatment if indicated). The first p... | [
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ferred treatment if indicated). The first pri-\nmary outcome measure was an adverse\nneonatal composite outcome includingbirth<37 weeks, birth weight $4.5 kg,\nbirth trauma, neonatal respiratory distresswithin 24 h of birth, phototherapy, stillbirth\nneonatal death, or shoulder dystocia. Early\nGDM treatment resulted in... | [
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GDM treatment resulted in a signifi cant\nbut modest improvement in the compositeadverse neonatal outcome (24.9% earlytreatment vs. 30.5% control, relative risk\n0.82 [0.68– 0.98]), with a suggestion of\nmore bene fit (per prespeci fied subgroup\nanalyses) among individuals who had\nthe OGTT at <14 weeks and among indi- | [
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the OGTT at <14 weeks and among indi-\nviduals with glycemic values in higherranges on their OGTTs (198). Therefore,S34 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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the bene fits of treatment for early abnor-\nmal glucose metabolism remain uncer-\ntain. Nutrition counseling and periodic“block ”testing of glucose levels weekly\nto identify individuals with high glucoselevels are suggested. Testing frequencymay proceed to daily, and treatmentmay be intensi fied, if the FPG is pre-\ndo... | [
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dominantly >110 mg/dL ( >6.1 mmol/L)\nprior to 18 weeks of gestation.\nBoth the FPG and A1C are low-cost\ntests. An advantage of the A1C test is its\nconvenience, as it can be added to the\nprenatal laboratories and does not re-\nquire an early-morning fasting appoint-ment. Disadvantages include inaccuracies\nin the pr... | [
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in the presence of increased red blood\ncell turnover and hemoglobinopathies(usually reads lower) and higher values\nwith anemia and reduced red blood cell\nturnover (199). A1C is not reliable forscreening for GDM or for preexisting diabe-\ntes at 15 weeks of gestation or later; if the\nfirst screening takes place at th... | [
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first screening takes place at this stage, one\ncannot differentiate between preexisting\ndiabetes and GDM with an A1C.\nGDM is often indicative of underlying\nb-cell dysfunction (200), which confers\nmarked increased risk for later develop- | [
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marked increased risk for later develop-\nment of diabetes, generally but not al-ways type 2 diabetes, in the mother afterdelivery (201,202). As effective preven-tion interventions are available (203,204),individuals diagnosed with GDM shouldreceive lifelong screening for prediabetesto allow interventions to reduce dia... | [
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risk and for type 2 diabetes to allow treat-\nment at the earliest possible time (205).\nDiagnosis\nGDM carries risks for the mother, fetus,and neonate. The Hyperglycemia and Ad-verse Pregnancy Outcome (HAPO) study\n(206), a large-scale multinational cohort | [
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(206), a large-scale multinational cohort\nstudy completed by more than 23,000pregnant individuals, demonstrated thatrisk of adverse maternal, fetal, and neonataloutcomes continuously increased as a func-tion of maternal glycemia at 24 –28 weeks\nof gestation, even within ranges previ-ously considered normal for pregna... | [
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For most complications, there was no\nthreshold for risk. These results have ledto careful reconsideration of the diagnos-tic criteria for GDM.\nGDM diagnosis ( Table 2.7 ) can be ac-\ncomplished with either of two strategies:1. The “one-step ”75-g OGTT derived\nfrom the IADPSG criteria, or\n2. The older “two-step ”app... | [
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from the IADPSG criteria, or\n2. The older “two-step ”approach with a\n50-g (nonfasting) screen followed by a\n100-g OGTT for those who screen posi-tive based on the work of Carpenter-Coustan ’s interpretation of the older\nO’Sullivan and Mahan (207) criteria.\nDifferent diagnostic criteria will identify | [
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Different diagnostic criteria will identify\ndifferent degrees of maternal hyperglyce-mia and maternal/fetal risk, leading someexperts to debate, and disagree on, opti-mal strategies for the diagnosis of GDM.\nOne-Step Strategy\nThe IADPSG de fined diagnostic cut points\nfor GDM as the average fasting, 1-h, and2-h PG va... | [
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viduals at 24 –28 weeks of gestation who\nparticipated in the HAPO study at which\nodds for adverse outcomes reached 1.75times the estimated odds of these outcomesa tt h em e a nf a s t i n g ,1 - h ,a n d2 - hP Gl e v e l sof the study population. This one-step strat-\negy was anticipated to signi ficantly increase\nth... | [
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the incidence of GDM (from 5 –6% to\n15–20%), primarily because only one abnor-\nmal value, not two, became suf ficient to\nmake the diagnosis (208). Many regional\nstudies have investigated the impact of\nadopting the IADPSG criteria on prevalence | [
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adopting the IADPSG criteria on prevalence\nand have seen a roughly one- to threefoldincrease (209). The anticipated increase inthe incidence of GDM could have a sub-stantial impact on costs and medical infra-structure needs and has the potential to\n“medicalize ”pregnancies previously cate-\ngorized as normal. A follo... | [
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gorized as normal. A follow-up study of\nindividuals participating in a study ofpregnancy OGTTs with glucose levelsblinded to caregivers found that 11 yearsafter their pregnancies, individuals who\nwould have been diagnosed with GDM by | [
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would have been diagnosed with GDM by\nthe one-step approach, as compared withthose without GDM, were at 3.4-foldhigher risk of developing prediabetes andtype 2 diabetes and had children with ahigher risk of obesity and increased body\nfat, suggesting that the larger group of in-\ndividuals identi fied as having GDM by ... | [
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dividuals identi fied as having GDM by the\none-step approach would benefi tf r o m\nthe increased screening for diabetes andprediabetes after pregnancy (210). TheADA recommends the IADPSG diagnos-\ntic criteria with the intent of optimizing | [
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tic criteria with the intent of optimizing\ngestational outcomes, because thesecriteria are the only ones based onpregnancy outcomes rather than endpoints such as prediction of subsequent\nmaternal diabetes.\nThe expected benefi ts of using IADPSG\ncriteria to the offspring are inferred fromintervention trials that focu... | [
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uals with lower levels of hyperglycemia\nthan those identi fied using older GDM di-\nagnostic criteria. Those trials found modestbenefits, including reduced rates of large-\nfor-gestational-age births and preeclamp-sia (211,212). It is important to note that80–90% of participants being treated for | [
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mild GDM in these two randomized con-trolled trials could be managed with life-\nstyle therapy alone. The OGTT glucose\ncutoffs in these two trials overlapped thethresholds recommended by the IADPSG,a n di no n et r i a l( 2 1 2 ) ,t h e2 - hP Gt h r e s h o l d\n(140 mg/dL [7.8 mmol/L]) was lower than | [
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(140 mg/dL [7.8 mmol/L]) was lower than\nthe cutoff recommended by the IADPSG(153 mg/dL [8.5 mmol/L]).\nNo randomized controlled trials of treat-\ning versus not treating GDM diagnosed by\nt h eI A D P S Gc r i t e r i ab u tn o tt h eC a r p e n t e r - | [
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t h eI A D P S Gc r i t e r i ab u tn o tt h eC a r p e n t e r -\nCoustan criteria have been published todate. However, a recent randomized trial oftesting for GDM at 24 –28 weeks of gesta- | [
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tion by the one-step method using IADPSGcriteria versus the two-step method using a1-h 50-g glucose loading test (GLT) and, ifpositive, a 3-h OGTT by Carpenter-Coustan\ncriteria identifi ed twice as many individuals\nwith GDM using the one-step method com- | [
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with GDM using the one-step method com-\npared with the two-step method. Despitetreating more individuals for GDM usingthe one-step method, there was no differ-\nence in pregnancy and perinatal complica-\ntions (213). However, concerns have beenraised about sample size estimates and un-anticipated suboptimal engagement... | [
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the protocol regarding screening and treat-\nment. For example, in the two-step group,165 participants who did not get countedas having GDM were treated for isolated\nelevated FPG >95 mg/dL ( >5.3 mmol/L)\n(214). The high prevalence of prediabetes\nin people of childbearing age may supportthe more inclusive IADPSG crit... | [
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Health and Nutrition Examination Survey\n(NHANES) data demonstrate a 21.5% prev-alence of prediabetes in people of repro-ductive age of 20 –44 years, which is\ncomparable to or higher than the preva-\nlence of GDM diagnosed by the one-step\nmethod (215).\nThe one-step method identi fies the | [
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method (215).\nThe one-step method identi fies the\nlong-term risks of maternal prediabetesand diabetes and offspring abnormal\nglucose metabolism and adiposity. Post\nhoc GDM in individuals diagnosed by thediabetesjournals.org/care Diagnosis and Classification of Diabetes S35\n©AmericanDiabetesAssociation | [
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one-step method in the HAPO cohort\nwas associated with higher prevalenceof IGT; higher 30-min, 1-h, and 2-h gluco-\nses during the OGTT; and reduced insulin\nsensitivity and oral disposition index intheir offspring at 10 –14 years of age com- | [
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p a r e dw i t ho f f s p r i n go fm o t h e r sw i t h o u tGDM. Associations of mother ’sf a s t i n g ,1 -\nh, and 2-h values on the 75-g OGTT were\ncontinuous with a comprehensive panel\nof offspring metabolic outcomes (216,217). In addition, HAPO Follow-up Study\n(HAPO FUS) data demonstrate that neo- | [
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(HAPO FUS) data demonstrate that neo-\nnatal adiposity and fetal hyperinsuline-mia (cord C-peptide), both higher across\nthe continuum of maternal hyperglyce-\nmia, are mediators of childhood body fat(218).\nData are lacking on how the treat-\nment of mother ’s hyperglycemia in\npregnancy affects her offspring ’sr i s ... | [
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pregnancy affects her offspring ’sr i s k\nfor obesity, diabetes, and other meta-\nbolic disorders (219,220). Additional\nwell-designed clinical studies are neededto determine the optimal intensity of\nmonitoring and treatment of individuals\nwith GDM diagnosed by the one-stepstrategy.\nTwo-Step Strategy | [
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with GDM diagnosed by the one-stepstrategy.\nTwo-Step Strategy\nIn 2013, the NIH convened a consensusdevelopment conference to considerdiagnostic criteria for diagnosing GDM\n(221). The 15-member panel had repre-\nsentatives from obstetrics and gynecol-ogy, maternal-fetal medicine, pediatrics,\ndiabetes research, biost... | [
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diabetes research, biostatistics, and other\nrelated fields. The panel recommended a\ntwo-step approach to screening that useda 1-h 50-g GLT followed by a 3-h 100-gOGTT for those who screened positive.\nThe American College of Obstetricians\nand Gynecologists (ACOG) recommendsany of the commonly used thresholds of | [
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130, 135, or 140 mg/dL for the 1-h 50-g\nGLT (222). Updated from 2014, a 2021U.S. Preventive Services Task Force sys-\ntematic review continued to conclude\nthat one-step versus two-step screeningis associated with increased likelihood of\nGDM (11.5% vs. 4.9%) but without im- | [
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GDM (11.5% vs. 4.9%) but without im-\nproved health outcomes. It reported thatt h eo r a lg l u c o s ec h a l l e n g et e s tu s i n g\nthresholds of 140 or 135 mg/dL had sen-\nsitivities of 82% and 93% and speci ficities\nof 82% and 79%, respectively, against\nCarpenter-Coustan criteria. FPG cutoffs of | [
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Carpenter-Coustan criteria. FPG cutoffs of\n85 mg/dL and 90 mg/dL had sensitivitiesof 88% and 81% and speci ficities of 73%\nand 82%, respectively, against Carpenter-Coustan criteria (223). The use of A1C at24–28 weeks of gestation as a screening\ntest for GDM does not function as well asthe GLT (224).Key factors cited ... | [
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their decision-making process were the\nlack of clinical trial data demonstratingthe bene fits of the one-step strategy and\nthe potential negative consequences of\nidentifying a large group of individuals\nwith GDM, including medicalization ofpregnancy with increased health care uti-lization and costs. Moreover, screen... | [
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with a 50-g GLT does not require fasting\nand therefore is easier to accomplish formany individuals. Treatment of higher-threshold maternal hyperglycemia, as\nidenti fied by the two-step approach, re-\nduces rates of neonatal macrosomia,\nlarge-for-gestational-age births (225), andshoulder dystocia without increasing sm... | [
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for-gestational-age births. ACOG currently\nsupports the two-step approach but notesthat one elevated value, as opposed totwo, may be used for the diagnosis ofGDM (222). If this approach is imple-\nmented, the incidence of GDM by the\ntwo-step strategy will likely increasemarkedly. ACOG recommends either oftwo sets of ... | [
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3-h 100-g OGTT Carpenter-Coustan or Na-\ntional Diabetes Data Group (226,227).Each is based on different mathematicalconversions of the original recommended\nthresholds by O ’Sullivan and Mahan (207),\nwhich used whole blood and nonenzy-\nmatic methods for glucose determination.A secondary analysis of data from a ran- | [
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domized clinical trial of identi fication and\ntreatment of mild GDM (228) demon-\nstrated that treatment was similarly bene-ficial in people meeting only the lower\nthresholds per Carpenter-Coustan (226)\nand in those meeting only the higher | [
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and in those meeting only the higher\nthresholds per National Diabetes DataGroup (227). If the two-step approach isused, it would appear advantageous to\nuse the Carpenter-Coustan lower diagnos-\ntic thresholds, as shown in step 2 inTable 2.7 .\nFuture Considerations\nThe con flicting recommendations from | [
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Future Considerations\nThe con flicting recommendations from\nexpert groups underscore the fact thatthere are data to support each strategy. Asystematic review of economic evalua-tions of GDM screening found that the\none-step method identi fied more cases\no fG D Ma n dw a sm o r el i k e l yt ob ec o s t - | [
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o fG D Ma n dw a sm o r el i k e l yt ob ec o s t -\neffective than the two-step method (229).The decision of which strategy to imple-ment must therefore be made based on\nthe relative values placed on factors that\nhave yet to be measured (e.g., willingnessTable 2.7 —Screening for and diagnosis of GDM\nOne-step strate... | [
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One-step strategy\nPerform a 75-g OGTT, with plasma glucose measurement when an individual is fasting and at\n1a n d2h ,a t2 4 –28 weeks of gestation in individuals not previously diagnosed with diabetes.\nThe OGTT should be performed in the morning after an overnight fast of at least 8 h. | [
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The diagnosis of GDM is made when any of the following plasma glucose values are met or\nexceeded:\n/C15Fasting: 92 mg/dL (5.1 mmol/L)\n/C151 h: 180 mg/dL (10.0 mmol/L)\n/C152 h: 153 mg/dL (8.5 mmol/L)\nTwo-step strategy\nStep 1: Perform a 50-g GLT (nonfasting), with plasma glucose measurement at 1 h, at | [
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24–28 weeks of gestation in individuals not previously diagnosed with diabetes.\nIf the plasma glucose level measured 1 h after the load is $130, 135, or 140 mg/dL (7.2,\n7.5, or 7.8 mmol/L, respectively),* proceed to a 100-g OGTT.\nStep 2: The 100-g OGTT should be performed when the individual is fasting. | [
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The diagnosis of GDM is made when at least two †of the following four plasma glucose\nlevels (measured fasting and at 1, 2, and 3 h during OGTT) are met or exceeded\n(Carpenter-Coustan criteria [226]):\n/C15Fasting: 95 mg/dL (5.3 mmol/L)\n/C151 h: 180 mg/dL (10.0 mmol/L)\n/C152 h: 155 mg/dL (8.6 mmol/L)\n/C153 h: 140 m... | [
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/C152 h: 155 mg/dL (8.6 mmol/L)\n/C153 h: 140 mg/dL (7.8 mmol/L)\nGDM, gestational diabetes mellitus; GLT, glucose load test; OGTT, oral glucose tolerancetest. *American College of Obstetricians and Gynecologists (ACOG) recommends any of the\ncommonly used thresholds of 130, 135, or 140 mg/dL for the 1-h 50-g GLT (222)... | [
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notes that one elevated value can be used for diagnosis (222).S36 Diagnosis and Classification of Diabetes Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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3. Prevention or Delay of\nDiabetes and AssociatedComorbidities:\nStandards of Care\nin Diabetes— 2024\nDiabetes Care 2024;47(Suppl. 1):S43 –S51 |https://doi.org/10.2337/dc24-S003American Diabetes Association\nProfessional Practice Committee *\nThe American Diabetes Association (ADA) “Standards of Care in Diabetes ”in- | [
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cludes the ADA ’s current clinical practice recommendations and is intended to\nprovide the components of diabetes care, general treatment goals and guide- | [
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lines, and tools to evaluate quality of care. Members of the ADA ProfessionalPractice Committee, an interprofessional expert committee, are responsible forupdating the Standards of Care annually, or more frequently as warranted. For adetailed description of ADA standards, statements, and reports, as well as theevidence... | [
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... |
and reports, as well as theevidence-grading system for ADA ’s clinical practice recommendations and a full | [
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list of Professional Practice Committee members, please refer to Introductionand Methodology. Readers who wish to comment on the Standards of Care are\ninvited to do so at professional.diabetes.org/SOC.\nFor guidelines related to screening for increased risk for type 2 diabetes (prediabe- | [
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tes), please refer to Section 2, “Diagnosis and Classi fication and of Diabetes. ”For\nguidelines related to screening, diagnosis, and management of type 2 diabetes inyouth, please refer to Section 14, “Children and Adolescents .”\nRecommendations\n3.1In people with prediabetes, monitor for the development of type 2 dia... | [
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0.07223014533519745,
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-0.021267591044306755,
0.01689152792096138,
0.023042600601911545,
-0.10393285006284714,
0.01... |
at least annually; modify based on individual risk assessment. E\n3.2In people with preclinical type 1 diabetes, monitor for disease progression\nusing A1C approximately every 6 months and 75-g oral glucose tolerance test | [
0.005611718632280827,
0.04208453372120857,
-0.06747803092002869,
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-0.04385702311992645,
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-0.08689573407173157,
-... |
(i.e., fasting and 2-h plasma glucose) annually; modify frequency of monitor-ing based on individual risk assessment based on age, number and type of\nautoantibodies, and glycemic metrics. E\nScreening for prediabetes and type 2 diabetes risk through an assessment of risk factors | [
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0.0654958039522171,
-0.05412912741303444,
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0.017288705334067345,
-0.04259960353374481,
-0.05525479093194008,
-0.05953063815832138,
0.00535980... |
(Table 2.5 ) or with an assessment tool, such as the American Diabetes Association risk\ntest ( Fig. 2.2 ), is recommended to guide whether to perform a diagnostic test for predi-\nabetes ( Table 2.2 ) and type 2 diabetes (Table 2.1 ) (see Section 2, “Diagnosis and | [
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-0.09093987196683884,
0.002071... |
Classi fication of Diabetes ”). Testing high-risk adults for prediabetes is warranted be-\ncause the laboratory assessment is safe and reasonable in cost, substantial time exists | [
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0.055490948259830475,
-0.06348779797554016,
0.007076949812471867,
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0.029366731643676758,
-0.03682130202651024,
0.020561696961522102,
-0.08851124346256256,
0.0... |
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