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©AmericanDiabetesAssociation | [
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for insulin administration (69). Proper insu-\nlin administration technique includes injec-tion or infusion (for CSII or AID systems)into appropriate body areas, injection orinfusion site rotation, appropriate careof injection or infusion sites to avoidinfection or other complications, and\navoidance of intramuscular (... | [
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avoidance of intramuscular (IM) insulin\ndelivery. Selection of method of admin-istration (vial and syringe, insulin pen,connected insulin pens/devices, or in-sulin pumps) will depend on a varietyof individual-speci fic factors and needs,\ncost and coverage, and individual prefer-\nences. Reassessment of the appropriate | [
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ences. Reassessment of the appropriate\nadministration technique via whichevermethod is used should be completed dur-ing routine follow-up.\nExogenously delivered insulin should\nbe injected into subcutaneous tissue, notintramuscularly. Recommended sites for\ninsulin administration include the abdo- | [
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insulin administration include the abdo-\nmen, thigh, buttock, and upper arm. Insu-lin absorption from IM sites differs fromthat in subcutaneous sites and is alsoinfluenced by the activity of the muscle.\nInadvertent IM injection can lead to un-predictable insulin absorption and vari- | [
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able effects on glucose and is associatedwith frequent and unexplained hypoglyce-\nmia. Risk for IM insulin delivery isincreased in younger, leaner individualswhen injecting into the limbs rather thantruncal sites (abdomen and buttocks) andwhen using longer needles. Recent evi-dence supports the use of short needles | [
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(e.g., 4-mm pen needles) as effective and\nw e l lt o l e r a t e dw h e nc o m p a r e dw i t hl o n -ger needles, including a study performedin adults with obesity (70).\nInjection or infusion site rotation is\nadditionally necessary to avoid lipohy-pertrophy, an accumulation of subcuta-\nneous fat in response to the... | [
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neous fat in response to the adipogenic\nactions of insulin at a site of multipleinjections. Lipohypertrophy appears assoft, smooth raised areas several centi-meters in breadth and can contribute toerratic insulin absorption, increased gly-cemic variability, and unexplained hypo-\nglycemic episodes. People treated with | [
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glycemic episodes. People treated with\ninsulin and/or caregivers should receiveeducation about proper injection or infu-sion site rotation and how to recognizeand avoid areas of lipohypertrophy. Asnoted in Table 4.1 , examination of insulin\ninjection sites for the presence of lipohy- | [
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pertrophy, as well as assessment ofadministration device use and injectiontechnique, are key components of a com-prehensive diabetes medical evaluationand treatment plan. Proper insulin injec-tion or infusion technique may lead tomore effective use of this therapy and, assuch, holds the potential for improvedclinical o... | [
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Noninsulin Treatments for Type 1\nDiabetes\nInjectable and oral glucose-lowering med-\nications have been studied for their ef fi-\ncacy as adjunct to insulin treatment of\ntype 1 diabetes. Pramlintide is based onthe naturally occurring b-cell peptide | [
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amylin and is approved for use in adultswith type 1 diabetes. Clinical trials havedemonstrated a modest reduction in A1C(0.3–0.4%) and modest weight loss\n(/C241 kg) with pramlintide (71). Similar results | [
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(/C241 kg) with pramlintide (71). Similar results\nhave been reported for several agentscurrently approved only for the treatmentof type 2 diabetes. The addition of met-formin in adults with type 1 diabetes wasassociated with small reductions in bodyweight, insulin dose, and lipid levels butdid not sustainably improve ... | [
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The largest clinical trials of glucagon-like\nSimplified overview of indications for Simplified overview of indications for ββ-cell replacement therapy in people with type 1 diabetes-cell replacement therapy in people with type 1 diabetes\nSevere diabetic chronic kidney disease\n(GFR <30 mL mln−1 [1.73 m]−2)Hypoglycemi... | [
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(GFR <30 mL mln−1 [1.73 m]−2)HypoglycemiaHypoglycemia\nKetoacidosisKetoacidosis\nImpaired kidney functionImpaired kidney function\nSimultaneous transplantationSimultaneous transplantation Living donor kidneyLiving donor kidney\nPancreas afterPancreas after\nkidneykidneyIslet afterIslet after\nkidneykidneySimultaneousSi... | [
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kidneykidneySimultaneousSimultaneous\npancreas andpancreas and\nkidneykidneySimultaneousSimultaneous\nislet and kidneyislet and kidneyPancreasPancreas\ntransplantationtransplantation\nalonealoneIsletIslet\ntransplantationtransplantation | [
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alonealoneIsletIslet\ntransplantationtransplantation\nalonealoneIntact/stable kidney functionIntact/stable kidney functionIncapacitating problems with exogenous insulin therapyIncapacitating problems with exogenous insulin therapy\nFailure of insulin-based management to prevent acuteFailure of insulin-based management ... | [
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complicationscomplicationsHypoglycemia unawarenessHypoglycemia unawarenessSevere metabolic complications\nBalancing surgical risk, metabolic need, and the choice of the individual with diabetes\nFigure 9.2 —Simpli fied overview of indications for b-cell replacement therapy in people with type 1 diabetes. The two main fo... | [
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ment therapy are whole-pancreas transplantation or islet cell transplantation. b-Cell replacement therapy can be combined with kidney transplan-\ntation if the individual has end-stage renal disease, which may be performed simultaneously or after kidney transplantation. All decisions about | [
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transplantation must balance the surgical risk, metabolic need, and the choice of the individual with diabetes. GFR, glomerular filtration rate.\nReprinted from Holt et al. (4).diabetesjournals.org/care Pharmacologic Approaches to Glycemic Treatment S161\n©AmericanDiabetesAssociation | [
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Table 9.1 —Examples of subcutaneous insulin treatment plans\nPlans Timing and distribution Advantages Disadvantages Adjusting doses\nPlans that more closely mimic normal insulin secretion\nInsulin pump therapy (also\nincluding AID systems: hybrid\nclosed-loop, low-glucosesuspend, CGM-augmented\nopen-loop, BGM-augmented | [
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open-loop, BGM-augmented\nopen-loop)Basal delivery of URAA or RAA;\ngenerally 30 –50% of TDD.\nMealtime and correction: URAA or\nRAA by bolus based on ICR and/or\nISF and target glucose, with\npremeal insulin /C2415 min\nbefore eating.Can adjust basal rates for varying\ninsulin sensitivity by time of day,for exercise, ... | [
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insulin sensitivity by time of day,for exercise, and for sick days.\nFlexibility in meal timing and\ncontent.\nPump can deliver insulin in\nincrements of fractions of units.\nPotential for integration with CGM\nfor AID systems.\nTIR % highest and TBR % lowest\nwith: hybrid closed-loop >low-\nglucose suspend >CGM-\naugm... | [
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glucose suspend >CGM-\naugmented open-loop >BGM-\naugmented open-loop.Most expensive plan.Must continuously wear one or more\ndevices.\nRisk of rapid development of ketosis\nor DKA with interruption of insulindelivery.\nPotential reactions to adhesives and\nsite infections.\nMost technically complex approach | [
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site infections.\nMost technically complex approach\n(harder for people with lowernumeracy or literacy skills).Mealtime insulin: if carbohydrate\ncounting is accurate, change ICR ifglucose after meal consistently outof target.\nCorrection insulin: adjust ISF and/or\ntarget glucose if correction doesnot consistently bri... | [
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range.\nBasal rates: adjust based on\novernight, fasting or daytime\nglucose outside of activity of\nURAA/RAA bolus.\nMDI: LAA 1flexible doses of URAA\nor RAA at mealsLAA once daily (insulin detemir or\ninsulin glargine may require twice-daily dosing); generally 30 –50% of\nTDD.\nMealtime and correction: URAA or | [
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TDD.\nMealtime and correction: URAA or\nRAA based on ICR and/or ISF andtarget glucose.Can use pens for all components.\nFlexibility in meal timing and\ncontent.\nInsulin analogs cause less\nhypoglycemia than human insulins.At least four daily injections.Most costly insulins.\nSmallest increment of insulin is | [
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Smallest increment of insulin is\n1 unit (0.5 unit with some pens).LAAs may not cover strong dawn\nphenomenon (rise in glucose in\nearly morning hours) as well as\npump therapy.Mealtime insulin: if carbohydrate\ncounting is accurate, change ICR if\nglucose after meal consistently out\nof target.\nCorrection insulin: ad... | [
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of target.\nCorrection insulin: adjust ISF and/or\ntarget glucose if correction does\nnot consistently bring glucose into\nrange.\nLAA: based on overnight or fasting\nglucose or daytime glucoseoutside of activity time course, orURAA or RAA injections.\nMDI plans with less flexibility\nFour injections daily with fixed | [
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MDI plans with less flexibility\nFour injections daily with fixed\ndoses of N and RAAPre-breakfast: RAA /C2420%\n of TDD.\nPre-lunch: RAA /C2410% of TDD.\nPre-dinner: RAA /C2410% of TDD.\nBedtime: N /C2450% of TDD.May be feasible if unable to\ncarbohydrate count.\nAll meals have RAA coverage.\nN is less expensive than LA... | [
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N is less expensive than LAAs.Shorter duration RAA may lead to\nbasal de ficit during day; may need\ntwice-daily N.\nGreater risk of nocturnal\nhypoglycemia with N.\nRequires relatively consistent\nmealtimes and carbohydrateintake.Pre-breakfast RAA: based on BGM\nafter breakfast or before lunch.\nPre-lunch RAA: based on... | [
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Pre-lunch RAA: based on BGM after\nlunch or before dinner.\nPre-dinner RAA: based on BGM after\ndinner or at bedtime.\nEvening N: based on fasting or\novernight BGM.\nContinued on p. S163S162 Pharmacologic Approaches to Glycemic Treatment Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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Table 9.1 —Continued\nPlans Timing and distribution Advantages Disadvantages Adjusting doses\nFour injections daily with fixed\ndoses of N and RPre-breakfast: R /C2420% of TDD.\nPre-lunch: R /C2410% of TDD.\nPre-dinner: R /C2410% of TDD.\nBedtime: N /C2450% of TDD.May be feasible if unable to\ncarbohydrate count.\nR can... | [
0.001275814138352871,
-0.021667588502168655,
-0.010152879171073437,
-0.02906050719320774,
-0.031887754797935486,
0.02222258597612381,
0.020846083760261536,
0.16112323105335236,
-0.09465529024600983,
-0.010915294289588928,
0.001691243378445506,
0.018715985119342804,
0.011213104240596294,
0.... |
carbohydrate count.\nR can be dosed based on ICR and\ncorrection.\nAll meals have R coverage.\nLeast expensive insulins.Greater risk of nocturnal\nhypoglycemia with N.\nGreater risk of delayed post-meal\nhypoglycemia with R.\nRequires relatively consistent\nmealtimes and carbohydrateintake.\nR must be injected at least... | [
0.015775814652442932,
0.03641446307301521,
-0.08762042224407196,
0.044581349939107895,
-0.01596984826028347,
0.018753284588456154,
0.04723721370100975,
0.09054585546255112,
-0.047484833747148514,
-0.03851193189620972,
-0.027500854805111885,
-0.016687149181962013,
-0.03195495903491974,
0.04... |
mealtimes and carbohydrateintake.\nR must be injected at least 30 min\nbefore meal for better effect.Pre-breakfast R: based on BGM after\nbreakfast or before lunch.\nPre-lunch R: based on BGM after\nlunch or before dinner.\nPre-dinner R: based on BGM after\ndinner or at bedtime.\nEvening N: based on fasting or\novernig... | [
-0.024451548233628273,
-0.01921660639345646,
0.007503791246563196,
0.020744990557432175,
-0.065374456346035,
0.03593432158231735,
-0.004132436588406563,
0.058641184121370316,
-0.05589951574802399,
-0.08020759373903275,
-0.004207253456115723,
0.0010463327635079622,
-0.033255256712436676,
0.... |
dinner or at bedtime.\nEvening N: based on fasting or\novernight BGM.\nPlans with fewer daily injections\nThree injections daily: N 1Ro r\nN1RAAPre-breakfast: N /C2440% TDD 1Ro r\nRAA/C2415% TDD.\nPre-dinner: R or RAA /C2415% TDD.\nBedtime: N /C2430% TDD.Morning insulins can be mixed in one\nsyringe.\nMay be appropriat... | [
-0.02422880008816719,
0.06388963013887405,
-0.04717117175459862,
0.048300955444574356,
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0.03344229981303215,
0.022144867107272148,
-0.04660141468048096,
-0.05378012731671333,
-0.0451374351978302,
0.006450694520026445,
-0.06755781918764114,
0.0462... |
syringe.\nMay be appropriate for those who\ncannot take injection in middle of\nday.\nMorning N covers lunch to some\nextent.\nSame advantages of RAAs over R.Least (N 1R) or less expensive\ninsulins than MDI with analogs.Greater risk of nocturnal\nhypoglycemia with N than LAAs.\nGreater risk of delayed post-meal\nhypog... | [
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0.021770145744085312,
-0.02331562340259552,
0.02231125347316265,
-0.02953832410275936,
-0.018560098484158516,
0.06864212453365326,
0.11574367433786392,
-0.04741334915161133,
0.019867215305566788,
-0.012031234800815582,
0.04497300460934639,
-0.0038444260135293007,
0.0... |
Greater risk of delayed post-meal\nhypoglycemia with R than RAAs.\nRequires relatively consistent\nmealtimes and carbohydrate\nintake.\nCoverage of post-lunch glucose often\nsuboptimal.\nR must be injected at least 30 min\nbefore meal for better effect.Morning N: based on pre-dinner\nBGM.\nMorning R: based on pre-lunch... | [
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0.025445643812417984,
-0.08537814021110535,
0.08431022614240646,
0.01594509370625019,
0.010643932968378067,
0.008600162342190742,
0.13173730671405792,
-0.058783017098903656,
0.01565568335354328,
-0.03743379935622215,
0.056728191673755646,
-0.01001893263310194,
0.01117... |
BGM.\nMorning R: based on pre-lunch BGM.\nMorning RAA: based on post-\nbreakfast or pre-lunch BGM.\nPre-dinner R: based on bedtime\nBGM.\nPre-dinner RAA: based on post-\ndinner or bedtime BGM.\nEvening N: based on fasting BGM.\nTwice-daily “split-mixed ”:N1Ro r\nN1RAAPr\ne-breakfast: N /C2440% TDD 1Ro r\nRAA/C2415% TDD... | [
-0.05873280018568039,
-0.038033436983823776,
-0.0059915222227573395,
0.031620703637599945,
-0.06703288108110428,
0.014304207637906075,
0.0015640499768778682,
0.06977919489145279,
-0.06828206777572632,
-0.050404950976371765,
-0.002348513575270772,
-0.031182358041405678,
-0.04307094216346741,
... |
RAA/C2415% TDD.\nPre-dinner: N /C2430% TDD 1Ro r\nRAA/C2415% TDD.Least number of injections for people\nwith strong preference for this.\nInsulins can be mixed in one syringe.\nLeast (N 1R) or less (N 1RAA)\nexpensive insulins vs. analogs.\nEliminates need for doses during the\nday.Risk of hypoglycemia in afternoon or\... | [
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0.03469836711883545,
-0.0471617616713047,
-0.030029920861124992,
0.04989062249660492,
0.1652604192495346,
-0.04205995425581932,
-0.023708034306764603,
-0.02885972335934639,
0.016976170241832733,
-0.0413026325404644,
0.041566... |
day.Risk of hypoglycemia in afternoon or\nmiddle of night from N.\nFixed mealtimes and meal content.Coverage of post-lunch glucose often\nsuboptimal.\nDifficult to reach targets for blood\nglucose without hypoglycemia.Morning N: based on pre-dinner\nBGM.\nMorning R: based on pre-lunch BGM.Morning RAA: based on post-\nbr... | [
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0.10096629709005356,
-0.04511323571205139,
0.08397268503904343,
0.00409157108515501,
0.025970090180635452,
0.0618961863219738,
0.08256539702415466,
-0.05130837485194206,
-0.03062143363058567,
-0.030917087569832802,
-0.0025079313199967146,
-0.04061087965965271,
0.0396... |
breakfast or pre-lunch BGM.\nEvening R: based on bedtime BGM.\nEvening RAA: based on post-dinner\nor bedtime BGM.\nEvening N: based on fasting BGM.\nAID, automated insulin delivery; BGM, blood glucose monitoring; CGM, continuous glucose monitoring; ICR, insulin-to-carbohydrate ratio; ISF, insulin sensitivity factor; LA... | [
-0.07421918213367462,
0.00035503122489899397,
-0.07808391749858856,
0.004016620572656393,
-0.07344529032707214,
-0.007479276042431593,
0.03393876180052757,
0.07713840901851654,
-0.04999401792883873,
-0.0093156723305583,
-0.040972623974084854,
0.00267678196541965,
-0.04362122341990471,
0.03... |
tiple daily injections; N, NPH insulin; R, short-acting (regular) insulin; RAA, rapid-acting analog; TBR, time below range; TDD, total daily insulin dose; TIR, time in range; URAA, ultra-rapid-acting analog.\nAdapted from Holt et al. (4).diabetesjournals.org/care Pharmacologic Approaches to Glycemic Treatment S163\n©Am... | [
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-0.02870120108127594,
-0.09042100608348846,
-0.040450651198625565,
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-0.01592169888317585,
0.05594038963317871,
0.08456455171108246,
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0.013707559555768967,
0.02049322985112667,
0.04085782542824745,
-0.04745422303676605,
-0.021... |
peptide 1 receptor agonists (GLP-1 RAs)\nin type 1 diabetes have been conductedwith liraglutide 1.8 mg daily, and resultsshowed modest A1C reductions ( /C240.4%),\ndecreases in weight ( /C245 kg), and reduc-\ntions in insulin doses (74,75). Similarly,sodium –glucose cotransporter 2 (SGLT2)\ninhibitors have been studied... | [
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0.04363568499684334,
0.09715898334980011,
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0.0013618957018479705,
-0.018191885203123093,
-0.07540277391672134,
0.04... |
inhibitors have been studied in clinical tri-\nals in people with type 1 diabetes, andresults showed improvements in A1C, re-duced body weight, and improved bloodpressure (76); however, SGLT2 inhibitoru s ei nt y p e1d i a b e t e sw a sa s s o c i a t e dw i t h\nan increased rate of DKA. The SGLT1/2 in-\nhibitor sota... | [
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-0.02049166150391102,
-0.11784007400274277,
0.01543976180255413,
-0.013992631807923317,
0.014030301943421364,
-0.011303694918751717,
0.12843748927116394,
0.015852266922593117,
-0.029673904180526733,
0.016225498169660568,
0.00914151594042778,
-0.0734536424279213,
0.02... |
hibitor sotagli flozin has been studied in\nclinical trials in people with type 1 diabe-\ntes, and results showed improvements inA1C and body weight (77); however, sota-gliflozin use was associated with an eight-\nfold increase in DKA compared with | [
0.029365217313170433,
0.027240393683314323,
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0.01253650151193142,
-0.05777087062597275,
-0.059939488768577576,
0.06547940522432327,
0.09866956621408463,
-0.031444910913705826,
-0.05552046373486519,
-0.020565854385495186,
0.014396438375115395,
-0.1107991561293602,
0.05... |
fold increase in DKA compared with\nplacebo (78). The studies that led to theapproved indication for heart failure (HF)excluded individuals with type 1 diabetesor a history of DKA (79,80). See section\nPRE-\nVENTION AND TREATMENT OF HEART FAILURE within\nSection 10, “Cardiovascular Disease and\nRisk Management, ”for in... | [
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0.013121898286044598,
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0.014413228258490562,
-0.035509996116161346,
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0.1385919451713562,
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0.035057295113801956,
-0.08998998254537582,
0.01... |
Risk Management, ”for information on risk\nmitigation with the use of SGLT inhibitors\nin those with type 1 diabetes. The risksand benefi ts of adjunctive agents continue\nto be evaluated, with consensus statementsproviding guidance on patient selection\nand precautions (81).\nThere are currently no approved thera- | [
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0.0018263786332681775,
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0.014965612441301346,
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0.06834693253040314,
0.015218275599181652,
0.12148124724626541,
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0.018179498612880707,
0.04409221187233925,
0.06670890003442764,
-0.006855888292193413,
0.0006... |
and precautions (81).\nThere are currently no approved thera-\npies for preservation of C-peptide or de-\nlaying the progression of clinical type 1diabetes. Higher C-peptide levels havebeen associated with better A1C, lower\nrisk of retinopathy, lower risk of nephropa- | [
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-0.06644031405448914,
0.010192354209721088,
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0.05171559378504753,
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0.13209058344364166,
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0.043697573244571686,
0.014236071147024632,
0.02238677255809307,
-0.11036941409111023,
0.04... |
risk of retinopathy, lower risk of nephropa-\nthy, and lower risk of severe hypoglycemia(82). Several therapies, including verapamiland monoclonal antibodies, are currentlyunder active investigation.\nSURGICAL TREATMENT FOR TYPE 1\nDIABETES\nPancreas and Islet Transplantation\nSuccessful pancreas and islet transplanta- | [
0.016648467630147934,
0.03639468550682068,
0.000446100631961599,
0.029699526727199554,
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0.055618781596422195,
0.11514124274253845,
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0.010125831700861454,
0.0024074125103652477,
0.048151303082704544,
-0.0464458130300045,
0.010... |
Successful pancreas and islet transplanta-\ntion can normalize glucose levels and miti-gate microvascular complications of type 1\ndiabetes. However, people receiving these | [
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0.016825683414936066,
-0.04557385295629501,
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0.08363252133131027,
0.04302329570055008,
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-0.011916606687009335,
0.06851383298635483,
-0.09194117039442062,
... |
diabetes. However, people receiving these\ntreatments require lifelong immunosup-pression to prevent graft rejection and/orrecurrence of autoimmune islet destruc-tion. Given the potential adverse effectsof immunosuppressive therapy, pancreas\ntransplantation should be reserved for | [
-0.02457515336573124,
0.08437057584524155,
0.011860723607242107,
-0.012398305349051952,
-0.06091836094856262,
0.04170752689242363,
0.13164517283439636,
0.10502566397190094,
0.002039967104792595,
0.016509724780917168,
0.0023580139968544245,
0.05370553210377693,
-0.03940625861287117,
0.04981... |
transplantation should be reserved for\npeople with type 1 diabetes undergoingsimultaneous kidney transplantation,following kidney transplantation, or for\nthose with recurrent ketoacidosis or se-\nvere hypoglycemia despite intensive gly- | [
-0.02394372969865799,
0.01701662316918373,
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0.07397469133138657,
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0.03243772312998772,
0.0037371814250946045,
-0.055353179574012756,
-0.01... |
vere hypoglycemia despite intensive gly-\ncemic management (83). In much of theworld, allogenic islet transplantation isregulated as an organ transplant. How-ever, in the U.S., allogenic islet transplan-tation is regulated as a cell therapy, andthefirst such allogeneic islet cell therapy, | [
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0.033412326127290726,
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0.028797725215554237,
0.001519385608844459,
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0.03557376191020012,
0.06194794550538063,
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0.03963030129671097,
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-0.... |
donislecel-jujn, was approved in 2023.Donislecel is indicated for the treatmentof adults with type 1 diabetes who areunable to approach their A1C goal be-cause of current repeated episodes ofsevere hypoglycemia despite intensivediabetes management and education.\nThe 2021 ADA/EASD consensus report | [
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-0.026897110044956207,
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0.005320222582668066,
0.0692545473575592,
0.036348335444927216,
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0.06880197674036026,
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-0.... |
The 2021 ADA/EASD consensus report\non the management of type 1 diabetesin adults offers a simplifi ed overview of\nindications for b-cell replacement ther-\napy in people with type 1 diabetes ( Fig.\n9.2)( 4 ) .\nPHARMACOLOGIC THERAPY FOR\nADULTS WITH TYPE 2 DIABETES\nRecommendations\n9.8Healthy lifestyle behaviors, di... | [
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0.029657507315278053,
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0.045794133096933365,
-0.09122738987207413,
0.03342868760228157,
0.08320534974336624,
0.061623770743608475,
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0.013003495521843433,
-0.06933315843343735,
0.05777721852064133,
-0.08730356395244598,
-0.0101... |
9.8Healthy lifestyle behaviors, dia-\nbetes self-management education\nand support, avoidance of therapeuticinertia, and social determinants of healthshould be considered in the glucose-lowering management of type 2 dia-\nbetes. A\n9.9A person-centered shared decision-\nmaking approach should guide the | [
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0.07332514226436615,
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0.022631876170635223,
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0.039575304836034775,
0.0972052812576294,
0.08717222511768341,
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0.0016335214022547007,
-0.03209000080823898,
0.046116914600133896,
-0.13719455897808075,
-0.0032... |
making approach should guide the\nchoice of pharmacologic agents foradults with type 2 diabetes. Considerthe effects on cardiovascular and re-nal comorbidities; effectiveness; hypo-glycemia risk; impact on weight, cost\nand access; risk for adverse reactions\nand tolerability; and individual prefer-ences ( Fig. 9.3 and... | [
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0.015108659863471985,
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0.043180953711271286,
-0.008103810250759125,
0.15052255988121033,
-0.06985020637512207,
-0.021717848256230354,
-0.03472556173801422,
0.06206301227211952,
-0.05297772213816643,
-... |
9.10 The glucose-lowering treatment\nplan should consider approaches thatsupport weight management goals(Fig. 9.3 andTable 9.2 ) for adults with\ntype 2 diabetes. A\n9.11 For adults with type 2 diabetes,\nuse pharmacological strategies that pro-\nvide suf ficient effectiveness to achieve\nand maintain the intended treat... | [
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0.07934893667697906,
0.006048681680113077,
0.02011280134320259,
-0.02700585126876831,
0.05319075658917427,
0.04535616189241409,
0.12624883651733398,
-0.09766749292612076,
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-0.00720983324572444,
0.04291822761297226,
-0.09672253578901291,
-0.018898... |
and maintain the intended treatment\ngoals. A\n9.12 Treatment modi fication (inten-\nsification or deintensi fication) for\nadults not meeting individualizedtreatment goals should not be de-layed. A9.13 Medication plan and medication-\ntaking behavior should be reevaluated at\nregular intervals (e.g., every 3 –6m o n t h ... | [
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0.0664859414100647,
0.0212451983243227,
-0.05420294031500816,
-0.07154454290866852,
0.050691958516836166,
0.019117269665002823,
0.08446379005908966,
-0.08506720513105392,
-0.04829627647995949,
0.06306733191013336,
0.07107697427272797,
-0.03531571850180626,
0.06795562... |
regular intervals (e.g., every 3 –6m o n t h s )\nand adjusted as needed to incorporatespecifi c factors that impact choice of\ntreatment ( Fig. 4.1 andTable 9.2 ).E\n9.14 Early combination therapy can\nbe considered in adults with type 2diabetes at treatment initiation to\nshorten time to attainment of indi-\nvidualize... | [
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0.001802154933102429,
0.02273460663855076,
0.027978450059890747,
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0.09884174913167953,
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0.12501847743988037,
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0.00767268892377615,
0.05900298431515694,
-0.0687171220779419,
0.042714986... |
shorten time to attainment of indi-\nvidualized treatment goals. A\n9.15 In adults with type 2 diabetes\nwithout cardiovascular and/or kidneydisease, pharmacologic agents shouldaddress both the individualized glyce-mic and weight goals ( Fig. 9.3 ).A\n9.16 In adults with type 2 diabetes | [
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0.03846604749560356,
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-0.... |
9.16 In adults with type 2 diabetes\nwho have not achieved their individual-ized glycemic goals, selection of subse-quent glucose-lowering agents shouldtake into consideration the individual-ized glycemic and weight goals as wellas the presence of other metabolic co-morbidities and the risk of hypoglyce-mia. A\n9.17 In... | [
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0.017037687823176384,
-0.0927899181842804,
-0.03805... |
9.17 In adults with type 2 diabetes\nwho have not achieved their individu-alized weight goals, additional weightmanagement interventions (e.g.,intensi fication of lifestyle modi fica-\ntions, structured weight managementprograms, pharmacologic agents, ormetabolic surgery, as appropriate) arerecommended. A\n9.18 In adults... | [
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9.18 In adults with type 2 diabetes\nand established or high risk of ath-erosclerotic cardiovascular disease,heart failure (HF), and/or chronic\nkidney disease (CKD), the treatment\nplan should include agent(s) that re-duce cardiovascular and kidney diseaserisk (e.g., sodium –glucose cotransporter | [
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-... |
2 inhibitor [SGLT2] and/or glucagon-likepeptide 1 receptor agonist [GLP-1 RA])(Fig. 9.3, Table 9.2 ,Table 10.3B ,a n d\nTable 10.3C ) for glycemic management\nand comprehensive cardiovascular riskr\neduction, independent of A1C and in\nconsideration of person-speci ficf a c t o r s\n(Fig. 9.3) (see Section 10, “Cardiova... | [
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(Fig. 9.3) (see Section 10, “Cardiovascular\nDisease and Risk Management,” for de-\ntails on cardiovascular risk reduction rec-ommendations). A\n9.19 In adults with type 2 diabetes\nwho have HF (with either reducedor preserved ejection fraction), anSGLT2 inhibitor is recommended, forglycemic management and prevention | [
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of HF hospitalizations (see Section 10,S164 Pharmacologic Approaches to Glycemic Treatment Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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“Cardiovascular Disease and Risk\nManagement,” for details on cardio-\nvascular risk reduction recommenda-\ntions). A\n9.20 In adults with type 2 diabetes\nw h oh a v eC K D( w i t hc o n firmed esti-\nmated glomerular filtration rate [eGFR]\nof 20 –60 mL/min per 1.73 m2and/or | [
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of 20 –60 mL/min per 1.73 m2and/or\nalbuminuria), an SGLT2 inhibitor shouldbe used for minimizing progression ofCKD, reduction in cardiovascular events,and reduction in hospitalizations for HF\n(Fig. 9.3); however, the glycemic bene-\nfits of SGLT2 inhibitors are reduced at\neGFR<45 mL/min per 1.73 m\n2(see\nSection 11,... | [
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2(see\nSection 11, “Chronic Kidney Disease and\nRisk Management ”for details on renal\nrisk reduction recommendations). A\n9.21 In adults with type 2 diabetes\nand advanced CKD (eGFR <30 mL/min\nper 1.73 m2), a GLP-1 RA is preferred\nfor glycemic management due to lower\nrisk of hypoglycemia and for cardiovas-cular eve... | [
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risk of hypoglycemia and for cardiovas-cular event reduction. B\n9.22 In adults with type 2 diabetes, | [
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9.22 In adults with type 2 diabetes,\ninitiation of insulin should be consid-ered regardless of background glucose-lowering therapy or disease stage ifthere is evidence of ongoing catabolism(e.g., unexpected weight loss), if symp-toms of hyperglycemia are present, orwhen A1C or blood glucose levels are veryhigh (i.e., ... | [
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0.003377... |
or blood glucose $300 mg/dL\n[$16.7 mmol/L]). E\n9.23 In adults with type 2 diabetes, a\nGLP-1 RA, including a dual glucose-dependent insulinotropic polypeptide(GIP) and GLP-1 RA, is preferred to in-sulin ( Fig. 9.4 ).A\n9.24 If insulin is used, combination | [
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9.24 If insulin is used, combination\ntherapy with a GLP-1 RA, including adual GIP and GLP-1 RA, is recom-mended for greater glycemic effective-ness as well as bene ficial effects on\nweight and hypoglycemia risk for adultswith type 2 diabetes. Insulin dosingshould be reassessed upon addition ordose escalation of a GLP-... | [
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9.25 In adults with type 2 diabetes,\nglucose-lowering agents may be contin-ued upon initiation of insulin therapy\n(unless contraindicated or not tolerated)\nfor ongoing glycemic and metabolicbenefits (i.e., weight, cardiometabolic,\nor kidney bene fits).A\n9.26 To minimize the risk of hypogly- | [
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or kidney bene fits).A\n9.26 To minimize the risk of hypogly-\ncemia and treatment burden whenstarting insulin therapy in adults with\ntype 2 diabetes, reassess the needfor and/or dose of glucose-lowering\nagents with higher hypoglycemia risk\n(i.e., sulfonylureas and meglitinides). A\n9.27 Monitor for signs of overbasa... | [
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0.0059... |
9.27 Monitor for signs of overbasaliza-\ntion during insulin therapy, such as basaldose exceeding /C240.5 units/kg/day,\nsignificant bedtime-to-morning or post-\nprandial-to-preprandial glucose differ-ential, occurrences of hypoglycemia( a w a r eo ru n a w a r e ) ,a n dh i g hg l y c e m i c\nvariability. When overbas... | [
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0.0... |
variability. When overbasalization is sus-\npected, a thorough reevaluation shouldoccur promptly to further tailor therapy\nto the individual ’s needs. E\n9.28 Routinely assess all people with\ndiabetes for financial obstacles that\ncould impede their diabetes manage-ment. Clinicians, members of the dia- | [
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betes care team, and social servicesprofessionals should work collabora-\ntively, as appropriate and feasible, to\nsupport these individuals by imple-menting strategies to reduce costs,\nthereby improving their access to\nevidence-based care. E\n9.29 In adults with diabetes and cost- | [
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evidence-based care. E\n9.29 In adults with diabetes and cost-\nrelated barriers, consider use of lower-cost medications for glycemic manage-ment (i.e., metformin, sulfonylureas,\nthiazolidinediones, and human insulin)\nwithin the context of their risks for hy-poglycemia, weight gain, cardiovascular\nand kidney events,... | [
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and kidney events, and other adverse\neffects. E\nThe ADA/EASD consensus report “Man-\nagement of Hyperglycemia in Type 2 Dia-\nbetes, 2022 ”(84) recommends a holistic,\nmultifaceted, person-centered approach\naccounting for the complexity of managingtype 2 diabetes and its complications acrossthe life span. Person-spe... | [
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fect choice of treatment include individu-alized glycemic goals (see Section 6,“Glycemic Goals and Hypoglycemia ”),\nin-\ndividualized weight goals, the individual ’s\nrisk for hypoglycemia, and the individual ’s\nhistory of or risk factors for cardiovascular,kidney, liver, and other comorbidities andcomplications of d... | [
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“Comprehensive Medical Evaluation and\nAssessment of Comorbidities, ”Section\n10, “Cardiovascular Disease and Risk\nManagement, ”and Section 11 “Chronic\nKidney Disease and Risk Management ”).\nIn addition, treatment decisions must con-\nsider the tolerability and side effectprofiles of medications, complexity of the | [
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medication plan and the individual ’sc a -\npacity to implement it given their specifi c\nsituation and context, and the access, cost,\nand availability of medication. Lifestyle\nmodifi cations and health behaviors that\nimprove health (see Section 5, “Facilitating\nPositive Health Behaviors and Well-being\nto Improve He... | [
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to Improve Health Outcomes ”)s h o u l db e\nemphasized along with any pharmacologictherapy. Section 13, “Older Adults,” and\nSection 14, “Children and Adolescents, ”\nhave recommendations speci fic for older\nadults and for children and adolescentswith type 2 diabetes, respectively. Sec-tion 10, “Cardiovascular Disease... | [
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Management, ”and Section 11, “Chronic\nKidney Disease and Risk Management, ”\nhave recommendations for the use ofglucose-lowering drugs in the manage-ment of cardiovascular disease and kid-\nney disease, respectively.\nChoice of Glucose-Lowering Therapy\nHealthy lifestyle behaviors, diabetes self- | [
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Healthy lifestyle behaviors, diabetes self-\nmanagement, education, and support,avoidance of clinical inertia, and social de-terminants of health should be considered\nin the glucose-lowering management of\ntype 2 diabetes. Pharmacologic therapyshould be guided by person-centeredtreatment factors, including comorbiditi... | [
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and treatment goals and preferences.\nPharmacotherapy should be started at thetime type 2 diabetes is diagnosed unlessthere are contraindications. Pharmaco-\nlogic approaches that provide the ef ficacy\nto achieve treatment goals should be con-\nsidered, such as metformin or other agents,including combination therapy, t... | [
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vide adequate ef ficacy to achieve and\nmaintain treatment goals (84). In adults\nwith type 2 diabetes and established/highrisk of atherosclerotic cardiovascular dis-\nease (ASCVD), HF, and/or chronic kidney\ndisease (CKD), the treatment plan shouldinclude agents that reduce cardiovascularand kidney disease risk (see Fi... | [
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9.2,S e c t i o n1 0 , “Cardiovascular Disease and\nRisk Management, ”and Section 11, “Chronic\nKidney Disease and Risk Management ”). In\ngeneral, higher-ef ficacy approaches have\ngreater likelihood of achieving glycemicgoals, with the following considered tohave very high ef ficacy for glucose lower-\ning: the GLP-1 R... | [
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ing: the GLP-1 RAs dulaglutide (high dose)\nand semaglutide, the dual glucose-depend-\nent insulinotropic polypeptide (GIP) andGLP-1 RA tirzepatide, insulin, combinationdiabetesjournals.org/care Pharmacologic Approaches to Glycemic Treatment S165\n©AmericanDiabetesAssociation | [
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-0.0069696... |
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Figure 9.3 —Use of glucose-lowering medications in the management of type 2 diabetes. ACEi, angiotensin-converting enzyme inhibitor; ACR, albumin-to-creati nine ratio; ARB, angiotensin receptor blocker; ASCVD, atherosclerotic cardio- | [
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vascular disease; CGM, continuous glucose monitoring; CKD, chronic kidney disease; CV, cardiovascular; CVD, cardiovascular disease; CVOT, cardiovascular outcomes trial; DPP-4i, dipeptidyl peptidase 4 inhibitor; eGFR, estimated glomerular | [
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filtration rate; GLP-1 RA, glucagon-like peptide 1 receptor agonist; HF, heart failure; HFpEF, heart failure with preserved ejection fraction; HFrEF , heart failure with reduced ejection fraction; HHF, hospitalization for heart failure; MACE, major | [
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adverse cardiovascular events; MI, myocardial infarction; SDOH, social determinants of health; SGLT2i, sodium-glucose cotransporter 2 inhibito r; T2D, type 2 diabetes; TZD, thiazolidinedione. Adapted from Davies et al. (84).S166 Pharmacologic Approaches to Glycemic Treatment Diabetes Care Volume 47, Supplement 1, Janua... | [
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©AmericanDiabetesAssociation | [
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