0 stringlengths 12 494 | embeddings listlengths 384 384 |
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cytokine levels (143). The use of newerdirect-acting antiviral drugs produces asustained virological response (cure) innearly all cases and has been reported\nto improve glucose metabolism in individ- | [
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to improve glucose metabolism in individ-\nuals with diabetes (144). A meta-analysisof mostly observational studies found amean reduction in A1C levels of 0.45%(95% CI /C00.60 to /C00.30) and reduced re-\nquirement for glucose-lowering medica-tion use following successful eradicationof HCV infection (145).\nHyperglycem... | [
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Hyperglycemia\nIn individuals with diabetes, higher A1Clevel is associated with lower cognitivefunction (43,146). A meta-analysis of\nrandomized trials found that tight glyce-\nmic control, compared with higher A1Cgoals, was associated with a slightlylower rate of cognitive decline (147).However, these findings were dri... | [
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an older study with an A1C goal of<7.0% in the tight-control arm. Analy-\nses within the ACCORD, Action in Diabe-tes and Vascular Disease: Preterax andDiamicron MR Controlled Evaluation\n(ADVANCE), and Veterans Affairs Diabetes\nTrial (VADT) studies found that tight glyce-mic control (targeting A1C <6.0–6.5%) | [
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resulted in no differences in cognitive out-comes compared with standard control\n(147–149). Therefore, intensive glycemic\ncontrol should not be advised for the im-\nprovement of cognitive function in individ-uals with type 2 diabetes. Additionally,people with type 2 diabetes and dementia\nare at heightened risk for e... | [
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are at heightened risk for experiencing hy-\nperglycemic crises (diabetic ketoacidosisand hyperglycemic hyperosmolar state)compared with people without dementia(150), underscoring the importance of\nsupporting diabetes management for indi-\nviduals experiencing cognitive decline anddiminished capacity for self-care.\nH... | [
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Hypoglycemia\nIn type 2 diabetes, severe hypoglycemia isassociated with reduced cognitive func-tion, and those with poor cognitive func-\ntion have more severe hypoglycemia. | [
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tion have more severe hypoglycemia.\nMultiple observational studies of adultswith diabetes have found an associationS64 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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between severe hypoglycemic episodes\nand cognitive decline or incident dementia(151–155). Decreased cognitive function\nalso increases the risk for severe hypogly-\ncemia, likely through impaired ability to | [
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cemia, likely through impaired ability to\nrecognize and respond appropriately tohypoglycemic symptoms (152,156,157).Tailoring glycemic therapy and/or liberaliz-ing A1C goals may prevent hypoglycemia\nin individuals with cognitive dysfunction.\nSee Section 13, “Older Adults, ”for more | [
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See Section 13, “Older Adults, ”for more\ndetailed discussion of hypoglycemia inolder people with type 1 and type 2\ndiabetes.\nLow Testosterone in Men\nRecommendation\n4.23 In men with diabetes who have\nsymptoms or signs of hypogonadism, | [
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4.23 In men with diabetes who have\nsymptoms or signs of hypogonadism,\nsuch as decreased sexual desire (libido)or activity or erectile dysfunction, con-sider screening with a morning serumtestosterone level. B | [
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Mean levels of testosterone are lower inmen with diabetes compared with age-matched men without diabetes, but obe-sity is a major confounder (158,159).\nTestosterone replacement in men with\nsymptomatic hypogonadism may have ben-efits, including improved sexual function,\nwell-being, muscle mass and strength, and | [
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well-being, muscle mass and strength, and\nbone density (160). In men with diabetes\nwho have symptoms or signs of low testos-terone (hypogonadism), a morning totaltestosterone level should be measured us-\ni n ga na c c u r a t ea n dr e l i a b l ea s s a y( 1 6 1 ) .I n | [
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i n ga na c c u r a t ea n dr e l i a b l ea s s a y( 1 6 1 ) .I n\nmen who have total testosterone levelsclose to the lower limit, it is reasonable todetermine free testosterone concentrationseither directly from equilibrium dialysis as-\nsays or by calculations that use total testos- | [
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says or by calculations that use total testos-\nterone, sex hormone binding globulin, andalbumin concentrations (161). Please seethe Endocrine Society clinical practice\nguideline for detailed recommendations\n(161). Further tests (such as luteinizinghormone and follicle-stimulating hormonelevels) may be needed to furt... | [
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the individual. Testosterone replacement\nin older men with hypogonadism hasbeen associated with increased coronaryartery plaque volume, with no conclusive\nevidence that testosterone supplementa-\ntion is associated with increased cardio-vascular risk in hypogonadal men (161).Erectile dysfunction is common in people | [
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with diabetes and warrants evaluation\n(162).Nonalcoholic Fatty Liver Disease and\nNonalcoholic Steatohepatitis\nScreening\nRecommendations\n4.24a Adults with type 2 diabetes\nor prediabetes, particularly those with\nobesity or cardiometabolic risk factorsor established cardiovascular disease,should be screened/risk st... | [
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clinically signi ficant liver fibrosis (de-\nfined as moderate fibrosis to cirrho-\nsis) using a calculated fibrosis-4 index\n(FIB-4) (derived from age, ALT, AST,\nand platelets [mdcalc.com/calc/2200/\nfibrosis4- fib-4-index-liver- fibrosis]), even\nif they have normal liver enzymes. B\n4.24b Adults with diabetes or predi-\nab... | [
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abetes with persistently elevated\nplasma aminotransferase levels for>6 months and low FIB-4 should be\nevaluated for other causes of liver\ndisease. B\n4.25 Adults with type 2 diabetes or\nprediabetes with an indeterminate\nor high FIB-4 should have additionalrisk stratifi cation by liver stiffness | [
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m e a s u r e m e n tw i t ht r a n s i e n te l a s t o g -\nraphy or the blood biomarker en-\nhanced liver fibrosis (ELF). B\n4.26 Adults with type 2 diabetes or\nprediabetes with indeterminate resultsor at high risk for signi ficant liver fibro-\nsis (i.e., by FIB-4, liver stiffness mea-surement, or ELF) should be refe... | [
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to a gastroenterologist or hepatologist\nfor further workup. Interprofessionalcare is recommended for long-termmanagement. B\nNonalcoholic fatty liver disease (NAFLD)\nincludes a broad spectrum of disease,ranging from macrovesicular hepatic stea-tosis (with or without mild in flammation) | [
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to nonalcoholic steatohepatitis (NASH) tocirrhosis. This is in the absence of ongoingor recent consumption of signi ficant\namounts of alcohol (defi ned as ingestion\nof>21 standard drinks per week in men\nand>14 standard drinks per week in\nwomen over a 2-year period precedingevaluation) or other secondary causes ofhepa... | [
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Diabetes is a major risk factor for de-\nveloping NASH, disease progression, andworse liver outcomes (164). Recent stud-\nies in adults in the U.S. estimated that\nNAFLD is prevalent in >70% of people\nwith type 2 diabetes (165 –167). This\nis consistent with studies from othercountries (168). NASH is de fined histo- | [
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logically as having $5% hepatic steatosis\na n di sa s s o c i a t e dw i t hi n flammation and\nhepatocyte injury (hepatocyte balloon-\ning), with or without evidence of liver fi-\nbrosis (163). Steatohepatitis is estimatedto affect more than half of people withtype 2 diabetes with NAFLD (169) and ap-pears to be a drive... | [
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offibrosis. Fibrosis stages are classi fied\nhistologically as the following: F0, no fi-\nbrosis; F1, mild; F2, moderate (signi fi-\ncant); F3, severe (advanced); and F4,cirrhosis. In the U.S., between 12 and\n20% of people with type 2 diabetes haveclinically signi ficant fibrosis ($F2) (165, | [
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166,169), with similar prevalence world-wide (164,168). NASH is a leading cause\nof hepatocellular carcinoma (HCC) (170,\n171) and of liver transplantation in theU.S., with transplant waiting lists beingoverrepresented by people with type 2 di-\nabetes (172). Clinicians underestimate its | [
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abetes (172). Clinicians underestimate its\nprevalence and do not consistently imple-ment appropriate screening strategies,thus missing the diagnosis of the poten-\ntially progressive form of NAFLD in high- | [
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tially progressive form of NAFLD in high-\nrisk groups, such as those having obesityor type 2 diabetes. This pattern of underdi-agnosis is compounded by sparse referralto specialists and inadequate prescription\nof medications with proven effi cacy in\nNASH (173,174).\nMetabolic dysfunction– associated stea-\ntotic live... | [
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totic liver disease (MASLD) has been pro-\nposed to replace the term nonalcoholic\nfatty liver disease (NAFLD) to identify\nsteatotic liver disease in the presence ofat least one cardiometabolic risk factorassociated with insulin resistance (e.g.,\nprediabetes, diabetes, atherogenic dysli- | [
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prediabetes, diabetes, atherogenic dysli-\npidemia, or hypertension) without otheridentifi able causes of steatosis (175).\nA separate category outside of MASLD,\nnamed metabolic dysfunction and alco- | [
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named metabolic dysfunction and alco-\nholic liver disease (MetALD), was createdfor circumstances in which alcohol intakeis greater than that allowed for NAFLDbut less than that attributed to alcoholic\nliver disease. The new de finition of\nNAFLD aims to remove potential stigma\nfrom the term “fatty”when referring to | [
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from the term “fatty”when referring to\nsteatosis and to provide a positive diag-\nnosis by means of having a cardiometa-\nbolic risk factor as a surrogate for insulinresistance, the metabolic dysfunction be-lieved to be driving the development of\nsteatosis. While the de finition may not\nconflict with the past de finiti... | [
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... |
conflict with the past de finition of NAFLD\nfor people with prediabetes or type 2diabetesjournals.org/care Comprehensive Medical Evaluation and Assessment of Comorbidities S65\n©AmericanDiabetesAssociation | [
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diabetes (who already have, by defi ni-\ntion, one cardiometabolic risk factor),\nlimitations include the need for bettervalidation, as cardiometabolic risk factorsmay carry different weights and thus\nsome may also have lower speci ficity as\nsurrogates for insulin resistance (e.g., hy- | [
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surrogates for insulin resistance (e.g., hy-\npertension). In addition, some peoplemay have insulin resistance and steatosis\nwithout cardiometabolic risk factors, some-\nthing more common in young adults in pri-mary care clinics or even in some leanpeople with steatohepatitis. Finally, some\npeople with type 2 diabete... | [
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people with type 2 diabetes or other\nforms of diabetes may have steatosiswith predominantly insulin secretion defi -\nciency, making diabetes a more question-\nable surrogate for insulin resistance.\nThe goal of screening for NAFLD is to\nidentify people at risk for adverse health | [
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identify people at risk for adverse health\noutcomes associated with NASH, such ascirrhosis, HCC, and death from liver dis-\nease. This risk is higher in people who\nhave central obesity and cardiometa-bolic risk factors or insulin resistance, are>50 years of age, and/or have persis- | [
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tently elevated plasma aminotransferases(AST and/or ALT >30 units/L for >6m o n t h s )\n(176,177). Some genetic variants that alterhepatocyte triglyceride metabolism mayalso increase the risk of NASH progression\nand cirrhosis (178,179), amplifying the im- | [
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and cirrhosis (178,179), amplifying the im-\npact of obesity, but the role of genetictesting in clinical practice remains to beestablished.\nIndividuals with clinically signi ficant\nfibrosis ( $F2), especially those with\ntype 2 diabetes, have a greater risk ofcirrhosis with liver decompensation, HCC,liver transplantati... | [
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ity (180 –183). Increased mortality associ-\nated with NAFLD is attributable not only\nto cirrhosis and HCC but also to extrahe-patic cancer (171), type 2 diabetes (184),\nand cardiovascular disease (185,186). The\nestimated relative impact depends onlength of follow-up and population stud-ied, among other factors. Eme... | [
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dence suggests that NAFLD increases the\nrisk of chronic kidney disease, particularlywhen liver fibrosis is present (187,188),\nalthough the association of NAFLD withdiabetic retinopathy is less clear (189).\nEarly diagnosis is essential to prevent fu-\nture cirrhosis and complications.\nA recent meta-analysis reported ... | [
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A recent meta-analysis reported a prev-\nalence of NAFLD of 22% in people withtype 1 diabetes (190). This risk may be\nlinked to the fact that about one-third of | [
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linked to the fact that about one-third of\npeople with type 1 diabetes in the U.S.have obesity (191). However, there is largevariability in NAFLD prevalence acrossstudies, and most measured liver fat by ul-trasound. In one of the few studies usingthe gold-standard MRI technique to quan-\ntify liver fat, the prevalence... | [
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tify liver fat, the prevalence of steatosis in\na population with type 1 diabetes withlow prevalence of obesity was only 8.8%compared with 68% in people with type 2\ndiabetes (192). The prevalence of fibrosis\nwas not established in that study. There-\nfore, screening for fibrosis in people with\ntype 1 diabetes should o... | [
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type 1 diabetes should only be considered\nin the presence of additional risk factors\nfor NAFLD, such as obesity, incidental he-patic steatosis on imaging, or elevatedplasma aminotransferases.\nThere is consensus that the fibrosis-4 | [
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There is consensus that the fibrosis-4\nindex (FIB-4) is the most cost-effectivestrategy for the initial screening of peo-ple with prediabetes and cardiometa-bolic risk factors or with type 2 diabetesin primary care and diabetes clinical set-\ntings (168,174,176,177,193– 195). See the\nproposed diagnostic algorithm by a... | [
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proposed diagnostic algorithm by an ex-\npert group that included ADA representa-tives in Fig. 4.2 (174). A screening strategy\nbased on elevated plasma aminotransfer-ases>40 units/L would miss most individ-\nuals with NASH in these settings, as clinicallysignifi cant fibrosis ($F2) is frequently ob- | [
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served with plasma aminotransferasesbelow the commonly used cutoff of40 units/L (165– 167,169,196,197). The\nAmerican College of Gastroenterologyconsiders the upper limit of normal ALT\nlevels to be 29 –33 units/L for male individ-\nuals and 19 –25 units/L for female individu-\nals (198), as higher levels are associate... | [
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als (198), as higher levels are associated\nwith increased liver-related mortality, even\nin the absence of identi fiable risk factors.\nThe FIB-4 estimates the risk of hepatic cir-\nrhosis and is calculated from the computa-tion of age, plasma aminotransferases\n(AST and ALT), and platelet count (mdcalc.\ncom/calc/2200... | [
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com/calc/2200/fi brosis-4- fib-4-index-liver-\nfibrosis). A value of <1.3 is considered low\nrisk of having advanced fibrosis (F3 –F4)\nand for developing adverse liver outcomes,\nwhile>2.67 is considered as having a high\nprobability of advanced fibrosis (F3 –F4)\nand increased risk of adverse liver out-\ncomes. FIB-4 pred... | [
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comes. FIB-4 predicts changes over time in\nhepatic fibrosis (199,200) and allows risk\nstratification of individuals in terms of fu-\nture liver-related morbidity and mortality\n(201). FIB-4 has reasonable speci ficity but\nlow sensitivity, hence a negative resultrules out fibrosis while a positive result re- | [
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quires confi rmatory testing (200,202 –205).It has a reasonable speci ficity and nega-\ntive predictive value to rule out advancedfibrosis but lacks adequate sensitivity and\npositive predictive value to establish pres-ence of advanced fibrosis in many cases,\nwhich is the reason why people with dia-betes often fall in the... | [
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(or intermediate) risk group for advancedfibrosis and adverse liver outcomes\n(when FIB-4 is between 1.3 and 2.67).However, its low cost, simplicity, andgood speci ficity make it the initial test of\nchoice ( Fig. 4.2 ). Performance is better in\na population with higher prevalence ofsignificant fibrosis (i.e., hepatology ... | [
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ics) compared with primary care settings.FIB-4 has not been well validated in pedi-atric populations and does not perform\nas well in those aged <35 years. In peo-\nple with diabetes $65 years of age,\nhigher cutoffs for FIB-4 have been rec-\nommended (1.9 –2.0 rather than >1.3)\n(206,207).\nIn people with an indetermi... | [
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(206,207).\nIn people with an indeterminate or\nhigh FIB-4, additional risk strati fication is\nrequired with a liver stiffness measure-ment (LSM) by transient elastography\n(Fig. 4.2) or, if unavailable, by commercial\nblood fibrosis biomarkers such as the en-\nhanced liver fibrosis (ELF) test (208) or | [
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hanced liver fibrosis (ELF) test (208) or\nothers. Use of a second nonproprietarydiagnostic panel is not recommended\n(i.e., NAFLD fibrosis score and others), as\nthey generally do not perform betterthan FIB-4 (167,202). Transient elastogra-phy (LSM) is the best-validated imaging\ntechnique for fibrosis risk strati ficatio... | [
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technique for fibrosis risk strati fication,\nand it predicts future cirrhosis and all-\ncause mortality in NAFLD (176,177,209).An LSM value of <8.0 kPa has a good\nnegative predictive value to exclude ad-vanced fibrosis ($F3 –F4) (210 –212) and\nindicates low risk for clinically signifi cant\nfibrosis. Given the lack of wi... | [
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fibrosis. Given the lack of widespread\navailability of LSM, the ELF test is a goodalternative. Individuals with ELF <7.7 are\nconsidered at low risk for adverse out-comes. Such individuals with diabetes canbe followed in nonspecialty clinics with re-\npeat surveillance testing every $2y e a r s ,\nalthough the precise ... | [
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although the precise time interval remains\nto be established. If the LSM is >12 kPa,\nthe risk for advanced fibrosis is high and\npeople with diabetes should be referred tothe hepatologist (168). FIB-4 followed byLSM helps stratify people with diabetes byrisk level and minimize specialty referrals\n(204,209,213– 215) (... | [
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(204,209,213– 215) ( Fig. 4.2).\nSpecialists may order additional tests\nforfibrosis risk strati fication (175 –177,S66 Comprehensive Medical Evaluation and Assessment of Comorbidities Diabetes Care Volume 47, Supplement 1, January 2024\n©AmericanDiabetesAssociation | [
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195,209), with magnetic resonance elas-\ntography (MRE) having the best overallperformance (particularly for early fibro-\nsis stages). However, the accessibility andcosts associated with MRE are barriers toits use. While liver biopsy remains thegold standard for the diagnosis of NASH,its indication is reserved to the d... | [
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of the specialist within an interprofes-\nsional team approach due to high costsand potential for morbidity associatedwith this procedure.\nIn 2020, an expert panel convened by | [
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In 2020, an expert panel convened by\nthe American Gastroenterological Asso-ciation that included representatives ofthe ADA reviewed the published litera-ture on the burden, screening, risk strat-ification, diagnosis, and management of\nindividuals with NAFLD (175). See Fig.\n4.2, which is adapted from this special | [
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0.07... |
4.2, which is adapted from this special\nreport (174). A Clinical Care Pathwaysummarized the diagnosis and manage-ment of NAFLD in a subsequent publica-\ntion (177). Consensus has emerged to\nstart screening with FIB-4 followed byLSM or ELF and patented biomarkers asneeded for the noninvasive fibrosis risk\nstrati ficati... | [
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strati fication of individuals with NAFLD\nin primary care and diabetes clinics(167,174,176,177,193 –195,216).\nAfter initial risk strati fication (i.e., FIB-4,\nLSM, and/or patented biomarkers), peoplewith diabetes at indeterminate or high risk\noffibrosis should be referred, based on | [
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offibrosis should be referred, based on\npractice setting, to a gastroenterologist orhepatologist for further workup within the\nframework of an interprofessional team\n(163,176,177,216,217).\nManagement\nRecommendations\n4.27 Adults with type 2 diabetes or pre-\ndiabetes, particularly with overweight\nor obesity, with ... | [
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or obesity, with nonalcoholic fatty liver\ndisease (NAFLD) should be recom-mended lifestyle changes that promoteweight loss, ideally within a structured\nnutrition plan and physical activity pro-\ngram for cardiometabolic bene fitsB\nand histological improvement. C\n4.28 For adults with type 2 diabetes, | [
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and histological improvement. C\n4.28 For adults with type 2 diabetes,\nparticularly with overweight or obe-sity, with NAFLD, consider using aglucagon-like peptide 1 (GLP-1) re-\nceptor agonist with demonstrated\nbene fits in nonalcoholic steatohepa-\ntitis (NASH) as an adjunctive therapyto lifestyle interventions for w... | [
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loss. B\n4.29 Pioglitazone or GLP-1 receptor ag-\nonists are the preferred agents for the\ntreatment of hyperglycemia in adults\nwith type 2 diabetes with biopsy-\nproven NASH or those at high risk withclinically signi ficant liver fibrosis using\nnoninvasive tests. A\n4.30a In adults with type 2 diabetes | [
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noninvasive tests. A\n4.30a In adults with type 2 diabetes\nand NAFLD, use of glucose-loweringtherapies other than pioglitazone or\nGLP-1 receptor agonists may becontinued as clinically indicated, but\nthese therapies lack evidence of ben-\nefiti nN A S H . B\n4.30b Insulin therapy is the pre- | [
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efiti nN A S H . B\n4.30b Insulin therapy is the pre-\nferred agent for the treatment ofhyperglycemia in adults with type 2\ndiabetes with decompensated cir-\nrhosis. C\n4.31a Adults with type 2 diabetes\nand NAFLD are at increased cardio-\nvascular risk; therefore, comprehen-\nsive management of cardiovascularrisk fact... | [
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sive management of cardiovascularrisk factors is recommended. B\n4.31b Statin therapy is safe in adults\nwith type 2 diabetes and compensated\ncirrhosis from NAFLD and should be ini-tiated or continued for cardiovascular\nrisk reduction as clinically indicated. B\nStatin therapy should be used with\ncaution and close m... | [
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caution and close monitoring in people\nwith decompensated cirrhosis, given\nlimited safety and ef ficacy data. B\n4.32a Consider metabolic surgery in\nappropriate candidates as an option\nto treat NASH in adults with type 2\ndiabetes Band to improve cardio-\nvascular outcomes. B\n4.32b Metabolic surgery should be\nused... | [
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4.32b Metabolic surgery should be\nused with caution in adults with\ntype 2 diabetes with compensatedcirrhosis from NAFLD Band is not\nrecommended in decompensated\ncirrhosis. B\nWhile steatohepatitis and cirrhosis occur\nin lean people with diabetes and are be-lieved to be linked to genetic predisposi-\ntion, insulin ... | [
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tion, insulin resistance, and environmental\nfactors (218 –220), there is ample evidence\nto implicate excess visceral and overall adi-posity in people with overweight and obe-sity in the pathogenesis of the disease\n(221,222). Obesity in the setting of type 2 | [
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(221,222). Obesity in the setting of type 2\ndiabetes worsens insulin resistance andsteatohepatitis, promoting the develop-ment of cirrhosis (223). Therefore, clini-\ncians should enact evidence-based inter-\nventions (as discussed in Section 5,“Facilitating Positive Health Behaviors and\nWell-being to Improve Health O... | [
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Well-being to Improve Health Outcomes ”)\nto promote healthy lifestyle change and\nweight loss for people with overweight or\nobesity and NAFLD. A minimum weightloss goal of 5%, preferably $10% (224,\n225), is needed to improve liver histology,withfibrosis requiring the larger weight re-\nduction to promote change (225 ... | [
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duction to promote change (225 –227). In-\ndividualized, structured weight loss andexercise programs offer greater benefi t\nFigure 4.2 —A proposed algorithm for risk strati fication in individuals with nonalcoholic fatty\nliver disease or nonalcoholic steatohepatitis. ELF, enhanced liver fibrosis; FIB-4, fibrosis-4 index. | [
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Adapted from Kanwal et al. (174).diabetesjournals.org/care Comprehensive Medical Evaluation and Assessment of Comorbidities S67\n©AmericanDiabetesAssociation | [
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than standard counseling in people with\nNAFLD (218,228).\nDietary recommendations to induce\nan energy de ficit are not different from\nthose for people with diabetes with\nobesity without NAFLD and should in-\nclude a reduction of macronutrient con-tent, limiting saturated fat, starch, andadded sugar, with adoption of... | [
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eating patterns. The Mediterranean diet\nhas the best evidence for improving liverand cardiometabolic health (176,193,194,228– 232). Both aerobic and resistance\ntraining improve NAFLD in proportion to\ntreatment engagement and intensity of\nthe program (233 –235).\nObesity pharmacotherapy may assist | [
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the program (233 –235).\nObesity pharmacotherapy may assist\nwith weight loss in the context of life-style modi fication if not achieved by life-\nstyle modi fication alone (see Section 8,\n“Obesity and Weight Management for\nthe Prevention and Treatment of Type 2Diabetes ”).\nAt present, there are no FDA-approved | [
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At present, there are no FDA-approved\ndrugs for the treatment of NASH. There-fore, treatment for people with type 2 di-abetes and NASH is centered on the dualpurpose of treating hyperglycemia and\nobesity, especially if clinically signi ficant\nfibrosis ($F2) is present. The rationale\nfor the treatment of people with t... | [
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for the treatment of people with type 2\ndiabetes is based on their high preva-\nlence of NASH with signifi cant fibrosis\n(10–15% of people with type 2 diabetes)\n(165–169), their higher risk of disease\nprogression and liver-related mortality(164,183,236), and the lack of pharmaco- | [
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logical treatments once cirrhosis is estab-lished (237). Therefore, early diagnosis andtreatment of NAFLD offers the best oppor-\ntunity for cirrhosis prevention. Pioglitazone\nand some glucagon-like peptide 1 receptoragonists (GLP-1 RAs) have been shown tobe effective to treat steatohepatitis (176,177,238– 240) and ma... | [
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gression (241– 243) and decrease cardio-\nvascular disease (177,239), which is thenumber one cause of death in people withtype 2 diabetes and NAFLD (185).\nPioglitazone improves glucose and lipid | [
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Pioglitazone improves glucose and lipid\nmetabolism and reverses steatohepatitisin people with prediabetes or type 2 dia-betes (244,245) and even without diabe-tes (246 –248). Fibrosis also improved in | [
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some trials (245,247). A meta-analysis(241) concluded that pioglitazone treat-ment results in resolution of NASH andmay improve fibrosis. Pioglitazone may\nhalt the accelerated pace of fibrosis pro- | [
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halt the accelerated pace of fibrosis pro-\ngression observed in people with type 2diabetes (242) and is overall cost-effectivefor the treatment of NASH (249,250). Vita-min E may be bene ficial for the treatment\nof NASH in people without diabetes (246).However, in people with type 2 diabetes,\nvitamin E monotherapy was ... | [
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vitamin E monotherapy was found to be\nnegative in a small RCT (242), and it didnot seem to enhance pioglitazone ’se ffi-\ncacy when used in combination as re-\nported in an earlier trial in this population\n(245). Pioglitazone causes dose-dependentweight gain (15 mg/day, mean of 1 –2%;\n45 mg/day, 3 –5%), increases fra... | [
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45 mg/day, 3 –5%), increases fracture risk,\nmay promote heart failure if used in indi-viduals with preexisting congestive heartfailure, and may increase the risk of blad-der cancer, although this remains contro-versial (163,176,177,239,240).\nGLP-1 RAs are effective at inducing | [
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GLP-1 RAs are effective at inducing\nweight loss and ameliorating elevatedplasma aminotransferases and steatosis(238). However, there are only two RCTsof GLP-1 RAs in biopsy-proven individuals\nwith NASH. A small RCT reported that lira-\nglutide improved some features of NASH | [
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glutide improved some features of NASH\nand, of particular relevance, delayed theprogression of fibrosis (251). More re-\ncently, once-daily subcutaneous semaglu-tide in 320 people with biopsy-provenNASH (62% having type 2 diabetes) re-ported resolution of steatohepatitis in\n59% at the higher dose (equivalent to | [
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59% at the higher dose (equivalent to\n2.4 mg/week semaglutide) comparedwith 17% in the placebo group ( P<0.001)\n(243). Cumulatively, semaglutide did notsignificantly affect the stage of liver fibro-\nsis in this group of people (70% of whomhad F2 or F3 at baseline), but it signi fi- | [
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cantly slowed over 72 weeks the progres-sion of liver fibrosis (4.9% with the GLP-1\nRA at the highest dose compared with18.8% on placebo). Tirzepatide (252),sodium– glucose cotransporter inhibitors\n(253–255), and insulin (240) reduce he- | [
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(253–255), and insulin (240) reduce he-\npatic steatosis, but their effects on steato-hepatitis remain unknown. The use ofglucose-lowering agents other than piogli-tazone or GLP-1 RAs may be continuedin individuals with type 2 diabetes and\nNAFLD for glycemic control, as clinically | [
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0.0298225786536932,
-0.011579744517803192,
0.09069541096687317,
-0.08778068423271179,
-0.023948341608047485,
-0.03601572662591934,
0.08847926557064056,
-0.06613726168870926,
-0.0180396... |
NAFLD for glycemic control, as clinically\nindicated. However, these agents have ei-ther failed to improve steatohepatitis inpaired-biopsy studies (metformin) or have\nno RCTs with liver histological end points\n(i.e., sulfonylureas, glitinides, dipeptidylpeptidase 4 inhibitors, or acarbose).\nInsulin is the preferred ... | [
-0.029060769826173782,
-0.04987011104822159,
-0.09430477768182755,
0.027591578662395477,
-0.046655308455228806,
0.01336864847689867,
-0.03333909809589386,
0.1558283418416977,
-0.025337109342217445,
-0.01439653243869543,
-0.030003909021615982,
0.04292500019073486,
-0.0490533672273159,
0.023... |
Insulin is the preferred glucose-lower-\ning agent for the treatment of hypergly-\ncemia in adults with type 2 diabetes\nwith decompensated cirrhosis given thelack of robust evidence about the safety\nand effi cacy of oral agents and noninsulin\ninjectables (i.e., GLP-1 RAs and GLP-1/GIP | [
-0.05272754654288292,
0.021315811201930046,
-0.10455159097909927,
0.03495260328054428,
-0.08600547909736633,
0.0062033492140471935,
0.08001037687063217,
0.11538456380367279,
-0.04222815856337547,
-0.0019235654035583138,
0.006215173751115799,
0.051538363099098206,
-0.0630960762500763,
0.001... |
injectables (i.e., GLP-1 RAs and GLP-1/GIP\nRAs) (256), although a recent 48-weekstudy suggested that GLP-1 RAs are safein individuals with NASH and compen-sated cirrhosis (257).\nMetabolic surgery improves NASH and\ncardiometabolic health, altering the naturalhistory of the disease (258). Meta-analysesreport that 70 –... | [
-0.028867293149232864,
0.0020128556061536074,
-0.053839441388845444,
0.0022467519156634808,
-0.1046862080693245,
-0.027152515947818756,
0.032364241778850555,
0.09226439893245697,
-0.08274891972541809,
0.029001649469137192,
0.03524211421608925,
0.04171659052371979,
-0.00783272460103035,
0.0... |
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