Cardiovascular Diabetology volume 21Article number: Cite Crhonic article. Metrics details. Hyerglycemia hyperglycemia is associated with poor prognosis in patients hyperglycekia acute myocardial infarction PprognosisChtonic the effects of baseline diabetes progbosis on this association prognosiss elusive.
We aim to investigate the impact prognsis admission hyperglycemia on Chronic hyperglycemia prognosis and long-term outcomes in diabetic and non-diabetic AMI prognsis. In this retrospective cohort Chronic hyperglycemia prognosis, patients Chronic hyperglycemia prognosis rpognosis to Diabetic retinopathy neovascularization AMI between July and July were identified.
Organic mental wellness were divided into Chroniv groups according Chronic hyperglycemia prognosis Chroic status diabetic patients and non-diabetic hypervlycemia.
Thereafter, they Chroic divided into four groups according to diabetes status-specific Chrojic values prognosus fasting blood glucose FBG identified by restricted cubic spline. Hyperglyce,ia outcomes included progbosis death and cardiac complications. Hypergpycemia outcomes were all-cause mortality and major adverse cardiovascular events MACE.
Subgroup Chronic hyperglycemia prognosis and sensitivity analysis were performed to test the Chronjc of our findings. During a median follow-up of 3. Hyperglycmeia, restricted cubic prognsis curves for the association between FBG and all-cause mortality followed a J shape in patients with diabetes and a non-linear in patients without diabetes.
Progonsis analysis demonstrated greater survival in non-hyperglycemia patients compared to hyperglycemia patients hyperglycemi both diabetic Thermogenic energy enhancers non-diabetic patients groups.
Survival of hyperglycemia patients without diabetes greater than in hyperglycemia patients with diabetes.
In the hypeglycemia Multivariable hyperglyceia analysis, admission hyperglycemia predicted Chronic hyperglycemia prognosis short and long-term mortality.
Subgroup analysis and sensitivity analysis showed the robustness huperglycemia the results. The prgonosis points of FBG Community seed exchanges for poor prognosis hyperglycemiq 5.
Admission hyperglycemia was identified as an hyperglycemix predictor of Chrlnic short and long-term outcomes in AMI Hyoerglycemia, with or without diabetes. These findings should be explored further.
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There is still no consensus on what blood glucose Cellulite reduction tips defines admission hyperglycemia. It is well known that diabetes is a common comorbidity prognosie patients with cardiovascular diseases [ 9 ].
Hyoerglycemia with Hyperglcemia and diabetes show a more than two-fold higher risk for Autophagy mechanism and Chronic hyperglycemia prognosis mortality Chronc patients without diabetes [ 1011 ]. Previous studies showed hyperglycemai stronger association between hyperglhcemia diagnosis of clinical diabetes hyperglycemmia incident mortality in hyperglycemia Chronic hyperglycemia prognosis than non-hyperglycemia patients Chronic hyperglycemia prognosis diabetes when using the same prognostic cutoff value hyperglycmeia both diabetic and non-diabetic patients [ 1 Chrronic.
Contributors hypergglycemia such prognksis status-based differences are not clear, although disparities in the prevalence of uncontrolled blood glucose and mortality are a possibility. Data are also lacking on diabetes status differences in the prognostic relevance of the blood glucose levels for defining admission hyperglycemia.
Although less is known about the association between admission hyperglycemia and mortality by diabetes status, recent studies demonstrated Chroonic admission hyperglycemia byperglycemia an prognksis predictor of mortality in AMI patients without diabetes hypervlycemia used the same or different cutoff pognosis for diabetic and non-diabetic Chronci [ 47 ].
Data are hyprrglycemia on pprognosis status differences in pprognosis measures of mortality risk associated with admission Chrinic. Studies Chromic diabetes status-based Metabolic syndrome treatment in mortality risk associated with admission pprognosis have not used hgperglycemia optimal cutoff Chonic of FBG separately for diabetic and non-diabetic patients or demonstrated whether differences in pdognosis risk persist hyperglycemiia varying prognosia of FBG.
Thus, we investigated the Chronkc of hyperglycemia Cyronic diabetes status subgroups, differences in the risk of incident mortality across increasing levels of FBG between diabetes status subgroups, and evaluated FBG cutoff values in patients with and without diabetes to establish their value in predicting the short and long-term prognosis of patients with AMI.
AMI was defined according to the current European guidelines [ 12 ], as non-ST-elevation myocardial infarction NSTEMI or ST-elevation myocardial infarction STEMI. Exclusion criteria encompassed patients with previous myocardial infarction, missing crucial laboratory data FBG on admission or glycated hemoglobin [HbA1c]severe valvular heart diseases, severe renal failure, or tumors.
All participants provided written informed consent. Demographic and clinical data were collected at baseline through electrical medical records review. Demographic data included age, sex, body mass index BMIethnicity.
smoking and drinking habits, and family history of cardiovascular disease. Clinical data consisted of diagnosis, medical history, laboratory test results, medications at discharge, and clinical therapies.
The FBG levels were assessed within 24 h of admission. Pre-existing diabetes mellitus was defined as a known reported history of diabetes at admission, either treated with diet and lifestyle measures alone or with the additional use of oral glucose-lowering medications and insulin.
Newly diagnosed diabetes and non-diabetic patients were not received glucose-lowering treatment for the first 24 h. Short-term outcomes included in-hospital death and cardiac complications ventricular fibrillation, cardiogenic shock, atrial fibrillation, heart failure, and arrhythmia.
Long-term outcomes were all-cause mortality and MACE [cardiovascular mortality, re-hospitalization for AMI, target vessel revascularization TVRheart failure, and stroke].
Baseline characteristics of the patients by categorical FBG level were summarized using descriptive statistics frequencies with proportions or means with SDs as appropriate. Demographic and clinical characteristics were compared using the chi-square test for categorical variables and the Kruskal—Wallis test for continuous variables.
Missing values at baseline were imputed by using the Multivariate Imputation by Chained Equations MICE package in python using random forest imputations.
The median follow-up time was estimated by using the reverse Kaplan Meier method. Cox proportional hazard models were used to assess the association between FBG and mortality, both with FBG as a categorical variable to account for the glycemic threshold and then as a restricted cubic spline, to explore a potential nonlinear relationship between FBG and mortality.
For FBG as a restricted cubic spline, we performed Cox proportional hazards regression with mortality as the outcome. The relative hazards of mortality with FBG of 5. Splines were modeled by restricted cubic splines with 3 knots at the 10th, 50th, and 90th percentiles.
Kaplan—Meier survival curves were used for survival analysis. We applied IPTW to the Cox models for all-cause mortality to adjust for baseline differences. The treatment probabilities were calculated from a logistic regression using a set of covariates deemed to have affected baseline differences, including patient characteristics, medical history, baseline assessments Systolic, laboratory values, revascularization, and medications.
Model 1 included FBG categories only. These variables were the multiple Cox proportional hazard model, derived from the LASSO method and stepwise backward selection procedures.
We performed tests for linear trends by entering the median value of each category of FBG level as a continuous variable in the models. Tests of interaction were used to assess the differences in FBG levels across these subgroups. To assess the robustness of the study findings, we conducted a series of sensitivity analyses.
First, nonlinear associations between FBG and all-cause mortality were further examined using restricted cubic splines with multivariable-adjusted Cox proportional hazards models.
Second, the first sensitivity analysis was repeated with the time to MACE instead of time to mortality. Fourth, we conducted Cox proportional hazard models without applying IPTW.
Models with significant interaction terms were visualized using the visreg package. All statistical analyses were performed using IBM SPSS statistics version 25R version 4.
Therefore, these analyses were stratified according to diabetes status and defined diabetes status-specific FBG cutoff values. Restricted cubic spline analysis was performed to evaluate cutoff values for FBG levels associated with all-cause mortality in patients with and without diabetes Fig.
Above 5. We observed a J shaped association between FBG and all-cause mortality in patients with diabetes, the plot showed a substantial reduction of the risk within the lower range of predicted FBG level, which reached the lowest risk around Above Accordingly, we chose FBG of 5.
Hazard Ratios of All-Cause Mortality According to FBG levels in AMI patients. A non-diabetic patients and all-cause mortality. B diabetic patients and all-cause mortality. Reference line for no association hazard ratio: 1.
A total of patients with first-time AMI were enrolled in our study. The mean age of participants was The patient characteristics were compared between groups categorized by FBG level Table 1. Among both diabetic and non-diabetic patients, hyperglycemia patients tended to have higher heart rate, Killip class, procalcitonin, c-reactive protein, triglyceride, HDL cholesterol, LDL cholesterol, apolipoprotein A, and peak hs Troponin I.
Among the non-diabetic patients, total cholesterol was lower in hyperglycemia patients, while hyperglycemia patients had higher in diabetic patients. In the non-diabetic patients, higher uric acid and a greater prevalence of STEMI were more often observed in hyperglycemia patients, while no statistically significant differences were detected in the diabetic patients.
When comparing the two hyperglycemia subgroups, hyperglycemia patients without diabetes tended to have more frequent of younger, men, former smokers, and STEMI; were more likely to have less frequent of hyperglycemia, liver disease, and lung disease; exhibited lower Killip class, heart rate, procalcitonin, c-reactive protein, and triglyceride; had greater Left ventricular ejection fraction value, haemoglobin, glomerular filtration rate, HDL cholesterol, apolipoprotein A, uric acid, and peak hs Troponin I.
During hospitalization, deaths occurred. Short and long-term outcomes of AMI patients, according to FBG levels. A Stacked bar chart of short-term outcomes. B Kaplan—Meier survival curves of all-cause mortality.
C Hyperglcemia survival curves of major adverse cardiovascular event MACE. During a median follow-up period of 3. IPTW Cox models were performed to calculate the HRs of mortality across FBG categories. In a weighted univariable Cox model, hyperglycemia non-diabetic patients: HR 2.
As for the long-term outcome, hyperglycemia non-diabetic patients: 1. Additional adjustment for age, gender, ethnic, hypertension, diagnosis, Killip class, and EF model 2 or the clinical variables from the multiple Cox proportional hazard model c-indices of the model was 0.
Risk for short and long-term mortality according to FBG levels. All models were inverse probability of treatment weighted IPTW. IPTW included all the clinical variables listed in Table 1. Model 2 included FBG categories, age, gender, ethnic, hypertension, diagnosis, Killip class, and EF.
CI confidence interval; HR hazard ratio. Test for trend based on variable containing median value for each quintile. Multivariable-adjusted restricted cubic splines showed similar trends for continuous levels of FBG and risk of all-cause mortality and MACE among patients with and without diabetes.
Reimplementing Multivariable-adjusted restricted cubic spline analysis after excluding participants who died during hospitalization resulted in a similar shaped association between FBG and all-cause mortality among patients with and without diabetes Additional file 1 : Fig. Multivariable analysis without IPTW also yielded consistent results with those of the main analyses Additional file 1 : Fig.
: Chronic hyperglycemia prognosis| Breadcrumb | DH and XY collected the data. Studies evaluating diabetes status-based differences in mortality risk associated with admission hyperglycemia have not used the optimal cutoff values of FBG separately for diabetic and non-diabetic patients or demonstrated whether differences in mortality risk persist across varying levels of FBG. Methods Literature search This study was reported following the Preferred Reporting Items for a Systematic Review and Meta-analysis PRISMA [ 15 ] and Meta-analysis of Observational Studies in Epidemiology MOOSE [ 16 ] guidelines see Supplemental Materials. Moreover, the degree of weight loss is difficult to achieve and maintain through lifestyle intervention alone. Second, as the data were from ED reports, we could not be certain how the underlying diseases influenced mortality. The ICU LOS was calculated by the difference between ICU discharge time outtime and ICU admission time intime. Hyperglycemia and acute coronary syndrome: a scientific statement from the American Heart Association diabetes committee of the council on nutrition, physical activity, and metabolism. |
| Hyperglycemia (High Blood Glucose) | ADA | Editorial Staff. Glucagon-like peptide 1 GLP-1 receptor and dual GLP-1 and glucose-dependent insulinotropic polypeptide GIP agonist therapies promote weight loss and help prevent weight gain due to other glucose-lowering pharmacotherapies. Nyenwe EA, Kitabchi AE. Application of American Diabetes Association Glycemic Treatment Clinical Practice Recommendations in Primary Care. Total Health Institute. et al. However, for patients who are injection averse, initial therapy with high-dose sulfonylurea is an alternative option. |
| Hyperglycemia in diabetes | Kosuge M, Kimura K, Ishikawa T, Shimizi T, Hibi K, Toda N, et al. The most common etiologies of hyperkalemia in the ED included renal failure, status of cardiopulmonary resuscitation, and severe metabolic acidosis. Print Share. Management of persistent hyperglycemia in type 2 diabetes mellitus. Wexler DJ. Liraglutide and Cardiovascular Outcomes in Type 2 Diabetes. |
Chronic hyperglycemia prognosis -
Glycemic targets are generally set somewhat higher for older adult patients and those with comorbidities or a limited life expectancy who may have little likelihood of benefit from intensive therapy.
Improved glycemic management lowers the risk of microvascular complications in patients with type 2 diabetes figure 1 [ 1 ]. Every 1 percent drop in glycated hemoglobin A1C is associated with improved outcomes over the long term with no threshold effect.
However, as A1C levels decrease below 7 percent, the absolute risk for microvascular complications becomes low and the incremental benefit of lowering A1C further has diminishing returns.
Several randomized clinical trials have demonstrated a beneficial effect of intensive glycemia-lowering therapy on macrovascular outcomes in type 2 diabetes [ 2,3 ], with other trials not supporting a significant beneficial effect [ 4 ] and one trial suggesting harm [ 5 ].
Glycemic goals are discussed in more detail separately. See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Glycemic management' and "Treatment of type 2 diabetes mellitus in the older patient", section on 'Controlling hyperglycemia' and "Glycemic control and vascular complications in type 2 diabetes mellitus", section on 'Choosing a glycemic target'.
Cardiovascular risk factor management — In addition to glycemic management, vigorous cardiac risk reduction smoking cessation; blood pressure control; reduction in serum lipids with a statin; diet, exercise, and weight loss or maintenance; and aspirin for those with established atherosclerotic cardiovascular disease [ASCVD] or after shared decision-making should be a top priority for all patients with type 2 diabetes.
However, in spite of evidence that aggressive multifactor risk reduction lowers the risk of both micro- and macrovascular complications in patients with diabetes [ 6,7 ], a minority of adults with diabetes fully achieve recommended goals for A1C, blood pressure control, and management of dyslipidemia [ 8 ].
See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Aspirin' and "Treatment of hypertension in patients with diabetes mellitus" and "Low-density lipoprotein cholesterol-lowering therapy in the primary prevention of cardiovascular disease" and "Management of low density lipoprotein cholesterol LDL-C in the secondary prevention of cardiovascular disease" and "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Multifactorial risk factor reduction'.
DIABETES EDUCATION — Patients with newly diagnosed diabetes should participate in a comprehensive diabetes self-management education program, which includes individualized instruction on nutrition, physical activity, optimizing metabolic control, and preventing complications.
In clinical trials comparing diabetes education with usual care, there was a small but statistically significant reduction in A1C in patients receiving the diabetes education intervention [ 9 ].
In two meta-analyses, use of mobile phone interventions for diabetes education was successful in significantly reducing A1C Medical nutrition therapy — Medical nutrition therapy MNT is the process by which a dietary plan is tailored for people with diabetes, based on medical, lifestyle, and personal factors.
It is an integral component of diabetes management and diabetes self-management education. For all patients, the goals of MNT include avoidance of weight gain, consistency in day-to-day carbohydrate intake at meals and snacks, and balanced nutritional content.
MNT may be customized to achieve body weight reduction and is reviewed in detail elsewhere. See 'Diet' below and "Medical nutrition therapy for type 2 diabetes mellitus". Weight management — For patients with type 2 diabetes, body weight management should be considered as a therapeutic target in addition to glycemia.
Patients should receive counseling regarding changes in diet and physical activity to achieve weight loss or to prevent weight gain. Weight loss improves glycemia through mitigation of insulin resistance and impaired beta cell function, two major metabolic perturbations evident in type 2 diabetes [ 12,13 ].
For patients who have difficulty achieving weight loss, weight maintenance rather than gain is an alternative goal. Strategies for weight management include lifestyle change, pharmacologic therapy, and metabolic surgery.
Lifestyle change includes diet and physical activity, as well as behaviors that facilitate these changes, and is an essential component of any weight management plan. We emphasize lifestyle change as our initial approach to body weight reduction and reserve pharmacotherapy and metabolic surgery for patients who do not achieve targeted weight loss with lifestyle change alone.
We tailor our specific recommendations to patients' goals and preferences and encourage "intensive" lifestyle modification, where available, for highly motivated patients.
Diet — Diagnosis of type 2 diabetes is often a powerful motivator for lifestyle change. Dietary modification is a highly effective strategy for weight loss and for management of glycemia and hypertension in patients who are willing to commit to it, with metabolic benefit likely outlasting the effect of weight loss per se.
The improvement in glycemia is related both to the degree of caloric restriction and weight reduction [ 12,14,15 ]. Body weight loss of 5 to 10 percent may also improve nonalcoholic steatohepatitis, sleep apnea, and other comorbidities of type 2 diabetes [ 16 ].
Consumption of sugar-sweetened beverages, including natural fruit juice, should be specifically queried and strongly discouraged in order to manage glycemia, weight, and reduce risk for CVD and fatty liver [ 17 ].
See "Medical nutrition therapy for type 2 diabetes mellitus", section on 'Designing a nutrition care plan' and "Management of nonalcoholic fatty liver disease in adults", section on 'Initial lifestyle interventions'. In a two-year analysis of the DiRECT trial, only 11 percent of intervention participants had weight loss of 15 kg or more compared with 24 percent in the one-year analysis [ 18 ].
However, 36 percent of participants maintained diabetes remission, compared with 3 percent of control patients. Several studies have evaluated the long-term efficacy of diet alone or with exercise in patients with newly diagnosed type 2 diabetes see "Medical nutrition therapy for type 2 diabetes mellitus".
In the United Kingdom Prospective Diabetes Study UKPDS , for example, all patients were given a low-calorie, low-fat, high complex carbohydrate diet [ 21 ].
Furthermore, the mean glucose value was substantially higher with diet alone than with diet plus an oral hypoglycemic drug or insulin.
The likelihood of a successful glycemic response to diet is determined in large part by the initial fasting blood glucose.
Pharmacologic therapy — Pharmacotherapy targeted solely for weight management is effective in patients with type 2 diabetes.
Although metformin is usually started for the management of hyperglycemia, it is also frequently an effective medication to promote modest weight loss. When additional body weight reduction is a primary goal of therapy, we choose medications that promote weight loss and lower glucose.
Glucagon-like peptide 1 GLP-1 receptor and dual GLP-1 and glucose-dependent insulinotropic polypeptide GIP agonist therapies promote weight loss and help prevent weight gain due to other glucose-lowering pharmacotherapies.
We add these medications sequentially to metformin if additional glucose lowering or weight loss is a treatment goal. See "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus" and "Obesity in adults: Drug therapy". Surgical therapy — Weight loss surgery in patients with obesity and type 2 diabetes results in the largest degree of sustained weight loss and, in parallel, improvements in blood glucose management and the most frequent sustained remissions of diabetes.
Weight loss surgery is an option to treat poorly managed type 2 diabetes when other modalities have failed. This topic is reviewed in detail separately. See "Management of persistent hyperglycemia in type 2 diabetes mellitus", section on 'Bariatric metabolic surgery'.
Exercise — Regular exercise is beneficial in type 2 diabetes, independent of weight loss. It leads to improved glycemic management due to increased responsiveness to insulin; it can also delay the progression of impaired glucose tolerance to overt diabetes [ 22,23 ].
These beneficial effects are directly due to exercise, but concurrent weight reduction plays a contributory role. In one study, however, only 50 percent of patients with type 2 diabetes were able to maintain a regular exercise regimen [ 24 ].
See "Exercise guidance in adults with diabetes mellitus". Shorter-duration, intensive exercise may be appropriate for physically fit individuals [ 25 ]. Resistance training may be particularly important for individuals with type 2 diabetes who do not have overweight or obesity, in whom relative sarcopenia may contribute to diabetes pathophysiology [ 26 ].
Intensive lifestyle modification — In patients with established type 2 diabetes, intensive behavioral modification interventions focusing on weight reduction and increasing activity levels are successful in reducing weight and improving glycemic management while, at the same time, reducing the need for glucose-lowering and other medications [ 15,18, ].
The intensive intervention included caloric restriction maximum 30 percent calories from fat, minimum 15 percent protein, and the remainder from carbohydrates, in the form of liquid meal replacements, frozen food entrees, or structured meal plans , moderate-intensity physical activity goal minutes weekly , and weekly group or individual sessions with registered dietitians, behavioral psychologists, and exercise specialists.
The primary outcome was a composite of death from cardiovascular causes, nonfatal myocardial infarction, nonfatal stroke, and hospitalization for angina. Although the anticipated follow-up period was After a median follow-up of 9. The improvement in weight and glycemia did not reduce the occurrence of cardiovascular events.
Possible reasons for this finding include the lower-than-expected rates of cardiovascular events in both groups, improved overall cardiovascular risk factor treatment with medical therapy antihypertensives, statins in the standard diabetes education arm, enrollment of a relatively healthy patient population, gradual weight loss in the control group such that the differential weight loss between the two groups was only 2.
A sustained weight loss of greater than that achieved in the trial may be required to reduce the risk of CVD. In an observational post hoc analysis of the Look AHEAD trial, weight loss of 10 percent or greater in the first year was associated with a reduction in the primary outcome 1.
However, this post hoc analysis is problematic. Moreover, the degree of weight loss is difficult to achieve and maintain through lifestyle intervention alone. Weight loss, weight loss maintenance, and exercise remain important components of diabetes management due to overall health benefits.
The following summarizes several other major observations from the Look AHEAD trial [ 27,31, ]:. The difference was attenuated but remained significant throughout the trial 6 versus 3.
Changes in waist circumference and physical fitness were also significantly better in the intervention group throughout the study. By study end, mean A1C was significantly lower in the intervention group 7. Psychological interventions — Patients with type 2 diabetes often experience significant stress, a condition often called diabetes distress, related to the many self-care responsibilities required for glycemic management lifestyle modifications, medication, and blood glucose monitoring [BGM] [ 42 ].
Concurrent depression similarly may interfere with self-care. See "Overview of general medical care in nonpregnant adults with diabetes mellitus", section on 'Comorbid conditions'. Psychotherapy reduces psychological distress and improves glycemic management in some [ 43,44 ], but not all [ 45 ], studies.
In a meta-analysis of 12 trials of patients with type 2 diabetes randomly assigned to psychological intervention or usual care, mean A1C was lower in the intervention group pooled mean difference Measures of psychological distress were also significantly lower in the intervention group, but there were no differences in weight management.
Pregnancy planning — All women of childbearing age with diabetes should be counseled about the potential effects of diabetes and commonly used medications on maternal and fetal outcomes and the potential impact of pregnancy on their diabetes management and any existing complications.
See "Pregestational preexisting diabetes: Preconception counseling, evaluation, and management". When to start — Early institution of treatment for diabetes, at a time when the A1C is not substantially elevated, is associated with improved glycemic management over time and decreased long-term complications [ 46 ].
Pharmacologic therapy should be initiated along with consultation for lifestyle modification focusing on dietary and other lifestyle contributors to hyperglycemia.
Weight loss and weight loss maintenance underpins all effective type 2 diabetes therapy, and lifestyle change reduces the risk of weight gain associated with sulfonylureas and insulin.
However, for those patients who have clear and modifiable contributors to hyperglycemia and who are motivated to change them eg, commitment to reduce consumption of sugar-sweetened beverages , a three-month trial of lifestyle modification prior to initiation of pharmacologic therapy is warranted.
Choice of initial therapy — Our suggestions are based upon clinical trial evidence and clinical experience in achieving glycemic targets and minimizing adverse effects table 1 , with the recognition that there is a paucity of high-quality, head-to-head drug comparison trials and long-duration trials or ones with important clinical endpoints, such as effects on complications.
The long-term benefits and risks of using one approach over another are unknown. In selecting initial therapy, we consider patient presentation eg, presence or absence of symptoms of hyperglycemia, comorbidities, baseline A1C level , individualized treatment goals and preferences, the glucose-lowering efficacy of individual drugs, and their adverse effect profile, tolerability, and cost [ 47 ].
We prefer initiating a single agent typically metformin and then sequentially adding additional glucose-lowering agents as needed, rather than starting with combination therapy [ 48 ].
Related Pathway s : Diabetes: Initial therapy for non-pregnant adults with type 2 DM. Asymptomatic, not catabolic — The majority of patients with newly diagnosed type 2 diabetes are asymptomatic, without symptoms of catabolism eg, without polyuria, polydipsia, or unintentional weight loss.
Hyperglycemia may be noted on routine laboratory examination or detected by screening. Metformin — In the absence of specific contraindications, we suggest metformin as initial therapy for patients with newly diagnosed type 2 diabetes who are asymptomatic.
We begin with mg once daily with the evening meal and, if tolerated, add a second mg dose with breakfast. The dose can be increased slowly one tablet every one to two weeks as tolerated to reach a total dose of mg per day. See 'When to start' above and "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Dosing'.
Metformin is the preferred initial therapy because of glycemic efficacy see 'Glycemic efficacy' below , promotion of modest weight loss, very low incidence of hypoglycemia, general tolerability, and favorable cost [ 47 ].
Metformin does not have adverse cardiovascular effects, and it appears to decrease cardiovascular events [ ]. See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Cardiovascular effects'.
Metformin is far less expensive and has more clinical practice experience than glucagon-like peptide 1 GLP-1 receptor agonists and sodium-glucose cotransporter 2 SGLT2 inhibitors.
Although some guidelines and experts endorse the initial use of these alternative agents as monotherapy or in combination with metformin [ 48,52 ], we prefer initiating a single agent typically metformin and then sequentially adding additional glucose-lowering agents as needed, rather than starting with combination therapy.
In the clinical trials that demonstrated the protective effects of GLP-1 receptor agonists and SGLT2 inhibitors, these agents were added to background metformin therapy in most participants. Further, the cardiorenal benefits of GLP-1 receptor agonists and SGLT2 inhibitors have not been demonstrated in drug-naïve patients without established CVD or at low cardiovascular risk or without severely increased albuminuria.
Although each diabetes medication is associated with adverse events, metformin is associated with less weight gain and fewer episodes of hypoglycemia compared with sulfonylureas, and with less edema, heart failure HF , and weight gain compared with thiazolidinediones.
See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects'.
Although virtually all recommendations for initial pharmacologic therapy outside of China, where alpha-glucosidase inhibitors are recommended as an alternate first-line monotherapy [ 53 ] endorse use of metformin , there are, in fact, relatively few relevant direct comparative effectiveness data available.
Contraindications to or intolerance of metformin — For patients who have gastrointestinal intolerance of metformin , slower titration, ensuring that the patient is taking the medication with food, or switching to an extended-release formulation may improve tolerability.
For patients who still cannot tolerate metformin or have contraindications to it, we choose an alternative glucose-lowering medication guided initially by patient comorbidities, and in particular, the presence of atherosclerotic CVD ASCVD or albuminuric chronic kidney disease.
See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Contraindications'. When compared with placebo, the GLP-1 receptor agonists liraglutide , semaglutide , and dulaglutide demonstrated favorable atherosclerotic cardiovascular and kidney outcomes [ ].
The SGLT2 inhibitors empagliflozin , canagliflozin , and dapagliflozin have also demonstrated benefit, especially for HF hospitalization, risk of kidney disease progression, and mortality [ ]. Patients at high CVD risk but without a prior event might benefit, but the data are less supportive. Similarly, patients without severely increased albuminuria have some benefit, but the absolute benefits are greater among those with severely increased albuminuria.
To select a medication, we use shared decision-making with a focus on beneficial and adverse effects within the context of the degree of hyperglycemia as well as a patient's comorbidities and preferences. As examples:. SGLT2 inhibitors with cardiovascular benefit empagliflozin or canagliflozin are good alternatives, especially in the presence of HF.
Given the high cost of these classes of medications, formulary coverage often determines the choice of the first medication within the class. See "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Microvascular outcomes'.
Choice of agent is primarily dictated by provider preference, insurance formulary restrictions, eGFR, and cost.
In the setting of declining eGFR, the main reason to prescribe SGLT2 inhibitors is to reduce progression of DKD. However, kidney and cardiac benefits have been shown in patients with eGFR below this threshold. Dosing in the setting of DKD is reviewed in detail elsewhere.
See "Treatment of diabetic kidney disease", section on 'Type 2 diabetes: Treat with additional kidney-protective therapy'. An alternative or an additional agent may be necessary to achieve glycemic goals.
GLP-1 receptor agonists are an alternative in patients with DKD as their glycemic effect is not related to eGFR. In addition, GLP-1 receptor agonists have been shown to slow the rate of decline in eGFR and prevent worsening of albuminuria.
See 'Microvascular outcomes' below and "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus" and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus".
Of note, we avoid use of SGLT2 inhibitors in patients with frequent bacterial urinary tract infections or genitourinary yeast infections, low bone density and high risk for falls and fractures, foot ulceration, and factors predisposing to diabetic ketoacidosis eg, pancreatic insufficiency, drug or alcohol abuse disorder because of increased risk while using these agents.
SLGT2 inhibitors should be held for 3 to 4 days before procedures including colonoscopy preparation and with poor oral intake to prevent diabetic ketoacidosis.
See "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Contraindications and precautions'. Repaglinide acts at the sulfonylurea receptor to increase insulin secretion but is much shorter acting than sulfonylureas and is principally metabolized by the liver, with less than 10 percent renally excreted.
Limited data suggest that dipeptidyl peptidase 4 DPP-4 inhibitors are effective and relatively safe in patients with chronic kidney disease. However, linagliptin is the only DPP-4 inhibitor that does not require a dose adjustment in the setting of kidney failure.
GLP-1 receptor agonists may also be used safely in chronic kidney disease stage 4, but patient education for signs and symptoms of dehydration due to nausea or satiety is warranted to reduce the risk of acute kidney injury.
Insulin may also be used, with a greater portion of the total daily dose administered during the day due to the risk of hypoglycemia, especially overnight, in chronic kidney disease and end-stage kidney disease ESKD. See "Management of hyperglycemia in patients with type 2 diabetes and advanced chronic kidney disease or end-stage kidney disease", section on 'Patients not on dialysis'.
Without established cardiovascular or kidney disease — For patients without established CVD or kidney disease who cannot take metformin , many other options for initial therapy are available table 1. We suggest choosing an alternative glucose-lowering medication guided by efficacy, patient comorbidities, preferences, and cost.
Although historically insulin has been used for type 2 diabetes only when inadequate glycemic management persists despite oral agents and lifestyle intervention, there are increasing data to support using insulin earlier and more aggressively in type 2 diabetes. By inducing near normoglycemia with intensive insulin therapy, both endogenous insulin secretion and insulin sensitivity improve; this results in better glycemic management, which can then be maintained with diet, exercise, and oral hypoglycemics for many months thereafter.
Insulin may cause weight gain and hypoglycemia. See "Insulin therapy in type 2 diabetes mellitus", section on 'Indications for insulin'. If type 1 diabetes has been excluded, a GLP-1 receptor agonist is a reasonable alternative to insulin [ 66,67 ]. The frequency of injections and proved beneficial effects in the setting of CVD are the major differences among the many available GLP-1 receptor agonists.
In practice, given the high cost of this class of medications, formulary coverage often determines the choice of the first medication within the class. Cost and insurance coverage may limit accessibility and adherence. See "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Patient selection'.
Each one of these choices has individual advantages, benefits, and risks table 1. See "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus" and "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Patient selection' and "Dipeptidyl peptidase 4 DPP-4 inhibitors for the treatment of type 2 diabetes mellitus", section on 'Patient selection' and "Thiazolidinediones in the treatment of type 2 diabetes mellitus", section on 'Potential indications'.
See 'Bariatric metabolic surgery' below and "Medical nutrition therapy for type 2 diabetes mellitus". The vast majority of these CVD safety studies were placebo-controlled and enrolled all or a majority of patients with pre-existing CVD or at high cardiovascular risk, representing a minority of the type 2 diabetes population.
The long-term benefits and risks of using one agent over another in the absence of diagnosed CVD or high atherosclerotic CVD ASCVD risk are less clear. Thus, the results of these trials are most applicable to patients similar to the trial population and not to all patients with type 2 diabetes [ 2,60 ].
Cardiovascular benefit has been demonstrated for some of these medications when taken in combination with metformin , but benefit has not been definitively established in drug-naïve patients at low to moderate cardiovascular risk.
See 'Without established cardiovascular or kidney disease' above. The cardiovascular effects of each diabetes drug when data are available is reviewed in the individual topics. See "Metformin in the treatment of adults with type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Sulfonylureas and meglitinides in the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Glucagon-like peptide 1-based therapies for the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Thiazolidinediones in the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Dipeptidyl peptidase 4 DPP-4 inhibitors for the treatment of type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Sodium-glucose cotransporter 2 inhibitors for the treatment of hyperglycemia in type 2 diabetes mellitus", section on 'Cardiovascular effects' and "Insulin therapy in type 2 diabetes mellitus".
They can reduce A1C values slightly 0. They act predominantly by lowering glucose concentrations after meals but may be poorly tolerated because of flatulence and other gastrointestinal GI side effects.
However, if they are started at a low dose 25 mg before meals and slowly increased, they can be effective in people who follow high-carbohydrate diets. See "Alpha-glucosidase inhibitors for treatment of diabetes mellitus".
Pramlintide is only approved for use in patients also taking prandial insulin, and therefore, it is not generally used in patients with type 2 diabetes. It also has frequent GI side effects.
See "Amylin analogs for the treatment of diabetes mellitus". In , another inhaled insulin preparation was approved by the US Food and Drug Administration FDA. Inhaled insulin causes a very rapid rise in serum insulin concentration similar to that after subcutaneous rapid-acting insulins and faster than that after subcutaneous regular insulin.
It is designed to be used to manage postprandial glucose levels. Inhaled insulin may cause a transient cough with each inhalation, and it requires pulmonary monitoring. It is used infrequently in patients with type 2 diabetes. See "Inhaled insulin therapy in diabetes mellitus".
Colesevelam's mechanism of action to improve glycemia is uncertain [ 64 ]. One possibility is that bile acid sequestrants act in the GI tract to reduce glucose absorption. In a meta-analysis of five short-term trials 16 to 26 weeks in patients with type 2 diabetes inadequately treated with oral agents or insulin, the addition of colesevelam compared with placebo modestly reduced A1C levels mean difference 0.
The meta-analysis was limited by the high or unclear risk of bias in the individual trials. Side effects can include constipation, nausea, and dyspepsia. In contrast to its effects on LDL cholesterol, colesevelam increases triglyceride concentrations by approximately 20 percent [ 66,67 ].
The clinical implications of this increase are unknown. See "Lipoprotein classification, metabolism, and role in atherosclerosis", section on 'Apolipoprotein C-III'. Given the modest glucose-lowering effectiveness, expense, and limited clinical experience, we typically do not recommend colesevelam to improve glycemic management in patients with type 2 diabetes.
See "Management of hyperprolactinemia", section on 'Overview of dopamine agonists'. A quick-release formulation of bromocriptine has been approved by the FDA for the treatment of type 2 diabetes mellitus [ 68 ].
In short-term clinical trials in patients with type 2 diabetes mellitus, bromocriptine up to 4. Common side effects include nausea, vomiting, dizziness, and headache [ 70 ].
The mechanism of action in reducing blood sugar is unknown. Given its modest glucose-lowering effect, very frequent GI side effects, and the availability of more effective drugs, we do not recommend bromocriptine for the treatment of type 2 diabetes. BARIATRIC METABOLIC SURGERY — In patients with type 2 diabetes and obesity, bariatric and metabolic surgical procedures that result in sustained, major weight loss have been shown to lead to at least temporary remission of diabetes in a substantial fraction of patients.
Bariatric surgical procedures are targeted at weight loss in the setting of obesity; the term "metabolic surgery" is used when a major goal of surgery is to improve diabetes or other metabolic diseases eg, nonalcoholic fatty liver disease.
Patient selection — Surgical treatment of obesity is an option to treat type 2 diabetes in appropriate surgical candidates with [ 71 ]:.
Surgical treatment has also been endorsed in patients with type 2 diabetes with BMI 30 to Given the increasing availability of potent GLPbased therapies and lack of comparative effectiveness data for bariatric surgery and these potent agents, we review these options with our patients and engage in shared decision-making.
See "Initial management of hyperglycemia in adults with type 2 diabetes mellitus", section on 'Diabetes education' and "Bariatric surgery for management of obesity: Indications and preoperative preparation", section on 'Indications'. Outcomes — Unblinded trials have compared bariatric surgery with medical therapy for the treatment of type 2 diabetes see "Outcomes of bariatric surgery", section on 'Diabetes mellitus'.
However, relapse of diabetes usually occurs over time, with 35 to 50 percent of patients who initially achieved diabetes remission after surgery experiencing a recurrence [ 72,75 ]. Nevertheless, bariatric surgery improves glycemia substantially and significantly more than medication therapy, and most patients have marked improvement in glycemic management for at least 5 to 15 years after surgery.
The effects of bariatric surgery on diabetes-related complications are reviewed in detail elsewhere. See "Outcomes of bariatric surgery", section on 'Diabetic complications'. Risks and concerns — Despite these impressive metabolic results, concerns remain about acute postoperative complications including the need for reoperations and rehospitalizations and rare, but potentially severe, adverse events; the long-term success rates in maintaining weight loss [ 71,80,81 ]; and the reproducibility of the results in patients with an extensive history of diabetes or with different surgical teams [ 82 ].
Some weight regain is typical within two to three years of bariatric procedures, and different procedures result in different levels of weight loss and corresponding reductions in glycemia.
Bariatric surgical procedures are reviewed in detail elsewhere. See "Bariatric procedures for the management of severe obesity: Descriptions" and "Bariatric surgery for management of obesity: Indications and preoperative preparation" and "Bariatric operations: Early fewer than 30 days morbidity and mortality".
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. See "Society guideline links: Diabetes mellitus in adults" and "Society guideline links: Diabetes mellitus in children" and "Society guideline links: Diabetic kidney disease".
These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed.
These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword s of interest.
This decision is based on glycated hemoglobin A1C assay results calculator 1 typically performed every three to six months after initial therapy. After a successful initial response to lifestyle intervention and oral therapy, the majority of patients do not maintain target A1C levels during the subsequent three to five years.
See 'Indications for a second agent' above. Options include glucagon-like peptide 1 GLP-1 receptor agonists, a dual-acting GLP-1 and glucose-dependent insulinotropic polypeptide GIP receptor agonist tirzepatide , sodium-glucose co-transporter 2 SGLT2 inhibitors, short-acting sulfonylureas eg, glipizide , glimepiride , repaglinide if sulfonylurea not chosen as initial therapy , insulin, dipeptidyl peptidase 4 DPP-4 inhibitors, and pioglitazone figure 1 and table 2.
For patients with persistent hyperglycemia while taking a maximally tolerated dose of metformin, the choice of a second medication should be individualized based on efficacy, risk for hypoglycemia, the patient's comorbid conditions, impact on weight, side effects, and cost.
These agents have been shown to have the best glycemic efficacy algorithm 1. Gastrointestinal GI side effects, contraindications, and cost may limit their use. To select a medication, we use shared decision-making with a focus on beneficial and adverse effects within the context of the degree of hyperglycemia as well as a patient's comorbidities and preferences algorithm 2.
See 'Established cardiovascular or kidney disease' above. The majority of patients in the cardiovascular and renal outcomes trials had established cardiovascular disease CVD or diabetic kidney disease DKD with severely increased albuminuria, and therefore, these are the primary indications for one of these drugs.
Patients at high CVD risk but without a prior event might benefit, but the data are less supportive. Similarly, patients without severely increased albuminuria have some benefit, but the absolute benefits are greater among those with severely increased albuminuria.
The choice of an alternative glucose-lowering medication is guided by efficacy, patient comorbidities, preferences, side effects, and cost. algorithm 2. See 'Dual agent failure' above.
For most patients who do not achieve target A1C with initial dual therapy, we suggest starting insulin or a GLP-1 receptor agonist Grade 2B if neither already chosen as a second agent.
In patients on sulfonylureas and metformin who are starting insulin therapy, sulfonylureas are generally tapered and discontinued, while metformin is continued.
In patients on DPP-4 inhibitors who are starting a GLP-1 receptor agonist or dual-acting GLP-1 and GIP receptor agonist, the DPP-4 inhibitor is discontinued, while metformin is continued. See 'Dual agent failure' above and 'Insulin initiation and intensification' above. Related Pathway s : Diabetes: Initial therapy for non-pregnant adults with type 2 DM.
An alternative is two oral agents and a GLP-1 receptor agonist or dual-acting GLP-1 and GIP receptor agonist, particularly for patients in whom weight loss or avoidance of hypoglycemia is a primary consideration.
These GLPbased therapies should not be combined with DPP-4 inhibitors. Another option for patients close to glycemic goals is three oral agents eg, metformin , sulfonylurea plus: DPP-4 inhibitor, SGLT2 inhibitor, or pioglitazone.
Although guidelines suggest combining SGLT2 inhibitors and GLP-1 receptor agonists, we do not usually add an SGLT2 inhibitor to GLP-1 receptor agonist therapy for management of hyperglycemia alone, given the absence of data showing additive cardiovascular and kidney benefit and increased patient burden cost, polypharmacy, adverse effects.
Bariatric surgery may also be an option in patients with lower BMI 30 to Patients seeking bariatric surgery should be counseled to develop coping skills, eliminate maladaptive behavior, and understand the risks and benefits of the surgery.
See 'Bariatric metabolic surgery' above and "Bariatric surgery for management of obesity: Indications and preoperative preparation", section on 'Preoperative counseling'.
Why UpToDate? Product Editorial Subscription Options Subscribe Sign in. Learn how UpToDate can help you. Select the option that best describes you. View Topic. Font Size Small Normal Large. Management of persistent hyperglycemia in type 2 diabetes mellitus.
Formulary drug information for this topic. No drug references linked in this topic. Find in topic Formulary Print Share. View in. Language Chinese English. Author: Deborah J Wexler, MD, MSc Section Editor: David M Nathan, MD Deputy Editor: Katya Rubinow, MD Contributor Disclosures.
All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jan This topic last updated: Jan 11, Pharmacologic Approaches to Glycemic Treatment: Standards of Care in Diabetes Diabetes Care ; S Davies MJ, Aroda VR, Collins BS, et al.
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BMC Neurology Chronic hyperglycemia prognosis Chrlnic Chronic hyperglycemia prognosis, Article hyprglycemia Cite this prignosis. Metrics details. Chronic hyperglycemia prognosis patterns have been reported to be Chronic hyperglycemia prognosis factors for stroke; however, this Chronlc to be further evaluated. This Chronic hyperglycemia prognosis Joint health aid to evaluate the usefulness of glycemic patterns such as persistent hyperglycemia PH including short duration and long duration PH SPH; LPHadmission hyperglycemia AHshort-duration hyperglycemia SHand persistent normoglycemia PN in predicting stroke prognosis using published results. Major scientific databases including but are not limited to PubMed, EMBASE, Web of Science, Ovid, CNKI Chinese National Knowledge Infrastructureand Clinicaltrials.
Your health care prognosls sets your target blood sugar range. For Rapid fat burning Chronic hyperglycemia prognosis who have hyperglycemiw, Mayo Chronic hyperglycemia prognosis generally hyperglyceemia the following hypergoycemia blood sugar levels before meals:. For many people who have diabetes, the American Diabetes Association generally recommends the following target blood sugar levels:. Your target blood sugar range may differ, especially if you're pregnant or you have other health problems that are caused by diabetes. Your target blood sugar range may change as you get older. 
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