More than 100,000 people with type 1 diabetes in England are to be offered an artificial pancreas, which experts believe could become the “holy grail” for managing the disease.

The groundbreaking device uses an algorithm to determine the amount of insulin that should be administered and reads blood sugar levels to keep them steady.

A world-first trial on the NHS found it was more effective at managing diabetes than current devices and required far less input from patients. The device is now set to be rolled out across the NHS in England after it won approval from the National Institute for Health and Care Excellence (Nice).

Mark Chapman, the interim director of medical technology at Nice, said: “Some people living with type 1 diabetes struggle to manage their condition, even though they are doing everything asked of them by their diabetes team. This technology is the best intervention to help them control their diabetes, barring a cure.”

In draft guidance published on Tuesday, an independent Nice committee recommended its use for managing blood glucose levels in people struggling to manage type 1 diabetes. The technology allows a patient to go about their day-to-day life without having to monitor if their blood glucose levels are too high or too low.

Women who are pregnant are also eligible, because blood glucose levels are harder to manage during this time. In total, about 105,000 people in England are set to be offered the technology.

Managing type 1 diabetes can be challenging, especially in young children, owing to variations in the levels of insulin required and unpredictability around how much patients eat and exercise. Children are particularly at risk of dangerously low (hypoglycaemia) and high (hyperglycaemia) blood sugar levels, which can damage the body or even lead to death.

The artificial pancreas is worn next to the body. It continually monitors blood glucose levels and automatically adjusts insulin delivered via a pump. It also eliminates the need for finger-prick tests to check blood sugar levels to prevent hypoglycaemic and hyperglycaemia attacks.

The draft Nice recommendations require NHS England to agree a cost-effective price for the device on behalf of relevant health bodies. Currently, the average annual cost for the technology is £5,744, higher than Nice considers a cost-effective use of NHS resources.

Although most of the NHS’s estimated £10bn annual spending on diabetes goes on type 2 diabetes, it is hoped the devices will help cut costs by ensuring less need for interventions for type 1 cases.

Prof Partha Kar, national specialty adviser for diabetes at NHS England, said: “This technology has been proven to give the best control for managing type 1 diabetes and should make things like amputations, blindness, and kidney problems possibly a thing of the past.” Kar, who has previously described the device as “not very far away from the holy grail of a fully automated system”, added: “We have seen fantastic results from the real-world trials which have taken place. The quality of life this technology gives to those using it is huge.”

The post NHS in England to offer artificial pancreas to help manage type 1 diabetes first appeared on Serene.

Alqahtani S. et al., J Endocrinol Metab. 2022;12(6):161-167, doi: https://doi.org/10.14740/jem848

Vascular disease including venous thromboembolism (VTE) is a common cause of death among patients with comorbid conditions such as diabetes mellitus . VTE results in a range of events from symptomless distal venous thrombus of deep veins to threatening deep venous thrombus and fatal pulmonary embolism. The  likelihood of VTE and its associated complications are higher in older patients than younger ones and the risk becomes two-fold with every decade of aging . This risk also varies by the sex of the patients with males being affected more by the second episode than females. The yearly incidence of VTE is between 1.5 and 3.0 cases per 1,000 individuals. The incidence of VTE is even higher among diabetic patients. For example, the data suggest the annual rate of VTE among diabetic patients was 432 per 100,000 population . VTE is considered as the third most common cause of cardiovascular disease following stroke and myocardial infarction . It seems that metformin being an antihyperglycemic drug prevents cardiovascular disease beyond glycemic control. However, despite the effects of metformin on glycemic control, its effects on venous thrombosis may be different. Overall, there is limited evidence supporting such beneficial effects with scarce evidence from well-conducted trials. Few epidemiological studies have shown that hypoglycemic agents such as metformin may have a direct effect on VTE . However, such evidence is not qualitatively synthesized both from observational and intervention studies, thereby limiting our understanding of the role of metformin in preventing VTE. Thus, we carried out a systematic review of the epidemiological studies assessing the role of metformin in preventing VTE. The findings of this review will help clinicians and researchers to plan further studies and make evidence-based clinical and policy decisions to treat the patients appropriately and reduce the burden of VTE and its associated morbidity and mortality.

Methods:

A systematic search of three main electronic databases including Embase, PubMed, and EBSCO was undertaken in 2021. Any study conducted between 2000 and 2021 that addressed the role of metformin in preventing venous thrombosis in patients diagnosed with type 2 diabetes mellitus was considered eligible.

Results:

Following a comprehensive review of the research articles based on the eligibility criteria, six articles were incorporated into the review. The findings of the review demonstrate that metformin was found to be associated with 22% to 58% risk reduction for venous thrombosis among diabetic patients. However, due to the observational studies included in the meta-analysis, the protective effect may not be independent of other risk factors or other variables.

Discussion:

This review was undertaken to summarize the evidence regarding the protective effect of metformin on VTE in diabetic patients. Overall the findings of the review demonstrated a protective effect of metformin among diabetic patients in terms of reducing venous thrombus formation. Though, limited evidence exists and perhaps there is a need to conduct more randomized controlled trials, the available evidence is suggestive of beneficial effects of metformin against VTE. This can be further confirmed by undertaking large intervention studies to endorse the findings. According to the current guidelines of the American Diabetes Association/European Association, metformin should be considered as either as a monotherapy or in combination for patients diagnosed with type 2 diabetes mellitus. This is even more beneficial for patients who are at risk of thrombus formation. Metformin being an insulin sensitizer can improve the function of vessels and related vascular abnormalities with few side effects in patients with type 2 diabetes mellitus . The potential mechanisms by which metformin may prevent venous thrombosis are by inhibiting platelet activation in vivo and in vitro [19]. The evidence suggests that platelets are involved in several biological processes such as clotting, vascular lesions, and activation of other platelets . This activity of platelets is markedly suppressed in the presence of metformin and it is mainly by suppression of platelet prothrombinase activity and by reducing extracellular mitochondrial release . This is consistent with the reduced platelet adhesive function after administering metformin. The animal studies suggest that metformin significantly suppressed aggregation of platelets and prevent both arterial and venous thrombosis in rat models [19]. And thrombus formation deteriorated in the rats treated with metformin . Besides, it has been found that metformin reduces the size and weight of arterial and venous thrombi and subsequently reduces the incidence of pulmonary embolism. Also, metformin reduces markers of endothelial activation such as Von Willebrand factor and it also decreases the inflammation and levels of plasminogen activator inhibitor . These potential mechanisms contribute to the protective effect of metformin in reducing thrombus formation and associated mortality in diabetic patients.

Conclusion and Implications:

for Future Overall, the existing studies included in this review demonstrate that metformin may be found protective against VTE, mainly in diabetic patients. Based on the available findings, metformin may be safely used in diabetic patients at risk of thromboembolism; however, we would recommend conducting more epidemiological studies particularly randomized controlled trials to assess the effect of metformin on VTE before making any definitive conclusions about the same. Considering the limited sample size of this review, more studies and their respective reviews are required to confirm these findings and these studies need to be undertaken both in developing and developed countries to confirm these findings and recommend the use of metformin on a broader scale for the prevention of thromboembolism in diabetic patients.

The post Protective Effect of Metformin on Venous Thrombosis in Diabetic Patients: Findings From a Systematic Review first appeared on Serene.

Ref: Michael Böhm, European Heart Journal (2022) 00, 1–12, https://doi.org/10.1093/eurheartj/ehac693

Empagliflozin reduced cardiovascular death and heart failure hospitalization in patients with preserved ejection fraction. Hypertension is the most common comorbidity and etiological trigger of heart failure with preserved ejection fraction (HFpEF) as pressure overload produces left ventricular hypertrophy, diastolic dysfunction, abnormal arterial-ventricular coupling, and other complications such as kidney failure. Sodium-glucose cotransporter 2 (SGLT2) inhibitors reduce systolic blood pressure (SBP) in patients with diabetes and hypertension, while in heart failure with reduced ejection fraction (HFrEF), only patients with a high baseline SBP had a significant and meaningful reduction. Registry data show an increase of heart failure outcomes and death for patients with SBP 140– 150 mmHg without differences between HFrEF and HFpEF. This U-shaped blood pressure (BP)-risk association might not be related to a causality rather than reflecting reverse causation as low BP selects patients with more advanced heart failure and frailty. In EMPEROR-Preserved (empagliflozin outcome trial in patients with chronic heart failure with preserved ejection fraction), we studied the effect of empagliflozin on SBP and its effects on heart failure outcomes and estimated glomerular filtration rate (eGFR) decline across baseline SBP levels in heart failure with ejection fraction >40%.

Methods and results:

The association of SBP and the treatment effects of empagliflozin in EMPEROR-Preserved (empagliflozin outcome trial in patients with chronic heart failure with preserved ejection fraction) was evaluated. Randomized patients (n=5988) were grouped according to SBP at baseline (130 mmHg, n=3118). The effect of empagliflozin on blood pressure, cardiovascular death or HF hospitalization (primary outcome), total HF hospitalizations, and rate of decline in estimated glomerular filtration rate was studied. Over a median of 26.2 months, the placebo-corrected decline was small and not significantly different across baseline SBP. On placebo, the risk of cardiovascular death or hospitalization for HF was 8.58 at >130 mmHg, 8.26 at 110–130 mmHg, and 11.59 events per 100 patient-years at 130 mmHg, P=0.08 vs. 110–130 mmHg). There was no evidence for baseline SBP moderating the effect of empagliflozin on risk of HF events (primary endpoint interaction P=0.69, recurrent HF hospitalizations interaction P=0.55). When comparing empagliflozin with placebo, SBP did not meaningfully associate with adverse events such as hypotension, volume depletion, and acute renal failure.

Discussion:

In EMPEROR-Preserved, there was a small placebo-corrected SBP decline by empagliflozin compared with placebo with an overall increase of SBP at low baseline SBP and a small drop of SBP at high baseline SBP on placebo and on empagliflozin possibly reflecting regression to the mean. In HFpEF, the outcome rates of the primary outcome were higher at low SBP ((<110 mmHg) but the treatment effect of empagliflozin on heart failure outcomes was not significantly related to baseline SBP with a similar risk reduction of heart failure hospitalization and cardiovascular death. Empagliflozin had minor effects on hypotension and volume depletion, while some fewer events were observed for acute renal failure (Structured Graphical Abstract).

HFpEF is a heterogeneous condition with hypertension being one of the most prevalent and possible etiological factors promoting the progression of hypertrophy to failure with more patients presenting with a history of hypertension in HFpEF than in HFrEF. A higher prevalence of high BP in HFpEF compared with HFrEF is shown by the finding that 52.0% of the patients had an SBP of >130 mmHg and 7.6% of EMPEROR-Reduced 28.2% were at >130 mmHg and 24.2% had an SBP of <110 mmHg.8 Patients with heart failure are often undertreated when SBP is low, although they have a worse prognosis than those with a higher SBP. Interestingly, the U- and J-shaped association of SBP and DBP on mortality appears to be similar in HFrEF and HFpEF. Herein, we show that the primary outcome and cardiovascular death was increased in patients at SBP <110 mmHg compared with >110 mmHg. This finding is similar to previous HFrEF trials with treatment effects of SGLT2 inhibitors and sacubitril/valsartan being similar across SBP groups. We extended those findings to HFpEF patients by showing that the effect of empagliflozin is similar across baseline SBP groups in EMPEROR-Preserved.

In EMPEROR-Preserved, 90.6% of patients had a history of hypertension. Although high SBP is a major driver for the development of HFpEF, we still found a significant number with normal or low SBP. Nevertheless, the proportion of patients with low SBP <110 mmHg is lower than in HFrEF.8 A reduced myocardial systolic or diastolic function has been speculated to be involved in drops of SBP over time, previously termed ‘decapitated hypertension’,  also observed in PARAGON-HF in HFpEF patients, and associated with increased HF events in HFrEF and HFpEF. Similar findings of an increased risk for cardiovascular outcomes at low SBP have also been shown in patients after myocardial infarction or stroke or known coronary artery disease. Nevertheless, in HFpEF as in HFrEF, SBP appears not to be an effect modifier of the cardio-renal effects of empagliflozin and, thus, might not contribute mechanistically to the treatment effect of empagliflozin.

As the effect of empagliflozin is maintained at SBP <110 mmHg, it is important that the protective effect does not come at a meaningfully increased cost of safety outcomes. There was only a slight increase of incident hypotension or volume depletion, while the incidence of acute renal failure was reduced. These observations are of clinical relevance as physicians are often reluctant to initiate treatment due to the fear of these adverse events at low SBP.

Conclusion:

In EMPEROR-Preserved, empagliflozin was effective and safe without SBP meaningfully moderating empagliflozin’s treatment effects. This analysis of EMPEROR-Preserved shows that empagliflozin can be used safely and effectively without blood pressure being a meaningful moderator of the drug benefit.

The post Empagliflozin, irrespective of blood pressure, improves outcomes in heart failure with preserved ejection fraction: the EMPEROR Preserved trial first appeared on Serene.

Ref: Diabetes Care 2022;45:1428–1437 | https://doi.org/10.2337/dc21-1957

Introduction

The incidence of unique form of diabetes among individuals with low body mass index (BMI; <19 kg/m²) has been long recognized. Formally classified as “malnutrition-related diabetes mellitus” (MRDM) by the World Health Organization (WHO), this form of diabetes has a high prevalence in low- and middle-income countries (LMICs). The WHO withdrew the MRDM category from diabetes classification in 1999, nevertheless; a substantial amount of data continued to support this unique and fairly prevalent form of diabetes. A correct assessment of patients’ metabolic defects may aid clinicians to appropriately tailor the clinical management in such patients.

Aim

To define the metabolic characteristics of individuals affected with MRDM

Patients Profile

• Patients with lower socioeconomic status (SES) and low BMI (BMI up to 19.5 kg/m²) (n=73)
• All patients were males (age; 19–45 years) with diabetes duration of at least 1 year and having moderate glycemic control (HbA1c 8–10%) and without micro- or macrovascular complications.
• Patients with “low BMI diabetes” (LD; n=20) in whom all forms of diabetes were excluded, were compared with demographically matched groups of patients with type 1 diabetes mellitus (T1DM; n=15), type 2 diabetes mellitus (T2DM; n=13), and a group of individuals without diabetes (lean non-DM; n=16, overweight non-DM; 9).

Results

• Individuals in the LD group had a lower total insulin secretory response as compared with the lean non-DM and the T2DM group.
• Individuals in the LD group also had significantly lower endogenous glucose production (EDP) when compared with patients in the T2DM group (Table 1).
• Individuals in the LD group had a significantly higher insulin-stimulated glucose uptake as compared with the patients in the T2DM group (R_d, peripheral insulin sensitivity), suggesting lower peripheral insulin resistance (Table 1).
• Individuals in the LD group had a significantly higher insulin resistance, as compared with the lean non-DM group. Individuals in the LD group also had significantly higher glucose levels at all time points as compared with the lean non-DM group.
• Patients in the LD groups also had significantly lower visceral adipose tissue and hepatocellular lipids as compared with patients in the T2DM group.

Conclusions

• This was a first-of-its kind study that comprehensively characterized insulin secretion, hepatic and peripheral insulin sensitivity, whole body composition, etc. in individuals with LD.
• The study demonstrated that the cardinal physiologic feature of LD was a defect in insulin secretory capacity as opposed to insulin resistance.
• Individuals from LMICs with LD had a unique metabolic profile, suggesting towards a distinct entity that warrants further investigation.

The post Lean Diabetes: A Unique form of Diabetes first appeared on Serene.

Adapted from Endocrine Today ByErin T. Welsh, MA, Oct-19, 2022

Use of continuous glucose monitoring among children and young adults with type 1 diabetes nearly doubled from 2017 to 2020 in the U.S. from 25% to 49% and was associated with lower HbA1c for users vs. non-users, according to registry data. The rate of CGM use among U.S. residents younger than 25 years remained less than that of their European peers, who saw an increase in use from 40% to 76% during the same period.

People aged less than 25 years using CGM in 2020 had lower HbA1c than those who didn’t use CGM. Data were derived from DeSalvo DJ, et al. Diabetes Technol Ther. 2022;doi:10.1089/dia.2022.0248.

“Clinical trials provide evidence that CGM improves glucose control and quality of life for children, adolescents and young adults,” Daniel J. DeSalvo, MD, director of strategic collaboration in the division of pediatric diabetes and endocrinology at Baylor College of Medicine at Texas Children’s Hospital, Houston, and colleagues wrote in Diabetes Technology & Therapeutics. “However, even as uptake of CGM in diabetes management is increasing, clinical outcomes vary.”

From 2017 to 2020, across all age ranges, use of CGM increased each year in both European and U.S. registries. In the U.S., use increased for those aged younger than 6 years from 34% to 55%; those aged 6 to younger than 12 years, from 29% to 51%; those aged 12 to younger than 18 years, from 22% to 43%; and those aged 18 to younger than 25 years, from 26% to 46%. CGM use in Europe was greater than that in the U.S. in all age groups in all years except for the18 to younger than 25 years age group in which use increased from 23% in 2017 to 58% in 2020.

Lower mean HbA1c was observed among CGM users younger than 25 years compared with nonusers regardless of the insulin delivery method used for all years (P < .001 for all). During 2020, mean HbA1c was 8.1% vs. 8.3% among users of an insulin pump with vs. without CGM, respectively, in the U.S., and 7.7% vs. 8%, respectively in Europe. Mean HbA1c was 8.7% vs. 9.1% for those using multiple daily injections with vs. without CGM, respectively, in the U.S., and 7.6% vs. 7.9%, respectively, for those in Europe. According to the researchers, these findings are similar to those observed in previous studies of real-world evidence of the steady increase of CGM use and the association of lower HbA1c compared with nonusers in youths with type 1 diabetes.

The post Continuous glucose monitoring (CGM) use increasing among young people, linked to lower HbA1c first appeared on Serene.

Adapted from Endocrine Today By Erin T. Welsh, MA, Sept 23, 2022

Source: de Vries SAG, et al. Abstract #469. Presented at: European Association for the Study of Diabetes Annual Meeting; Sept. 19-23, 2022; Stockholm (hybrid meeting).

Researchers observed sex disparities among children with type 1 diabetes, according to a presenter at the European Association for the Study of Diabetes annual meeting.

Girls with type 1 diabetes tended to have higher HbA1c, BMI and insulin dose compared with boys, among other outcomes. 

“We noted that a younger age at disease onset increases risk, cardiovascular complications and also is associated with reduced life expectancy. That makes it very important to identify risk factors already present at an early age in patients,” Silvia A. G. de Vries, MSc, MD-PhD candidate in the department of vascular medicine at Amsterdam University Medical Centers, said during a presentation. “We also know, similar to type 2 diabetes, that in type 1 diabetes there is a greater excess risk of cardiovascular disease and also with mortality in adult females. But what we do not know is if sex influences care and outcomes in children.”

Researchers identified 90 observational studies from MEDLINE records through June 15, 2021, focusing on type 1 diabetes in children that mentioned sex differences. Studies included 30 with data clinical patient profiles, 25 with data on glycemic control, 14 with data on treatment, 20 with data on complications, 14 with data on comorbidities and 15 with data on quality of life.

In most studies, BMI, dyslipidemia, HbA1c and insulin dose were all higher among girls in all age categories. Insulin pump therapy was more often used by girls compared with boys. Researchers also observed a higher likelihood of a diabetic ketoacidosis diagnosis, hospitalization and lower quality of life scores among girls. However, boys more often experienced hypoglycemia and partial remission than girls. According to de Vries, reasons behind these differences may be biological, including differences in hormones at puberty, body composition and fat distribution; psychological, including disease-related attitudes and behaviors; behavioral, such as physical activity, nutrition and presentation of symptoms; and the influence of the treatment team and caregiver approach.

The post Girls with type 1 diabetes may have worse cardiometabolic metrics than boys first appeared on Serene.

Ref: Diabetes  Obes Metab.2022;24:1061–1071, DOI: 10.1111/dom.14670

Introduction

Patients with type-2 diabetes mellitus (T2DM) are predisposed towards developing non-alcoholic fatty liver disease (NAFLD). Nearly 20% patients with NAFLD also have hepatic fibrosis, which is a strong predictor of NAFLD-mortality. Recent studies have demonstrated the beneficial impact of empagliflozin treatment on hepatic steatosis and fibrosis in T2DM cohorts.

Aims

• To evaluate the impact of empagliflozin on risk for NAFLD-related steatosis and fibrosis
• To determine the association between risk categories and cardiorenal outcomes in EMPA-REG OUTCOME trial

Results

• At baseline, 73% and 84% had high steatosis risk by DSI and HIS, respectively; and 23% and 4% had high risk of advanced fibrosis by NFS and FIB-4, respectively.
• The proportion of patients at risk of high steatosis dropped slightly over time, amongst the patients treated with empagliflozin, but not amongst those treated with placebo (Table 1).
• Empagliflozin treatment, as compared with placebo, did not improve the proportion of patients at high fibrosis risk over time.
• At all time-points, as compared with placebo, empagliflozin reduced body weight across all steatosis and fibrosis risk groups.
• As per the NFS and FIB-4 stratification of fibrosis risk, patients at high risk of advanced fibrosis had substantially higher incidence rates of CV death, first hospitalization due to heart failure (HF), first hospitalization for HF or CV death and all-cause mortality compared to the respective groups at low risk of advanced fibrosis.
• The impact of empagliflozin on cardiorenal and all-cause mortality outcomes remained consistent across all risk groups.

Conclusions

• Treatment with empagliflozin may improve steatosis but not fibrosis risk in individuals with T2DM and pre-existing CVD.
• High risk categories of fibrosis were associated with higher incidence of CV events
• Treatment with empagliflozin was associated with improved cardiorenal outcomes and mortality, independent of steatosis and fibrosis risk.

The post Impact of Empagliflozin on Markers of Liver Steatosis and Fibrosis, and their Association with Cardiorenal Outcomes first appeared on Serene.

Abstract

Aim

Patients with type 2 diabetes mellitus exhibited autonomic nervous system (ANS) dysfunction and comorbidities with depressive or anxiety symptoms were related to poor glycaemic control. Heart rate variability (HRV) converted from electrocardiogram (ECG) has been used as the ANS index. The study aimed to explore the associations between depression, anxiety, HRV, and glycaemic control in patients with type 2 diabetes mellitus.

Methods

The Patient Health Questionnaire-9 (PHQ-9) and Generalized Anxiety Disorder-7 (GAD-7) questionnaires were used to assess depressive and anxiety symptoms in 647 patients with type 2 diabetes mellitus (mean age was 63 ± 10 years, 56 % males). The ECG raw signals were collected from a 5-min sitting and resting baseline and then transformed to HRV indices referring ANS activation. Blood glucose and lipid profiles including glycated hemoglobin (HbA1c), high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglyceride were obtained from the electronic medical records.

Results

Ninety-nine (15 %) participants had depressive symptoms and 59 (9 %) had anxiety symptoms. Depression and HbA1c were negatively correlated with parasympathetic activation. Depression and anxiety were positively correlated with sympathetic activation. After controlling for demographic data and lipid profiles, depression was a significant positive predictor for HbA1c levels; and HRV indices (lnLF and lnHF) were the significant negative predictors for HbA1c levels. Mediation effect analysis showed that depression was a mediator between parasympathetic activation and glycaemic control.

Conclusions

Lower parasympathetic activation and higher depressive symptoms may affect glycaemic control in patients with type 2 diabetes mellitus. Intervention programs targeting to increase parasympathetic activities and reducing depression could be further tested for their effects on glycaemic outcomes for potential clinical use.

Highlights

• Depression was positively correlated with glycated haemoglobin (HbA1c).

• Depression was a mediator between parasympathetic activation (lnHF) and HbA1c.

• Sympathetic activation, parasympathetic activation, and depression predicted HbA1c levels.

The post Association of depression and parasympathetic activation with glycaemic control in type 2 diabetes mellitus (T2DM) first appeared on Serene.

Introduction

Chronic kidney disease (CKD) is one of the most common complications of type 2 diabetes mellitus (T2DM). Progression of CKD is associated with poor health outcomes and increased healthcare expenditures. Considering the substantial increase in CKD in T2DM patients, it is important to get a better understanding regarding the prevalence and progression of CKD. However, not many real-world studies have explored the progression of CKD based on the established markers, in T2DM patients.

Aim

• To determine the prevalence of newly recognized CKD and subsequent disease progression using laboratory-based markers in a large administrative claims data source in the US

Patient Profile

• Adult patients (age ≥18 years) with T2DM and laboratory evidence of newly recognized CKD (at least two laboratory results indicating reduced estimated glomerular filtration rate or at least two laboratory results indicating elevated urine albumin: creatinine ratio 90–365 days apart

Methods

Study Design

• A retrospective, population-based cohort study

Outcomes

• Last observed CKD stage in follow-up, based on an eGFR and/or UACR laboratory result

Results

• Data of 65,731 and 23,035 patients with T2DM was available for the analysis of eGFR (estimated Glomerular Filtration Rate) – and UACR (Urine Albumin-to-Creatinine Ratio )-based CKD stage progression, respectively.
• Amongst patients assessed based on their eGFR progression, ~50% had no change in their eGFR over a median period of 1-1.5 years.
• Over a median period of 1.8–2.3 years, disease progression from CKD Stages 3a, 3b and 4 to the next closest stage was seen in 16.9%, 11.8% and 10.2% of patients. Over a median period of 1.3-1.8 years, ~31% patients exhibited improvement in their eGFR levels. Over a median period of 3.5 years, 2% patients had disease progression over two eGFR stages
• Amongst patients assessed based on their UACR progression, ~64% had no change in their UACR progression over a median period of 1.3 years
• Over a median period of ~2 years, 10.4% patients with UACR Stage A2 on the index date progressed to the next stage. Increased UACR values were observed in ~28% of patients over a median follow-up of 1.5 years. On the contrary, <5% of patients regressed from Stage A3 to A1 during all available follow-ups
• Overall, CKD worsening was observed in nearly 10–17% of patients over a median follow-up of 2 years.
• Overall, nearly one-third of patients experienced an increase in eGFR values or a decrease in UACR values during follow-up.

Highlights

• Data of 65,731 and 23,035 patients with T2DM was available for the analysis of eGFR (estimated Glomerular Filtration Rate) – and UACR (Urine Albumin-to-Creatinine Ratio)-based CKD stage progression, respectively.
•  
• Overall, CKD worsening was observed in nearly 10–17% of patients over a median follow-up of 2 years.

• Overall, nearly one-third of patients experienced an increase in eGFR values or a decrease in UACR values during follow-up.

Conclusions

• A substantial proportion of T2DM patients with newly recognized CKD had disease progression over a relatively short period of time. Prompt identification of these patients with rapid CKD progression is critical to address their unmet therapeutic needs.

Future studies that would determine the clinical characteristics of these high-risk patients are warranted to inform earlier diagnostic and therapeutic interventions that would retard the disease progression.

The post Rapid Progression of CKD in T2DM first appeared on Serene.

Objective:

To evaluate the effectiveness and safety of vildagliptin or vildagliptin/metformin combination among patients with type 2 diabetes mellitus (T2DM) uncontrolled on insulin in a real-world setting in Egypt.

Study Design:

This 12-week, prospective, observational study enrolled T2DM patients. Primary endpoint was mean change in glycated haemoglobin (HbA1c) from baseline to Week 12. Secondary endpoints included mean change in body weight, insulin dosage and safety after 12 weeks.

Results:

• Significant reduction in HbA1c by Vildagliptin and Vildagliptin/metformin treatment group was observed at week 12.               ( Figure-1)

Figure1

• 27.1% of the patients achieved HbA1c <7% in Vildagliptin / metformin and 11.1% in Vildagliptin group at week 12 ( Figure-2)

Figure2

• Decrease in body weight of patients at week 12 in both Vildagliptin / metformin (p=0.0055) groups was noted  ( Figure 3)

Figure3

• A significant reduction in the daily insulin dose was observed in the Vildagliptin / metformin group (p<0.0001) (Figure-4)

Figure4

• A significant decrease in FPG and PPG was observed in both the groups

FPG (Fasting Plasma Glucose):

• Vildagliptin: 52.7 ± 62.3 mg/dL (p=.0023)
• Vildagliptin / metformin: 51.43 ± 41.7 mg/dL (p=.0001)

PPG (Postprandial Glucose):

• Vildagliptin:  73.3 ± 91.3 mg/dL (p=.0034)   
• Vildagliptin / metformin: 81.82 ± 59.7 mg/dL (p<.0001)

• No serious adverse events were observed throughout the study

Conclusion

• Vildagliptin with/without metformin as an add-on to insulin resulted in good glycaemic control and was well tolerated without any hypoglycaemic events.

The post Effectiveness, safety, and tolerability of vildagliptin or vildagliptin/metformin combination in patients with type 2 diabetes uncontrolled on insulin (The OMEGA study) first appeared on Serene.