Project description:BackgroundBenign prostatic hyperplasia (BPH) is strongly related to type 2 diabetes. Recent evidence has been inconsistent regarding the effect of BPH medications on glucose homeostasis. This study examined the risk of poor glycemic control associated with finasteride and tamsulosin use in individuals with type 2 diabetes.MethodsWe conducted a retrospective cohort study with a new-user, active-comparator design, utilizing nationwide pharmaceutical dispensing and hospitalization databases in New Zealand. The study cohort consisted of men with type 2 diabetes who were prescribed finasteride (n = 1,259) or tamsulosin (n = 580). Inverse probability treatment weighting using propensity scores was applied to create a weighted population with balanced baseline covariates. Cox proportional hazard models were fitted to estimate the risk.ResultsDuring a median follow-up of 2.4 years for finasteride users and 1.6 years for tamsulosin users, the incidence rates were 564 per 10,000 person-years and 409 per 10,000 person-years in tamsulosin users and finasteride users, respectively. After applying inverse probability treatment weighting, tamsulosin users did not have a significantly higher risk of poor glycemic control compared with finasteride users (weighted hazard ratio 1.27, 95 % confidence interval 0.95-1.72). Sensitivity analyses addressing confounding and protopathic bias yielded similar risk estimates.ConclusionsWe found that there was a non-differential risk of poor glycemic control between tamsulosin users and finasteride users during long-term use.
Project description:IntroductionPatients with diabetes mellitus type 2 (DM2) are at high risk for micro- and macrovascular disease. Here, we explore the degree of traditional risk factor control in the baseline visit of a cohort of DM2 outpatients.MethodsDIACORE (DIAbetes COhoRtE) is a prospective cohort study of 3000 adult DM2 outpatients. Here, we present results from the baseline visit. Sociodemographic and anthropometric variables, cardiovascular risk factors, comorbidities and medication were assessed by interview and medical exams. Serum-creatinine based estimated glomerular filtration rate (eGFRcrea) and urinary albumin-creatinine ratio (UACR) were determined for classification of chronic kidney disease (CKD). The proportion of patients with adequate control of traditional risk factors (blood pressure<140/90mmHg, HbA1c<7.5%, LDL<100mg/dl) was calculated in 2892 patients with non-missing data in 9 relevant variables within each KDIGO 2012 CKD class.ResultsIn the analyzed baseline data (n = 2892, 60.2% men), mean (standard deviation) values for age, DM2 duration and HbA1c were 65.3 (9.3) years, 10.3 (8.4) years and 6.9% (1.1) respectively. Of these 2892 patients, 18.7% had CKD stage 3 or higher, 25.7% had UACR≥30mg/g. Adequate blood pressure, HbA1c and LDL control was achieved in 55.7%, 78.5% and 34.4%, respectively. In 16.4% of patients (473), all three risk factors were below recommended targets. The proportion of adequate risk factor control was similar across KDIGO eGFRcrea classes. Adequate blood pressure and HbA1c control were significantly associated with lower UACR category without and with controlling for other risk factors (p<0.0001, p = 0.0002, respectively).ConclusionIn our study of patients with diabetes mellitus type 2, we observed a low level of risk factor control indicating potential for risk reduction.
Project description:BACKGROUND:The management of hyperglycaemia and associated cardiovascular risk factors in patients with type 2 diabetes mellitus (T2DM) may reduce diabetes-related complications. The strategy to broaden the knowledge base of primary care professionals to improve health care has mainly been prompted by the current reality of limited resources and access to specialized care. The main objective of this study is to assess the effectiveness of comprehensive interventions focused on treatment intensification, decrease clinical inertia and reduce possible barriers to treatment adherence in patients with poorly controlled diabetes in a primary care setting. METHODS:This is a two-phase mixed method study, whose aims are the development of complex interventions and the assessment of their effectiveness. The main study outcome is a change in glycated haemoglobin (HbA1c) levels. The INTEGRA study is divided into two phases. Phase 1: A qualitative study with a phenomenological approach using semi-structured interviews with the objective of determining the factors related to the participants and health care professionals that influence the development and implementation of a specific intervention strategy aimed at patients with poor glycaemic control of T2DM in primary care. Phase 2: Exploratory intervention study to be conducted in Primary Health Care Centres in Catalonia (Spain), including 3 specific health care areas. The intervention study has two arms: Intervention Group 1 and 2. Each intervention group will recruit 216 participants (the same as in the control group) between the ages of 30 and 80 years with deficient glycaemic control (HbA1c > 9%). The control group will be established based on a randomized selection from the large SIDIAP (Sistema d'Informació per al desenvolupament de la Investigació en Atenció Primària) database of patients with comparable socio-demographic and clinical characteristics from the three provinces. DISCUSSION:This study is a comprehensive, pragmatic intervention based on glycaemic treatment intensification and the control of other cardiovascular risk factors. It is also aimed at improving treatment adherence and reducing clinical inertia, which could lead to improved glycaemic control and could likewise be feasible for implementation in the actual clinical practice of primary care. TRIAL REGISTRATION:Clinicaltrials.gov . registration number. NCT02663245; January 25, 2016.
Project description:IntroductionPrior primary studies have examined the prevalence and factors associated with glycaemic control among patients with type 2 diabetes mellitus, but studies with evidence-based synthesis of the primary data remained unknown. Hence, we aimed to determine the prevalence of poor glycemic control and identify determinants of poor glycemic control in patients with type 2 diabetes in Ethiopia.MethodsWe performed searches in the online databases of PubMed, Google Scholar, Scopus, Science Direct, and the Cochrane Library. Microsoft Excel was used to extract data, and STATA statistical software (v. 16) was used for analysis. Publication bias was explored by forest plots, Begg's rank test, and Egger's regression test. To check for heterogeneity, I2 was computed. Subgroup analysis was conducted based on region and publication year. In addition, the pooled odds ratio for associated factors was calculated.ResultsOut of 1,045 studies assessed, 23 studies were included fulfilling our inclusion criteria. In all, 6,643 individuals were enrolled in the study. It was estimated that 61.11% of type 2 diabetes patients had poor glycemic control (95% CI, 57.14-65.19). The subgroup analysis by study region and publication year revealed that the highest prevalence was observed in the Addis Ababa region (68.57%) and studies published before 2019 (61.76%), respectively. Poor glycemic control was associated with older age > 50 years (AOR = 2.12; 95% CI: 1.27-2.97), not attending formal education (AOR = 3.60; 95% CI: 2.75, 4.46), having diabetes for longer duration (10 years; AOR = 2.57; 95% CI: 1.65-3.49), having comorbidity (AOR = 2.43; 95% CI: 2.05-2.80), and low adherence to diabetes management (AOR = 3.67; 95% CI: 2.41-4.92).ConclusionOur findings indicate a high prevalence of poor glycemic control among people with type 2 diabetes in Ethiopia. Being older, not attending formal education, having a longer duration of diabetes, having comorbidity, and having low adherence to diabetes management were all associated. Therefore, we recommend health organizations implement measures to monitor and control patients' blood glucose levels. Patient education and training of healthcare professionals could serve as a short-term strategy to achieve adequate glycemic control.Systematic review registrationPROSPERO, identifier CRD42022349792, https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42022349792.
Project description:PurposePrevious studies have revealed lower prostate specific antigen concentrations in men with type 2 diabetes, paralleling the reported lower prevalence of prostate cancer in diabetic men. Data are lacking on prostate specific antigen in men with type 1 diabetes whose insulin and obesity profiles differ from those with type 2 diabetes mellitus. In this study we examined the relationship between long-term glycemic control and prostate specific antigen in men with type 1 diabetes mellitus.Materials and methodsTotal prostate specific antigen was measured at one time in 639 men in the EDIC, the observational followup of participants in the DCCT. The relationship between DCCT/EDIC weighted mean hemoglobin A1c and log prostate specific antigen was assessed using linear regression modeling after adjusting for age, body mass index, total testosterone, statin and thiazide medication use, diabetes duration, and DCCT randomization arm and cohort.ResultsMedian subject age was 52 years, body mass index was 28.4 kg/m(2) and DCCT/EDIC time-weighted hemoglobin A1c was 7.9%. Median prostate specific antigen was 0.64 ng/ml (IQR 0.43, 1.05). Prostate specific antigen increased significantly with age (p <0.0001) and with lower time-weighted hemoglobin A1c (p <0.0001). Each 10% increase in hemoglobin A1c was accompanied by an 11% reduction in prostate specific antigen (p=0.0001).ConclusionsProstate specific antigen decreases as hemoglobin A1c increases in men with type 1 diabetes mellitus. This relationship is independent of age, body mass index, androgen levels, medication use and measures of diabetes severity, which suggests that factors related to glycemia may directly affect prostate specific antigen levels.
Project description:BackgroundGlycaemic control in women with diabetes is critical to satisfactory pregnancy outcome. A systematic review of two randomised trials concluded that there was no clear evidence of benefit from very tight versus tight glycaemic control for pregnant women with diabetes.MethodsA systematic review of observational studies addressing miscarriage, congenital malformations and perinatal mortality among pregnant women with type 1 and type 2 diabetes was carried out. Literature searches were performed in MEDLINE, EMBASE, CINAHL and Cochrane Library. Observational studies with data on glycated haemoglobin (HbA1c) levels categorised into poor and optimal control (as defined by the study investigators) were selected. Relative risks and odds ratios were calculated for HbA1c and pregnancy outcomes. Adjusted relative risk estimates per 1-percent decrease in HbA1c were calculated for studies which contained information on mean and standard deviations of HbA1c.ResultsThe review identified thirteen studies which compared poor versus optimal glycaemic control in relation to maternal, fetal and neonatal outcomes. Twelve of these studies reported the outcome of congenital malformations and showed an increased risk with poor glycaemic control, pooled odds ratio 3.44 (95%CI, 2.30 to 5.15). For four of the twelve studies, it was also possible to calculate a relative risk reduction of congenital malformation for each 1-percent decrease in HbA1c, these varied from 0.39 to 0.59. The risk of miscarriage was reported in four studies and was associated with poor glycaemic control, pooled odds ratio 3.23 (95%CI, 1.64 to 6.36). Increased perinatal mortality was also associated with poor glycaemic control, pooled odds ratio 3.03 (95%CI, 1.87 to 4.92) from four studies.ConclusionThis analysis quantifies the increase in adverse pregnancy outcomes in women with diabetes who have poor glycaemic control. Relating percentage risk reduction in HbA1c to relative risk of adverse pregnancy events may be useful in motivating women to achieve optimal control prior to conception.
Project description:Type 2 diabetes (DM2) is a disease that hinders tuberculosis (TB) control strategies worldwide. TB infection, progression, morbidity, treatment success, adverse effects, relapse, and mortality are worse in these susceptible populations. Therefore, expanding the partially known molecular mechanisms leading to TB-DM2 comorbidity may be essential to face both epidemics. Consequently, a transcriptomic study was conducted on TB-DM2 comorbidity, associated with patients with DM2 who have poor glycaemic control (PDM2), since they have a higher risk of getting TB. Human blood samples from healthy controls (CTRL, HbA1c < 6.5%), TB ( HbA1c < 6.5%), TB-DM2, DM2 (HbA1c < 8.9%), and PDM2 (HbA1c > 10%) groups (n=4 each) were analyzed using high-density human GE 4X44K v2 differential expression microarrays.
Project description:Abstract Background An emerging field of research concerns the deleterious effects of type 2 diabetes mellitus (T2DM) on bone. Our group has previously reported a hemoglobin A1c (A1c) threshold of 7% where bone impairment occurs as reflected by reduction in bone turnover markers and deterioration in bone microarchitecture and strength. However, whether poor glycemic control is also associated with underlying derangements in cellular flux remains unclear. Methods Analysis of the baseline data from 42 consecutive men aged 35-65 enrolled in a clinical trial (NCT03887936) at the Michael E DeBakey VA Medical Center, Houston, TX, who were able to provide the outcomes of interest. Inclusion criteria were average fasting morning testosterone from 2 measurements of <300 ng/dl, T2DM and BMI<35 kg/m2. The following variables were assessed: A1c by high performance liquid chromatography; testosterone and estradiol by LC/MS; bone turnover markers and sex hormone binding globulin by ELISA; quantification of osteoblast (OB) progenitors and osteoclast (OC) precursors by flow cytometry; areal bone mineral density (aBMD) and body composition by DXA; and bone microarchitecture and strength by high resolution peripheral quantitative computerized tomography. Results Participants with poorly controlled T2DM (A1c>7%) had significantly lower percent of OB progenitors in circulation than those with A1c≤7% (1.12 ± 0. 079% v 1.47 ± 0.11% of non-B non-T non-NK cells, p=0. 02) when controlling for age, duration of T2DM, free testosterone, and 25-hydroxyvitamin D levels. Higher levels of free testosterone were associated with smaller percentage of OB progenitors (r = -0.31, p = 0. 05). Although the percent of OC precursors in circulation (cells that were dual CD14CD11b+, CD14MCSFR+, or CD14CD120b+) was not significantly related to A1c, it was positively associated with percent of OB progenitors in peripheral blood (r = 0.34, p = 0. 03; r = 0.35, p = 0. 02; r = 0.39, p = 0. 01) respectively. There was a significant positive association between OB progenitors and visceral adipose tissue (VAT) volume (r=0.41, p=0. 009). Although there was no association between osteoblast progenitors and osteocalcin levels (product of mature OBs), osteocalcin negatively correlated with VAT (r=-0.47, p=0. 002). There was no association between OB progenitors and OC precursors with aBMD or bone microarchitecture parameters. Conclusions Poor glycemic control is associated with fewer circulating OB progenitors, as was higher free testosterone levels while the converse was true for VAT. It is possible that the former harms cell viability, while the latter two affect differentiation of OB progenitors into mature OB's; with testosterone promoting, and visceral adipose tissue (via unknown mediators) retarding maturation as suggested by the negative association between osteocalcin and VAT. The positive association between OB progenitors with circulating OC precursors is consistent with the physiologic crosstalk between OB and OC which appears to be preserved in patients with T2D. Presentation: No date and time listed
Project description:In a cohort of adults with type 1 diabetes, we examined the prevalence of hypomagnesemia and the correlation of serum magnesium levels with metabolic determinants, such as glycaemic control (as HbA1c), inflammatory markers and circulating cytokines. Furthermore, we assessed if a surrogate for insulin resistance is essential for the possible association of serum magnesium with metabolic determinants. Individuals with type 1 diabetes, aged above 18 years, were included and clinical characteristics were obtained from questionnaires and clinical records. In venous blood samples we measured cytokines and adipose-tissue specific secretion proteins. Serum magnesium concentrations were measured and correlated with clinical data and laboratory measurements using univariate and multivariate regression models. Hierarchical multiple regression of serum magnesium with insulin resistance was adjusted for diabetes and potential magnesium confounders. The prevalence of hypomagnesemia (serum magnesium levels < 0.7 mmol/L) was 2.9% in a cohort consisting of 241 individuals with type 1 diabetes. The magnesium concentration in the cohort was not associated with HbA1c (r = - 0.12, P-value = 0.068) nor with any inflammatory marker or adipokine. However, insulin dose (IU/kg), a surrogate measure of resistance in type 1 diabetes, moderated the association of serum magnesium (mmol/L) with HbA1c (mmol/mol) with a B coefficient of - 71.91 (95% CI: - 119.11; -24.71), P-value = 0.003) and Log10 high-sensitivity C-reactive protein (Log10 mg/L) - 2.09 (95% CI: - 3.70; - 0.48), P-value = 0.011). The association of low serum magnesium levels with glycaemic control (HbA1c) and high-sensitivity C-reactive protein in individuals with type 1 diabetes is limited to subjects using a high insulin dose and suggests that insulin resistance, a type 2 diabetes feature, is a prerequisite for hypomagnesemia.