BMJ Open Diabetes Research & Care最新文献

Elevated serum uric acid levels are an independent predictor of occurrence and development of chronic kidney disease (CKD) and are strongly associated with prognosis. Several clinical trials have demonstrated the benefits of sodium-glucose cotransporter-2 (SGLT-2) inhibitors. To evaluate and rank the effects and safety of various SGLT-2 for serum uric acid levels in patients with CKD. We performed a systematic PubMed, Embase, Scopus, and Web of Science search, including studies published before July 1, 2023. Two researchers independently extracted data on study characteristics and outcomes and assessed study quality using the Cochrane Collaboration's risk of bias tool 2. The gemtc package of R software was used to perform network meta-analysis within a Bayesian framework. The primary outcome was serum uric acid levels, and the secondary outcome was adverse events. Effect sizes are reported as standardized mean differences (SMDs), risk ratio (RR), and 95% CI, respectively. The certainty of evidence was evaluated using Grading of Recommendations, Assessment, Development and Evaluations (GRADE) criteria. Eight RCTs (9367 participants) were included in this meta-analysis. The results of the paired meta-analysis showed that SGLT-2 inhibitors significantly reduced serum uric acid levels in patients with CKD compared with the placebo group (SMD -0.22; 95% CI -0.42 to -0.03; GRADE: low). Pooled analysis of any adverse events reported in the included studies showed similar incidence rates in the SGLT-2 inhibitor and placebo groups (RR: 0.99; 95% CI 0.97 to 1.00; p=0.147; GRADE: high). Subgroup analysis showed a statistically significant difference only for tofogliflozin. Further network meta-analysis showed that dapagliflozin 10 mg and ipragliflozin 50 mg may be the most effective in reducing uric acid levels. SGLT-2 inhibitors significantly reduced serum uric acid levels in patients with CKD, and dapagliflozin 10 mg and ipragliflozin 50 mg may be the optimal dosages. SGLT-2 inhibitors hold great promise as an antidiabetic therapeutic option for patients with CKD who have elevated serum uric acid levels. PROSPERO registration number: CRD42023456581.

Introduction: Diabetic foot ulcer (DFU) is a disabling complication of diabetes mellitus. Here, we attempted to assess whether long-term intrafemoral artery infusion of low-dose urokinase therapy improved DFUs and decreased cardiovascular events in patients with DFUs.

Research design and methods: This trial was a single-center, randomized, parallel study. A total of 195 patients with DFU were randomized to continuous intrafemoral thrombolysis or conventional therapy groups. The continuous intrafemoral thrombolysis group received continuous intrafemoral urokinase injection for 7 days, and conventional therapy just received wound debridement and dressing change. Then, a follow-up of average 6.5 years was performed.

Results: Compared with conventional therapy, at the first 1 month of intervention stage, the ulcers achieved a significant improvement in continuous intrafemoral thrombolysis group including a complete closure (72.4% vs 17.5%), an improved ulcer (27.6% vs 25.8%), unchanged or impaired ulcer (0% vs 56.7%). During the 6.5-year follow-up, for the primary outcome of ulcer closure rate, continuous intrafemoral thrombolysis therapy obtained a better complete healing rate (HR 3.42 (95% CI 2.35 to 4.98, p<0.0001)). For the secondary outcome of cardiovascular disease events, continuous intrafemoral thrombolysis therapy had a lower incidence of cardiovascular events (HR 0.50 (95% CI 0.34 to 0.74, p<0.0001)). Importantly, intrafemoral thrombolysis therapy decreased the incidence of cardiovascular death (HR 0.42 (95%CI 0.20 to 0.89, p=0.0241)). Additionally, continuous intrafemoral thrombolysis therapy improved local skin oxygenation and peripheral neuropathy as well as glycolipid metabolic profiles when compared with conventional therapy group (p<0.05).

Conclusions: Continuous intrafemoral thrombolysis therapy has a better therapeutic efficacy to improve DFUs and decrease cardiovascular events.

Trial registration number: NCT01108120.

Introduction: Women with a history of gestational diabetes mellitus (GDM) are at high risk of developing type 2 diabetes, while the exact mechanisms underlying its pathophysiology are still unclear. We investigated the association of glucagon-like peptide-1 (GLP-1) response to oral glucose with parameters of glycemic control in women with previous GDM in the prospective PPSDiab (Prediction, Prevention, and Subclassification of Type 2 Diabetes) study.

Research design and methods: Glucose metabolism parameters and GLP-1 secretion were analyzed during oral glucose tolerance test (OGTT) in women with previous GDM (n=129) and women with a history of normal glucose tolerance (n=67) during pregnancy (controls). First- and second-phase insulin and GLP-1 secretion in relation to plasma glucose (PG) levels were assessed, and development of pre-diabetes was analyzed after 5-year follow-up among women with previous GDM and a normal glycemic state at baseline (n=58).

Results: The area under the curve (AUC during the OGTT 0-120 min) of PG and insulin but not GLP-1 differed significantly between post-GDM women and controls. However, women with previous GDM had a significantly decreased GLP-1 response in relation to PG and plasma insulin during the second phase of the OGTT. After a follow-up of 5 years, 19.0% post-GDM women with a normal glycemic state at the baseline visit developed abnormal glucose metabolism. The total, first- and second-phase AUC GLP-1/PG and GLP-1/insulin ratios were not associated with development of abnormal glucose tolerance.

Conclusions: Women with previous GDM showed a reduced GLP-1 response in relation to PG and insulin concentrations indicating early abnormalities in glucose metabolism. However, the altered GLP-1 response to oral glucose did not predict progression to pre-diabetes and type 2 diabetes in the first 5 years after GDM.

Introduction: Insulin resistance and defects in pancreatic beta cells are the two major pathophysiologic abnormalities that underlie type 2 diabetes. In addition, visceral fat area (VFA) is reported to be a stronger predictor for diabetes than body mass index (BMI). Here, we tested whether the performance of diabetes prediction models could be improved by adding HOMA-IR and HOMA-β and replacing BMI with VFA.

Research design and methods: We developed five prediction models using data from a cohort study (5578 individuals, of whom 94.7% were male, and 943 had incident diabetes). We conducted a baseline model (model 1) including age, sex, BMI, smoking, dyslipidemia, hypertension, and HbA1c. Subsequently, we developed another four models: model 2, predictors in model 1 plus fasting plasma glucose (FPG); model 3, predictors in model 1 plus HOMA-IR and HOMA-β; model 4, predictors in model 1 plus FPG, HOMA-IR, and HOMA-β; model 5, replaced BMI with VFA in model 2. We assessed model discrimination and calibration for the first 10 years of follow-up.

Results: The addition of FPG to model 1 obviously increased the value of the area under the receiver operating characteristic curve from 0.79 (95% CI 0.78, 0.81) to 0.84 (0.83, 0.85). Compared with model 1, model 2 also significantly improved the risk reclassification and discrimination, with a continuous net reclassification improvement index of 0.61 (0.56, 0.70) and an integrated discrimination improvement index of 0.09 (0.08, 0.10). Adding HOMA-IR and HOMA-β (models 3 and 4) or replacing BMI with VFA (model 5) did not further materially improve the performance.

Conclusions: This cohort study, primarily composed of male workers, suggests that a model with BMI, FPG, and HbA1c effectively identifies those at high diabetes risk. However, adding HOMA-IR, HOMA-β, or replacing BMI with VFA does not significantly improve the model. Further studies are needed to confirm our findings.