This study aimed to clarify the clinical significance of perinatal changes in fibroblast growth factor 21 and their association with postpartum metabolic outcomes in women with gestational diabetes mellitus.

This single-center retrospective observational study used prospectively collected residual serum samples to investigate longitudinal changes in serum fibroblast growth factor 21 concentrations at approximately 26 (T1) and 36 (T2) weeks of gestation and within 7 days postpartum (T3) in 45 women with gestational diabetes mellitus and 30 controls. Associations between fibroblast growth factor 21 concentrations and postpartum metabolic outcomes were evaluated in the gestational diabetes mellitus group.

Serum fibroblast growth factor 21 concentrations increased significantly from T1 to T2 and remained elevated at T3, irrespective of gestational diabetes mellitus status, as assessed using the Friedman test with post hoc comparisons. In women with gestational diabetes mellitus, fibroblast growth factor 21 showed predictive performance for postpartum insulin resistance, as assessed using the homeostasis model assessment of insulin resistance. Receiver operating characteristic analysis showed the highest area under the curve for predicting postpartum insulin resistance at T1 (area under the curve, 0.871; bootstrap 95% confidence interval, 0.732-0.973). Fibroblast growth factor 21 concentrations appeared to decline during the early postpartum period, as indicated by significantly lower T3/T1 ratios in samples from postpartum Days 5-7 compared with those from Days 1-4.

These findings suggest that perinatal fibroblast growth factor 21 dynamics may reflect physiological changes in insulin sensitivity and that fibroblast growth factor 21 concentrations measured during pregnancy may serve as a complementary indicator for postpartum metabolic risk stratification in women with gestational diabetes mellitus. Further validation is needed before clinical application.

To evaluate the appropriateness of antiplatelet use across dementia subtypes in older adults and to identify factors associated with inappropriate antiplatelet use.

This population-based retrospective study enrolled adults aged ?65 years with dementia evaluated at a tertiary geriatric outpatient clinic at Gulhane Training and Research Hospital between 2016 and 2025. Antiplatelet (aspirin or clopidogrel) use was categorized as appropriate use, underuse, overuse, or appropriate non-use according to the 2021-2024 European Society of Cardiology guidelines. Multivariable logistic regression analyses were performed to identify the factors associated with inappropriate antiplatelet use.

Among 683 older adults with dementia, 40.7% received antiplatelet therapy. Antiplatelet underuse and overuse were observed in 16.8% and 16.1% of the participants, respectively. Underuse was most prevalent in vascular dementia (38.9%), whereas overuse was most prevalent in Alzheimer disease (20.2%) and frontotemporal dementia (19.0%). In multivariable analyses, antiplatelet overuse was independently associated with diabetes mellitus (odds ratio [OR] 4.31; 95% confidence interval [CI] 1.66-11.16) and inversely associated with current smoking (OR 0.06; 95% CI 0.06-0.67). Antiplatelet underuse was independently associated with female sex (OR 4.44; 95% CI 1.52-12.92).

Our findings highlight the gaps between guideline recommendations and real-world practice and support the need for individualized dementia-sensitive antiplatelet treatment strategies.

In recent years, with the increasing prevalence of cervical spondylosis, neck-shoulder syndrome, and scapulohumeral periarthritis, dorsocervical fat pad (DCFP) has become more commonly observed and is no longer considered exclusively a rare disease entity. Consequently, there is a growing need for safer, more effective, and minimally invasive therapeutic strategies to manage the rising number of patients presenting with DCFP.

A total of 42 patients diagnosed with DCFP in our hospital between December 2023 and January 2025 were enrolled in this study. The cohort comprised 23 male and 19 female patients, with a mean age of 37.69 years, a mean height of 164.42 cm, and a mean body weight of 58.64 kg. Among these patients, 17 had a history of hypertension, four had diabetes mellitus, 27 were diagnosed with neck-shoulder myofascial pain syndrome, and 31 presented with cervical spondylosis. Following four sessions of combined cupping and acupuncture therapy, therapeutic efficacy was evaluated by assessing changes in DCFP volume, head-and-neck range of motion, neck disability index (NDI) scores, body mass index, and the occurrence of adverse reactions RESULTS: After four treatment sessions, significant overall differences were observed in DCFP length, width, and thickness across the three time points (P < 0.001), with the most pronounced improvement noted in thickness. Additionally, NDI scores decreased significantly compared to baseline (P < 0.001). Following treatment, flexion range of motion (FF-ROM), extension range of motion (E-ROM), left lateral flexion range of motion (LLF-ROM), and right lateral flexion range of motion (RLF-ROM), all showed significant increases relative to pretreatment values (all P < 0.001). No significant change in BMI was detected before and after treatment (P = 0.598).

The combination of acupuncture and cupping therapy demonstrates significant efficacy in reducing the volume parameters of DCFP, particularly in decreasing thickness. Furthermore, this therapeutic approach improves head-and-neck range of motion and enhances cervical function and esthetic appearance in affected patients.

This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Diabetic nephropathy (DN) is a leading cause of end-stage renal disease, with proximal tubular injury and oxidative stress playing pivotal roles in its progression. The AMPK-Nrf2 signaling axis is a key regulator of antioxidant defense, but its modulation by Aloin in DN-relevant renal models remains insufficiently characterized. Aloin, a natural anthraquinone glycoside from Aloe species, exhibits antioxidant, anti-inflammatory, and anti-fibrotic properties in non-renal systems. This study investigated whether Aloin protects renal cells from high-glucose-induced injury and whether AMPK and Nrf2 contribute to these protective responses.

Human renal proximal tubular epithelial cells (HK-2) and human renal glomerular endothelial cells (HRGECs) were exposed to high glucose (HG, 30 mM) for 48 h with or without Aloin (25 or 50 µM). Functional assays included CCK-8 cell viability, colony formation, and wound healing migration analysis. mRNA expression of oxidative stress-related, inflammatory, fibrotic, and phenotype-associated markers, including VIM and CDH1, was quantified by reverse transcription-quantitative polymerase chain reaction (RT-qPCR). siRNA-mediated knockdown of PRKAA1 (AMPK) or NFE2L2 (Nrf2) was performed to assess mechanistic involvement, with gene silencing confirmed by RT-qPCR and Western blotting. For exploratory in vivo validation, male db/db mice received oral Aloin at 25 mg/kg/day for 8 weeks, while age-matched db/m and db/db mice received vehicle (n = 6 per group).

HG exposure reduced proliferation and clonogenic capacity while increasing wound closure under serum-free conditions in both HK-2 cells and HRGECs, accompanied by upregulation of TNF, CCL2, TGFB1, COL1A1, and VIM, and downregulation of NFE2L2, SOD1, PRKAA1, and CDH1. Aloin treatment dose-dependently restored proliferation, reduced migration, and normalized gene expression patterns, with 50 µM producing near-complete reversal toward normal glucose controls. PRKAA1 knockdown in HK-2 cells and NFE2L2 knockdown in HRGECs substantially attenuated Aloin-associated protective responses, supporting the functional involvement of AMPK and Nrf2 in these cell-specific effects.

Aloin attenuated high-glucose-induced injury in cultured renal tubular epithelial and glomerular endothelial cells, with loss-of-function experiments supporting the involvement of AMPK and Nrf2 in these responses. Exploratory validation in db/db mice further showed reductions in albuminuria, serum creatinine, and mesangial matrix expansion, accompanied by restoration of renal AMPK-Nrf2 signaling. However, the 25 and 50 µM concentrations used in vitro cannot be directly equated with the 25 mg/kg/day oral dose used in mice, and plasma exposure, renal tissue concentrations, pharmacokinetics, and systemic safety were not determined. Additional pharmacokinetic, dose-ranging, and toxicological studies are required before the therapeutic relevance of Aloin can be established.

Diabetes mellitus and persistent proteinuria are major determinants of cardiovascular morbidity, graft dysfunction, and mortality after kidney transplantation. Although sodium-glucose cotransporter-2 (SGLT2) inhibitors have demonstrated substantial cardiorenal benefits in chronic kidney disease, data regarding their use in kidney transplant recipients remain limited. This study aimed to evaluate the clinical effects of dapagliflozin on proteinuria, graft function, glycemic measures, treatment burden, and observed safety events in diabetic kidney transplant recipients.

We conducted an exploratory retrospective 1:1 clinically matched cohort study of diabetic kidney transplant recipients followed between 2010 and 2022. Among 282 transplant recipients, 68 had diabetes mellitus. Eighteen patients initiated dapagliflozin 10 mg/day and were included in the all-treated tolerability cohort; three discontinued treatment before completing 3 months because of patient preference unrelated to documented adverse events, leaving 15 recipients who received dapagliflozin for at least 12 months in the efficacy cohort. Fifteen diabetic kidney transplant recipients not receiving SGLT2 inhibitor therapy were selected as 1:1 clinically matched comparable controls according to prespecified matching criteria. Primary outcomes were changes in proteinuria and eGFR. Secondary outcomes included HbA1c, fasting plasma glucose, insulin requirements, antihypertensive medication burden, and observed safety events.

Thirty diabetic kidney transplant recipients were included in the 12-month efficacy analysis (15 dapagliflozin-treated recipients and 15 1:1 clinically matched comparable controls). Baseline demographic, transplant-related, renal, and glycemic characteristics were broadly comparable between groups. Proteinuria decreased more in the dapagliflozin group than in controls (median change, - 157 [- 310 to - 52] vs. -12 [- 48 to + 25] mg/day; Hodges-Lehmann location-shift estimate, - 171 mg/day; 95% CI, - 310 to - 32; p = 0.009), while eGFR remained stable (between-group difference in ΔeGFR, + 1.6 mL/min/1.73 m²; 95% CI, - 1.8 to + 5.0; p = 0.31). HbA1c decreased from 8.10% (65 mmol/mol) to 7.10% (54 mmol/mol) in the dapagliflozin group, whereas it decreased from 8.18% (66 mmol/mol) to 7.80% (62 mmol/mol) in controls. Greater reductions were also observed in fasting plasma glucose and daily insulin dose. Two urinary tract infections requiring oral antibiotics occurred in the dapagliflozin group and one in controls. No genital infections, diabetic ketoacidosis, acute rejection, graft loss, cardiovascular events, severe infections requiring hospitalization, or deaths were observed.

In this exploratory 1:1 clinically matched cohort of selected diabetic kidney transplant recipients, dapagliflozin use was associated with reduced proteinuria, improved glycemic measures, and lower treatment burden over 12 months, without observed major graft-related or serious infectious events. However, the retrospective design, small sample size, selected cohort, and treatment-completer efficacy analysis preclude causal inference and definitive safety conclusions. Larger prospective multicenter studies are required before routine implementation in transplant practice can be recommended.

Diabetes mellitus (DM) is increasingly prevalent in people with HIV, with reported prevalence estimates generally ranging from 5% to 15% across contemporary cohorts. It represents a major contributor to both microvascular and macrovascular disease. People with HIV are at increased risk of insulin resistance and type 2 diabetes due to chronic immune activation, antiretroviral therapy-related metabolic effects, and traditional cardiometabolic risk factors. In this context, DM is associated with accelerated atherosclerosis, earlier onset of microvascular injury, and adverse cardiovascular outcomes. Glycaemic screening and management remain suboptimal in this population, and HbA1c may underestimate dysglycaemia in selected patients. This narrative review critically appraises current evidence on diabetes-related vascular complications in people with HIV, identifies key pathophysiological and clinical gaps, and highlights priorities for improved screening, risk stratification, and integrated management.

We aimed to probe the European Society of Cardiology (ESC) guideline recommended electrocardiographic (ECG) criteria for degree of under detection of left ventricular hypertrophy (LVH) across clinically relevant subgroups in a contemporary general population and if ECG-threshold recalibration could promote diagnostic equity.

We studied participants in the Copenhagen General Population Study. Cardiac computed tomography (CT) was used to define CT-LVH, and ECG-LVH was defined according to ESC guideline: Sokolow-Lyon, Cornell voltage, or Sokolow-aVL criteria. Diagnostic performance was assessed using Poisson regression across subgroups defined by age above 60 years, sex, overweight (BMI ≥ 25 kg/m²), hypertension, diabetes mellitus, obstructive pulmonary disease, and physical activity. ECG-thresholds were recalibrated to 95% specificity while maximizing sensitivity across all subgroups with disparities in both measures. Recalibration was performed in 50% of the population and validation in the remaining 50%.

We studied 9392 participants with median age of 60 years, of whom 58% were women. By CT 839 (9%) had CT-LVH. The guideline ECG-LVH definition had overall 20% sensitivity and 96% specificity. Sensitivity was lower in women than men (15% versus 26%; P < 0.001) and individuals with overweight compared to normal weight (16% versus 23%; P = 0.005). The recalibrated ECG-thresholds provided overall 36% sensitivity and 91% specificity in the validation cohort with consistent sensitivity and specificity across subgroups. The new recalibrated ECG criteria promoted diagnostic equity in LVH detection across sex and BMI subgroups, increasing overall sensitivity at a slight specificity cost.

To investigate the association of concurrent diabetes mellitus and poor sleep with cognitive decline in a community-based population.

Cognitively normal adults aged 40 years or older were followed-up for 4 years. Cognitive decline was defined as a decrease of ≥ 4 points on the Chinese Mini-Mental Status from baseline. Sleep quality was assessed using the Pittsburgh Sleep Quality Index. Logistic regression was employed to evaluate associations of diabetes and poor sleep status with cognitive decline.

Among 1218 participants, 30 (2.46%) developed cognitive decline during follow-up. Participants with concurrent diabetes and poor sleep had higher odds of cognitive decline (adjusted OR = 5.74, 95% CI: 1.58 - 18.81). The association of the concurrent presence of poor sleep and diabetes with cognitive decline was evident mainly when poor sleep was defined by poor subjective sleep quality, short sleep duration, low sleep efficiency, frequent sleep disturbances, or severe daytime dysfunction (adjusted ORs, 4.17-10.23; all P < 0.05), rather than prolonged sleep latency. The application of broader criteria for dysglycemia (adjusted OR = 4.10, 95% CI: 1.23 - 12.82) corroborated the robustness of these findings.

The co-occurrence of diabetes and poor sleep was associated with higher odds of cognitive decline, suggesting the clinical potential of integrated interventions in preserving cognitive health.

To estimate the prevalence of undiagnosed, symptomatic heart failure (HF) and progression of HF in a contemporary cohort of patients with type 2 diabetes (T2D).

This was an epidemiologic, 2-year prospective cohort study that enrolled outpatients with T2D, diagnosed within the prior 10 years, with high/very high cardiovascular risk but no HF history. Prevalence and incidence of symptomatic HF (ACC/AHA stages C/D) and cardiovascular-related healthcare resource utilization (HCRU) rates were estimated.

From 20-Jul-2020 to 31-Oct-2022, 241 consecutive patients [61.8% males, median (IQR) age 63.0 (57.0-69.0) years] were enrolled; 0.8% (95% CI: 0.00-1.98) had symptomatic (stage C) HF; 91.3% (95% CI: 87.73-94.85) stage A and 7.9% (95% CI: 4.48-11.29) stage B HF. During follow-up, 2.8% (6/215) of evaluable patients experienced HF progression [time-to-progression, median (range): 19.8 (5.9-24.1) months]. Incidence rate of symptomatic HF among patients with preclinical (stage A/B) HF at enrollment was 0.44/100 patient-years (95% CI: 0.11-1.77). Cardiovascular-related HCRU were reported by 54.7% (87/159) of patients, corresponding to incidence rate of 51.68 encounters/100 patient-years.

Whereas the low prevalence of symptomatic HF and low rate of HF-progression likely reflect effective monitoring and intervention at preclinical HF stages, the substantial healthcare-burden highlights an unmet need regarding implementation of HF preventive management strategies in patients with T2D.

Clusterin is a multifunctional glycoprotein involved in lipid transport, complement regulation, and oxidative/inflammatory stress responses, pathways relevant to insulin resistance and metabolic stress in gestational diabetes mellitus (GDM). However, its role in established GDM remains insufficiently defined. This study aimed to compare maternal serum clusterin in established GDM and normoglycemic controls and explore associations with the need for insulin therapy and perinatal outcomes.

This prospective single-center case-control study included 88 singleton pregnancies at 24-28 weeks' gestation (44 GDM, 44 controls). Fasting serum clusterin was measured by enzyme-linked immunosorbent assay after completion of GDM screening and, in women who subsequently required insulin, before insulin initiation.

Clusterin was lower in GDM than in controls (1.46 [0.76-2.81] vs 2.56 [1.31-3.98] ng/mL; p = 0.018). Within GDM, women who subsequently required insulin had lower clusterin than those managed with diet alone (1.14 [0.54-1.63] vs 2.26 [1.32-3.98] ng/mL; p = 0.005). In exploratory Firth penalized regression, higher clusterin remained inversely associated with the need for insulin therapy after adjustment for selected clinical and glycemic covariates (adjusted odds ratio per 1 ng/mL increase, 0.50; 95% CI 0.27-0.91; p = 0.024). Clusterin alone showed modest discrimination for GDM (AUC 0.646, 95% CI 0.537-0.745), whereas its discrimination for insulin therapy was higher but imprecise because of the small subgroup and wide confidence interval (AUC 0.748, 95% CI 0.595-0.867). Clusterin did not significantly discriminate the composite adverse perinatal outcome in either the overall cohort or the GDM subgroup.

Maternal serum clusterin was reduced in established GDM and was associated with the subsequent need for insulin therapy, suggesting a possible link with metabolic severity. These exploratory findings are hypothesis-generating and require validation before use in treatment stratification.