The associations between different definitions of prediabetes and diabetes with mortality and life expectancy remain unclear. Clarifying these associations is essential for informing hyperglycemia management policies. We aimed to compare the prevalence of prediabetes and newly diagnosed diabetes across different glycemic indicators and diagnostic criteria, and to examine their associations with mortality and life expectancy.

We analyzed data from 141,945 adults from a nationally representative cohort study in China. Cox proportional hazards regression models were used to estimate hazard ratios (HRs). Using fasting plasma glucose (FPG), 2-hour postload glucose (2hPG), and hemoglobin A1c (HbA1c) levels, prediabetes was defined according to the American Diabetes Association (ADA), World Health Organization (WHO), or International Expert Committee (IEC) criteria, and newly diagnosed diabetes according to the ADA criteria.

Prediabetes prevalence varied widely across glycemic indicators, ranging from 3.0% to 26.1%, while newly diagnosed diabetes prevalence ranged from 2.6% to 4.4%. Over a median follow-up of 9.0 years, a total of 6,924 deaths were documented. Compared with people with normoglycemia, prediabetes defined by FPG (either ADA or WHO criteria) was not significantly associated with increased risks of all-cause or cardiovascular disease (CVD) mortality (all P>0.05). In contrast, prediabetes defined by 2hPG or HbA1c (either ADA or IEC criteria) was each associated with higher risks of all-cause mortality (HRs: 1.13-1.23; all P<0.001) and CVD mortality (HRs: 1.12-1.25; all P<0.001). Prediabetes defined by 2hPG or HbA1c, but not FPG, was associated with 1.1-2.3 years reduction in life expectancy, with the largest loss observed for IEC HbA1c. In addition, diabetes defined by FPG, 2hPG or HbA1c was each significantly associated with higher risk of all-cause and CVD mortality (HRs: 1.25-1.51), and reduction in life expectancy (2.0-3.7 years). Furthermore, the 2hPG-based definition of prediabetes and diabetes was associated with mortality risk, independent of FPG and HbA1c levels.

These findings suggest that reliance on FPG alone may fail to identify certain individuals at elevated mortality risk. In contrast, 2hPG and HbA1c provide additional prognostic information beyond FPG.

Physical activity (PA) plays a crucial role in the management of Type 2 Diabetes Mellitus (T2DM). Despite its known benefits, many individuals living with T2DM face challenges in maintaining regular PA. General practitioners (GPs) are often seen as key facilitators of lifestyle change, yet little is known about how individuals living with T2DM perceive PA and the role of GPs in promoting it. This study aims to explore the personal perceptions, motivators, and barriers related to PA among individuals living with T2DM, and to understand their expectations for GP support within the primary care setting.

A qualitative study was conducted in primary care settings in Germany. Participants were recruited from self-help groups and GP practices across Hesse, Bavaria, and Berlin. Semi-structured interviews were conducted with 13 individuals living with T2DM. Interviews were transcribed verbatim and analysed using an inductive-deductive thematic analysis approach (Braun and Clarke) informed by the Health Belief Model.

Participants recognised PA as essential for diabetes management and reported diverse experiences and challenges. Motivators included fear of complications, self-efficacy, enjoyment, goal-setting, and perceived health benefits. However, self-efficacy played a complex role—while it encouraged PA, it also increased feelings of personal responsibility, sometimes resulting in stress, guilt, or excessive self-monitoring. Barriers included comorbidities, lack of companionship, time constraints, and reluctance. Participants valued GP support, valuing a partnership-relationship, while also feeling motivated through authorities. Suggestions for GP involvement included tailored PA counselling, regular follow-up, structured goal-setting, and addressing emotional aspects of diabetes.

PA was widely acknowledged as important, yet its adoption was influenced by personal and contextual factors. Self-efficacy played a dual role, acting as both a motivator and a psychological burden. GPs were seen as important in PA promotion, but their support needed to be flexible and personalised.

The online version contains supplementary material available at 10.1186/s12875-026-03344-z.

The SPAST gene encodes spastin, a microtubule-severing protein. Pathogenic variants in this gene are commonly associated with autosomal dominant Spastic paraplegia type 4 (SPG4), a neurodegenerative disorder presenting with progressive lower limb spasticity. Severe phenotypes involving more extensive neurological impairment are rare.

We report the first known case of an adolescent with a rare pathogenic SPAST variant (NM_014946.4: c.1507C > T; NP_055761.2: p. [Arg503Trp]) presenting with spastic quadriplegia. Additional features included severe intellectual disability, absent speech, dysphagia, and epilepsy, manifestations infrequently reported in association with SPAST mutations. He was born prematurely at 32 weeks of gestation after a complicated antenatal period due to the development of preeclampsia at 23 weeks and gestational diabetes mellitus at 26 weeks.

The patient's clinical presentation represents one of the most severe phenotypes described in the literature for SPAST-related disorders. The identification of a genetic cause provided a more satisfactory and specific diagnosis than the previously presumed etiology of perinatal asphyxia. This case broadens the phenotypic spectrum of SPAST-related disease and highlights the role of genetic testing in the diagnostic workup of complex neurological conditions.

We report the first case of a pathogenic variant in the SPAST gene and quadriplegia and one of the most severe clinical phenotypes described in the literature in association with variants in this gene. This report underscores the importance of considering SPAST mutations in patients with atypical or severe neurodevelopmental presentations. Genetic diagnosis enables more accurate prognosis, individualized medical care, and appropriate genetic counseling for families.

Diabetic foot is among the most frequent complications of diabetes mellitus (DM), with potentially dramatic consequences ranging from chronic wounds to major lower-limb amputations. The Tardivo Algorithm is a simple prognostic scoring system designed to support risk stratification and structured longitudinal reassessment in routine clinical care.

To describe the real-world implementation and feasibility of dynamic risk reassessment using the Tardivo Algorithm in a prospective observational cohort of patients with diabetic foot managed in a vascular surgery outpatient setting, and to explore associations between baseline risk stratification and clinical outcomes.

This prospective observational cohort study was conducted in a routine outpatient clinic for complex wounds. Adult patients with diabetic foot were classified according to the Tardivo Algorithm at baseline and underwent structured serial reassessments at each follow-up visit as part of usual multidisciplinary care. No comparator group was included. Patients were followed for 6-18 months, and outcomes were descriptively recorded as minor amputation, major amputation, wound in process of healing, or complete healing.

A total of 42 patients were followed for up to 18 months. Mean initial Tardivo score was 7.6 ± 4.8, with 19% classified as high risk (≥12 points). Limb preservation was observed in 94.3% of participants, and complete healing occurred in 57%, with a mean healing time of 5.05 ± 1.95 months. Higher baseline Tardivo scores were positively associated with peripheral arterial disease (r = 0.740; p < 0.001), while healing time correlated with both PAD (r = 0.547; p = 0.006) and prior amputations (r = 0.523; p = 0.009). These correlations were not independent in multivariable models. Findings reflect associations observed in a real-world, structured outpatient care model.

In this prospective real-world cohort, structured application of the Tardivo Algorithm was feasible and allowed dynamic clinical monitoring. Clinical outcomes observed during follow-up are described within the context of this non-controlled design and should be interpreted as observational associations rather than indicators of therapeutic effect. Controlled studies are required to determine the independent impact of algorithm-guided reassessment and adjunctive therapies.

Metabolic Syndrome (MetS) is a cluster of metabolic abnormalities including abdominal obesity, impaired glucose metabolism, hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and hypertension. It is diagnosed when at least three of these five criteria are present. Individuals with MetS are at increased risk of developing type 2 diabetes mellitus and cardiovascular disease. Beyond these well-established complications, infertility has emerged as an underrecognized consequence of metabolic dysfunction. Infertility, defined as failure to achieve pregnancy after one year of regular unprotected intercourse, affects approximately 10-15% of couples worldwide, with nearly 20% of cases classified as idiopathic.

This review aims to examine the impact of metabolic syndrome and its components on male and female infertility and to highlight the potential mechanisms linking metabolic disturbances with impaired reproductive function.

A narrative review of current literature was conducted, focusing on the relationship between metabolic syndrome components - obesity, dyslipidemia, hyperinsulinemia, and hypertension - and reproductive health outcomes. Evidence from clinical, epidemiological, and experimental studies evaluating reproductive dysfunction in both males and females was analyzed.

Metabolic syndrome exerts significant adverse effects on reproductive health in both women and men. In women, it is associated with reduced ovulation, impaired oocyte competence, diminished follicular reserve, anovulation, and increased risk of ovarian pathology. In men, MetS contributes to reduced sperm count, impaired sperm motility and viability, poor semen quality, erectile dysfunction, and prostate-related disorders. Early identification and proper management of metabolic syndrome may play a crucial role in reducing the burden. Addressing metabolic abnormalities through lifestyle modification and appropriate medical interventions could improve reproductive outcomes.

Diabetic osteoporosis (DOP) is a diabetes mellitus (DM) complication, defined by diminished bone density and a significantly increased fracture risk due to disorders in bone metabolism, making it a key clinical concern. Growth differentiation factor-15 (GDF-15), a transforming growth factor-β superfamily member, has broad target specificity and exerts diverse biological effects through multiple signaling pathways, drawing attention to its role in metabolic diseases. GDF-15 has been implicated in the regulation of osteoblast- and osteoclast-related processes. It is abnormally expressed in DOP patients and may be correlated with disease progression, potentially mediated by insulin resistance, hyperglycemic toxicity, ferroptosis, and inflammatory responses. Although some biological functions of GDF-15 have been elucidated, its specific pathways in this disease and clinical application value warrant further studies. This review summarizes recent advances in basic and clinical research, elucidates the pathophysiological mechanisms behind GDF-15 in DOP, and provides theoretical support and research directions for GDF-15-based targeted therapeutic strategies.

Medical therapy is the first-line treatment for lower urinary tract symptoms (LUTS) secondary to benign prostatic hyperplasia (BPH). However, predictors of treatment failure in men with small prostate volume (<30 ml) remain poorly defined. This study aimed to develop and temporally validate a simple bedside risk score for predicting medical therapy failure in this specific subgroup.

We performed a retrospective cohort study of 201 men aged ≥50 years with IPSS ≥8 and prostate volume <30 ml who started medical therapy between 2015 and 2025. Treatment failure was defined as surgical intervention, acute urinary retention or IPSS worsening by ≥4 points. Independent predictors were identified using multivariable logistic regression. A practical integer risk score was derived from the strongest predictors. Temporal validation was conducted by splitting the cohort chronologically (derivation set 2015-2020, n = 120; validation set 2021-2025, n = 81).

During a median follow-up of 24 months, 66 patients (32.8%) experienced treatment failure. Independent predictors included higher IPSS, greater BPH Impact Index, increased intravesical prostatic protrusion, lower maximum flow rate, higher post-void residual volume and diabetes mellitus. The bedside risk score stratified patients into low-risk (0-3 points: 11.0% failure), moderate-risk (4-7 points: 32.9%) and high-risk (8-13 points: 77.5%) categories. The model demonstrated good discrimination (AUC 0.789; bootstrap-corrected 0.782) and maintained strong performance in temporal validation (derivation AUC 0.799; validation AUC 0.821).

This novel bedside risk score reliably predicts medical therapy failure in small-volume BPH using readily available clinical parameters. It may enable early risk stratification and timely intervention, particularly in populations with high diabetes prevalence.

Whether pre-operative central sensitization (CS) affects post-operative outcomes after arthroscopic rotator cuff repair (ARCR) remains unclear. This study aimed to evaluate the potential association between pre-operative CS and post-operative pain and function for 2 years in patients who underwent ARCR for small-to-medium rotator cuff tears.

Sixty patients with small-to-medium full-thickness rotator cuff tears who underwent ARCR and were followed up for 24 months post-operatively were enrolled. The presence or absence of CS was evaluated using the Japanese version of the Central Sensitization Inventory (short form). Patients were divided into 2 groups according to the presence or absence of CS, with scores ≥10 defined as CS. Baseline demographic and radiologic factors (eg, smoking status, diabetes mellitus, occupation, tear size, and fatty infiltration) were recorded and compared between groups. Post-operative outcomes, including pain (numerical rating scale), shoulder range of motion, muscle strength, and clinical scores (Constant, American Shoulder and Elbow Surgeons), were assessed at 3, 6, 12, 18, and 24 months. Rotator cuff integrity was evaluated by magnetic resonance imaging (MRI) at 3, 6, 12, and 24 months post-operatively.

CS was present in 45% of patients. There were no significant differences in baseline demographic, clinical, or radiologic factors, as well as in pre-operative shoulder joint range of motion, strength, or pain between the groups with and without CS. Patients with CS exhibited significantly less improvement in pain on motion, abduction strength, and clinical scores at multiple time points up to 18 months; by 24 months, however, these differences had diminished.

Pre-operative CS may be associated with delayed improvement in post-operative motion-related pain and clinical scores after ARCR, although its long-term impact appears limited. Clinicians should consider pre-operative CS among factors that may affect post-operative functional recovery, particularly in the first 18 months, with no apparent difference by 24 months.

Diabetic retinopathy (DR), a complication of diabetes, damages microvascular of retina through various molecular pathways. Emerging evidence points to miRNAs as key players in progression of DR. This study aims to investigate whether miR-103a-3p contributes to pathological processes of DR through MFN2.

Serum samples were collected from type 2 diabetes mellitus patients and divided into NDR, NPDR, and PDR groups based on fundus lesions. miR-103a-3p levels in each group were quantified by qRT-PCR. ARPE-19 cells were cultured under high-glucose (HG). Cell viability and apoptosis rates were evaluated by CCK-8 assay and flow cytometry. Activities of MDA and GSH-Px were detected by specific kits. Luciferase reporter gene confirmed MFN2 as a direct target of miR-103a-3p.

Clinical sample detection revealed that miR-103a-3p levels were higher in NPDR and PDR patients compared to control and NDR groups, and it was an independent risk factor for DR. In vitro experiments confirmed that HG treatment greatly increased miR-103a-3p levels, decreased cell viability, accelerated apoptosis, elevated MDA content, and reduced GSH-Px activity, while transfection of miR-103a-3p inhibitor reversed these effects. Using luciferase reporter assay, we identified MFN2 as a direct target of miR-103a-3p. Moreover, rescue experiments demonstrated that silencing MFN2 effectively reversed the cell functions induced by miR-103a-3p inhibitor.

miR-103a-3p is upregulated in DR and accelerates its progression by directly targeting and inhibiting MFN2 expression. This study suggested the molecular mechanism of miR-103a-3p/MFN2 axis in DR, identifying a novel potential target for early diagnosis and therapy of DR.

Carotid artery plaque (CAP) and sarcopenia are notable complications in patients with type 2 diabetes mellitus (T2DM). This study aims to explore whether the inflammatory biomarkers neutrophil-to-lymphocyte ratio (NLR) and systemic inflammatory response index (SIRI) mediate the association between sarcopenia and CAP in such patients.

Sarcopenia was diagnosed using the criteria of the Asian Working Group for Sarcopenia (AWGS 2019), and CAP was assessed by carotid ultrasonography. Inflammatory biomarkers including NLR and SIRI were calculated, with their natural logarithm-transformed values (Ln-NLR, Ln-SIRI) derived. Restricted cubic spline (RCS) analysis, univariate and multivariate logistic regression analyses were used to investigate the associations among these inflammatory biomarkers, sarcopenia and CAP. Additionally, mediation analysis was performed to explore the mediating role of these inflammatory biomarkers.

A total of 749 patients with T2DM were enrolled in this study. The prevalence of CAP and sarcopenia in the study was 58.9% (n=441) and 33.9% (n=254), respectively. Patients with CAP had significantly higher levels of NLR, SIRI, and a higher prevalence of sarcopenia than those without CAP (all p < 0.05). RCS analysis revealed linear correlations of NLR and SIRI with both sarcopenia and CAP (all p for nonlinear > 0.05). Multivariate logistic regression analysis showed that sarcopenia (adjusted odds ratio (aOR) = 1.67, 95% confidence interval (CI): 1.10-2.54, p = 0.016), NLR (aOR = 1.63, 95% CI: 1.01-2.66, p = 0.047), SIRI (aOR = 1.23, 95% CI: 1.01-1.59, p = 0.046), Ln-NLR (aOR = 1.77, 95% CI: 1.10-2.80, p = 0.037), and Ln-SIRI (aOR = 1.38, 95% CI: 1.02-1.74, p = 0.035) were independently and positively associated with CAP. Mediation analysis further indicated that NLR and SIRI partially mediated the association between sarcopenia and CAP, with mediated proportions of 10.39% and 11.40%, respectively. Similarly, Ln-NLR and Ln-SIRI also exerted partial mediating effects, with mediated proportions of 9.73% and 9.29%.

Sarcopenia is an independently positively associated factor for CAP in patients with T2DM. NLR and SIRI may partially account for the association between sarcopenia and CAP.

Not applicable.