Athletes with diabetes increasingly participate in endurance running, benefiting from physiological adaptations and technological advances like continuous glucose monitoring (CGM) for glycemic control. So far, no comprehensive review summarizing the current knowledge has been performed. To identify the prevalence of long-distance runners with diabetes, their performance, methods used for blood glucose monitoring and glycemic control. PubMed, Medline Ovid, Scopus, SPORTDiscus, Cochrane databases, CINAHL, and Web of Science were systematically searched until April 2024 using key terms related to long-distance running and diabetes. An updated search applying the identical strategy was conducted on May 3rd, 2026, to capture subsequently published literature. This study included original research articles, case reports, and case studies published in English or German in peer-reviewed journals, utilizing both quantitative and qualitative methodologies. Eligibility criteria encompassed runners with a confirmed diagnosis of diabetes mellitus, irrespective of type, who participated in endurance events of at least half-marathon distance, including half-marathons, marathons, ultra-marathons, and other ultra-endurance competitions. Patients with prediabetic state, gestational diabetes, or after pancreatic islet-cell transplantation were excluded. For quality assessment, we used the Joanna Briggs Institute of Analytical Cross-Sectional Studies or the Joanna Briggs Institute of Analytical Case Report critical appraisal tool. A total of 656 studies were identified, with 22 meeting the inclusion criteria, comprising 99 runners with diabetes (99.0% Type 1, 1.0% Type 2 diabetes mellitus). Among them, 50.0% used CGM, 27.2% had an insulin pump, 63.6% administered insulin via multiple daily injections, and the method of insulin application was not specified in 7.0% of runners. The weighted mean HbA1c was 7.4% (95% CI 6.9-8.1). Time-in-range varied by race distance: 40-100% for half-marathoners, 51.6% for marathoners, and 47-73% for ultra-marathoners. No cases of symptomatic hypoglycemia were observed during the races. However, asymptomatic late-onset hypoglycemia (occurring 6-15 h post-exercise) was reported in 27 runners. The most common insulin adjustment strategy before competitive races was a 50-80% reduction of basal insulin. Despite limited research, evidence suggests that with proper preparation and multidisciplinary support, athletes with diabetes can safely participate in endurance events, including ultra-marathons, while maintaining stable glycemic control. PROSPERO-CRD42024539281.
Most people with type 2 diabetes have metabolic dysfunction-associated steatotic liver disease (MASLD), yet fewer than 2% experience major adverse liver outcomes within 10 years. Because progression to end-stage liver disease is uncommon, identifying the small subset of individuals at highest risk remains a central clinical challenge. Liver fibrosis is the strongest prognostic determinant in MASLD, and a range of blood-based and imaging tests are used to assess the likelihood of advanced fibrosis (AF) in the clinic. Since 2023, major medical societies have recommended systematic screening for MASLD-related AF in individuals with type 2 diabetes, driven by reports suggesting a high prevalence of up to 20-40%. This review critically examines the evidence underlying these recommendations while providing a clinically oriented guide to diagnosing MASLD in type 2 diabetes. Re-analysis of data from prevalence studies suggests that the burden of AF in type 2 diabetes has been substantially overestimated and may be below 5-10%, which has profound implications for both the rationale for screening and its expected yield. Simulations and emerging real-world evidence suggest that current non-invasive tests may refer 30-50% of patients for costly second-line testing and 15% for specialist evaluation, while generating high false-positive rates and missing more than a third of all AF cases. Moreover, it remains uncertain whether diagnosing AF in type 2 diabetes currently leads to meaningful changes in management or outcomes. Existing cost-effectiveness analyses rely on assumptions about disease burden and therapeutic benefit that are not supported by available data. Together, these considerations call for a more rigorous, evidence-based approach to evaluating liver disease risk in type 2 diabetes and other populations.
Diabetes mellitus is a major and growing contributor to morbidity and mortality. Indian Council of Medical Research-India Diabetes study reports a prevalence of 11.4% for diabetes and 15.3% for prediabetes in India. Diabetes is described in depth in ancient Ayurveda texts, from aetiology to pre-clinical, clinical features, complications, and its stage-wise management. The current study has the potential to explore whether lowering glycemic control at the level of haemoglobin affects endogenous insulin production by examining C-peptide and insulin levels. The current study is designed as a randomized, double-blind, placebo-controlled, multicenter, two-arm clinical trial enrolling 220 participants across two Indian sites. Adults with diagnosed Type-2 diabetes mellitus on oral hypoglycemic agents (OHAs) with glycated haemoglobin (HbA1c) between 8% and 10% will be randomized (1:1) to receive either an Ayurvedic Formulation, Varadi Kwath Ghana Vati, or a matched placebo, administered twice daily after meals as an adjunct to standard OHAs therapy for 180 days. The primary outcome is the mean change in HbA1c from baseline to 90 and 180 days. Secondary outcomes include the proportion of participants achieving optimal glycemic control, i.e., HbA1c ≤7%; changes in fasting C-peptide, fasting insulin, lipid profile, liver function tests, and renal function tests at baseline, 90, and 180 days. Treatment effects will be estimated as between-group differences in mean changes ± standard deviation (SD), reported with 95% confidence intervals, with statistical significance set at p < .05. Following the lead from the classical anti-diabetic action of Varadi Kwath ingredients, i.e., Haritaki (Terminalia chebula Retz), Bibhitaki [Terminalia bellirica (Gaertn.) Roxb.], Amalaki (Phyllanthus emblica L.), Daruharidra (Berberis aristata DC.), Musta (Cyperus rotundus L.), and Devdaru (Cedrus deodara Roxb. Ex D.Don). The drug will be evaluated through HbA1c and the indigenous production of C-peptide and insulin through the study. CTRI/2026/01/100208, Registered on: 02/01/2026, Registered Prospectively. © 2026 Wiley Periodicals LLC.
The risk of diabetic ketoacidosis (DKA) is increased following the severe acute respiratory syndrome coronavirus 2 infection, "COVID-19," however, little evidence is available regarding the prevalence and outcomes of DKA in newly diagnosed patients with diabetes in the Middle East and African countries. Our objective was to conduct a systematic review of case reports detailing the prevalence and outcomes of DKA in COVID-19 infected in the above referenced countries. Our search encompassed Medline (via PubMed), Embase (via OVID), Web of Science, Scopus, grey literature sources such as Open Access Theses and Dissertations (OATD), and the reference lists of the included studies. The results of the current meta-analysis study showed that 17 studies met the search criteria and a total of 22 patients (15 patients with newly type 1 diabetes and seven patients with newly diagnosed type 2 diabetes). About 69.5% of the patients were of Arabian ethnicity. Body mass index (BMI) was reported only for seven patients, with a mean of 25.04 k g/m2. Two patients died in patients with newly diagnosed type 2 diabetes, giving a mortality rate of 14.3%, while all patients were in type 1 diabetes, who had DKA survived. Covid 19 infection in patients with new diabetes from the Middle East and African countries was associated with increased risk of DKA with high mortality in patients with newly diagnosed type 2 diabetes.
The Diabetes Prevention Program (DPP) was a randomized clinical trial designed to prevent type 2 diabetes (T2D) in adults with prediabetes. The DPP Outcomes Study (DPPOS) is the 30-year follow-up of this cohort, focusing on T2D, prediabetes, and related complications. Cognitive assessments began in 2009 and expanded in 2022 to examine cognitive impairment, including Alzheimer's disease (AD) and AD related dementias (ADRD), in the surviving cohort. To support these aims, the National Alzheimer's Coordinating Center Uniform Data Set version 3 (NACC-UDSv3), the standardized framework used by Alzheimer's Disease Research Centers, was implemented in DPPOS in 2022 to enable data sharing with NACC. These forms were complemented by cognitive tests administered in DPPOS. We aimed to integrate the NACC-UDSv3 into the existing longitudinal DPPOS framework while maintaining fidelity to its structure and developing automated reports to streamline cognitive outcomes adjudication. Items from the 16 NACC-UDSv3 data forms were compared with those already collected within DPPOS to integrate overlapping similar items, add missing NACC-UDSv3 items, and create a dataset harmonized with NACC-UDSv3. Forms were adapted for electronic data capture (EDC) using the MIDAS (Multimodal Integrated Data Acquisition System, George Washington University). Automated reports integrated current and prior neuropsychological scores to support adjudications. In the first wave of the DPPOS-AD/ADRD study, 1561 cognitive adjudications were successfully completed using the harmonized DPPOS and NACC-UDSv3 data implemented into MIDAS. The DPPOS-AD/ADRD project demonstrated that NACC-UDSv3 can be successfully integrated into a long-standing longitudinal cohort not originally designed for AD/ADRD research. The harmonization, electronic capture, and automated adjudication processes may provide a practical framework for other cohorts seeking to incorporate NACC-UDSv3 to align with national AD/ADRD research standards.
Clinical trials of interventions to preserve beta cell function in new-onset type 1 diabetes frequently employ participant-reported outcome measures (PROMs). However, the expected changes in PROMs scores immediately following diagnosis and their association with residual beta cell function, metabolic markers and continuous glucose monitoring (CGM) are unclear. Repeated PROMs including Paediatric Quality of Life Inventory diabetes module (PedsQL) and hypoglycaemia fear survey (HFS) were recorded from participants aged 10-18 years with newly diagnosed type 1 diabetes and their parents in two clinical trials: CLOuD (N=97, hybrid closed loop [HCL] vs multiple daily injections [MDI]) and USTEKID (N=72, ustekinumab immunotherapy vs placebo). Scores were compared with serial mixed meal-stimulated C-peptide levels (AUC C-peptide), HbA1c and CGM data. PedsQL and HFS scores for children/adolescents and their parents showed wide variation between individuals but did not change substantially within individuals over the first 48 months from diagnosis. Baseline scores were highly predictive of scores at 12-48 months (p<0.001). PedsQL scores were higher (better) in those reported by children/adolescents than by their parents (p<0.01). In contrast, HFS scores were higher in parents than children (p<0.001), indicating more fear. Strong correlations were observed between child and parent scores (p<0.001). No significant improvement in these scores was detected following intervention (ustekinumab or HCL). Meta-analysis revealed modest but statistically significant associations between HbA1c and PedsQL (β(std)=-0.11; 95% CI -0.20, -0.03) and HFS (β(std)=0.11; 95% CI 0.00, 0.21), and between CGM time in range and PedsQL (β(std)=0.14; 95% CI 0.03, 0.26) but not HFS (β(std)=-0.05; 95% CI -0.16, 0.06). Beta cell function (AUC C-peptide) was strongly associated with HbA1c (β(std)=-0.29; 95% CI -0.39, -0.20) and CGM time in range (β(std)=0.41; 95% CI 0.30, 0.52). Higher beta cell function showed a trend towards better PedsQL (β(std)=0.11; 95% CI -0.03, 0.25) and lower HFS (β(std)=-0.05; 95% CI -0.17, 0.07) but this did not reach statistical significance. PedsQL and HFS scores changed little during the first 48 months after diagnosis of type 1 diabetes. These scores showed modest but statistically significant associations with measures of glucose management (HbA1c and CGM time in range), whereas the relationships with residual beta cell function (C-peptide) were weaker and did not reach significance. The modest size of these effects suggests current PROMs capture only limited aspects of the clinical benefit associated with beta cell preservation. Future research should incorporate psychometric instruments that are specifically adapted for young people using modern diabetes technologies and undergoing disease-modifying therapy, to ensure outcomes are meaningfully represented in early-stage type 1 diabetes trials.
Type 1 diabetes and disordered eating (T1DE) affects 8-37.1% of adults and is associated with high rates of morbidity and mortality. The absence of a standardised case definition of T1DE and its severity hinders effective screening, diagnosis and treatment. This systematic review aimed to (1) synthesise existing case definitions and diagnostic criteria for T1DE in adults and (2) identify key characteristics to inform consensus for future diagnostic criteria. A systematic review was conducted following the Preferred Reporting Items for Systematic reviews and Meta-Analysis (PRISMA) guidelines. Eligible studies involved adults (≥18 years) with type 1 diabetes assessing disordered eating; paediatric studies, mixed samples without disaggregated data, non-empirical designs and non-English publications were excluded. PubMed, MEDLINE, EMBASE, CINAHL and PsycINFO were searched up to November 2025 for peer-reviewed studies involving adults with T1DE. Qualitative and quantitative data on definitions, diagnostic criteria and assessment tools were extracted. Study quality was appraised using a modified Graphical Appraisal Tool for Epidemiological studies (GATE) checklist. Due to heterogeneity of data, a narrative synthesis of findings was performed to describe current definitions of T1DE. Sixty-one studies met the inclusion criteria, with a pooled sample of 111,208 participants (76% women) from over 22 countries. T1DE was defined using a heterogeneous array of terms, diagnostic frameworks and assessment tools (29 distinct methods). The Diabetes Eating Problem Survey-Revised (DEPS-R) was the most used questionnaire, but many studies relied on criteria adapted from general eating disorder classifications or generic questionnaires. Approximately three-quarters of the studies assessed insulin omission behaviours, but the operationalisation of the cognitions for insulin omission varied widely. Beyond physiological markers such as HbA1c and BMI, studies explored various diabetes-related and psychological constructs, although often considering diabetes and disordered eating separately rather than as an integrated condition. This systematic review highlights the lack of a unified, evidence-based definition of T1DE, resulting in inconsistent screening, diagnostic and reporting practices. Establishing clear, consistent, evidence-based diagnostic criteria and screening questionnaires for T1DE is critical to improving early detection and developing targeted interventions. These findings provide a foundation for refining T1DE definitions as a stepping stone to an international consensus definition. PROSPERO registration no. CRD420250223622 FUNDING: King's College London and King's College Hospital through the KMRT KCH Joint Research Committee studentship. This work was also conducted as part of the National Institute for Health Research (NIHR; CS-2017-17-023)-funded STEADY project (Safe management of people with Type 1 diabetes and EAting Disorders studY). NZ's salary was part-funded by the NIHR via the NIHR Clinician Scientist award to MS; JT and KI are part-funded by the NIHR Mental Health Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King's College London. MS was funded through her NIHR Clinician Scientist Fellowship (CS-2017-17-023).
Background and Objectives: Diabetes mellitus is a major systemic modifier of oral infection, periodontal inflammation, and tissue healing. Persistent hyperglycemia may intensify oxidative stress, immune dysfunction, dysbiotic biofilm activity, and advanced glycation end-product/receptor signaling, thereby reducing the predictability of periapical and periodontal healing. In patients with endo-periodontal lesions, these mechanisms may interact with pulpal infection and periodontal breakdown, complicating diagnosis, prognosis, and therapeutic sequencing. This review summarizes current evidence on diabetes, glycated hemoglobin (HbA1c), and endo-periodontal outcomes and proposes an HbA1c-guided clinical framework for risk stratification and treatment planning. Materials and Methods: A structured narrative review with an expert-informed clinical framework was conducted using the literature published between January 2016 and December 2025. Eligible sources included consensus reports, clinical practice guidelines, systematic reviews, meta-analyses, umbrella reviews, randomized and non-randomized clinical studies, observational studies, and selected mechanistic studies or contemporary narrative reviews with direct relevance to the framework. Case reports, animal studies, and in vitro investigations without direct relevance to the clinical framework were excluded from the main synthesis. Results: Diabetes is associated with increased periodontal severity, impaired periodontal treatment response, a higher prevalence of radiolucent periapical lesions in root-filled teeth, delayed periapical healing, and increased non-retention of endodontically treated teeth. Periodontal therapy is safe in diabetic patients and may be associated with modest reductions in HbA1c, especially when baseline metabolic control is poor. Conclusions: HbA1c should complement, not replace, pulpal testing, periodontal charting, and radiographic assessment. The proposed framework prioritizes endodontic infection control when pulpal necrosis or active intracanal infection is present, adapts periodontal intervention to metabolic risk, and postpones elective surgical or regenerative procedures in poorly controlled diabetes until medical stabilization is achieved.
Type 1 diabetes (T1D) impacts more than 9 million individuals globally. Despite a century since the isolation and clinical introduction of insulin, exogenous insulin injections remain the primary form of treatment for T1D. While continuous glucose monitoring systems and optimized insulin delivery reduce life-threatening hypoglycemic events, they do not provide a permanent cure. Transplantation of pancreatic islets offers a potential long-term solution. Recent advances in stem cell-derived islets (SC-islets) have shown remarkable promise in both clinical and research settings. This article highlights recent clinical reports in the use of SC-islets to restore islet function and their versatility as a platform for disease modeling and drug screening while emphasizing current strategies aimed at overcoming their limitations and enhancing their therapeutic potential. We also discuss exciting emerging approaches that expand investigations beyond pancreatic endocrine cells to encompass nonendocrine cell types in the pancreas, offering a unique bird's-eye view into pancreatic biology and insights into cellular cross talk in health and disease. Our aim is for this article to serve as a resource for up-to-date advances in SC-islet research and to highlight novel platforms for studying diabetes pathogenesis in unprecedented ways, accelerating progress toward a permanent cure. Stem cell-derived islets provide a renewable source of insulin-producing cells for studying diabetes and developing regenerative therapies. Stem cell-derived islets are still functionally immature in comparison with primary human islets, underscoring the need for deeper insights into β-cell biology to improve their fidelity. Nonetheless, they serve as a powerful platform for diabetes disease modeling. Emerging technological advances, including spatial multiomics and multicellular organoid development, are revealing key roles for non-β-cell and nonislet cell types in pancreatic diseases. Integrating these emerging tools is critical for broadening our understanding of diabetes pathophysiology and may enable us to view the disease from previously unexplored perspectives.
Continuous glucose monitoring (CGM) has increasingly been incorporated into studies examining cognitive function in people with diabetes. This scoping review systematically maps how CGM has been applied in cognitive research among individuals with diabetes to characterize current methodological approaches, identify key knowledge gaps, and inform future research. A scoping review was conducted following Arksey and O'Malley's framework. A systematic search of five electronic databases (PubMed, CINAHL, Cochrane Library, EMBASE, PsycINFO) was performed. Cognitive outcomes were extracted and mapped to the International Classification of Functioning, Disability and Health framework. Twenty-one studies met the inclusion criteria. CGM data completeness was consistently high, with 84-100% of expected CGM data captured, supporting the feasibility of intensive glucose monitoring in cognitive research in diabetes. Considerable heterogeneity was observed in cognitive domains and assessment tools. Most studies evaluated executive function, memory, and attention, whereas psychomotor, language, and perceived cognitive functions were less frequently assessed. More than 10 distinct instruments were used to assess memory and executive function. Across studies, similar cognitive domains were examined regardless of the specific CGM metrics employed. Research examining CGM and cognitive function in diabetes is characterized by substantial methodological variability in both CGM metrics and cognitive assessments. These findings underscore the need for greater standardization to improve cross-study comparability and to advance CGM-informed cognitive research, including the development of personalized interventions to support cognitive health through optimized glucose management in people with diabetes.
Diabetes care is characterized by the widespread use of plastics. With plastic-associated endocrine-disrupting chemicals (EDCs) implicated in diabetes pathogenesis, this review examines how medical plastics relate to diabetes and related disorders and proposes interventions to improve the situation. Plastic-associated EDCs and micro-/nanoplastics (MNPs) are linked to metabolic dysfunction. Medical care exposes patients to these agents; however, the precise contribution of diabetes care to these exposures and their associated adverse health effects remains poorly defined. Diabetes care is an increasingly important contributor to plastic pollution and climate change, yet inadequate systems exist to mitigate its environmental impact. Plastic-associated EDCs and MNPs remain an underappreciated metabolic health threat. Mitigating the deleterious impacts of plastics on human and planetary health requires concerted actions from manufacturers, scientists, policymakers, professional organizations, healthcare providers, and patients. Doing so has the potential to improve metabolic health and promote health equity.
Background and Objectives: Atrial fibrillation (AF) and related arrhythmias carry a substantial psychosocial burden that current cardiology guidelines do not systematically address. Whether economic strain and type 2 diabetes mellitus (T2DM) cluster with high perceived stress in arrhythmia outpatients remains untested in Arab populations. The objective of this study was to estimate the prevalence of high perceived stress and to identify its independent sociodemographic and clinical correlates in Saudi outpatients with cardiac arrhythmia, with an a priori focus on income insufficiency and type 2 diabetes mellitus. Materials and Methods: Between December 2025 and January 2026, 282 adults with clinician-documented arrhythmia attending a tertiary cardiology clinic in Saudi Arabia completed a structured questionnaire including an Arabic 10-item Perceived Stress Scale (PSS-10) previously validated in Arabic-speaking populations. High perceived stress was defined as a PSS-10 score of 20 or higher. A theoretically specified multivariable logistic regression with Firth penalisation identified independent correlates. Three sensitivity analyses were prespecified, and the latent structure of the Arabic PSS-10 was examined by split-sample exploratory and confirmatory factor analysis. Reporting follows the Strengthening the Reporting of Observational Studies in Epidemiology (STROBE) statement. Results: Sixty-nine participants (24.5%; 95% confidence interval [CI], 19.7-29.9) met the high-stress threshold (mean PSS-10 15.5; standard deviation [SD] 9.1). Income insufficiency (adjusted odds ratio [aOR] 2.09; 95% CI, 1.16-3.78; p = 0.014) and T2DM (aOR 2.51; 95% CI, 1.39-4.55; p = 0.002) were independently associated with high perceived stress; age and sex were not. The Arabic PSS-10 showed a two-factor structure (62.8% common variance) with acceptable confirmatory fit (root mean square error of approximation [RMSEA] = 0.078; 90% CI, 0.058-0.098; comparative fit index [CFI] = 0.945; Tucker-Lewis index [TLI] = 0.927; standardised root mean square residual [SRMR] = 0.052) and excellent reliability (Cronbach's α = 0.92). Conclusions: Roughly one in four Saudi outpatients with cardiac arrhythmia reports high perceived stress. The burden concentrates among those with income insufficiency or T2DM. Brief PSS-10 screening paired with onward referral to financial-navigation and diabetes-distress support warrants prospective evaluation as a low-cost, scalable component of routine arrhythmia care, with longitudinal designs needed to establish temporal sequence and intervention efficacy.
Determine whether and how alternative payment models (APMs) impact diabetes care and outcomes. Explain what APMs are and highlight key principles of effective APMs. Provide a conceptual model for how APMs can support transformation to evidence-based population health delivery models that improve diabetes outcomes. Advanced APMs with shared savings or global budgets, along with quality incentives, tended to improve diabetes and composite chronic condition outcomes, and can reduce Medicare Part A hospital and Part B outpatient costs. Advanced APMs, particularly models with global budgets that hold health care organizations accountable for total cost of care and quality of care, can improve diabetes outcomes and reduce costs. Careful design and implementation of APMs are essential to provide the appropriate mix of incentives, support, and risk for participants to succeed in APMs and develop effective population health management models.
Annexin A5 (ANXA5) is a Ca2+-dependent phosphatidylserine (PS)-binding protein classically employed as an apoptosis biomarker. Accumulating evidence now positions ANXA5 as a multifunctional regulator of membrane homeostasis, immunometabolism, and cellular adaptation to metabolic stress across the spectrum of diabetes mellitus (DM). This review synthesizes current mechanistic and translational insights identifying ANXA5 as a candidate molecular determinant of diabetic pathophysiology. Its conserved α-helical architecture and dual-promoter transcriptional regulation enable reversible, high-affinity PS binding and assembly of a two-dimensional (2D) crystalline lattice that underpins its diverse biological functions. In the pancreas, ANXA5 has been shown to inhibit islet amyloid polypeptide (IAPP) aggregation and shields β-cell membranes from amyloid-induced injury; it has also been proposed to modulate mitochondrial Ca2+ homeostasis via VDAC1-associated pathways. In insulin-responsive peripheral tissues, ANXA5 has been hypothesized to modulate insulin signaling fidelity and facilitate glucose uptake through putative IRS-1 interactions and lipid raft stabilization, although direct in vivo validation remains outstanding. In the diabetic endothelium, hyperglycemia-induced dysfunction of acid sphingomyelinase impairs ANXA5-mediated membrane resealing, thereby precipitating Ca2+ overload, inflammasome activation, and a prothrombotic state. Experimental studies further suggest that ANXA5 may promote M2 macrophage polarization and suppress TGF-β/Smad2/3 signaling, indicating potential roles in immunomodulation and fibrosis attenuation. Importantly, distinct disease contexts shape ANXA5 biology: in T2D, glucolipotoxic stress and IAPP aggregation drive ANXA5-dependent protective responses, whereas in T1D, circulating anti-ANXA5 autoantibodies may neutralize membrane-protective functions and amplify vascular injury risk. Emerging translational applications include recombinant ANXA5 (NEXUS) and Diannexin, although prospective clinical validation remains limited. To facilitate interpretation of the literature, we introduce an evidence-grading framework that distinguishes diabetes-validated mechanisms from biologically supported, incompletely validated, and speculative pathways.
Immune checkpoint inhibitors are widely used in the treatment of malignant tumors. Although the incidence rate of type 1 diabetes induced by these inhibitors is low, the damage to pancreatic β cells is irreversible and the treatment effect of steroids is poor, which requires clinical attention. This article reports a case of a 69-year-old patient with poorly differentiated adenocarcinoma of the stomach and colon who developed this disease during treatment with Sintilimab combined with the SOX regimen. After insulin treatment, her blood glucose levels gradually stabilized. Based on the literature, we explore the pathogenesis, diagnostic difficulties, and current treatment status centered around insulin replacement therapy. We emphasize the need for clinicians to strengthen blood glucose monitoring during treatment with immune checkpoint inhibitors, identify symptoms early, and optimize diagnosis and treatment to improve patient prognosis.
To address the systemic financial and equity burdens of preventable diabetes-related lower-extremity amputations, this perspective evaluates current structural failures in US healthcare financing and proposes a scalable, prevention-oriented framework. Current fee-for-service models consistently reimburse expensive disease deterioration while neglecting early surveillance. Meanwhile, omitting preventive foot metrics from federal quality frameworks renders early intervention organizationally invisible. In response, this analysis incorporates data from a peer-reviewed, 5-year implementation study within a medically complex population using low-overhead, multilingual, digital patient education and risk-stratified surveillance. This low-friction intervention model achieved a diabetic foot ulcer rate of 2.8% and a major amputation rate of 0.43%, significantly outperforming the federal Healthy People 2030 benchmark of 0.55%. To replicate these results nationally, public payers must integrate risk-stratified podiatric surveillance into core quality reporting frameworks, expand reimbursement codes for asynchronous digital education, and formally classify patient-centered education as vital health infrastructure. Such policy prioritization will mitigate profound health disparities, reduce avoidable public spending, and preserve patient mobility.
Immune checkpoint inhibitors-induced diabetes mellitus (ICI-DM) is a rare but potentially life-threatening endocrine immune-related adverse event, often characterized by abrupt onset of insulin deficiency and frequent presentation with diabetic ketoacidosis and difficulty with daily management with the available therapies. Lung cancer patients represent a substantial proportion of reported cases, reflecting the widespread use of PD-1/PD-L1 inhibitors in thoracic oncology. We report on the case of an elderly patient with metastatic lung adenocarcinoma treated with pembrolizumab who developed severe DM requiring permanent insulin therapy and leading to treatment discontinuation. The patient was subsequently followed over a prolonged period, during which oncological disease remained under sustained control despite immunotherapy interruption. We describe the clinical course, diagnostic workup, and multidisciplinary management, and review current guideline recommendations addressing acute metabolic management, diabetic treatment, and decision-making regarding continuation of immunotherapy. This case highlights the complexity of managing ICI-DM in real-world clinical practice. The current guidelines may help in broad terms. Although guidelines have been published, they remain cursory. Nevertheless, therapeutic decisions should ultimately be individualized through close multidisciplinary collaboration.
Gestational diabetes (GDM) is a frequent health problem associated with both short- and long-term adverse outcomes for mother and child. Standard management includes lifestyle interventions and, when necessary, pharmacologic therapy. However, the effectiveness and timely initiation of pharmacological therapy depend on accurate glucose monitoring. Continuous glucose monitoring (CGM) systems have emerged as valuable tools in diabetes care, providing real-time information on glycemic variability and enabling more individualized therapeutic interventions. In this narrative review, we explore the role of CGM in the early detection of dysglycemia, its diagnostic and prognostic value, and its ability to identify specific glycemic patterns during pregnancies complicated by GDM. We also assess its role in optimizing lifestyle interventions and guiding pharmacotherapeutic strategies. Current evidence suggests that CGM supports clinical decision-making and patient engaging by providing real-time glucose data. This facilitates earlier identification of hyperglycemic patterns, more precise treatment changes and improved glucose control. Furthermore, CGM use has been associated with improved neonatal and maternal outcomes. Despite these promising findings, barriers such as cost and limited access persist. Although the existing evidence remains relatively limited, it supports the integration of CGM into routine care of women with GDM as part of a comprehensive and personalized treatment strategy. Larger clinical trials are needed to fully understand the benefits and optimal use of CGM in GDM, as well as its impact on pregnancy outcomes, glycemic control and psychological well-being.
To assess the effect of tirzepatide, a glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide agonist, on cardiovascular outcomes and mortality in subjects with overweight/obesity, or type 2 diabetes mellitus (T2DM). We searched MEDLINE, Embase and CENTRAL up to January 14, 2026, selecting randomized controlled trials studying tirzepatide in adults with T2DM or overweight/obesity with a minimum follow-up of 24 weeks. We independently extracted data and assessed risk of bias and quality of evidence. We conducted meta-analysis using a fixed-effects model. Trial sequential analysis (TSA) was employed to assess if current information support definitive conclusions. We included 22 trials encompassing 29,023 participants. Overall risk of bias was low. Tirzepatide was associated with a reduction in MACE (OR 0.87, 95% CI 0.79-0.94; high certainty); TSA estimated that sample size was sufficient for definitive conclusions. A dose-response association was observed, with 2.8% lower odds of MACE for every 1 mg increase in tirzepatide dose. Tirzepatide was associated with a reduction in all-cause mortality (OR 0.84, 95% CI 0.75-0.93), however no association was observed for individual components of MACE or heart failure hospitalizations. Tirzepatide is associated with a significant reduction in MACE in subjects with T2DM or overweight/obesity.
The identification of reliable biomarkers of ageing represents a major challenge in biomedical research, particularly in the context of increasing life expectancy and the growing burden of chronic diseases. Among potential candidates, the ABO blood group system has attracted interest as a stable genetic trait potentially associated with inter-individual variability in ageing-related outcomes. This narrative review critically examines current evidence linking ABO blood groups to age-related diseases and biological mechanisms of ageing. A structured search of major biomedical databases was performed, focusing primarily on studies published in the last five years and complemented by seminal earlier reports. Current findings indicate associations between ABO phenotypes and several chronic conditions, including cardiovascular disease, thrombotic disorders, diabetes, cancer, allergies, and cognitive disorders, which substantially contribute to morbidity and mortality in older adults. However, data are contradictory and dependent on ethnicity, genetic background and environmental factors. Non-O blood groups consistently exhibit a higher risk of thrombotic and cardiovascular events, likely mediated by differences in coagulation factors, endothelial function, and hemostatic balance. ABO-related phenotypic variation may also influence processes implicated in ageing, including vascular dysfunction, chronic low-grade inflammation, immune remodeling, glycosylation pathways, cellular senescence, and host-microbiome interactions. However, evidence supporting a direct relationship between ABO blood groups and longevity remains inconsistent and appears to be population dependent. Overall, current data suggest that ABO blood groups are unlikely to represent independent biomarkers of ageing, but rather modest, context-dependent modifiers of biological pathways contributing to susceptibility to age-related diseases. Further longitudinal and mechanistic studies are needed to clarify their role in healthy and pathological ageing trajectories. SUMMARY: ABO blood group system has been associated with susceptibility to several age-related diseases (ARDs). Non-O blood groups show a higher risk of thrombotic and cardiovascular events. Although some studies also suggest a relationship between ABO phenotype and longevity, findings remain inconsistent and appear to vary across populations. Potential mechanisms linking ABO blood groups to ageing include effects on inflammation, vascular function, immune responses, and host-microbiome interactions. Overall, current evidence indicates that ABO blood group is unlikely to represent an independent biomarker of ageing, but rather a modest and context-dependent factor that can influence aging-related mechanisms and contribute to the ARD development.