Immune checkpoint inhibitors (ICIs) significantly improve prognosis and survival outcomes in cancer patients by enhancing immune function, thereby providing new therapeutic hope for cancer patients. However, with the widespread clinical application of ICIs, an increasing number of immune-related adverse events (irAEs) have been reported. Immune checkpoint inhibitor-induced type 1diabetes mellitus (ICI-T1DM) is a rare but potentially life-threatening irAE, usually presenting as acute onset and easily progressing to diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar state (HHS), which poses a serious threat to patients' safety. This study reports a case of DKA in an 81-year-old female patient diagnosed with cervical squamous cell carcinoma without history of diabetes mellitus, which developed after multiple cycles of Cadonilimab. The patient's blood glucose levels were effectively controlled via insulin therapy and fluid resuscitation, and a definitive diagnosis of ICI-T1DM was confirmed. Taking this case as a starting point, this article reviews the epidemiology, clinical characteristics, pathogenesis, and clinical management strategies of ICI-T1DM, aiming to enhance clinicians' awareness of ICI-T1DM, especially the endocrine toxicity of dual-target ICIs such as cadonilimab, and provide practical reference for ensuring the safety of ICI therapy in cancer patients.

Hemoglobin A1c (HbA1c) is a critical biomarker used for the diagnosis and management of diabetes. However, nonglycemic genetic variations may affect the accuracy of HbA1c measurements.

We presented a clinical evaluation of a type 2 diabetic patient with an SLC4A1 (solute carrier family 4 member 1) gene mutation, characterized by high blood glucose and low HbA1c, and estimated the carrier frequency of SLC4A1 variants in Chinese population.

A 56-year-old patient with type 2 diabetes presented with a low HbA1c level, an elevated glycated albumin percentage (GA), normal hemoglobin and albumin levels, hemolysis, and increased red blood cell osmotic fragility. Exome sequencing revealed a heterozygous mutation in SLC4A1 gene (c.1239_1241del), which is associated with hereditary spherocytosis. Further research indicates that around 0.756% of individuals in China carry pathogenic or likely pathogenic SLC4A1 variants.

We report the SLC4A1 c.1239_1241del variant, which perturbs HbA1c via nonglycemic mechanisms, likely through a reduction in the erythrocyte lifespan, and similar variants may not be rare in Chinese population.

At the start of the COVID-19 pandemic, there were concerns that some antidiabetic medications might worsen outcomes, though anti-inflammatory properties suggested possible benefits. Many observational studies examined antidiabetic medications use and COVID-19 outcomes. Meta-analyses showed that insulin was linked to worse outcomes, while metformin, sodium-glucose cotransporter 2 (SGLT-2) inhibitors, and glucagon-like peptide-1 (GLP-1) agonists were associated with better outcomes. Findings on dipeptidyl peptidase-4 (DPP-4) inhibitors, pioglitazone, and sulfonylureas were mixed-showing neutral, beneficial, or negative effects. However, randomized controlled trials (RCTs) testing these medications after SARS-CoV-2 infection found no effect on COVID-19 outcomes, implying that their anti-inflammatory effects do not translate into meaningful clinical benefits during acute infection. This discrepancy prompts questioning what observational studies actually measured. Given that many studies applied robust statistical methods, their results are unlikely solely due to confounding or indication bias. We hypothesize that these studies reveal broader cardiovascular effects and illuminate diabetes management more than they inform COVID-19 pathology. Their findings align with current 2022 American Diabetes Association/European Association for the Study of Diabetes (ADA/EASD) consensus guidelines for the management of type 2 diabetes mellitus endorsing metformin, SGLT-2 inhibitors, and GLP-1 agonists as first-line therapies, recommending cautious early insulin use, and reserving DPP-4 inhibitors, sulfonylureas, and pioglitazone for selective cases. This is applicable regardless of COVID-19 status. Further research should determine whether infection-related clinical endpoints, such as mortality or hospitalization from COVID-19 or other infections, might serve as valid surrogate markers for cardiovascular outcomes.

This study aimed to evaluate the clinical characteristics, symptom presentation, and management outcomes of patients diagnosed with paroxysmal supraventricular tachycardia (PSVT) at King Hamad University Hospital (KHUH), a tertiary care center. It examined the influence of demographics, comorbidities, and sex on treatment responses to pharmacologic and non-pharmacologic interventions, including cardioversion.

A retrospective observational study was conducted on 427 adult patients with PSVT (ICD-10: I47.1, confirmed by chart review) between January 2018 and early 2024. Data were extracted from the KHUH HOPE electronic medical records system. Descriptive statistics summarized baseline characteristics; chi-square tests examined categorical associations. Kaplan-Meier analyses for the cardioversion subgroup (n = 18) are presented as exploratory and descriptive only.

Females comprised 56.9% of the cohort (mean age 52.8 ± 15.2 years). Palpitations were the most common symptom (94.4%). Of 219 patients who received adenosine, 177 (80.8%) achieved cardioversion with the first dose, 25 (11.4%) with the second, and 17 (7.8%) with the third. Vagal maneuvers showed reduced success in patients with structural heart disease and diabetes mellitus. Electrical cardioversion was required in 18 patients (4.2%). Pacemaker implantation was documented in 3 patients (0.7%) for co-existing conduction disease, not as a PSVT treatment. Comorbidities significantly influenced outcomes: hypertension was associated with favorable vagal maneuver response, while heart failure and ischemic heart disease correlated with poor response across all modalities.

PSVT generally responds well to first-line treatments. However, individualized strategies are warranted for patients with structural heart disease or significant comorbidities. Observed sex-based and age-related response differences are descriptive and require multivariable validation.

Type 1 diabetes mellitus (T1DM) involves autoimmune β-cell destruction, but insulin resistance may also influence disease outcomes. Vitamin D modulates insulin sensitivity and immune function, and hypovitaminosis D is common in T1DM. This systematic review evaluates clinical and mechanistic evidence on the association between hypovitaminosis D and insulin resistance in T1DM. A Preferred Reporting Items for Systematic Reviews and Meta‑Analyses (PRISMA) framework was applied for a systematic search of PubMed^®, BMJ Journals, Scopus^®, IEEE Xplore^®, and Web of Science™, including articles published until 7 March 2026. Studies assessing vitamin D status and insulin resistance measures in T1DM populations were included. Risk of bias was evaluated using the Cochrane Risk of Bias 2 tool and the Newcastle-Ottawa Scale. Narrative synthesis was performed due to methodological heterogeneity. Eight studies (one controlled trial, two prospective cohorts, and five cross-sectional) were included. Hypovitaminosis D prevalence ranged from 47 to 79%. Six studies reported significant associations between low vitamin D levels and markers of insulin resistance, including a positive correlation with estimated glucose disposal rate (eGDR), as well as associations with higher insulin requirements and greater odds of insulin resistance. Mechanistic studies demonstrated preserved β-cell function with sufficient vitamin D and identified vitamin D receptor (VDR) polymorphisms as effect modifiers. Supplementation trials showed conflicting results, and longitudinal analysis revealed no significant association over time. Risk of bias was low in one study, good in five, and fair in two. Hypovitaminosis D is prevalent in T1DM and associated with insulin resistance in cross-sectional studies, with supportive mechanistic evidence. However, interventional and longitudinal data remain inconsistent. Vitamin D may be a marker of metabolic dysregulation, but its therapeutic role in improving insulin resistance requires further robust investigation.

This study aims to assess the predictive value of dietary antioxidants in diabetes-cancer comorbidity using interpretable machine learning (ML) models and to identify key clinical factors. Data were sourced from the National Health and Nutrition Examination Survey (NHANES) 2007-2010 and 2017-2018 cycles, including 44 dietary antioxidants, as well as demographic, lifestyle, and health-related features. 8 ML models (Random Forest, light Gradient Boosting Machines [LightGBM], Logistic Regression, Decision Tree, Multilayer Perceptron, Naïve Bayes, Kernel k-Nearest Neighbors, and Support Vector Machine with Radial Basis Function) were trained, with preprocessing steps for multicollinearity, class imbalance (SMOTE), and data normalization. Model performance was evaluated using AUC, accuracy, Brier scores, and calibration plots. SHapley Additive exPlanations (SHAP) values were applied to interpret feature importance. Data from 8644 participants were analyzed, including 272 individuals with confirmed diabetes-cancer comorbidity. After removing collinear features, the ML model included 30 dietary antioxidant features and 10 baseline features. The Random Forest model achieved optimal performance (AUC = 0.996, accuracy = 0.978, brier score = 0.0241), followed by LightGBM (AUC = 0.993). SHAP analysis revealed that while advanced age, cardiovascular disease, and hypertension were the primary drivers of comorbidity probability, dietary antioxidants are also influential factors. Specifically, polyphenols (daidzein, malvidin, pelargonidin, cyanidin) and essential minerals (magnesium) emerged as the most influential nutritional features. The high accuracy of the Random Forest and LightGBM models underscores their clinical utility in risk stratification for diabetes-cancer comorbidity. While advancing age and cardiometabolic dysfunction primarily drives the probability of diabetes-cancer comorbidity. This study establishes dietary antioxidants, particularly polyphenols such as daidzein and malvidin, as predictive factors for diabetes-cancer comorbidity.

Diabetes is a significant disease that affects individuals of all ages and may lead to the development of systemic and ocular complications, ultimately resulting in a poor quality of life (QoL). The use of health-related quality of life (HRQoL) measures is important for identifying disparities and those at risk, thereby promoting early intervention. This study aimed to examine the HRQoL and associated factors in Ghanaian children and adolescents with type 1 diabetes mellitus (T1DM).

A cross-sectional study involving children and adolescents with T1DM aged 5-19 years was conducted. Demographic and clinical data of participants were recorded. Participants completed the PedsQL Generic Scales questionnaires. SPSS Version 25.0 was used in analyzing the data. Logistic regression was used in analyzing risk factors associated with poor QoL. p-values < 0.05 were considered statistically significant.

Data from 46 children and adolescents with T1DM were analyzed. A female preponderance of 35/46 (76.1%) was observed. The overall mean HRQoL score for participants was 73.9 ± 18.7. Sex was the only risk factor associated with poor self-reported HRQoL in children and adolescents with T1DM. Female children and adolescents with T1DM were 13 times more likely to have poor self-reported HRQoL compared with their male counterparts (OR = 13.2; 95% CI = 1.9-91.0; p = 0.009). There were no significant associations with age, duration of diabetes, glycemic control, number of hypoglycemic and diabetic ketoacidosis episodes, hypertension, or nephropathy.

Self-reported QoL of children and adolescents with T1DM was poor. Female children and adolescents with T1DM are more likely to have poor self-reported QoL.

Metformin is derived from the plant Galega officinalis with the blood-glucose-lowering properties. Although its early development was hindered by the toxicity issues associated with other guanidine derivatives and the rise of insulin therapies, it ultimately established its position as a first-line oral hypoglycemic agent for addressing insulin resistance and managing hyperglycemia through extensive clinical validation. With a nearly 70-year history in diabetes treatment, the mechanisms by which metformin modulates blood glucose have been widely studied and refined. Recent investigations into combination therapies, fixed-dose formulations, and novel applications underscores a broader therapeutic potential beyond glycemic control. This paper aims to review the development trajectory of metformin, consolidate the latest evidence for its clinical benefits, and critically appraise its future directions and constraints.

Objective biomarkers that reflect systemic inflammation in pediatric allergic rhinitis to support clinical diagnosis. We aimed to evaluate serum levels of endocan (a marker of endothelial activation) and eosinophil-derived neurotoxin (EDN; reflecting eosinophil degranulation) in children with AR and investigate their diagnostic performance and associations with disease severity and conventional inflammatory markers. In this prospective case-control study, 85 children with AR and 67 healthy controls were enrolled. Serum endocan and EDN were measured via sandwich ELISA. Primary outcomes included group comparisons of biomarker levels and their diagnostic accuracy determined by receiver operating characteristic (ROC) curve analysis. Serum endocan and EDN levels were significantly elevated in children with AR compared to controls (both p < 0.001). Both biomarkers demonstrated high diagnostic performance, with an area under the curve (AUC) of 0.931 for endocan and 0.929 for EDN, showing greater diagnostic accuracy than absolute eosinophil counts (AUC, 0.871). Endocan and EDN showed a strong intercorrelation (r = 0.88, p < 0.001) and significant positive correlations with total IgE and eosinophil counts. However, no significant associations were observed between these biomarkers and disease severity, symptom control scores, or allergen sensitization patterns.

Serum endocan and EDN are significantly elevated in children with AR and demonstrate high diagnostic discrimination in this cohort. These findings suggest that endocan and EDN may serve as promising complementary biomarkers for the objective assessment of allergic inflammation in children, although further multicenter studies are needed to confirm their clinical utility.

• Allergic rhinitis (AR) is common in childhood and involves systemic inflammatory pathways; however, objective biomarkers to support diagnosis in pediatric practice remain limited. • Endocan and eosinophil-derived neurotoxin (EDN) reflect endothelial activation and eosinophil degranulation, respectively, and have been studied in other atopic and inflammatory conditions.

• This study concurrently evaluates serum Endocan and EDN in children with AR in a prospective case-control design. • Both biomarkers demonstrated high discriminatory performance (AUC∼ 0.93 in this cohort) and showed greater diagnostic accuracy than absolute eosinophil counts . • Endocan and EDN are largely independent of generalized systemic inflammatory indices (NLR, SII, SIRI), supporting specificity for the endothelial- eosinophilic axis in pediatric AR.

Chronic inflammation plays a pivotal role in carcinogenesis, particularly in upper gastrointestinal (UGI) cancers. However, the contribution of dietary inflammation to UGI cancer risk in the Chinese population remains insufficiently explored. This study investigated the association between energy-adjusted dietary inflammatory index (E-DII) and UGI cancer incidence in high-risk regions of China.

This prospective cohort study included 43,153 participants enrolled between 2017 and 2019 in the National Cohort of Esophageal Cancer. The E-DII score, based on 22 dietary parameters, quantified dietary inflammation. Cox proportional hazards regression models were used to assess the relationship between E-DII scores and incident UGI cancer, with adjustments for age, sex, residence, lifestyle factors, medical history, and pathological diagnoses. Subgroup and sensitivity analyses were conducted to address potential confounding effects.

Over a median follow-up of 55 months, 527 participants developed UGI cancer. Higher E-DII scores were associated with increased UGI cancer risk (hazard ratio [HR] for highest vs. lowest quartile: 1.75; 95% confidence interval [CI]: 1.28-2.40; P for trend = 0.001). Significant associations were observed for esophageal cancer (HR = 1.81; 95% CI 1.03-3.18; P for trend = 0.050) and gastric cancer (HR = 1.69; 95% CI 1.16-2.47; P for trend = 0.009). Subgroup analyses and sensitivity tests confirmed the robustness of these findings.

This study highlights the role of dietary inflammation in increasing UGI cancer risk and suggests that promoting anti-inflammatory dietary patterns may serve as an effective preventive measure in high-risk populations.