Vestibulocochlear infarct, most commonly associated with infarction of a terminal branch of the anterior inferior cerebellar artery, presents with acute vertigo and sensorineural hearing loss. It often mimics peripheral vestibular disorders and may show no abnormal findings on neuroimaging, making the diagnosis particularly challenging. Without appropriate treatment, permanent unilateral hearing loss can significantly impair patients' quality of life. This review synthesizes findings from recent studies regarding the clinical characteristics, diagnostic approach, and therapeutic strategies of this condition. Patients typically present with prolonged vertigo (>24 hours), unilateral hearing loss, tinnitus, and imbalance. On examination, peripheral signs such as a positive head impulse test or horizontal-rotatory nystagmus may be observed, while the only indicator of a central origin is the hearing loss, often subtle or unnoticed even by the patient. Vascular comorbidities, including hypertension and diabetes mellitus, constitute key risk factors. Diagnostic difficulties arise from overlap with idiopathic sudden sensorineural hearing loss and vestibular neuritis; a vascular origin may account for up to 15-20% of acute audio-vestibular syndromes in high-risk populations. Early thrombolysis or antiplatelet therapy may improve outcomes, though thrombolysis is rarely administered due to the lack of imaging evidence. For diagnosis, video head impulse testing, audiometry, and MR neuroimaging are essential. Management relies on vestibular and auditory rehabilitation for persistent vertigo and secondary stroke prevention. Our review highlights the underdiagnosis of vestibulocochlear stroke and advocates for an integrated neuro-otological and vascular diagnostic protocol in patients presenting with vertigo and hearing loss to facilitate faster and more effective treatment. Orv Hetil. 2026; 167(33): 1309-1317.

Night Eating Syndrome (NES) is an eating disorder associated with circadian rhythm disruption, but its clinical relevance in metabolic diseases remains unclear. This study aimed to determine the prevalence of NES in individuals with type 1 and type 2 diabetes and to examine its associations with glycemic control and metabolic risk markers within each subtype. This cross-sectional study included 500 patients with diabetes (108 with type 1 and 392 with type 2). NES was assessed using the Night Eating Questionnaire (NEQ), with a score ≥ 25 indicating NES. Group comparisons, correlation analyses, and binary logistic regression were performed to identify factors independently associated with metabolic syndrome. The overall prevalence of NES was 23.2%, with no significant difference between type 1 and type 2 diabetes. In exploratory analyses conducted separately within each subtype, NEQ scores in type 1 diabetes showed weak positive correlations with fasting glucose and glycated hemoglobin (HbA1c), while in type 2 diabetes NEQ scores showed weak positive correlations with waist circumference, triglycerides, and the atherogenic index of plasma. In multivariable analysis, the NEQ score was independently associated with metabolic syndrome (odds ratio [OR] 1.08, 95% confidence interval [CI] 1.046-1.122). NES is common among individuals with diabetes and, in the overall diabetic population, is independently associated with metabolic syndrome. These findings suggest that NES may represent a clinically relevant metabolic phenotype in diabetes. Given the cross-sectional design, prospective studies are needed; however, early identification of NES may support a more comprehensive metabolic risk assessment.

BACKGROUND: Vitamin D is an important immunomodulator in host defense against , yet most tuberculosis-related research has focused on the vitamin D receptor (VDR). The contribution of vitamin D metabolism genes, particularly cytochrome P450 (CYP) enzymes, remains less clearly defined. METHODS: We conducted a narrative review examining the role of major vitamin D-metabolizing enzymes, including CYP2R1, CYP27A1, CYP27B1, and CYP24A1, in tuberculosis susceptibility, immune regulation, and treatment response, with additional focus on diabetes mellitus as a major comorbidity. Evidence from genetic association studies, observational studies, mechanistic experiments, and clinical data was synthesized. RESULTS: Vitamin D metabolism enzymes influence intracellular vitamin D activation and inactivation, affecting antimicrobial peptide production, autophagy, cytokine signaling, and macrophage-mediated clearance of . Genetic and epigenetic variation in these pathways may contribute to differences in tuberculosis risk and prognosis. Diabetes mellitus may further disrupt these mechanisms through chronic hyperglycemia, oxidative stress, inflammation, impaired macrophage and T-cell function, and alterations in vitamin D metabolism, potentially increasing tuberculosis susceptibility and worsening outcomes. However, direct evidence for several enzymes remains limited. Inconsistent findings from vitamin D supplementation trials suggest that circulating 25(OH)D may not accurately reflect functional vitamin D activity at infection sites. Current evidence is largely mechanistic, observational, and genetic, with few interventional studies. CONCLUSION: Vitamin D metabolism genes represent an underexplored but potentially important component of tuberculosis pathophysiology, particularly in patients with diabetes. Future work should prioritize genetically stratified host-directed approaches to identify patients most likely to benefit from vitamin D-based interventions.

BACKGROUND Despite the well-established epidemiological association between diabetic kidney disease (DKD) and coronary artery disease (CAD) in patients with T2DM, which reflects a core feature of cardiovascular-kidney-metabolic (CKM) syndrome, the underlying molecular mechanisms connecting these 2 conditions remain unclear. Within this integrated pathophysiological framework, the potential role of lipocalin-2 (LCN2) was investigated. MATERIAL AND METHODS A total of 917 participants with T2DM were stratified into an overall cohort and a BMI-, age-, and sex-matched sub-cohort. Serum LCN2 levels were measured. Immunohistochemistry was performed on cardiac and renal tissues from high-fat diet/streptozotocin-induced diabetic mice. Renal tubular (HK-2) and cardiomyocyte (H9c2) cells were treated with recombinant LCN2 to assess inflammatory responses. RESULTS DKD severity was identified as an independent risk factor for CAD in patients with T2DM. Serum LCN2 levels were significantly elevated in patients with DKD or CAD, and were closely correlated with DKD severity and B-type natriuretic peptide levels. Logistic regression analysis further indicated that an elevated serum LCN2 level served as an independent risk factor for the presence of DKD or CAD. Importantly, mediation analysis revealed that increased serum LCN2 may partially mediate the bidirectional association between DKD and CAD. Consistent with these clinical findings, animal experiments demonstrated concurrent upregulation of LCN2 in both the heart and kidney tissues of diabetic mice. Recombinant LCN2 dose-dependently increased interleukin-6 and tumor necrosis factor-a mRNA expression in HK-2 and H9c2 cells. CONCLUSIONS LCN2 may represent a potential biomarker and partial mediator between DKD and CAD in T2DM, potentially contributing to CKM-related organ crosstalk.

Diabetes mellitus is strongly associated with metabolic dysfunction-associated steatotic liver disease (MASLD). For many years, MASLD has not been recognised as either a common pathophysiological feature of type 2 diabetes or a diabetes-related complication. This special issue of Diabetologia puts the liver in focus in the context of diabetes. This review discusses current challenges in, and emerging opportunities for, the diagnosis and management of MASLD and fibrosis in type 2 diabetes. Up to 95% of cases of MASLD remain undiagnosed because there are no accepted recommendations for assessing steatosis, whereas non-invasive tests overestimate the prevalence of MASLD progression in type 2 diabetes. Of note, the combination of type 2 diabetes and metabolic syndrome features is a strong predictor of liver disease outcomes, but CVD is the major cause of death in non-cirrhotic MASLD. MASLD is heterogeneous including subtypes linked to common genetic variants, for example PNPLA3 I148M, which increases the risk of liver disease but may protect against CVD. Recent approval of drugs targeting hepatic energy metabolism or promoting weight loss is promising for achieving fibrosis remission, but people with type 2 diabetes will still require complex multifactorial management. Achieving a significant increase in diagnostic rates of at-risk metabolic dysfunction-associated steatohepatitis (MASH) will require a paradigm shift, including greater awareness among clinicians, including diabetologists and endocrinologists, and expansion of community-based diagnostic capabilities accompanied by analyses of the cost-effectiveness of prevention and treatment.

Acute kidney injury (AKI) is a common and potentially serious complication, yet population-level data on its burden and determinants remain limited. We quantified AKI incidence, temporal trends, and risk factors across a complete healthcare system. We conducted a population-based cohort study including all adult residents of Stockholm, Sweden (2017-2021) using the SCREAM project. AKI events requiring hospitalization or occurring during hospital stays were identified using a composite algorithm incorporating laboratory-based KDIGO creatinine criteria, ICD-10 diagnoses, and acute dialysis procedure codes. We calculated annual incidence rates, temporal trends using Poisson regression, and incidence rate ratios for selected demographic, clinical, and laboratory-defined risk factors. Among approximately 1.9 million adults annually, 0.6-0.7% experienced AKI each year (71-95 per 10,000 person-years). AKI occurred in 5.8-7.8% of hospitalizations, with only 30% reaching KDIGO stage 2-3. From 2017 to 2021, AKI incidence increased by 26% (95% CI 1.23-1.29). Populations at highest risk of AKI were largely consistent over the years, and included older adults, men, and individuals with uncontrolled diabetes, prior AKI, hypertension, heart failure, kidney transplantation, and multiple myeloma. Lower eGFR and higher albuminuria were associated with markedly higher AKI risk in a graded manner. COVID-19 infection was associated with a six-fold higher AKI risk in 2020, but marked attenuation in 2021 suggests it does not explain the overall upward trend. This region-wide analysis quantifies the contemporary burden of AKI and identifies high-risk populations that may benefit from targeted prevention and monitoring strategies.

BACKGROUND: Diabetes is of great interest globally, given the associated health and economic costs. It may impact long-term systemic and oral health with unfavourable outcomes when undetected or poorly controlled, leading to various oral manifestations, including premature tooth loss and reduced quality of life. Early detection can enable early diagnosis, intervention and improve treatment and health outcomes. AIMS: To synthesise evidence on risk‑targeted screening and early case‑detection protocols for Type 2 Diabetes (T2D) that incorporate HbA1c or glucose point-of-care testing (POCT) using finger‑stick (FSB) or gingival crevicular blood (GCB) with a clinical risk assessment, to ascertain the value and potential impact of chair-side testing if implemented in primary care dental settings. METHODS: Electronic databases were searched using a pre-defined strategy, identifying 21 eligible studies; nine studies focused primarily on identifying at-risk individuals through finger-stick testing and twelve through gingival crevicular blood testing. Returned articles and grey literature were screened and used as supportive material for later discussion. A descriptive synthesis of 21 articles was undertaken, with focus of the review on multi-stage chair-side diabetes screening protocols incorporating risk questionnaires and periodontal examinations and HbA1c or glucose POCT testing. RESULTS: Chair-side HbA1c-or glucose POCT may identify potentially new T2D cases. Identification rates were shown to range between 20-66%. CONCLUSION: When a POCT is added as part of a two-staged screening protocol, it enhances the ability to identify more cases correctly and is easily integrated into the dental appointment for chair-side screening. Gingival crevicular blood may be used as an alternative blood source; however, the screening method has limitations. Therefore, the most promising solution seems to be a multi-staged predictive model involving tandem risk questionnaires, periodontal examination, and capillary testing with a chair-side POCT.

Diabetes Mellitus is a major metabolic disorder affecting over 800 million people worldwide, with significant health risks including cardiovascular diseases, kidney failure, and neuropathy. Among women, diabetes during pregnancy - both pre-existing and gestational - poses severe complications for maternal and fetal health. This study develops a comprehensive mathematical model capturing the dynamics of diabetes among women, emphasizing pregnancy-associated transitions. The total female population is divided into fertile and non-fertile groups, each further subdivided into eleven compartments representing different diabetic and pregnancy states. The model incorporates hereditary factors, social transmission, comorbidities, and lifestyle influences. Using a system of nonlinear differential equations, the work demonstrates positivity, boundedness, and quasi-steady-state (QSS) reduction, thereby simplifying the high-dimensional system while retaining essential pregnancy dynamics. This framework provides insight into how social interactions, lifestyle changes, and pregnancy contribute to diabetes progression, offering a foundation for targeted public health strategies to manage diabetes in women of reproductive age. Partial Rank Correlation Coefficient (PRCC) analysis shows that equilibrium diabetes prevalence is controlled by demographic inflow, whereas pregnancy complications are driven by progression dynamics.

BACKGROUND: Diabetic foot ulcers (DFUs) arise from interacting clinical, microbial, and host processes, yet public datasets differ substantially in design, scale, and evidentiary strength. METHODS: We curated eight public DFU cohorts and defined an evidence hierarchy. PRJNA287759 was reprocessed from raw 16 S reads; outcome tests used one baseline sample per patient (74 healed and 15 non-healed/adverse). GSE134431 compared 13 DFU with 8 diabetic foot skin samples using limma. Host discrimination underwent fold-confined leave-one-sample-out validation, 100 repeated nested five-fold analyses, 200 label permutations, and independent rank-score evaluation in GSE80178. RESULTS: Baseline diversity and community structure did not differ by outcome (Shannon P = 0.159; Observed ASVs P = 0.669; PERMANOVA R2 = 0.0157, P = 0.142). Rothia was the only nominal genus (P = 0.0307), and none survived FDR correction across prevalence thresholds. GSE134431 yielded 2,873 differentially expressed genes with coherent epidermal repair enrichment. Host leave-one-sample-out AUC was 0.990 (95% CI 0.964-1.000), repeated nested-CV median AUC was 0.981 (95% interval 0.952-1.000), and permutation P was 0.00995. The GSE80178 score separated 6 DFU from 3 diabetic foot skin samples (exact P = 0.0238; AUC = 1.000), although this external comparison was small. CONCLUSIONS: Host expression provides the strongest evidence, whereas microbiome findings remain exploratory. The repair framework synthesizes parallel evidence without demonstrating causal coupling or a clinically deployable biomarker.

Historically the development of amyloid-β plaques and tau neurofibrillary tangles have been used as the hallmarks of Alzheimer's disease (AD). However, there is increasing evidence suggests that these pathological hallmarks are secondary to deeper metabolic defect in the brain. AD is progressively being recognized as a metabolic synaptic disorder characterized by insulin resistance, impaired cellular energy homeostasis, mitochondrial dysfunction, and synaptic degeneration. Synaptic plasticity is closely linked to the insulin-sensitive system of glucose utilization, mitochondrial activity, and local protein synthesis that render the synapses highly sensitive to the malfunction of the metabolic system. Recent discoveries highlight the important role of exosomes in mediating communication between neural cells by transferring regulatory miRNAs across neuronal networks. Exosomal miRNAs regulate insulin signaling, synaptic gene expression, mitochondrial function, and neuroinflammation. In AD, exosomal miRNA profiles are significantly altered, with enrichment of miR-29, miR-34a, miR-146a, and miR-21, alongside depletion of synapse-supporting miR-132. These changes contribute to insulin resistance, impaired glucose transporter trafficking, dendritic spine destabilization, and reduced expression of synaptic proteins such as PSD-95 and synaptophysin, ultimately leading to cognitive decline. Importantly, neuron-derived exosomes can cross the blood-brain barrier, making their miRNA cargo promising biomarkers and therapeutic targets for early AD diagnosis and precision treatment.

PURPOSE: Tirzepatide and semaglutide are widely used for type 2 diabetes mellitus (T2DM) and obesity. However, the blood pressure-related adverse event profiles associated with tirzepatide and semaglutide remain unclear. This study systematically evaluated hypertension- and hypotension-related treatment-emergent adverse events (TEAEs) that occurred when using tirzepatide and semaglutide for the treatment of T2DM or obesity. METHODS: A comprehensive search was performed in PubMed, Scopus, Web of Science, Embase, CENTRAL, and ClinicalTrials.gov from inception to September 26, 2025. Pooled risk ratios (RRs) with 95% confidence intervals (CIs) were estimated using a random-effects model, with subgroup analyses performed. RESULTS: This meta-analysis of 32 randomized controlled trials (RCTs), enrolling 47,332 participants, revealed distinct differences in the blood pressure-related safety profiles of tirzepatide and semaglutide. Tirzepatide was associated with a lower risk of hypertension-related events (RR = 0.40, 95% CI [0.26-0.60]; p < 0.001). This potent antihypertensive effect was accompanied by an increased risk of hypotension-related events (RR = 2.45, 95% CI [1.35-4.45]; p = 0.003), particularly at higher doses (RR = 2.58, 95% CI [1.38-4.81]; p = 0.003). Semaglutide exhibited a relatively neutral blood pressure-related safety profile, showing no significant association with either hypertension-related events (RR = 0.81, 95% CI [0.57-1.15]; p = 0.233) or hypotension-related events (RR = 1.39, 95% CI [0.81-2.36]; p = 0.232), although potential protective signals were observed in high-dose subgroups. CONCLUSION: Tirzepatide reduces hypertension-related adverse events but increases dose-dependent hypotension risk in patients with T2DM or obesity. These distinct hemodynamic safety profiles support individualized treatment decisions based on baseline blood pressure and cardiometabolic risk.

PURPOSE OF REVIEW: Persistence with glucagon-like peptide-1 (GLP-1)-based therapies is important for sustained weight loss and glycemic control in adults with coexisting obesity and type 2 diabetes. This narrative review examined how persistence has been defined and measured, real-world patterns of continuation and discontinuation, factors associated with persistence, reasons for discontinuation, and supportive strategies in this population. RECENT FINDINGS: Seven studies met the inclusion criteria, with follow-up ranging from 6 months to 2 years. Persistence generally declined over time and often fell below 60% by 12 to 24 months, although estimates varied by refill-gap definitions and analytic approaches. Discontinuation reached 64.1% at 2 years in one large cohort, and treatment interruption with reinitiation was common. Persistence varied by age, income, gastrointestinal adverse events, weight reduction, body mass index-related measures, GLP-1 agent, formulation, and dosing schedule. Only two studies reported patient-level reasons for discontinuation, most commonly adverse effects, and none described structured behavioral or supportive strategies. Persistence with GLP-1-based therapies among adults with obesity and type 2 diabetes is variable and often declines within the first one to two years. More consistent definitions, closer attention to patient experiences, and routine-care support strategies are needed to improve long-term continuation.

OBJECTIVE: Metabolic dysfunction-associated steatotic liver disease (MASLD) is a systemic disorder associated with cardiovascular, renal, and metabolic comorbidities. We evaluated cardiovascular disease (CVD), four-domain cardiovascular-renal-hepatic-metabolic (CRHM) involvement, and their associations with non-invasive liver-related scores in patients with type 2 diabetes mellitus (T2DM) and MASLD. METHODS: We retrospectively analyzed 216 patients with T2DM and MASLD. A study-specific four-domain CRHM phenotype was defined as the coexistence of T2DM, MASLD, chronic kidney disease (CKD), and atherosclerotic CVD. FIB-4, AST-to-ALT ratio (AAR), APRI, Hellenic Score II, Fibrotic NASH Index (FNI), and CORE model were evaluated. RESULTS: CVD was present in 75/216 participants (34.7%). Among 206 participants with sufficient classification data, 35 (17.0%) had the four-domain CRHM phenotype. Patients with CVD had higher Hellenic Score II, creatinine, glycated hemoglobin, FNI, and CORE scores, and lower HDL. FNI showed modest discrimination for CVD (AUROC 0.65; 95%CI 0.56-0.74), while FNI combined with Hellenic Score II showed higher discrimination (AUROC 0.80; 95%CI 0.72-0.87). Participants with CRHM phenotype had higher APRI and FIB-4 and lower platelet counts. FIB-4 was independently associated with CRHM (OR 5.4; 95%CI 1.6-18.6) and showed moderate discriminative ability (AUROC 0.69; 95%CI 0.56-0.83). FIB-4 combined with CORE showed greater discriminative ability (AUROC 0.81; 95%CI 0.70-0.92). CONCLUSIONS: In patients with T2DM and MASLD, liver-related scores showed distinct associations with cardiovascular and multidomain disease burden. FNI was associated with CVD, whereas FIB-4 was associated with a study-specific four-domain CRHM phenotype. These findings are exploratory and require external validation.

PURPOSE: Although intensive weight management achieves considerable success in diabetes remission, individual response varies substantially. We aimed to evaluate the predictive ability of early β-hydroxybutyrate (BHB) for type 2 diabetes (T2D) remission following an intensive dietary intervention in Southeast Asian individuals, and explore the metabolomic signatures associated with remission. METHODS: We analysed 45 adults with obesity and T2D (age:42 ± 10 years, 66.7% male, body mass index:33.7 ± 4.2 kg/m²) who completed 12 weeks of total diet replacement (TDR; ~800 kcal/day) in a secondary care setting. Blood BHB levels were measured at week 2 of TDR using point-of-care testing (POCT). Metabolomic analysis was performed on baseline and post-TDR plasma samples from 33 participants using nuclear magnetic resonance spectroscopy. Remission was defined as HbA1c < 6.5% and fasting plasma glucose<7 mmol/L without glucose-lowering medications. RESULTS: Following TDR, 64.4% of participants achieved remission with 8.2% mean weight loss. Increasing remission rates were observed across POCT-BHB tertiles (p-trend=0.001), with the highest tertile independently associated with remission (risk ratio:3.11, 95% CI:1.63-5.94, p < 0.001). Addition of POCT-BHB to a base model (baseline age, sex, weight, and HbA1c) increased the area under the receiver operating characteristic curve from 0.72-0.94. The optimal POCT-BHB cut-off value was 0.575 mmol/L, yielding 72.4% sensitivity and 93.8% specificity. Metabolomic analysis revealed that remitters exhibited enhanced ketone metabolism and distinct lipoprotein remodelling. CONCLUSION: In this real-world implementation of an intensive weight management programme, our preliminary findings identified week 2 POCT-BHB as a potentially useful biomarker for predicting diabetes remission in clinical practice.

BACKGROUND: The atherogenic index of plasma (AIP) and inflammatory indices may reflect the burden of atherosclerosis. This study evaluated their predictive value for obstructive coronary artery disease (CAD) in patients with non-ST-elevation myocardial infarction (NSTEMI). METHODS: This retrospective study included 624 NSTEMI patients undergoing coronary angiography. Patients were classified as having obstructive or non-obstructive CAD. Demographic, clinical, laboratory, and echocardiographic characteristics were compared. Independent predictors were identified using multivariable logistic regression, and discriminative performance was assessed by receiver operating characteristic analysis. RESULTS:           The obstructive CAD group was significantly older (64.3 ± 12.3 vs. 57.4 ± 14.2 years; p < 0.001) with higher prevalence of males (63.3% vs. 50.8%; p = 0.003), hypertension (52.1% vs. 30.2%; p < 0.001), and diabetes mellitus (47.6% vs. 28.9%; p < 0.001). Inflammatory markers were markedly elevated: NLR [4.2 vs. 1.9; p < 0.001], PLR [140.9 vs. 119.1; p < 0.001], SII [1113.3 vs. 520.1; p < 0.001], and CRP [0.4 vs. 0.2 mg/dL; p < 0.001]. AIP was significantly higher [0.71 vs. 0.46; p < 0.001]. ROC analysis demonstrated that NLR (AUC = 0.764) and SII (AUC = 0.738) had the highest discriminative ability, while AIP showed limited performance (AUC = 0.563). In multivariable analysis, independent predictors included age (OR = 1.031), hypertension (OR = 1.645), diabetes (OR = 1.547), PLR (OR = 1.004), CRP (OR = 1.156), and AIP (OR = 2.413; all p < 0.05). CONCLUSION: AIP was independently associated with obstructive CAD beyond traditional risk factors and inflammatory indices, despite modest standalone discriminative ability. These findings are hypothesis-generating and require prospective validation with clinical outcomes before routine clinical implementation.

Flavonoids exhibit a wide range of biological activities, including antioxidant, anti-inflammatory, antidiabetic, antitumor, antiproliferative, and hemorheological effects. This review discusses the hemorheological activity of flavonoids and the underlying mechanisms. The hemorheological activity of flavonoids and flavonoid complexes has been studied in both in vitro and in vivo models of myocardial infarction, arterial hypertension, atherosclerosis, cerebrovascular insufficiency, pancreatitis, hepatitis, and rheumatoid arthritis, as well as in aging animals. Flavonoids are known to decrease whole blood viscosity, reduce red blood cell (RBC) aggregation, improve RBC deformability, and even, in some cases, decrease fibrinogen levels and plasma viscosity. The key mechanisms underlying the hemorheological effects of flavonoids are the following: (1) antioxidant protection from oxidative stress and (2) stabilization of membrane fluidity. The antioxidant effect is mediated through neutralization of reactive oxygen species outside RBCs, within the RBC membrane, and in the cytoplasm, thereby protecting RBC membranes (both lipid and protein constituents) from oxidative damage. Flavonoids also contribute to the maintenance and enhancement of endogenous antioxidant defense systems in RBCs. Clinical trials of flavonoid-based agents have demonstrated both hemorheological activity and therapeutic efficacy in patients with diabetes mellitus, coronary heart disease, venous insufficiency, dyscirculatory encephalopathy, arterial hypertension, and other conditions. The introduction of effective and low-toxicity flavonoid preparations with hemorheological activity into treatment regimens for conditions associated with hyperviscosity syndrome may enable the development of new therapeutic strategies for many diseases and improve patient outcomes.

PURPOSE: Primary care follow-up of women with previous GDM is often lacking. Little is known about effective approaches to improve follow-up and promote a healthy lifestyle. METHOD: Semi-structured individual interviews were conducted with 17 purposively sampled women with previous GDM in southern Sweden. The interviews were audio-recorded, transcribed verbatim, and qualitative content analysis was performed. RESULTS: Three main categories were found: "a missed proactive opportunity caused by insufficient GDM follow-up", "need for a holistic approach to health and wellbeing", and "ambivalence toward tech-enhanced lifestyle management". Women with previous GDM felt abandoned by healthcare after labour, since follow-up in primary care was lacking. Follow-up was viewed as proactive and requested, preferably in the form of a holistic approach to health. Motherhood and future T2DM risk were the strongest motivators for healthy lifestyle behaviours. Overall, they were cautiously optimistic regarding digital solutions in facilitating follow-up and lifestyle improvement. The capability opportunity motivation-behavior (COM-B) framework was applied, highlighting key determinants of women's ability to make lifestyle changes. CONCLUSIONS: Promoting a healthy lifestyle among women with prior GDM requires efforts at multiple levels to reduce long-term diabetes risk. Structured primary care follow-up and person-centred lifestyle support can be potentially enhanced through digital health interventions.

AIMS: Diabetes mellitus (DM) is a severe metabolic disease characterized by increased blood glucose levels due to reduced insulin action or secretion. This study aimed to synthesize new polyhydroquinoline (PHQ)-based acyl hydrazide derivatives and assess their potential as dual inhibitors of α-amylase and α-glucosidase enzymes. MATERIALS AND METHODS: Various acyl hydrazide derivatives of PHQ were synthesized via a multi-step reaction and structurally deduced through modern spectroscopic techniques. These compounds were evaluated for their studies, while molecular docking was performed to gain mechanistic insights into their biological activities. RESULTS AND DISCUSSION: In the series, compound (2c) emerged as the most potent inhibitor against both enzymes (IC = 0.44 ± 0.07 µM and 0.17 ± 0.01 µM, respectively), showing greater efficacy than acarbose. Density functional theory (DFT) analysis revealed valuable insights into the electronic properties and showed the best correlation with the biological targets. Moreover, molecular docking analysis showed good binding interactions with the active sites of both enzymes, which was supported by the experimental activities. CONCLUSION: These integrated experimental and computational results demonstrate that the polyhydroquinoline scaffold represents a promising platform for developing next-generation antidiabetic therapeutics with enhanced efficacy and favorable safety profiles.

BACKGROUND: Coronary stent fracture is an uncommon mechanical complication of percutaneous coronary intervention (PCI) that may lead to adverse outcomes such as in-stent restenosis, thrombosis, and, rarely, coronary artery aneurysm (CAA) formation. The coexistence of stent fracture and a saccular coronary aneurysm represents a particularly high-risk scenario requiring careful diagnostic assessment and individualized management. CASE SUMMARY: A 65-year-old man with long-standing hypertension and type 2 diabetes mellitus presented with recurrent rest angina and evidence of inducible myocardial ischaemia. Coronary angiography revealed multivessel coronary artery disease, and the patient underwent staged PCI with rotational atherectomy and implantation of overlapping drug-eluting stents in the left anterior descending artery. Follow-up imaging identified an abnormal contrast-filled structure adjacent to the proximal stent, initially suspected to represent plaque extrusion or aneurysm formation. Optical coherence tomography (OCT) later demonstrated a type IB stent fracture associated with a saccular CAA measuring ∼5 mm in diameter and 10 mm in length. The lesion was successfully treated with implantation of a covered coronary stent under OCT guidance, achieving complete aneurysm exclusion and restoration of normal coronary flow. DISCUSSION: Stent fracture complicated by CAA is a rare but clinically relevant complication of PCI. High-resolution intracoronary imaging plays a crucial role in establishing the diagnosis, characterizing aneurysm morphology, and guiding treatment. In selected cases, OCT-guided implantation of a covered stent offers an effective percutaneous strategy for aneurysm exclusion while preserving vessel patency.

BACKGROUND: Metabolic syndrome (MetS) is increasingly prevalent among premenopausal women and is associated with a higher risk of subclinical atherosclerosis. This study investigated whether composite metabolic indices are more strongly associated than conventional metabolic markers with subclinical coronary artery disease (CAD) detected by coronary computed tomography angiography (CCTA). The potential contribution of oxidative stress markers to early atherosclerosis risk assessment was also evaluated in premenopausal Iranian women. METHODS: In this cross-sectional case-control study, 101 women aged 30-50 years who were referred for CCTA were enrolled and classified into MetS and control groups according to The National Cholesterol Education Program, Adult Treatment Panel III (NCEP-ATP III) criteria. Demographic, biochemical, metabolic, oxidative stress, and CCTA data were collected. Atherosclerotic burden was assessed using coronary calcium score, plaque number, plaque volume, and percentage of stenosis. Composite metabolic indices, including Triglyceride glucose (TyG), Atherogenic Index of Plasma (AIP) and others were calculated and correlated with imaging findings. RESULTS: Women with MetS exhibited significantly higher coronary plaque numbers, greater lesions volume, and more extensive calcium accumulation compared to the control group. They also demonstrated poorer metabolic health and elevated oxidative stress, as reflected by lower Total Antioxidant Capacity (TAC) and higher levels of Malondialdehyde (MDA) and Superoxide Dismutase (SOD). While traditional lipid levels showed a weak association with plaque metrics, composite indices (TyG and AIP) demonstrated a strong correlation with plaque burden and CAD risk. Oxidative stress markers may also play a supportive role in the assessment of early vascular injury. CONCLUSION: MetS is strongly associated with early coronary atherosclerosis in women of reproductive age. Composite indices, especially TyG and AIP, outperform conventional metabolic markers in predicting plaque burden. Their combined use with oxidative stress markers may improve early cardiovascular risk stratification and support targeted preventive strategies in premenopausal women.

PURPOSE: T-SPOT.TB is an interferon-γ release assay that aids in detecting infection but cannot distinguish latent infection from active tuberculosis. False-negative results may delay diagnosis and treatment in patients with active pulmonary tuberculosis (PTB). This study investigated factors associated with false-negative T-SPOT.TB results in bacteriologically confirmed PTB. PATIENTS AND METHODS: This retrospective cohort study included 4,931 adults with bacteriologically confirmed PTB hospitalized at Fuzhou Pulmonary Hospital, Fujian Province, China, between January 2018 and September 2025. The primary outcome was a false-negative T-SPOT.TB result. Demographic characteristics, comorbidities, radiological findings, inflammatory markers, and T-lymphocyte subset counts were collected. Multivariable logistic regression was used to identify independent predictors, while restricted cubic spline (RCS) analyses explored potential nonlinear dose-response relationships. RESULTS: False-negative T-SPOT.TB results occurred in 437 patients (8.86%). Compared with patients with positive results, those with false-negative results were older (median, 61 vs 57 years), had higher neutrophil-to-lymphocyte ratios (NLR; 3.85 vs 3.25), and had lower CD4⁺ T-cell counts (540 vs 594 cells/μL) (all <0.001). Older age (OR=1.007, 95% CI: 1.001-1.014; =0.024), chronic obstructive pulmonary disease (OR=1.848, 95% CI: 1.273-2.682; =0.001), and elevated NLR (OR=1.018, 95% CI: 1.002-1.035; =0.026) were independent risk factors. Diabetes mellitus, cavitary lesions, airway lesions, and higher CD4⁺ T-cell counts were independently associated with a reduced risk of false-negative results. RCS analyses demonstrated nonlinear associations for NLR ( for nonlinearity <0.001) and CD4⁺ T-cell count ( for nonlinearity=0.002), with a marked increase in false-negative risk above an NLR of 2.96 and below a CD4⁺ T-cell count of 490.7 cells/μL. CONCLUSION: Advanced age, chronic obstructive pulmonary disease, elevated NLR, and reduced CD4⁺ T-cell counts increase the likelihood of false-negative T-SPOT.TB results. In high-risk patients with TB-compatible imaging, a negative T-SPOT.TB result should not preclude further microbiological evaluation or diagnostic investigation.

Diabetes is a leading cause of chronic kidney disease, yet gaps in the use of guideline-directed therapies persist in primary care. In 2025, our group developed and validated community pharmacist-led prescribing algorithms for individuals with an estimated glomerular filtration rate ≥30 mL/min/1.73 m, targeting angiotensin-converting enzyme inhibitors or angiotensin receptor blockers, sodium-glucose cotransporter-2 inhibitors, and nonsteroidal mineralocorticoid receptor antagonists. To address the evolving therapeutic landscape, we developed and validated a semaglutide-specific algorithm to complement this approach. Algorithm development and validation followed Lynn's method. A two-part questionnaire per algorithm item assessed content and face validity, with nephrology clinicians (nephrologists and kidney pharmacists) and community pharmacists rating items using Likert scales. Content validity was measured using item-level (I-CVI) and scale-level (S-CVI/Ave) indices, while face validity was assessed by level of agreement to five statements per round. The algorithm was iteratively revised between rounds. Ten nephrology clinicians (five per round for three rounds) and 12 community pharmacists (six per round for two rounds) participated. For clinicians, the I-CVI ranged from 0.6 to 1.0, with an overall S-CVI/Ave of 0.89 across three rounds. Among pharmacists, all items met the prespecified content validity threshold for both rounds (I-CVI ≥0.83; P < 0.05). Face validity exceeded the 70% consensus threshold for both validator groups. This study adds a validated semaglutide-specific algorithm to our existing pharmacist-led care model, expanding a suite of algorithms to support uptake of disease-modifying therapies for individuals with type 2 diabetes and chronic kidney disease in primary care. Implementation and evaluation in Nova Scotia community pharmacy clinics are underway.

Diabetes mellitus is among the strongest independent risk factors for severe influenza, hospitalization, and influenza-associated acute respiratory distress syndrome (ARDS). The mechanistic basis of this association, and its clinical implications for immunomodulatory therapy, has been examined extensively in basic immunology and virology but is rarely synthesized for the practicing intensivist. This narrative review synthesizes the mechanistic basis by which diabetes predisposes to severe influenza and to translate the established pathogen-driven versus host-driven lung injury framework into a bedside-relevant heuristic for immunomodulatory decision-making. PubMed/MEDLINE and the Cochrane Library were searched from inception through April 2026, integrating evidence across innate and adaptive immunology, viral pathogenesis, and clinical trial data. The review was guided by the SANRA framework. Diabetes plausibly impairs early antiviral containment through disruption of type I interferon signaling, alveolar macrophage function, neutrophil-mediated barrier defense, and CD8 T-cell responses, predominantly demonstrated in vitro and in murine models with supportive observational human data. The resulting prolonged viral replication, superimposed on baseline endothelial vulnerability, may contribute to rapid, severe lung injury. The framework applies most directly to type 2 diabetes; mechanistic differences between type 1 and type 2, and between acute glucose-driven and chronic structural mechanisms, are addressed. Available observational and meta-analytic evidence consistently associates corticosteroids with worse outcomes in influenza pneumonia. Selective adjunctive strategies, most notably mTOR inhibition with sirolimus and combination clarithromycin-naproxen-oseltamivir, show early hypothesis-generating signals but require confirmatory trials. This synthesis is intended as hypothesis-generating, not definitive.

AIM: To map the available evidence on nurse-led interventions on type 2 diabetes management for minority ethnic groups in the World Health Organisation (WHO) European region. BACKGROUND: Although research on nurse-led interventions for type 2 diabetes mellitus is well-established, the extent of nurse-led interventions for minority ethnic groups in the World Health Organisation (WHO) European region is not well explored. DESIGN: Scoping review design according to Joanna Briggs institute (JBI). METHODS: A systematic search of published English articles was carried out in 6 electronic databases (PubMed, CINAHL, MEDLINE, Sabinet, Scopus, EBSCO host) and 2 search engines (Google, Google Scholar). Population (minority ethnic groups with type 2 diabetes mellitus), Concept (nurse-led interventions), and Context (World Health Organisation European region) were used to define the inclusion and exclusion criteria. The three-step search strategy was used to find 322 eligible articles. The identified articles were imported into the Systematic Review Web app, Rayyan, in preparation for selection. The selection process involved the title and abstract initially followed by full text screening of potentially relevant papers. RESULTS: Fourteen (14) articles were included. Results showed minimal relevant publications per year between 2006 and 2018; an increase between 2019 and 2021 (n = 5), with a greater number from the UK (n = 7). Four studies were reviews, followed by quantitative (n = 4), qualitative (n = 4),and mixed methods (n = 2). The implemented nurse-led interventions included culturally sensitive (n = 5), Self-management (n = 3), community based enhanced care package (n = 2), psychological (n = 1), web and mHealth technologies (n = 1), Group-based diabetes education model (n = 1), Type 2 diabetes lifestyle (n = 1). CONCLUSIONS: Findings suggest that nurse-led interventions on type 2 diabetes management improve self-care knowledge, skills, and behaviour change. In addition, patients are empowered, and this improves non-pharmacological lifestyle change. Furthermore, it improves the knowledge and skills of nurses in type 2 diabetes management. RELEVANCE TO CLINICAL PRACTICE: This review will promote the development of culturally specific interventions for type 2 diabetes mellitus for ethnic minority groups in the United Kingdom. This will enhance proper care and improve the quality of life among the population affected. PATIENT AND PUBLIC CONTRIBUTION: No patient or public contribution. TRIAL REGISTRATION: Open Science Framework; https://doi.org/10.17605/osf.10/4D6Q9.