Backgroud and Objectives: To evaluate conventional Doppler indices and the novel middle cerebral artery (MCA) diastolic deceleration area (DDA) in pregnancies complicated by gestational diabetes mellitus (GDM), and to explore their associations with perinatal outcomes. Prospective case-control study conducted at a tertiary referral perinatology center. Materials and Methods: The study included 83 women with GDM and 92 healthy controls. Standard fetal biometric and Doppler parameters-umbilical artery, MCA, ductus venosus, cerebroplacental ratio, and umbilicocerebral ratio-were assessed, alongside calculation of MCA DDA. Perinatal outcomes were recorded. Results: Most conventional Doppler indices did not differ between groups, except for lower MCA dicrotic notch velocity and higher ductus venosus time-averaged maximum velocity in the GDM group. MCA DDA values did not differ significantly between GDM and control groups (6.67 [5.02-8.20] vs. 7.05 [5.21-8.39] cm·s, p = 0.444) and showed no difference between insulin- and diet-controlled subgroups (p > 0.05). MCA DDA showed significant correlations with gestational age, MCA peak systolic velocity, and birth weight. However, after adjustment for potential confounders, gestational age remained the only independent determinant of MCA DDA. The multivariable analysis evaluating composite adverse neonatal outcomes was limited by the small number of adverse events (n = 14). Conclusions: MCA DDA did not differ between GDM and control pregnancies and primarily reflected gestational age-related physiological variation rather than diabetes specific hemodynamic changes. However, its relationship with adverse neonatal outcomes remains uncertain and requires further investigation in larger prospective studies.

Contrast-induced nephropathy (CIN), now more accurately referred to as contrast-induced acute kidney injury (CI-AKI), remains a major cause of hospital-acquired acute kidney injury (AKI) and is associated with increased morbidity and mortality, particularly in high-risk patients. This condition occurs following the intravascular administration of iodinated radiocontrast media (RCM), especially in individuals with pre-existing chronic kidney disease (CKD), diabetes mellitus, heart failure, advanced age, or exposure to high contrast volumes. The pathophysiology of CI-AKI is multifactorial and involves renal hemodynamic alterations, direct tubular toxicity, oxidative stress, inflammatory activation, and endothelial dysfunction, ultimately leading to tubular injury and reduced glomerular filtration rate (GFR). Traditional diagnostic markers such as serum creatinine (sCr) and estimated glomerular filtration rate (eGFR) are limited by low sensitivity and delayed response, prompting growing interest in novel biomarkers, including cystatin C (CysC), β-2 microglobulin (β-2M), Interleukin-18 (IL-18), Kidney Injury Molecule-1 (KIM-1), Neutrophil Gelatinase-Associated Lipocalin (NGAL), and osteopontin (OPN), which allow earlier detection and risk stratification. Preventive strategies remain the cornerstone of management and include optimizing hydration protocols, minimizing contrast dose, selecting low- or iso-osmolar agents, and individualized risk assessments. Despite extensive research into pharmacological and procedural interventions, no effective treatment for established CI-AKI exists, underscoring the critical importance of prevention and ongoing investigation into safer contrast agents and innovative prophylactic approaches.

Background and Objectives: Continuous glucose monitoring (CGM) improves glycemic control in type 2 diabetes (T2DM), but its effects on diabetes-related distress and quality of life (QoL), particularly in patients on intensive insulin therapy, are less well studied. Aim: We aim to assess the impact of CGM on glycemic control, diabetes distress, and QoL in adults with T2DM on intensified insulin therapy. Materials and Methods: This prospective observational study included 226 adults with T2DM using multiple daily insulin injections or basal-bolus therapy. CGM was initiated at baseline. HbA1c, fasting glucose, and lipid profile were measured at baseline, 3, 6, 9, and 12 months. Diabetes-related distress (DDS-17) and quality of life (MDQoL-17) were assessed at the same time points. Longitudinal changes were analyzed using linear mixed-effects models. Results: Mean age was 66 ± 9.1 years; 55% were male. HbA1c decreased from 8.56 ± 1.87% to 7.20 ± 0.90% at 3 months (p < 0.001) and remained improved at 12 months (7.21 ± 1.04%). Diabetes distress declined significantly over time (β = -0.025/month; p = 0.001). Older age and lower income were associated with higher distress. Quality of life improved significantly during follow-up; higher income predicted better QoL, while greater distress predicted poorer QoL. HbA1c did not independently influence QoL. CGM metrics (GMI, mean glucose, TIR, glycemic variability) remained stable after initial improvement. Conclusions: In 226 insulin-treated T2DM patients, implementation of CGM as part of a structured insulin intensification strategy was associated with sustained improvements in glycaemic control, reduced diabetes-related distress, and enhanced quality of life over 12 months. These findings support routine CGM use and highlight the importance of addressing psychosocial outcomes in diabetes care.

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is highly prevalent among patients with type 2 diabetes (T2D) and has been increasingly recognized as a potential contributor to cardiovascular (CV) disease. However, the relationship between MASLD and subclinical/clinical atherosclerosis remains controversial, with inconsistent findings across imaging modalities and study populations. Methods: A systematic review was conducted according to PRISMA guidelines and registered in PROSPERO (CRD420261347480). Literature searches were performed across the PubMed, Scopus, and Web of Science library databases from 1 January 2016 to 27 March 2026, using the terms: "MASLD AND (type 2 diabetes OR type 2 diabetes mellitus OR T2DM) AND atherosclerotic plaque" for each of the three databases. Inclusion criteria comprised original full-text English-language studies, published in the last 10 years and conducted in adults, reporting data regarding the evaluation of atherosclerosis in patients with T2D and MASLD/NAFLD. Exclusion criteria are letters to the editor, expert opinions, case reports, conference or meeting abstracts, reviews, and redundant publications; having unclear or incomplete data; and being performed in vitro (cell cultures) or in animal models. The quality of included studies was assessed using the Newcastle-Ottawa Scale. Results: The included studies, predominantly cross-sectional and a single longitudinal study, as well as different modalities of evaluating atherosclerosis, showed heterogeneous findings. MASLD is associated with increased carotid plaque progression, including in lean individuals. Its relationship with carotid intima-media thickness (CIMT) is inconsistent across studies, with some reporting higher values and others finding no significant association after adjustment. Hepatic fibrosis appears more strongly linked to vascular aging than steatosis alone, with variability likely due to differences in study methods and populations. Conclusions: The presence of both MASLD and T2D may be associated with atherosclerosis across different stages, from subclinical changes to clinically manifest disease, particularly at more advanced stages such as plaque presence or progression, whereas its relationship with early markers like pulse wave velocity or CIMT remains inconsistent. Liver fibrosis may represent a stronger determinant of atherosclerosis than hepatic steatosis alone. Although the evidence base is limited and largely derived from a small number of predominantly cross-sectional studies, further standardized and prospective research is warranted to better define these relationships and evaluate CV risk stratification in patients with T2D.

Background and Objectives: Healthcare-associated infections (HAIs) remain a relevant complication in coronary care units (CCUs), particularly among patients with cardiac dysfunction requiring invasive monitoring and prolonged hospitalization. In this setting, infection occurrence may reflect the cumulative interaction between baseline biological vulnerability and care-related exposure. This study aimed to explore whether a simple cumulative framework integrating these components can describe patterns of HAI occurrence and support early identification of patients at risk for severe infectious complications and sepsis. Materials and Methods: The retrospective cohort study included 870 consecutive adult patients admitted to a tertiary-care CCU. A four-component cumulative framework was constructed using reduced left ventricular ejection fraction (LVEF < 40%), diabetes mellitus, urinary catheterization, and CCU length of stay > 5 days. Each component contributed one point (range 0-4). HAIs were defined according to CDC/NHSN criteria and required microbiological confirmation. Associations between cumulative burden and infection occurrence were assessed using trend analysis and exploratory modeling. Results: HAI occurrence increased progressively across cumulative framework levels, demonstrating a stepwise pattern from low to higher vulnerability strata (p for trend < 0.001). A substantial proportion of infections clustered in patients with higher cumulative values, despite representing a minority of the cohort. Increasing cumulative burden was accompanied by higher observed infection occurrence, supporting a graded association between cumulative vulnerability and infection occurrence. Conclusions: In CCU patients, HAI occurrence appears to reflect the accumulation of biological vulnerability and care-related exposure during hospitalization. A simple cumulative framework may support early identification of patients requiring closer preventive attention and contribute to improved awareness of severe infectious complications in cardiac critical care. Prospective validation is warranted.

Background and Objectives: Diabetes mellitus (DM) is a major global health concern, with diabetes-related foot disease (DFD) representing one of its most severe complications, often resulting in chronic infection, osteomyelitis, and limb amputation. Conventional therapies frequently fail in refractory cases, necessitating novel adjunctive strategies. Ozone therapy (OT) possesses antimicrobial, immunomodulatory, and oxygen-enhancing properties, while negative pressure wound therapy (NPWT) facilitates granulation, exudate removal, and tissue perfusion. This study explored the combined efficacy of OT and NPWT in advanced DFD. Materials and Methods: An exploratory, retrospective, observational cohort study was conducted at a specialized wound care center in Gdańsk, Poland, between 2019 and 2022. The study included 30 patients (n = 30) with refractory DFD involving both soft tissue and bone infection who had not responded to previous conventional treatment. The analyzed treatment approach consisted of surgical debridement, application of topical ozonated preparations, and (NPWT) with instillation of ozonated saline administered over a six-week period. Clinical outcomes included wound healing assessed using the Wagner classification and wound volume reduction, pain intensity measured using the Numeric Rating Scale (NRS), inflammatory biomarkers (C-reactive protein [CRP] and procalcitonin [PCT]), and microbiological characteristics of wound cultures. Statistical analyses were performed using the Wilcoxon signed-rank test and the chi-square test, and regression modeling was applied to identify potential predictors of therapeutic response. Statistical significance was defined as p < 0.05. Results: By week six, 100% of ulcers improved to Wagner stage ≤1, with 26.7% achieving stage 0. Median wound volume decreased from 5.5 cm³ to 0 cm³ (p < 0.001). Pain scores declined from 7.2 ± 0.96 points to 0.2 ± 0.5 points (p < 0.001). CRP and PCT levels decreased significantly (p < 0.001), and microbiological clearance was observed in all cases. Higher body mass index (BMI) was associated with poorer pain reduction. Conclusions: The combination of standard wound care with OT and NPWT was associated with clinically relevant improvements in wound healing, infection control, systemic inflammation, and pain reduction in patients with refractory DFD. Although limited by a non-controlled design and small cohort size, these findings support further randomized controlled trials to define the role of this combined approach in integrated diabetic foot care.

Background and Objectives: Anemia is a frequent complication of chronic kidney disease (CKD), primarily attributed to erythropoietin deficiency. Interstitial fibrosis (IF), which disrupts the renal interstitium where erythropoietin-producing cells reside, may contribute to anemia independent of glomerular filtration rate (GFR). However, data in primary glomerulonephritis (PGN) are limited and conflicting. Materials and Methods: In this nationwide multicenter registry analysis (TSN-GOLD), 2794 adults with biopsy-proven PGN were included. Interstitial fibrosis was graded semi quantitatively (0-3). Anemia was defined according to KDIGO/WHO criteria. Multivariable logistic regression models were constructed to evaluate the independent association between IF severity and anemia, adjusting for age, sex, eGFR, log-transformed proteinuria, hypertension, diabetes mellitus, and biopsy diagnosis. Interaction between IF and eGFR was assessed. A predefined subgroup analysis was performed in patients with preserved renal function (eGFR ≥ 60 mL/min/1.73 m²). Results: Anemia was present in 34.4% of patients. Although moderate-to-severe IF was more frequent among anemic patients (p < 0.001), IF severity was not independently associated with anemia in multivariable analysis (p-trend = 0.72). Female sex and lower eGFR were independently associated with anemia. A statistically significant IF×eGFR interaction was observed (p = 0.0029), indicating effect modification across renal function levels. The model demonstrated moderate discrimination (AUC = 0.705). In patients with preserved renal function, IF severity was not associated with anemia. Conclusions: In this large multicenter cohort of PGN patients, interstitial fibrosis severity was not independently associated with anemia after adjustment for renal function and clinical covariates. These findings suggest that the association between interstitial fibrosis and anemia in PGN appears largely mediated by renal functional status rather than fibrosis severity alone.

Background/Objectives: Type 1 diabetes (T1D) and multiple sclerosis (MS) are autoimmune, multifactorial, organ-specific disorders mediated by immune cells. Their co-occurrence has been partially attributed to shared genetics and environmental factors. We aimed to dissect the shared genetic architecture between T1D and MS using large-scale genome-wide association studies (GWASs) and colocalization analyses. Methods: We applied a Bayesian colocalization framework to two large-scale GWAS data sets: a T1D study comprising 18,942 cases and 501,638 controls, and an MS GWAS including 14,802 cases and 26,703 controls. Results: We identified 26 shared colocalizing association signals between T1D and MS. Among them, seven loci (EOMES, RGS14, DLL1, ZNF438/ZEB1, SESN3, WARS1/SLC25A47, and IRF8) were novel for T1D and two (UBAC2 and LAT) for MS. Several signals showed supportive evidence in additional datasets and demonstrated functional annotation characteristics consistent with disease involvement. Conclusions: Colocalization can be a powerful discovery tool for disorders with co-divided genetic architecture, as prioritizing shared rather than individual causal variants may enhance the detection of novel loci. Our findings indicate that T1D and MS predominantly share general autoimmune susceptibility signals (17/26), rather than disease-specific (private), often with opposite direction of effect (9/26), underscoring their immunological heterogeneity.

Effective sick-day management, including ketosis home management aimed at preventing diabetic ketoacidosis (DKA), is essential for families living with a child/adolescent with type 1 diabetes (T1D).

Adolescents living with T1D and caregivers of younger children living with T1D were invited to participate in an interview consisting of five parts: (I) demographic data, (II) subjective self-ratings on competence in ketosis home management, (III) objective assessment of competence in ketosis home management using a standardized clinical case scenario consisting of 10 management steps, in which participants were asked to describe the actions they would take to prevent DKA, and (IV) practical demonstrations to objectively assess skills in (IVa) urine dipstick self-testing and (IVb) insulin administration, (V) household availability of (Va) urine dipsticks and (Vb) insulin cartridges.

(I) We enrolled 61 adolescents and 79 caregivers. (II) Competence in ketosis home management was subjectively self-rated as good to very good. (III) Adolescents reported 4 (median; Q25/Q75 3/5) and caregivers 5 (4/5) of 10 management steps. Never self-testing ketone levels was reported by 33% of adolescents and 11% of caregivers. (IVa) At least one handling error occurred in 100% of adolescents' and in 98% of caregivers' practical demonstrations of urine dipstick self-testing and in (IVb) 98% of adolescents' and 98% of caregivers' insulin administrations. (Va) Altogether urine dipsticks were available in 43% of households, whereas (Vb) insulin cartridges were available in 78% of households.

Our results demonstrate a mismatch between challenges in ketosis home management and high subjective self-ratings.

Diabetic neuropathy is one of the most common chronic complications of diabetes mellitus and could lead to foot ulcerations, lower-limb amputations, increased mortality and reduced quality of life. This study examines the level of GPIHBP1 to assess its diagnostic and prognostic values across the metabolic continuum.

This is an observational monocentric study, including 160 patients with type 2 diabetes mellitus, obesity without carbohydrate metabolism disorders and healthy controls. Clinical data and laboratory results were collected, and serum levels of GPIHBP1 were measured using an ELISA. The presence of DPN for the diabetes group was assessed using corneal confocal microscopy and NDS. The statistical analyses included t-tests, Pearson's correlation analysis, and ROC analysis to explore associations and the predictive values of the biomarker.

The GPIHBP1 levels increased progressively, with the lowest levels observed in the control group, higher levels in patients with obesity, and the highest levels in those with diabetes mellitus. Higher GPIHBP1 levels were observed in patients with peripheral diabetic neuropathy compared to those without. GPIHBP1 demonstrated moderate discriminative performance for the presence of diabetes, diabetic neuropathy and nephropathy. GPIHBP1 levels were also associated with renal function parameters and markers of vascular involvement. After adjustment for confounders, including estimated glomerular filtration rate (eGFR), the association between GPIHBP1 and diabetic neuropathy remained statistically significant although attenuated. Higher levels were observed in patients with coronary artery disease, and a positive correlation was established with mean IMT and sudomotor dysfunction score.

Circulating GPIHBP1 levels are associated with diabetes mellitus and its micro- and macrovascular complications, particularly diabetic neuropathy. Its measurement could enhance early diagnosis and personalized management of T2DM, and, while these findings support a potential role of GPIHBP1 as a biomarker of metabolic and vascular dysfunction, its clinical utility requires confirmation in longitudinal studies.