Roxana Daniela Brata

Background: Contemporary management of type 2 diabetes mellitus (T2DM) extends beyond glycemic control and requires comprehensive assessment of cardiovascular, renal, metabolic, and anthropometric factors. Nevertheless, clinical status is often summarized predominantly by glycated hemoglobin (HbA1c), potentially overlooking concurrent non-glycemic abnormalities. This study evaluated the prevalence and coexistence of cardiorenal-metabolic abnormalities among patients with HbA1c <7.0% at six months. Methods: This retrospective observational study included adults with T2DM routinely followed in a specialized outpatient diabetes clinic. The primary descriptive analysis included participants with HbA1c <7.0% at the six-month assessment (T1). Seven non-glycemic cardiorenal-metabolic domains were evaluated at T1: LDL cholesterol, HDL cholesterol, triglycerides, body mass index, blood pressure, estimated glomerular filtration rate, and urinary albumin-to-creatinine ratio. An unweighted descriptive count of domains outside study-defined analytical thresholds was calculated (range, 0–7). An exploratory Poisson regression model examined associations between selected baseline characteristics and the number of affected domains, excluding baseline variables that directly corresponded to components of the T1 count to minimize mathematical coupling. Results: Among 809 participants, 385 (47.6%) had HbA1c <7.0% at six months and were included in the primary descriptive analysis. Concurrent non-glycemic abnormalities were common, particularly for blood pressure, LDL cholesterol, triglycerides, body mass index, and HDL cholesterol. The median number of domains outside study-defined analytical thresholds was three (IQR 3–4), and only three participants (0.8%) had values within all seven thresholds. In the exploratory multivariable model, none of the evaluated demographic, glycemic, or treatment-related baseline characteristics was independently associated with the number of domains outside study-defined thresholds. Conclusions: HbA1c <7.0% at six months did not necessarily coincide with favorable values across other clinically relevant cardiovascular, metabolic, anthropometric, and kidney-related domains in patients with T2DM. The unweighted domain count provides a descriptive summary of concurrent non-glycemic abnormalities but should not be interpreted as a validated measure of risk, prognosis, or clinical risk stratification. These findings support comprehensive, individualized assessment beyond glycemic status alone.

Background: Contemporary antidiabetic therapy has evolved from a glucose-centered approach toward integrated cardiometabolic risk reduction. However, real-world evidence regarding treatment patterns and their association with glycemic and cardiovascular–renal profiles remain limited. Methods: This retrospective observational study included 250 adults with type 2 diabetes mellitus receiving non-insulin glucose-lowering therapy in routine specialist clinical practice. Demographic, clinical, biochemical, and pharmacological data were extracted from medical records. Glycemic control was assessed using HbA1c levels and HbA1c variation, while cardiovascular–renal parameters included estimated glomerular filtration rate (eGFR), C-reactive protein (CRP), lipid profile, blood pressure, and heart failure prevalence. Comparative analyses and multivariate logistic regression were performed. Results: The cohort had a mean age of 61.8 ± 11.3 years, and all patients had type 2 diabetes mellitus (100.0%). Obesity, metabolic syndrome, hypertension, ischemic heart disease, and chronic kidney disease were highly prevalent. Metformin was the most frequently prescribed therapy (58.8%), followed by GLP-1 receptor agonists (28.8%) and SGLT-2 inhibitors (27.6%). Patients receiving GLP-1 receptor agonists or SGLT-2 inhibitors showed numerically lower HbA1c values and greater HbA1c reductions compared with conventional therapies. However, differences in HbA1c, CRP, and eGFR were not statistically significant after correction for multiple comparisons. Longer diabetes duration independently predicted poor glycemic control, whereas increasing age was associated with a lower probability of HbA1c > 7%. Conclusions: Contemporary antidiabetic therapies were associated with favorable numerical cardiometabolic trends, although these associations did not remain statistically significant after multiple-comparison correction. The findings should therefore be considered exploratory and hypothesis-generating.

Background: Type 2 diabetes mellitus (T2DM) is strongly associated with atherosclerotic cardiovascular disease (ASCVD), yet the independent contribution of diabetes duration to cardiovascular burden remains incompletely understood. While prolonged disease exposure is presumed to increase vascular risk, the extent to which this association is independent of chronological aging and metabolic factors remains unclear. Methods: We conducted a real-world, cross-sectional study including 250 adults with T2DM followed in a tertiary outpatient clinic. Diabetes duration was analyzed both as a continuous variable and across four predefined strata (0–4, 5–9, 10–14, and ≥15 years). The primary outcome was the presence of a composite ASCVD endpoint. Logistic regression models were constructed in unadjusted, adjusted (age, sex, BMI, HbA1c), and extended forms including additional cardiometabolic variables. Interaction, nonlinear, and sensitivity analyses were also performed. Results: ASCVD prevalence increased numerically across duration strata (76.9%, 83.3%, 86.5%, and 93.8%, respectively), although the linear trend did not reach statistical significance (p = 0.118). In unadjusted analysis, each additional year of diabetes was associated with increased odds of ASCVD (OR 1.09; 95% CI 1.02–1.17; p = 0.012), but this association was attenuated after adjustment (OR 1.04; 95% CI 0.96–1.13; p = 0.328) and remained non-significant in extended models (OR 1.05; 95% CI 0.95–1.15; p = 0.347). Conclusions: In this high-risk clinical cohort, the association between diabetes duration and prevalent ASCVD was attenuated after multivariable adjustment, particularly after accounting for age and cardiometabolic covariates. These findings suggest substantial overlap between chronological aging, cumulative metabolic exposure, and cardiovascular burden in patients with T2DM. Due to the cross-sectional design and potential residual confounding, the results should be interpreted as hypothesis-generating.

Background/Objectives: Horizontal alveolar ridge resorption following tooth loss often compromises implant placement and requires augmentation procedures to restore adequate bone volume. This pilot case series descriptively evaluated the clinical, radiographic, and histological outcomes of lateral ridge augmentation (LRA) using a collagenated porcine-derived xenograft combined with autogenous bone. Methods: Three consecutive partially edentulous patients presenting with severe horizontal ridge deficiency (residual bone width ≤ 4 mm) underwent LRA using a mixture of porcine-derived xenograft and autogenous bone covered with a resorbable collagen membrane. After a healing period of 3–5 months, core biopsies were harvested at implant placement and subjected to histological and histomorphometric analysis, including TRAP staining. Results: All sites healed uneventfully without intraoperative or postoperative complications. Radiographic evaluation demonstrated substantial horizontal bone gain, allowing placement of standard-diameter implants. Histological analysis revealed newly formed trabecular bone, residual graft material, and well-vascularized connective tissue, indicating active bone regeneration and biomaterial integration. TRAP-positive multinucleated giant cells (MNGCs) were observed at the biomaterial interface, suggesting ongoing remodeling. Long-term follow-up (mean 54.2 months) showed stable implant function without biological or mechanical complications. Conclusions: Within the limitations of this pilot case series, LRA using a collagenated porcine-derived xenograft combined with autogenous bone demonstrated preliminary favorable clinical, radiographic, and histological outcomes.

Background: Post-infarction heart failure (HF) remains a major contributor to morbidity and mortality despite advances in reperfusion and pharmacological management. However, the combined influence of clinical background, myocardial injury, neuro-hormonal activation, and angiographic disease on HF severity is not fully defined. Methods: We retrospectively analyzed 181 patients with confirmed myocardial infarction treated in a tertiary cardiology center. Demographics, cardiovascular risk factors, prior chronic HF, inflammatory markers (CRP, fibrinogen, ESR, leukocyte indices), and high-sensitivity troponin (hs-Tn) were measured at admission (pre-intervention), immediately after percutaneous coronary intervention (PCI), and at 48 h, angiographic lesion distributions were collected. HF severity was graded on a five-level scale and further dichotomized as no/mild HF (grade 0–1) versus moderate–severe HF (grade ≥ 2). Group comparisons and multivariable logistic regression were used to identify independent determinants of severe HF. Results: Moderate–severe HF occurred in 42.5% of patients (77/181). Compared to HF 0–1, the HF ≥ 2 group was older (64.0 vs. 60.5 years, p = 0.042) and exhibited substantially higher systemic inflammation (CRP 41.5 vs. 9.75 mg/L, p < 0.001; fibrinogen 435 vs. 346 mg/dL, p = 0.0002; ESR 28 vs. 18 mm/h, p = 0.0004). hs-Tn levels and NT-proBNP were significantly elevated in HF ≥ 2 (NT-proBNP 3449 vs. 1243 pg/mL, p = 0.0003), while left ventricular ejection fraction was reduced. Prior HF increased the likelihood of HF ≥ 2 (54.5% vs. 33.7%, p = 0.0078), and conservative therapy was associated with adverse outcomes (87.5% vs. 40.5%, p = 0.0235). In multivariable analysis, NT-proBNP remained the only independent predictor of moderate–severe HF, while CRP showed a positive but non-significant trend after adjustment. Conclusions: Post-MI HF severity reflects the combined influence of myocardial injury, neurohormonal stress, and systemic inflammatory activation. However, in multivariable analysis, NT-proBNP emerged as the dominant independent predictor of moderate–severe HF, while CRP reflected an associated but non-independent inflammatory signal.

Background: Length of stay (LOS) reflects healthcare utilization but may also capture patient clinical trajectories. We investigated the relationship between LOS categories, organ support requirements, and in-hospital mortality. Methods: This retrospective observational study included 1332 consecutive adult ICU patients in a tertiary-care center. ICU LOS patterns were categorized using median-based and predefined cutoffs. Multivariable logistic regression was used to identify independent predictors of in-hospital mortality. Results: Prolonged ICU LOS was associated with higher crude mortality (61.0% vs. 43.5%, p < 0.001). However, in LOS-adjusted models, mortality was independently associated with mechanical ventilation (aOR 29.89, 95% CI 17.92–49.86), inotropic support (aOR 4.94, 95% CI 3.50–6.97), hemodialysis (aOR 5.43, 95% CI 2.52–11.72), older age, and diabetes mellitus. Prolonged LOS was not independently associated with mortality (aOR 0.93, p = 0.630). Conclusions: LOS reflects underlying disease severity rather than acting as an independent driver of mortality. Integrating LOS pattern assessment with markers of organ dysfunction may improve risk stratification and resource planning in hospitalized populations.

Background: Multimorbidity frequently involves overlapping neuro-psychic, cardiometabolic, and renal disturbances, yet clinical assessment often relies on diagnosis-based comorbidity counts that may not fully capture cumulative physiological stress. We developed the Neuro–Cardio–Renal Stress Index (NCR-SI) as a pragmatic composite framework to describe multisystem burden using routinely available clinical data. Methods: This cross-sectional study analyzed electronic medical record data from adult patients with chronic conditions. NCR-SI integrates three domains: neuro-psychic burden (text-derived indicators and psychotropic medication use), cardiometabolic stress (triglyceride–glucose index and cardiometabolic diagnoses), and renal function (MDRD-estimated eGFR staging). Importantly, this study is not intended to demonstrate incremental predictive value over individual components or established comorbidity indices. Rather, it presents NCR-SI as a transparent, domain-based descriptive framework and reports its internal coherence and distribution across clinically recognizable multimorbidity contexts. Results: A total of 148 patient records were screened; 143 patients met complete-case criteria and were included in the main NCR-SI analyses. NCR-SI ranged from 0 to 10 (median 5). Higher scores were observed in renometabolic profiles. NCR-SI showed expected structural associations with declining renal function (eGFR; ρ ≈ −0.71), moderately with the TyG index (ρ ≈ 0.42), and weakly with medication burden. Correlation with age-adjusted CCI was minimal (ρ ≈ 0.09), indicating limited overlap with diagnosis-based comorbidity counts. Domain-specific correlations were consistent with predefined score construction rules, particularly between the renal domain and eGFR, and between the cardiometabolic domain and TyG. Conclusions: NCR-SI provides a pragmatic, integrative descriptor of neuro-cardio-renal stress using routinely collected clinical data. Rather than replacing established comorbidity indices, NCR-SI may complement them by summarizing multidimensional physiological burden patterns. NCR-SI is proposed as a research-oriented, hypothesis-generating descriptive framework. External validation in independent cohorts and longitudinal evaluation against clinically meaningful outcomes (e.g., hospitalization, mortality, functional status, healthcare utilization) are required before any claims of clinical performance can be made.

Background/Objective: Advanced peri-implantitis presents a significant challenge in contemporary implant dentistry and sometimes necessitates implant removal when regenerative therapies are no longer reliable. Protocols for staged bone reconstruction, re-implantation, and definitive prosthetic rehabilitation following peri-implantitis continue to evolve. This study aims to present a clinical case of advanced peri-implantitis with vertical interproximal bone loss managed with a staged surgical and prosthetic approach and review current concepts in implant removal, bone regeneration, re-implantation, and soft-tissue management. Methods: A patient with peri-implantitis affecting two maxillary implants underwent treatment over one year. The initial surgical stage included removal of the failing implants and reconstruction of the defects using guided bone regeneration with a composite graft of 50% xenogeneic bone substitute and 50% autogenous bone, covered by a barrier membrane. After six months of healing, a second surgical stage was performed, involving placement of two new implants in positions 2.2 and 2.4, additional bone augmentation, and soft tissue grafting to enhance soft tissue volume and the width of keratinized gingiva following mucogingival line rebounce. After an additional six months of osseointegration, full maxillary prosthetic rehabilitation was completed in August 2025. Results: Clinical and radiographic assessments demonstrated successful bone regeneration, stable implant integration, adequate peri-implant soft-tissue conditions, and favorable functional and esthetic outcomes at follow-up. The case is discussed in the context of current evidence regarding indications for implant removal, regenerative strategies after explantation, timing of re-implantation, and the importance of keratinized gingiva and prosthetic design in long-term peri-implant health. Conclusions: Staged explantation, guided bone regeneration, delayed re-implantation, and comprehensive soft-tissue and prosthetic management may represent a viable treatment strategy in selected cases of advanced peri-implantitis.

Background: Type 2 diabetes mellitus (T2DM) is characterized by chronic low-grade inflammation that contributes to cardiometabolic complications. While diabetes duration reflects cumulative metabolic exposure, its relationship with systemic inflammatory burden remains insufficiently defined. We aimed to investigate inflammatory patterns across diabetes duration and to explore their metabolic and cardio–renal correlates. Methods: This real-world cross-sectional study included 250 adults with T2DM. Diabetes duration was analyzed both continuously and across four predefined strata (0–4, 5–9, 10–14, and ≥15 years). Inflammatory burden was assessed using C-reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Given the skewed distribution of CRP, log-transformed CRP was used in regression analyses. Nonlinear associations were evaluated using quadratic regression models. This approach was selected because preliminary descriptive analyses suggested a non-monotonic relationship between diabetes duration and CRP levels. Inclusion of a quadratic term allowed formal testing of a potential curvilinear association between diabetes duration and inflammatory burden. Spearman correlations were performed to assess associations with metabolic, renal, and cardiovascular variables. Results: CRP showed a nonlinear cross-sectional association across diabetes duration strata. Median CRP values were higher in early (0–4 years: 0.62 mg/L) and long-standing diabetes (≥15 years: 0.77 mg/L) compared with intermediate-duration groups (p = 0.063). Quadratic regression confirmed a U-shaped relationship (adjusted β_duration = −0.079, p < 0.001; β_duration² = 0.0027, p < 0.001; R² = 0.326). ESR differed significantly across duration strata (p = 0.002), with the highest levels observed in long-standing diabetes. CRP correlated positively with BMI (ρ = 0.151; p = 0.017) and triglyceride-to-HDL ratio (ρ = 0.215; p < 0.001), but not with HbA1c. Both CRP and ESR were more strongly associated with functional CKD (ρ = 0.350 and 0.429, respectively; p < 0.001) than with ASCVD. Conclusions: Inflammatory burden in T2DM shows a nonlinear cross-sectional pattern across diabetes duration, characterized by elevated levels in early and long-standing disease. Systemic inflammation appears more closely linked to renal dysfunction than to established cardiovascular disease. These findings support a cardio–renal–inflammatory axis in which prolonged diabetes exposure contributes to renal decline, which in turn amplifies systemic inflammatory activation.

Background: Glycated hemoglobin (HbA1c) is widely used for the diagnosis and monitoring of diabetes mellitus; however, its interpretation is largely based on fixed diagnostic thresholds. This study moves beyond describing a glycemic continuum by translating the non-linear HbA1c–microvascular relationship into an individualized risk estimation framework. Methods: In this cross-sectional observational study, adult subjects from a real-world clinical cohort were analyzed using HbA1c as a continuous variable. Associations between HbA1c and metabolic parameters were assessed using correlation analysis. Linear regression was applied to evaluate the relationship between HbA1c and cumulative diabetes-related complication burden. Non-linear associations between HbA1c and the risk of presenting at least one complication were explored using restricted cubic spline logistic regression models. Additional risk estimation analyses focused on the HbA1c gray zone (5.5–6.4%). Results: HbA1c showed a strong continuous association with fasting plasma glucose (ρ = 0.73, p < 0.001) and was positively associated with cumulative complication burden (β = 0.016 per 1% increase in HbA1c, p = 0.009). Non-linear modeling revealed a progressive increase in complication risk beginning below the diagnostic threshold for diabetes, with an inflection of the risk curve within the HbA1c gray zone. Individuals within this interval exhibited a higher prevalence and increased odds of presenting at least one complication compared with lower HbA1c values, although some estimates did not reach statistical significance. Conclusions: HbA1c acts as a continuous and non-linear marker of metabolic stress, with potentially biologically meaningful increases in complication risk emerging below traditional diagnostic thresholds. We demonstrate a non-linear acceleration of microvascular risk within the 5.5–6.4% interval, rather than a simple linear gradient. These findings support the concept of a glycemic risk continuum and highlight the clinical relevance of the HbA1c sub-diagnostic interval for early risk stratification and preventive strategies.