<p><strong>Aim </strong>To identify predictors of all-cause mortality and 6-month rehospitalisation in patients with hypertensive crisis, focusing on inflammatory indices, metabolic markers measured at admission, and antihypertensive treatment profiles.</p> <p><strong>Methods </strong>This prospective observational study included 210 adult patients with hypertensive crisis. Demographic, clinical, and therapeutic data were collected, including data on comorbidities, antihypertensive drug use, and treatment adherence. Laboratory parameters obtained at admission included neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), systemic immune-inflammation index (SII), pan-immune-inflammation value (PIV), homocysteine, and uric acid. Patients were followed for 12 months. Multivariate logistic regression and receiver operating characteristic (ROC) curve analyses were conducted to identify independent predictors.</p> <p><strong>Results </strong>Mortality occurred in 10.9% of patients, and 27.1% were rehospitalised within 6 months. Deceased patients exhibited significantly higher levels of PLR (p=0.0329), SII (p=0.0355), homocysteine (p=0.0488), and uric acid (p=0.021). In multivariate analysis, homocysteine (OR=3.55; p&lt;0.001), uric acid (OR=1.03; p=0.007), PLR (OR=1.04; p=0.047), and SII (OR=1.01; p=0.030) remained independently associated with mortality. Chronic kidney disease (OR=2.15, p=0.012) and poor treatment adherence (OR=1.92; p=0.017) were also significant predictors. ROC analysis demonstrated moderate discriminative power, with AUC values of 0.68 for PLR, 0.66 for SII, 0.65 for homocysteine, and 0.63 for uric acid.</p> <p><strong>Conclusion</strong> Elevated inflammatory indices and metabolic markers, particularly homocysteine and uric acid, were independently associated with increased mortality risk. Additionally, chronic kidney disease and suboptimal adherence to antihypertensive therapy significantly contributed to adverse outcomes. These findings underscore the importance of comprehensive risk assessment and personalised management in this high-risk population.</p>

BACKGROUND Inflammation-driven mechanisms play a central role in adverse outcomes after non-ST-elevation myocardial infarction (NSTEMI), yet simple, widely available biomarkers for early risk stratification remain insufficiently defined. Hemogram-derived indices and iron-related inflammatory markers may provide complementary prognostic information. OBJECTIVE To evaluate the prognostic significance of the mean platelet volume-to-monocyte ratio (MMR) and serum ferritin in predicting major adverse cardiovascular events (MACE) in patients with NSTEMI, and to assess the association of angiotensin-converting enzyme (ACE) inhibitor therapy with clinical outcomes. METHODS This prospective cohort study included 170 consecutive NSTEMI patients admitted to the University Clinical Center Tuzla between February 2022 and January 2023. All patients received dual antiplatelet therapy and high-intensity statins. The baseline evaluation included a complete blood count, serum ferritin, and C-reactive protein. MMR was calculated as the ratio of mean platelet volume to absolute monocyte count. Patients were followed for 12 months for the occurrence of MACE, defined as cardiovascular death, non-fatal myocardial infarction, urgent revascularization, stroke, or hospitalization for heart failure. RESULTS During follow-up, 103 patients (60.6%) experienced MACE. Admission MMR (18.1 ± 11.7 vs 13.2 ± 5.5; P = 0.003) and ferritin levels (284 ± 396 vs 152 ± 109 µg/L; P = 0.001) were significantly higher in patients with events. In multivariable analysis, both MMR (odds ratio [OR] 1.06, 95% confidence interval [CI] 1.02-1.11; P = 0.008) and ferritin (OR 1.28 per 100 µg/L, 95% CI 1.10-1.55; P = 0.003) independently predicted MACE, while ACE inhibitor therapy was associated with a lower risk (OR 0.24, 95% CI 0.08-0.70; P = 0.01). The combined model demonstrated good discriminative performance (AUC 0.72; 95% CI 0.64-0.80). CONCLUSION AND RELEVANCE Elevated admission MMR and ferritin were independently associated with a higher 1-year risk of MACE in patients with NSTEMI. ACE inhibitor therapy was associated with improved outcomes, although causality cannot be inferred. These findings suggest that readily available inflammatory biomarkers may complement established clinical parameters for early risk stratification and support continued guideline-directed pharmacotherapy in NSTEMI.

Severe hypoglycemia increases the risk of cardiovascular disease (CVD) in people with diabetes. Large cohort studies and scientific statements show that severe hypoglycemia is linked to higher rates of coronary heart disease, cardiovascular events, and mortality in both type 1 and type 2 diabetes. This risk is especially high in individuals with significant vascular risk, such as older adults and those with multiple cardiovascular risk factors. Hypoglycemia triggers several pathophysiological changes that increase cardiovascular risk. These include activation of the sympathoadrenal system, promotion of proinflammatory and prothrombotic states, arrhythmogenic changes, and increased hemodynamic stress. Experimental evidence shows that recurrent hypoglycemia worsens microvascular dysfunction and promotes adverse cardiac remodeling, especially in people with diabetes. While the link between hypoglycemia and cardiovascular events is well established, the causality remains debated. Hypoglycemia may directly contribute to cardiovascular disease or indicate underlying vulnerability, especially in patients with advanced disease or comorbidities. Minimizing hypoglycemic episodes is recommended for all patients with diabetes, particularly those with established cardiovascular disease, due to the clear association with adverse outcomes.

Background Dilatation of the common bile duct (CBD) after cholecystectomy is frequently observed during follow-up imaging; however, its extent and clinical implications remain incompletely defined. Distinguishing physiological postoperative ductal enlargement from pathological dilatation is essential to avoid unnecessary diagnostic evaluation. This study aimed to compare CBD diameter in post-cholecystectomy patients with non-operated controls and to assess its association with time since surgery, age, and body mass index (BMI). Materials and methods This retrospective observational study included 165 adult patients who underwent abdominal ultrasound examination, comprising 91 post-cholecystectomy patients and 74 controls with an intact gallbladder. The CBD diameter was measured in the suprahilar segment. Group differences were evaluated using independent t-tests and chi-square tests. Logistic and linear regression analyses were used to assess predictors of CBD dilatation and continuous diameter change. All multivariable models were adjusted for age, sex, and BMI. Results CBD diameter was significantly greater in post-cholecystectomy patients compared with controls (6.61 mm vs. 4.56 mm; p < 0.001). Dilatation ≥7 mm occurred in 38.5% of post-cholecystectomy patients versus 5.4% of controls (p < 0.001), and prior cholecystectomy remained a strong independent predictor of dilatation after adjustment (aOR = 14.583; 95% CI: 4.449-47.807). Using a fixed ≥7 mm cutoff, increasing age was associated with lower odds of categorical CBD dilatation, whereas sex and BMI were not significant predictors. Linear regression analyses demonstrated a significant positive association between CBD diameter and both time elapsed since surgery and age, indicating gradual ductal enlargement over time. Marked dilatation (>10 mm) was uncommon and did not reach statistical significance in relation to cholecystectomy. Conclusion Cholecystectomy is associated with measurable and progressive enlargement of the CBD. While CBD diameter increases gradually with advancing age and postoperative duration, categorical dilation thresholds are more strongly influenced by surgical status than by age alone. Recognition of this expected postoperative anatomical pattern may help clinicians avoid unnecessary imaging and interventions in asymptomatic patients.

Background Acute cholecystitis (AC) is one of the most common surgical emergencies with a wide range of clinical outcomes. Early identification of patients at risk for postoperative complications is essential for optimizing surgical decision-making and resource allocation. Hemogram-derived indices such as the systemic immune-inflammation index (SII) and neutrophil-to-lymphocyte ratio (NLR), in addition to biochemical markers, may provide prognostic value beyond traditional risk factors. Materials and methods This retrospective single-center study included 210 patients admitted to the University Clinical Center Tuzla with AC between January 2024 and January 2025. Demographic, clinical, and laboratory data were collected. Receiver operating characteristic (ROC) analysis was performed to identify optimal cut-off values for predicting complications. Multivariate logistic regression was adjusted for age, sex, diabetes mellitus, hypertension, and other baseline comorbidities, in addition to SII, NLR, glucose, and creatinine. Results Four variables emerged as independent predictors of complications: SII > 950 remained an independent predictor after full adjustment (p = 0.002) with a sensitivity of 78% and specificity of 72%. It yielded the highest discriminatory accuracy among the evaluated markers, with an area under the curve (AUC) of 0.81 (95% confidence interval (CI) 0.75-0.87). No formal comparison with TG18 grading was performed. In contrast, baseline comorbidities such as diabetes mellitus and hypertension did not retain significance after adjustment. Conclusion SII, NLR, glucose, and creatinine independently predicted complications in AC, with SII emerging as the strongest predictor among the evaluated variables. These findings suggest that incorporating hemogram-derived indices into preoperative assessment may enhance risk stratification. However, the retrospective single-center design and potential confounding related to the surgical approach warrant cautious interpretation.

Glioblastoma (GBM) remains a major clinical challenge due to limited therapeutic success despite standard treatments including surgery, radiotherapy, and temozolomide (TMZ). Recent evidence links hyperglycemia to cancer progression, and altered glucose metabolism has emerged as a key factor in GBM development. Metformin, an antidiabetic drug, has shown promise in improving survival in GBM patients, possibly due to its ability to cross the blood-brain barrier and target metabolic pathways involved in tumor growth. Preclinical studies suggest metformin may enhance TMZ efficacy by acting on glioma stem cells and overcoming resistance mechanisms. Its activation of AMPK and modulation of Wnt signaling further support its therapeutic potential. However, while early studies and clinical trials have explored metformin’s safety and efficacy, its direct impact on GBM survival remains unclear. Ongoing research aims to clarify its mechanisms and identify responsive patient subgroups. Novel strategies, including PPARγ agonists and nanoerythrosome-based drug delivery systems, are also under investigation to improve metformin’s therapeutic profile. Rigorous clinical trials and mechanistic studies are essential to determine the role of metformin as adjunct therapy in GBM treatment.

Aim This study compared the extent of coronary artery calcification in patients with and without type 2 diabetes mellitus (T2DM) using Coronary Computed Tomography Angiography (CCTA). Methods This retrospective, observational cohort study included 107 patients who underwent CCTA at the Clinical Centre of the University of Sarajevo between July and December 2024. Patients were divided into two groups: those with T2DM (n=51) and those without T2DM (n=56). Laboratory parameters, demographic data, and calcium scores were analysed. The calcium score was categorised into six groups based on cardiovascular risk and the comparison was made using appropriate statistical analysis. Results Patients with T2DM had significantly higher calcium scores than non-diabetic patients (p=0.0001). In the T2DM group, 35.3% of patients had a calcium score >400, indicating high cardiovascular risk. Patients without diabetes were more frequently classified into lower-risk categories (p=0.0001). A significant correlation was found between calcium score and age (r=0.442, p=0.001) and gender (r=-0.218, p=0.024), with men having higher calcium scores. Additionally, total cholesterol, LDL, and uric acid levels were significantly higher in diabetic patients (p=0.005; p=0.025; p=0.03, respectively). Conclusion This study confirms a strong association between T2DM and increased coronary artery calcification. Age and male gender are significant predictors of higher calcium scores. Further research is needed to explore these relationships, particularly within the Bosnian population. Keywords Coronary angiography, coronary artery calcification, coronary disease, diabetes mellitus type 2.

Introduction: Non-ST elevation myocardial infarction (NSTEMI) carries a substantial risk of early major adverse cardiovascular events (MACE) despite advances in therapy. Easily obtainable biochemical and echocardiographic markers may improve early risk stratification, particularly in patients managed without revascularization. This prospective study assessed the prognostic significance of inferior vena cava (IVC) diameter, serum uric acid, homocysteine, and selected hematological indices in predicting 90-day MACE in NSTEMI patients treated with conservative medical therapy. Unlike prior studies that examined these biomarkers individually, our study integrates biochemical (uric acid, homocysteine), echocardiographic (IVC diameter), and hemogram-derived indices into a combined model for early risk stratification in conservatively treated NSTEMI patients. Methods: A total of 170 consecutive NSTEMI patients admitted to the University Clinical Center Tuzla between February 2022 and January 2023 were included. All patients received guideline-directed medical therapy. Clinical, echocardiographic, and laboratory data were obtained within 24 hours of admission. The primary endpoint was MACE (cardiac death, reinfarction, or urgent coronary revascularization) within 90 days. Logistic regression identified independent predictors; discriminatory ability was assessed using receiver operating characteristic (ROC) analysis, and Kaplan-Meier curves evaluated event-free survival. Results: MACE occurred in 87 patients (51.2%). Compared to event-free patients, those with MACE had larger IVC diameters (20.25 ± 2.52 mm vs. 18.36 ± 2.16 mm; p < 0.001), higher uric acid (432.8 ± 47.3 μmol/L vs. 358.9 ± 44.6 μmol/L; p < 0.001), and elevated homocysteine levels (18.42 ± 4.13 μmol/L vs. 13.39 ± 2.88 μmol/L; p < 0.001). In multivariate analysis, uric acid (OR per 10 μmol/L = 1.32; 95% CI: 1.05-1.65; p = 0.015) and homocysteine (OR per 1 μmol/L = 1.23; 95% CI: 1.06-1.42; p = 0.005) remained independent predictors. ROC analysis showed excellent discrimination for homocysteine (AUC: 0.844) and uric acid (AUC: 0.830). IVC diameter was associated with lower MACE-free survival (log-rank p = 0.036) but lost significance after adjustment. Conclusion: Elevated homocysteine and uric acid independently predicted 90-day MACE in NSTEMI patients managed without revascularization. While IVC diameter was not independently predictive, its combination with biochemical markers may enhance risk stratification and guide early post-discharge management. These findings warrant validation in larger multicenter studies.