Search Results (1,304)

Background: Stroke-associated pneumonia (SAP) is a common complication after acute ischemic stroke and contributes to worse recovery and greater resource use. Nutritional and inflammatory dysregulation have been implicated in both SAP susceptibility and adverse prognosis. Objective: To examine whether admission inflammatory and nutritional markers are associated with the development of SAP and with short-term functional prognosis. Methods: We performed a retrospective single-centre cohort study of consecutive patients with acute ischemic stroke admitted between 1 January 2015 and 31 December 2024 ($N=303;SAPn=108,non-SAPn=195$). Admission laboratory indices (albumin, CRP, fibrinogen, WBC, PCT, and prealbumin) in the first 24 h and clinical variables were analysed. Multivariable logistic regression identified factors independently associated with SAP; the relationship between SAP and early functional recovery was assessed in adjusted outcome models. A nomogram integrating key predictors was developed and its apparent discrimination is reported. Results: SAP occurred in 35.6% of patients. Factors independently associated with SAP included nasogastric tube placement (OR: 7.02, 95% CI: 3.50–14.62), venous thromboembolism (OR: 3.20, 95% CI: 1.62–6.31), cognitive impairment (OR: 2.90, 95% CI: 1.32–6.36), and elevated inflammatory markers (WBC OR: 1.52, 95% CI: 1.28–1.80; fibrinogen OR: 1.37, 95% CI: 1.02–1.84; CRP OR: 1.01, 95% CI: 1.00–1.03). Higher admission serum albumin was associated with lower odds of SAP (OR: 0.92, 95% CI: 0.86–0.98). The nomogram showed strong apparent discrimination (AUC: 0.90, 95% CI: 0.86–0.94). After multivariable adjustment, SAP remained associated with poorer short-term functional improvement (adjusted OR: 6.99, 95% CI: 3.05–17.54) and greater healthcare utilization (median length of stay: 39.6 vs. 30.6 days; median cost: USD 12,836 vs. 6585). Conclusion: In this retrospective cohort, admission markers of nutritional depletion and inflammatory activation were associated not only with increased likelihood of SAP, but also with adverse early functional outcomes. These association-based findings support early risk stratification using routine admission markers; prospective studies and external validation are required before clinical implementation. Full article

Endovascular aneurysm repair (EVAR) is a widely used minimally invasive treatment for abdominal aortic aneurysms. However, postoperative type II endoleak (T2EL) remains a relevant complication associated with a risk of aneurysm rupture and the need for repeated imaging follow-up, resulting in exposure to ionizing radiation. Identification of biological factors predisposing to T2EL may improve risk stratification. This pilot study aimed to investigate whether disturbances in hemostasis are associated with early T2EL development after EVAR. A total of 103 patients treated with EVAR for symptomatic or asymptomatic abdominal aortic aneurysms in a tertiary vascular center were prospectively enrolled. Blood samples were collected preoperatively and one month postoperatively to assess fibrinogen, prothrombin fragment F1+2 (F1+2), thrombin–antithrombin complex (TAT), tissue plasminogen activator antigen (tPA), plasminogen activator inhibitor-1 (PAI-1) activity, and platelet activity. Computed tomography angiography (CTA) during follow-up was used to detect endoleaks and calculate their volume. Patients with T2EL had significantly lower levels of prothrombin fragment F1+2 and higher PAI-1 activity compared with patients without endoleak. No significant association was observed between the analyzed biomarkers and endoleak volume. These findings suggest that reduced thrombin generation and impaired fibrinolysis may contribute to endoleak formation after EVAR and warrant further investigation in larger, confirmatory studies. Full article

Antioxidants, such as phenolic compounds, are essential for mammal physiology. Significant research made on the gut–brain axis has produced volumes of evidence indicating that some plant-derived phenolic compounds can reach brain cells to exert protective effects on them, mainly by maintaining and/or restoring redox homeostasis. Their systemic uptake and transport might be determined by the phenolic’s physicochemical properties, along with complex interactions with protein transporters and carriers, including GLUT, SGLT1, ABC transporters (P-glycoprotein, breast cancer resistance protein), albumin, fibrinogen, organic anion and cation transporters, and MATE1. The present work focuses on the chemical interactions and transport pathways of some phenolic compounds to reach brain cells. Full article

Background: Complicated acute pyelonephritis (AP) is a severe upper urinary tract infection associated with systemic inflammation, organ dysfunction, and the risk of sepsis. The increasing prevalence of antimicrobial-resistant (AMR) organisms can alter clinical management. This study aimed to characterize the biological profile of inpatients with complicated AP and to eventually identify laboratory markers associated with risks of sepsis and AMR infections. Material and Methods: A retrospective observational analysis on 553 adult inpatients diagnosed with complicated AP between 2021 and 2025 was conducted in a tertiary center. Demographic, clinical, and biological parameters were analyzed, including inflammatory markers and renal and hepatic markers. Results: Group characteristics included a mean age of 63.82 ± 15.67 years, and 63% were female. At admission, inflammatory markers were raised, with leukocytosis (15.6 ± 5.8 × 10³/µL), neutrophilia (10.1 ± 4.7 × 10³/µL), and elevated C-reactive protein (CRP) (median 43.2 mg/dL). Coagulation activation was significant with elevated fibrinogen of 747 ± 145 mg/dL and D-dimer with a median level of 1249 ng/mL, of which 58% exceeded 1000 ng/mL. Mild to moderate renal impairment was frequently observed (creatinine 1.69 ± 0.76 mg/dL). In multivariate analysis, no biological parameter proved to be an independent predictor of AMR status among organisms. Discussion and Conclusions: Inpatients with complicated AP showed a pronounced inflammatory and procoagulant biological profile that did not vary between AMR pathogen and non-AMR pathogen infections. This suggests that the clinical value of biomarkers, such as leukocyte and neutrophile, CRP, D-dimer, fibrinogen, procalcitonin, urea, and creatinine, lies primarily in assessing disease severity rather than predicting antimicrobial resistance. The microbiological profile was dominated by Gram-negative pathogens, particularly Escherichia coli, although a heterogeneous spectrum of microorganisms was identified. Full article

Novel pharmacological approaches advocate developing multitarget drugs, that is, molecules capable of simultaneously acting on two or more pharmacological targets to produce synergistic effects from a single compound in each disease. This strategy may help reduce required doses and prevent drug–drug interactions typically associated with polypharmacy. Coumarins are natural products with diverse pharmacological activities, including antioxidant, anti-inflammatory, anticancer, neuroprotective, cardioprotective, and antithrombotic effects. The pleiotropic actions of these molecules suggest that modifying the coumarin structure could yield new multi-target antiplatelet agents with greater efficacy and safety than those currently available in clinical practice. In this work, we began with a theoretical approach using molecular docking and designed three coumarins that simultaneously inhibited platelet aggregation induced by epinephrine, collagen, and ADP. Experimentally, we evaluated the structure activity relationship of three coumarins: (A) 6,7-dimethoxy-3-(1H-pyrrol-1-yl)-2H-chromen-2-one, (B) 7,8-dimethoxy-3-(1H-pyrrol-1-yl)-2H-chromen-2-one, and (C) 3-(1H-imidazol-1-yl)-6,7-dimethoxy-2H-chromen-2-one. In silico studies suggest that compounds B and C may exhibit antagonistic interactions at the α₂-adrenergic, GPVI collagen, and P₂Y₁₂ ADP receptors. Additionally, molecular docking indicates essential interactions between the compounds and the GPIIb/IIIa fibrinogen receptor. Full article

Acute coronary syndromes (ACS) are a major cause of mortality worldwide, and although interventional treatment has significantly improved mortality and morbidity related to ischemic heart disease, there is constant concern about optimizing drug treatment. In this regard, multiple studies have been conducted on inflammation in myocardial infarction (MI), starting from its implications in the atherosclerosis process. The aim of this review is to analyse the current evidence related to the subject and the correlation between the inflammatory state at presentation and the prognosis of patients with MI, identifying key points, possible therapeutic limitations, and future research directions. Both innate and acquired immune components are involved in the inflammatory cascade, with an increase in inflammatory cell and cytokine levels. To analyse the degree of inflammation and determine when it is excessive, numerous inflammatory markers have been studied, from acute phase proteins such as high-sensitivity C-reactive protein (hsCRP) and fibrinogen, to the ratios between inflammatory cells and interleukins involved in the main inflammatory pathways. Their association with post-infarction mortality and morbidity has been observed, but they must be integrated into the clinical context for the selection of patients who would benefit most from their reduction. New anti-inflammatory therapies are being studied in light of these findings, and progress is expected. Early trials with non-selective anti-inflammatory drugs have highlighted the importance of selective inhibition so as not to disrupt healing, and drugs are now being studied that target specific pathways that are exacerbated in infarction and lead to excessive remodelling. Several inflammatory pathways have been investigated but the results are inconclusive in terms of improving prognosis, requiring further studies to formulate future therapeutic indications. Full article

Background and Objectives: Severe COVID-19 frequently fulfills Sepsis-3 criteria and is characterized by thrombo-inflammation and endothelial injury. We evaluated whether a bedside endothelial activation index (EAI = D-dimer/fibrinogen) identifies biologically distinct phenotypes and relates to interleukin-6 (IL-6) response after therapeutic plasma exchange (TPE), and whether baseline IL-6 predicts a ≥50% IL-6 reduction. Methods: Retrospective single-center ICU cohort of adults with SARS-CoV-2 infection, sepsis-related organ dysfunction, and ≥1 TPE session (n = 51). Patients were stratified by median EAI (low vs. high). Outcomes included peri-procedural biomarker/physiology changes (post–baseline), IL-6 responder status (≥50% reduction), correlations with IL-6 reduction (%), and multivariable predictors of response. Results: Compared with low EAI (n = 25), high EAI (n = 26) had higher baseline D-dimer (6.2 vs. 2.2 µg/mL) and lower fibrinogen (2.9 vs. 7.1 g/L) (both p < 0.001). Low EAI showed larger CRP decreases (ΔCRP −84.0 vs. −2.3 mg/L; p = 0.001) and larger fibrinogen falls (Δ −3.1 vs. −0.4 g/L; p < 0.001), while high EAI had larger D-dimer decreases (Δ −2.5 vs. −0.6 µg/mL; p = 0.004) and a modest SOFA improvement (Δ −0.3 vs. +0.1; p = 0.026). IL-6 responders (n = 20) had higher baseline IL-6 than non-responders (365.2 vs. 47.1 pg/mL; p < 0.001). Baseline IL-6 independently predicted response (per doubling: OR 1.94, 95% CI 1.27–2.95; p = 0.002), while age reduced odds (OR 0.91/year, 95% CI 0.84–0.99; p = 0.032). IL-6 reduction correlated with ΔCRP (ρ = −0.41; p = 0.003) and ΔPaO₂/FiO₂ (ρ = 0.37; p = 0.01). Conclusions: EAI stratifies distinct thrombo-inflammatory patterns around TPE, while baseline IL-6 is the dominant predictor of achieving large IL-6 reductions. To emphasize the novelty and clarify the study objective, this exploratory analysis used a phenotype-stratified framework to test whether a simple bedside endothelial activation index could enrich biological response assessment to adjunctive TPE. The prespecified primary outcome was achievement of a ≥50% IL-6 reduction after completion of the TPE course; secondary outcomes included peri-procedural biomarker, oxygenation, SOFA, and ICU endpoints. Full article

This study aimed to systematically elucidate the antihyperlipidemic mechanism of paeoniflorin, and we adopted an integrated multi-omics strategy to screen the key molecular targets and regulatory pathways involved in its action, followed by experimental validation to verify the potential regulatory effects of paeoniflorin on the screened targets and metabolic processes. Rats with high-fat diet-induced hyperlipidemia received paeoniflorin treatment. Liver histopathology was evaluated using hematoxylin–eosin and Oil Red O staining. Serum levels of total cholesterol, triglycerides, low-density lipoprotein cholesterol, high-density lipoprotein cholesterol, alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, total bile acids, activated partial thromboplastin time, prothrombin time, thrombin time, and fibrinogen were measured using a biochemical analyzer. Integrated multi-omics analyses were performed to investigate paeoniflorin’s lipid-lowering mechanism. Critical pathways and targets identified were validated using Western blotting. Paeoniflorin alleviated pathological liver damage in hyperlipidemic rats and improved blood lipid levels, coagulation function, and liver function markers. Multi-omics analyses verified that paeoniflorin downregulated the expression of TREM-1, TLR4, NF-κB, TNF-α, and IL-1β, thereby alleviating hepatic inflammation. Paeoniflorin also upregulated the expression of low-density lipoprotein receptors (LDLR), liver X receptor alpha (LXRα), and ATP-binding cassette subfamily G member 1 (ABCG1), while downregulating proprotein convertase subtilisin/kexin type 9 (PCSK9) expression, contributing to balanced cholesterol metabolism. Paeoniflorin normalized glycerophospholipid and branched-chain amino acid metabolism, which correlated with reduced inflammation and improved cholesterol metabolism. Paeoniflorin ameliorates hyperlipidemia through multitarget mechanisms, potentially by suppressing the TREM-1-TLR4-NF-κB signaling pathway to reduce inflammation and by regulating cholesterol metabolism via the PCSK9-LDLR and LXRα-ABCG1 pathways. Full article

Background: Thrombosis in light chain amyloidosis (LCA) occurs in the context of multiple organ dysfunction and inflammation. Conventional coagulation tests (screening) may not sufficiently capture the procoagulant substrate in the inflammatory/therapeutic dynamics. Methods: A total of 61 consecutive patients with LCA were prospectively included in the study. Clinical data, including organ involvement, time of diagnosis, treatment phase, DOAC exposure and thrombosis history were systematically recorded and subjected to screening. Specialized hemostasis tests such as APTT/PT, fibrinogen, D-dimer, TEG and TGT were performed and conventional times were analyzed in the subgroup without DOAC. Results: The prevalence of documented thrombosis was 32.8%, and thrombosis status was associated with TEG positivity and more strongly with TGT positivity. Hypercoagulability was identified in 50.8% by TEG and 41.0% by TGT, regardless of whether APTT/PT were within the reference values. APTT/PT did not predict thrombosis recurrence (p > 0.05), which was predicted by TEG (p = 0.0027) and TGT (p = 0.0006). An inflammation/fibrin turnover panel (CRP, fibrinogen, D-dimer) predicted TEG positivity (p < 0.0001), but not TGT, and was correlated with assessment at diagnosis, daratumumab-based therapy, and cardiac involvement. Conclusions: Global tests (TEG/TGT) promptly correlate with thrombosis recurrence in our cohort and provide crucial information in addition to clotting times for thrombotic phenotyping. Inflammation can influence TEG, so the decision to recommend the tests and the timing of their performance should be adapted to the clinical, biological, and therapeutic context. Full article

Background: Preoperative differentiation between uncomplicated and complicated paediatric appendicitis remains challenging. This study aimed to evaluate the diagnostic performance of routine admission biomarkers and blood cell count-derived inflammatory indices for severity stratification and to determine whether fibrinogen provides additional predictive value beyond commonly used markers. Methods: We conducted a retrospective single-centre study (2018–2025) using electronically recorded clinical data. Patients with suspected appendicitis were identified through appendicitis-related ICD-10 codes and diagnostically validated. The final analytical cohort required complete admission laboratory data, including C-reactive protein (CRP), fibrinogen, and complete blood count parameters. Derived inflammatory indices included the neutrophil-to-lymphocyte ratio (NLR) and the systemic immune-inflammation index (SII). Diagnostic discrimination and multivariable prediction models were evaluated to assess the ability of these markers to distinguish complicated from uncomplicated appendicitis. Results: Of 1518 screened records, 1132 patients met inclusion criteria (620 complicated; 512 uncomplicated). Complicated appendicitis was associated with higher inflammatory markers and longer hospital stay (all p < 0.001). CRP demonstrated the strongest univariable discrimination (area under the curve [AUC] 0.785), while fibrinogen showed lower performance (AUC 0.744). A combined model including CRP, NLR, and SII achieved good discrimination (AUC 0.812), with minimal improvement after adding fibrinogen (AUC 0.813). In multivariable analysis, log-transformed CRP and SII remained independently associated with complicated appendicitis (both p < 0.001). A rule-out probability threshold of 0.303 achieved 90% sensitivity (negative predictive value 0.803), whereas a CRP cut-off ≥92.24 mg/L showed high specificity (0.943) and positive predictive value (0.900). Conclusions: Routine admission biomarkers and inflammatory indices derived from complete blood counts can support severity stratification in paediatric appendicitis. CRP and SII provide meaningful predictive information, whereas fibrinogen contributes little additional discriminatory value beyond CRP-based models. These findings suggest that a small set of routinely available laboratory markers may assist early risk stratification, although external validation is required before clinical implementation. Full article

Yamakagashi (Rhabdophis tigrinus) is a widely distributed snake species in Japan. Yamakagashi causes venom-induced consumption coagulopathy (VICC) when the amount of infused venom is high, and bites can be fatal if antivenom treatment is delayed. However, yamakagashi antivenom is an unapproved treatment, and its storage capacity is limited, preventing its prompt administration. Therefore, we investigated the application of commercially available drugs, namely tranexamic acid and antithrombin III, in the treatment of VICC caused by yamakagashi venom in a rat model. Furthermore, we investigated the combination of each drug with recombinant thrombomodulin α. Administration of tranexamic acid or antithrombin III alone failed to extend rat survival or correct changes in blood coagulation markers, such as prothrombin time, fibrinogen concentrations, and D-dimer levels, in yamakagashi venom-treated rats. However, combined administration of recombinant thrombomodulin α and tranexamic acid extended rat survival and partially restored blood coagulation markers. Therefore, the combination of recombinant thrombomodulin α and tranexamic acid might represent a useful therapeutic regimen for yamakagashi venom exposure. Full article

Background: Early rebleeding after endoscopic variceal ligation (EVL) represents a serious complication in patients with cirrhosis and is associated with poor short-term outcomes. This study aimed to identify independent predictors of early rebleeding after EVL, with a particular focus on distinguishing factors associated with variceal rebleeding from those related to post-banding ulcer (PBU) bleeding, and to assess predictors of six-week mortality. Methods: We conducted a retrospective cohort study including 217 cirrhotic patients who underwent first emergency EVL for an index episode of esophageal variceal bleeding at a tertiary referral center. Early rebleeding was defined as recurrent upper gastrointestinal bleeding occurring between days 6 and 42 after the index EVL. Results: Early rebleeding occurred in 38/217 patients (17.5%): 27/38 (71.1%) variceal rebleeding and 11/38 (28.9%) PBU rebleeding. In multivariable logistic regression analysis, lower hemoglobin (OR = 0.19, 95% CI: 0.067–0.539, p = 0.002) and a higher albumin–bilirubin (ALBI) grade (OR = 24.94, 95% CI: 1.134–548.342, p = 0.041) were independently associated with increased odds of early variceal rebleeding, whereas a higher number of bands applied during index EVL (OR = 0.52, 95% CI: 0.302–0.896, p = 0.019) was independently associated with reduced odds of rebleeding, with excellent model discrimination (area under the curve [AUC] 0.981; 95% CI: 0.959–1.000). For PBU rebleeding, lower fibrinogen level was the only independent predictor (OR = 0.957, 95% CI: 0.916–1.000, p = 0.047), with strong discriminative performance (AUC 0.945; 95% CI: 0.909–0.982). Model for End-Stage Liver Disease (MELD) score, serum albumin, platelet count, and PBU rebleeding independently predicted six-week mortality. Conclusions: Markers of liver function, along with endoscopic parameters, predict early rebleeding after EVL, emphasizing the importance of the complete assessment of cirrhotic patients for refined risk stratification and tailored post-EVL management. Full article

Background/Objectives: Pelvic injuries are frequently associated with severe hemorrhage and may contribute to early trauma-induced coagulopathy (TIC). Whether pelvic injury is independently associated with TIC beyond overall injury severity remains unclear. The objective of this study was to evaluate the association between pelvic injury and TIC in severe trauma patients. Methods: We conducted a retrospective single-center study including adult severe trauma patients (injury severity score > 15) admitted between January 2012 and July 2020. Patients with moderate to severe traumatic brain injury (because of its specific coagulopathy and mortality), inter-hospital transfer, pregnancy, or long-term anticoagulant or antiplatelet therapy were excluded. Pelvic injury was defined as any traumatic lesion involving the pelvic girdle identified on admission computed tomography. TIC was defined by an international normalized ratio (INR) > 1.2 and/or fibrinogen < 1.5 g/L and/or platelet count < 100 G/L. Multivariable logistic regression was performed to identify factors associated with TIC. Results: Among 388 included patients (79.6% male, median age 39 years), 114 (29.4%) had a pelvic injury. TIC was present in 160 patients (41.3%), and TIC prevalence was significantly higher in patients with pelvic injury (n = 73–64.0%) compared to those without (n = 87–31.8%) (p < 0.001). After multivariate analysis, TIC was independently associated with pelvic injury (OR 2.81, 95% CI 1.63–4.89), shock index > 0.9 (OR 1.94, 95% CI 1.12–3.37), hemoglobin < 10 g/dL (OR 4.27, 95% CI 1.77–11.49), and lower base excess values on admission (OR per unit increase 0.92, 95% CI 0.87–0.97). Injury severity score and number of lesions (AIS ≥ 3) were not independently associated with TIC. Conclusions: Pelvic injury was independently associated with TIC after adjustment for injury severity, number of severe injuries, and markers of hemodynamic and metabolic shock, including shock index, hemoglobin level, and base excess. These findings suggest that patients with pelvic injury may represent a high-risk subgroup for early coagulopathy, supporting the need for early recognition and adapted resuscitation strategies. Further prospective studies are required to explore underlying mechanisms. Full article

Background: Acute coronary syndrome (ACS) remains a leading cause of morbidity and mortality worldwide, and improved risk stratification beyond conventional biomarkers is needed. Novel laboratory-derived indices reflecting systemic inflammation and immunonutritional status including the inflammatory prognostic index (IPI), prognostic nutritional index (PNI), and aggregate index of systemic inflammation (AISI) may provide integrated prognostic information in ACS. Methods: In this cohort study, 2400 participants were included: 800 controls, 800 patients with non-ST-elevation myocardial infarction (NSTEMI), and 800 with ST-elevation myocardial infarction (STEMI). Results: Compared with controls, NSTEMI and STEMI patients were younger and exhibited higher body mass index, blood pressure, heart rate, and progressively worse glycemic indices (fasting glucose and HbA1c; all p < 0.001). Lipid parameters were significantly higher in ACS groups versus controls (p < 0.001). Cardiac biomarkers were markedly elevated in ACS, with significantly higher troponin I and CK-MB levels in STEMI than NSTEMI and controls (both p < 0.001). Inflammatory and renal parameters (CRP, fibrinogen, urea, creatinine) were increased in ACS, most prominently in STEMI. Composite indices demonstrated strong inter-correlations, including a strong positive correlation between AISI and IPI (r ≈ 0.91, p < 0.001), while PNI correlated inversely with CONUT score (r ≈ −0.70, p < 0.001). The Gensini score differed significantly among groups and was highest in NSTEMI (p < 0.001). Survival was significantly lower in STEMI than NSTEMI (log-rank p = 0.005), with RMST of 315.5 days in NSTEMI versus 299.4 days in STEMI. In multivariable Cox regression, STEMI presentation independently predicted higher mortality risk (HR 1.26, 95% CI 1.04–1.53; p = 0.018), and higher Gensini score was also independently associated with mortality (HR 1.01 per point; 95% CI 1.00–1.02; p = 0.036). Higher PNI was independently protective (HR 0.997; 95% CI 0.993–1.000; p = 0.045), whereas age and CONUT score were not significant in the adjusted model. Conclusions: Novel laboratory-derived systemic inflammatory and nutrition-related indices particularly IPI and AISI as markers of inflammatory burden and PNI as a marker of immunonutritional balance provide clinically relevant prognostic information in ACS. STEMI presentation is associated with shorter survival, and all-cause mortality is independently related to STEMI status, greater angiographic severity (higher Gensini score), and lower PNI. These readily available indices may offer incremental value for risk stratification in NSTEMI and STEMI when integrated with conventional clinical and angiographic assessment. Full article

Long COVID is associated with persistent fatigue, exercise intolerance, and microcirculatory dysfunction. Altered red blood cell (RBC) rheology, including impaired deformability and increased aggregation, may contribute to these symptoms, yet the effects of exercise interventions remain unclear. This longitudinal pilot study tested whether an individualized, symptom-responsive exercise program improves RBC rheology in Long COVID. A total of 170 (110 f/60 m) participants entered a five-phase training protocol; 15 completed all phases and formed a predefined finisher subgroup. RBC aggregation and deformability, hematological parameters, and coagulation- and iron-related markers were assessed across phases; RBC morphology was additionally analyzed in finishers at baseline and completion. In the total cohort, aggregation indices decreased across training phases, accompanied by prolonged aggregation half-time, while hematological, coagulation, and iron markers remained largely unchanged. The deformability changes were not uniform in the full cohort; however, finishers showed a deformability shift after completion. Importantly, morphologically abnormal RBC decreased in finishers, and these changes correlated with deformability, suggesting that improved rheology is linked to reduced RBC abnormalities. Prospectively, larger controlled studies are needed to confirm these results and to evaluate whether exercise-induced rheological improvements translate into functional and symptomatic benefits. Full article