Search Results (694)

Background: COVID-19 is associated with coagulopathy and increased mortality. The ABO blood group system has been implicated in modulating susceptibility to SARS-CoV-2 infection and disease severity, but its relationship with viral RNAemia, spike gene mutations, and thrombosis remains underexplored. Methods: We analyzed 446 hospitalized COVID-19 patients between 2021 and 2022. SARS-CoV-2 RNAemia was assessed via RT-qPCR on whole blood, and spike gene mutations were identified through whole-genome sequencing in RNAemia-positive samples. ABO blood groups were determined by agglutination testing, and thrombotic events were evaluated using coagulation markers. Statistical analyses included chi-square tests and Kruskal–Wallis tests, with significance set at p < 0.05. Results: RNAemia was detected in 26.9% of patients, with no significant association with ABO blood group (p = 0.175). Omicron was the predominant variant, especially in blood group A (62.5%). The N501Y mutation was the most prevalent in group O (53.2%), and K417N was most prevalent in group B (36.9%), though neither reached statistical significance. Thrombotic events were significantly more common in blood group A (OR = 2.08, 95% CI = 1.3–3.4, p = 0.002), particularly among RNAemia-positive patients. Conclusions: ABO blood group phenotypes, particularly group A, may influence thrombotic risk in the context of SARS-CoV-2 RNAemia. While no direct association was found between blood group and RNAemia or spike mutations, the observed trends suggest potential host–pathogen interactions. Integrating ABO typing and RNAemia screening may enhance risk stratification and guide targeted thromboprophylaxis in COVID-19 patients. Full article

Background: COVID-19-associated coagulopathy (CAC) is a complex condition, with high rates of thrombosis, high levels of inflammation markers and hypercoagulation (increased levels of fibrinogen and D-Dimer), as well as extensive microthrombosis in the lungs and other organs of the deceased. It resembles, without being identical, other coagulation disorders such as sepsis-DIC (SIC/DIC), hemophagocyte syndrome (HPS) and thrombotic microangiopathy (TMA). Platelets (PLTs), key regulators of thrombosis, inflammation and immunity, are considered an important risk mediator in COVID-19 pathogenesis. Platelet index MPV/PLT ratio is reported in the literature as more specific in the prognosis of platelet-related systemic thrombogenicity. Studies of MPV/PLT ratio with regards to the severity of COVID-19 disease are limited, and there are no references regarding this ratio to the outcome of COVID-19 disease at specific time points of hospitalization. The aim of this study is to evaluate the relationship of COVID-19 mortality with the red cell distribution width–coefficient of variation (RDW-CV), platelets and MPV/PLT ratio parameters. Methods: Values of these parameters in 511 COVID-19 hospitalized patients were recorded (a) on admission, (b) as mean values of the 1st and 2nd week of hospitalization, (c) over the total duration of hospitalization, (d) as nadir and zenith values, and (e) at discharge. Results: As for mortality (survivors vs. deceased), statistical analysis with ROC curves showed that regarding the values of the parameters on admission, only the RDW-CV baseline was of prognostic value. Platelet parameters, absolute number and MPV/PLT ratio had predictive potential for the disease outcome only as 2nd week values. On the contrary, with regards to disease severity (mild/moderate versus severe/critical), only the MPV/PLT ratio on admission can be used for prognosis, and to a moderate degree. On multivariable logistic regression analysis, only the RDW-CV mean hospitalization value (RDW-CV mean) was an independent and prognostic variable for mortality. Regarding disease severity, the MPV/PLT ratio on admission and RDW-CV mean were independent and prognostic variables. Conclusions: RDW-CV, platelets and MPV/PLT ratio hematological parameters could be of predictive value for mortality and severity in COVID-19 disease, depending on the hospitalization timeline. Full article

Background/Objectives: Pregnancy is associated with increased procoagulant conditions, and when combined with obesity, it can elevate the risk of thrombosis. The study aims to assess thrombosis risk markers during pregnancy in relation to obesity. Methods: Somatically healthy women aged 18–42 years with spontaneous pregnancies who did not receive specific antithrombotic treatment were enrolled in the study (n = 97). The participants were divided into groups based on pregestational BMI: the first group consisted of patients who had a BMI ≤ 25 (n = 42), and the second group consisted of patients who were overweight (BMI > 25) and obese (BMI > 30) (n = 55). The control group comprised healthy, non-pregnant, non-obese women (n = 10). Results: Fibrinogen levels, elevated during pregnancy, were higher in the II and III trimesters, with gestational period having a greater influence than BMI. Moderate D-dimer accumulation was observed regardless of obesity, but higher levels were seen in obese women during the III trimester, indicating the dissolution of intravascular fibrin deposits. Soluble fibrin was significantly higher in obese and overweight women during the II trimester and elevated in both groups during the III trimester, correlating with D-dimer accumulation and indicating thrombus formation. A decrease in platelet aggregation ability was observed correlating with D-dimer and soluble fibrin patterns. Conclusions: A significant accumulation of thrombosis risk markers was observed in the III trimester compared to the II, occurring earlier in obese and overweight pregnant women and indicating a higher risk of thrombotic complications in obesity. Full article

Inflammatory Bowel Disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), results from dysregulated immune responses that drive chronic intestinal inflammation. Neutrophils, as key effectors of the innate immune system, contribute to IBD through multiple mechanisms, including the release of reactive oxygen species (ROS), pro-inflammatory cytokines, and neutrophil extracellular traps (NETs). NETs are web-like structures composed of DNA, histones, and associated proteins including proteolytic enzymes and antimicrobial peptides. NET formation is increased in IBD and has a context-dependent role; under controlled conditions, NETs support antimicrobial defense and tissue repair, whereas excessive or dysregulated NETosis contributes to epithelial injury, barrier disruption, microbial imbalance, and thrombotic risk. This review examines the roles of neutrophils and NETs in IBD. We summarize recent single-cell and spatial-omics studies that reveal extensive neutrophil heterogeneity in the inflamed gut. We then address the dual role of neutrophils in promoting tissue damage—through cytokine release, immune cell recruitment, ROS production, and NET formation—and in supporting microbial clearance and mucosal healing. We also analyze the molecular mechanisms regulating NETosis, as well as the pathways involved in NET degradation and clearance. Focus is given to the ways in which NETs disrupt the epithelial barrier, remodel the extracellular matrix, contribute to thrombosis, and influence the gut microbiota. Finally, we discuss emerging therapeutic strategies aimed at restoring NET homeostasis—such as PAD4 inhibitors, NADPH oxidase and ROS pathway modulators, and DNase I—while emphasizing the need to preserve antimicrobial host defenses. Understanding neutrophil heterogeneity and NET-related functions may facilitate the development of new therapies and biomarkers for IBD, requiring improved detection tools and integrated multi-omics and clinical data. Full article

Background: Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most common malignancies associated with thrombotic events. While there is research present on various techniques of portal vein reconstruction, there is limited published data on the techniques and/or considerations of reconstruction in the setting of complete portal vein occlusion. We therefore sought to analyze and present our experience of this clinical scenario. Methods: This was a retrospective analysis of a prospectively collected database. All patients who underwent portal vein resection and/or reconstruction during a pancreatic resection were included. Post-operatively, all patients underwent a contrast-enhanced CT scan on post-operative day 1 to assess for any portal vein thrombus. Results: Pancreatic resection with portal vein reconstruction was performed in 183 patients. Complete PV occlusion was seen in 12 patients at the time of surgery. In those patients with an occluded PV, reconstruction options included primary repair with end-end anastomosis (n = 2) or use of an interposition graft (n = 9). Interposition graft conduits included the left renal vein (n = 6), tubularized bovine pericardium (n = 3), and femoral vein (n = 1). Post-operative portal vein thrombus was seen in 4/12 patients. The majority of patients (n = 7) were discharged on therapeutic anticoagulation, 4 were discharged on an antiplatelet, and 1 patient received neither. Conclusions: Based on our series, we would recommend attempting PV reconstruction in these patients with an interposition graft (with autologous left renal vein or bovine pericardium). We believe that with this technique, the post-operative thrombosis risk is similar to PV reconstructions in non-occluded patients. Full article

Myeloproliferative neoplasms (MPNs) are chronic blood cancers characterized by overproduction of blood cells, leading to increased thrombotic and ischemic risk. Patients frequently experience symptoms including fatigue, abdominal discomfort, and complications from thrombotic events, which significantly impact the quality of life (QoL). Many patients inquire about complementary and integrative medicine (CIM) approaches, including nutritional interventions and supplements, creating opportunities for healthcare providers to engage in meaningful discussions guided by the principle of safety. This review examines the current evidence for integrative approaches in MPN management, focusing on nutrition, microbiota, supplements, mind–body techniques, and acupuncture. We analyze the available data on anti-inflammatory interventions, QoL improvement strategies, and treatment tolerance enhancement. The review provides clinicians with evidence-based guidance for safely integrating complementary therapeutic approaches with conventional MPN treatment. This integrative approach represents an opportunity to develop more comprehensive and personalized therapeutic paradigms in hematology while ensuring that complementary interventions serve as adjuncts to evidence-based medical treatment. Full article

Sinusoidal Obstruction Syndrome/Veno-Occlusive Disease (SOS/VOD) is a severe complication of hematopoietic cell transplantation (HCT). Furthermore, emerging evidence suggests the potential role of complement activation and endothelial injury in SOS/VOD pathogenesis. In this study, we aimed to identify potential distinct pathogenic genetic variants between SOS/VOD and other endothelial injury syndromes following HCT, such as transplant-associated thrombotic microangiopathy (TA-TMA). For this aim, genomic DNA from 30 SOS/VOD patients and 30 controls with TA-TMA was analyzed. Using Next-Generation Sequencing (NGS), variants in complement-related genes (CFH, CFI, CFB, CFD, C3, CD55, C5, CD46, and thrombomodulin/THBD) and ADAMTS13 were examined. Out of 426 detected variants, 20 were classified as pathogenic. In SOS/VOD patients, variants were identified in ADAMTS13 (4), CFH (3), C3 (2), and CFB (1) genes. One of the variants has been recognized as the strongest genetic predictor of ADAMTS13 activity. Controls exhibited more variants in complement-related genes, particularly CFH, CFI, and C3. The genetic differences between SOS/VOD and TA-TMA highlight different pathogenic mechanisms, offering the potential for targeted risk assessment and therapy in HCT recipients. Full article

Background: The enzyme A Disintegrin and metalloprotease with thrombospondin type 1 motif, member 13 (ADAMTS13) regulates hemostasis by cleaving von Willebrand factor (VWF) multimers. ADAMTS13–VWF axis dysregulation leads to different thrombotic conditions. This study investigated changes in ADAMTS13 activity during major cardiac procedures and their relationship to VWF changes and clinical complications. Methods: A total of 628 ADAMTS13 activity and inhibitor measurements were carried out in 168 patients who underwent cardiac surgery. ADAMTS13 activity was measured after the initiation of anesthesia and daily for up to 6 days postoperatively via Technozym chromogenic ELISA. The von Willebrand factor antigen (VWF:Ag) and collagen binding (VWF:CB) were also measured. Clinical complications and correlations with liver function biomarkers were also assessed. Results: ADAMTS13 activity significantly decreased during surgery, with mean values markedly decreasing from preoperative to postoperative measurements (p = 0.01). A clear inverse relationship between ADAMTS13 activity and the VWF:CB/VWF:AG ratio was observed, indicating that increased high-molecular-weight VWF multimers are associated with decreased ADAMTS13 activity. Correlation analyses (CHE, Spearman’s rho = 0.39) indicated that the reduction in ADAMTS13 activity was not attributable to impaired liver synthesis but likely resulted from peripheral consumption, potentially influenced by surgical stress. Conclusions: Perioperative reductions in ADAMTS13 activity are associated with an accumulation of high-molecular-weight VWF multimers and a higher incidence of postoperative complications. These results demonstrate that ADAMTS13 could be a useful perioperative risk biomarker for cardiac surgery patients. Full article

Venous thromboembolism (VTE) represents a significant complication of cancer immunotherapy, with emerging evidence suggesting distinct pathophysiological mechanisms compared to traditional chemotherapy-associated thrombosis. This narrative review examines the epidemiology and pathogenesis of VTE in patients receiving immunotherapies for cancer including immune checkpoint inhibitors (ICIs), chimeric antigen receptor (CAR) T-cell therapy, bispecific T-cell engagers (BiTEs), among others. Real-world studies demonstrate a wide range of VTE incidence rates in ICI recipients, with potential mechanisms including exacerbated underlying interleukin-8-mediated inflammatory pathways and consequent neutrophil extracellular trap (NET) formation. CAR T-cell therapy is associated with unique hemostatic challenges, including concurrent thrombotic and bleeding risks related to cytokine release syndrome. Current risk assessment tools show limited predictive utility in patients receiving immunotherapies for cancer, highlighting the need for novel stratification models. Future research priorities include developing immunotherapy-specific risk prediction tools, elucidating mechanistic pathways linking immune activation to thrombosis, and establishing evidence-based and tailored thromboprophylaxis strategies. As cancer immunotherapy continues to evolve, understanding and mitigating thrombotic complications remains crucial for optimizing patient outcomes. Full article

Myeloproliferative neoplasms (MPNs) are clonal hematopoietic disorders characterized by excessive proliferation of one or more myeloid lineages, frequently accompanied by an elevated risk of thrombotic events. Matrix metalloproteinases (MMPs), a family of zinc-dependent endopeptidases, are implicated in numerous inflammatory and vascular pathophysiological processes. In this study, we analyzed the association between selected MMP polymorphisms, rs1799750, rs243865, rs3025058, rs3918242, and rs17576, and thrombotic risk as well as clinical characteristics in patients with MPNs. Genotyping was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. Among the polymorphisms analyzed, a statistically significant association was identified between the MMP-9 rs3918242 CT genotype and an increased risk of arterial thrombosis (OR = 4.206, CI 1.337–13.234, p = 0.014). Moreover, rs3918242 CT was associated with thrombotic events (both arterial and venous thrombosis combined), suggesting a potential contributory role in the prothrombotic phenotype observed in MPNs (OR = 3.200, CI 1.110–9.258, p = 0.031). These findings indicate that genetic variation in MMP-9, particularly rs3918242, may serve as a predictive marker for vascular complications in MPN patients. Further studies with larger cohorts are warranted to confirm these associations and to elucidate the molecular mechanisms underlying the contribution of MMP polymorphisms to thrombosis in MPNs. Full article

Background: Chronic kidney disease (CKD) is an established global health problem, with the increased prevalence of vascular inflammation, accelerated atherogenesis, and thrombotic risk all contributing to overall cardiovascular risk. The major CKD-specific risk factor is presumed to be the accumulation of uremic toxins in circulation and tissues, further accelerating the progression of CKD and its co-morbidities, including those of bone mineral disorders and cardiovascular diseases. Materials and Methods: In our narrative review, we focused on non-traditional cardiovascular risk factors, as they evolve with declined kidney function and are potentially further modulated by the choice of kidney replacement therapy. Results: Based on the data from the literature to date, the pre-eminent role of non-traditional risk factors emerges to mediate inflammation and increased cardiovascular mortality. In particular, patients receiving hemodialysis (HD) display dramatically increased CVD-mediated mortality. This intensified state of inflammation may be linked to the direct exposure of the bloodstream to a bio-incompatible environment in HD; for both complement-mediated and non-complement-mediated reactions, the possible contribution of neutrophil extracellular traps and complement activation-related pseudoallergy are reviewed in detail. Conclusions: Our narrative review emphasizes key elements of a bio-incompatible HD environment that may contribute to increased cardiovascular mortality in patients receiving HD. Summarizing these results may provide conceptual opportunities to develop new therapeutic targets. Full article

Objectives: We aimed to quantify the damage burden measured using the Damage Index for Antiphospholipid Syndrome (DIAPS) in patients with antiphospholipid syndrome (APS) and identify patients with high damage as well as any correlations of damage with subclinical atherosclerosis. Methods: Patient damage was assessed via DIAPS. Based on demographic, clinical and laboratory characteristics, patients were divided into two subgroups: thrombotic APS patients with high vs. low damage, and non-thrombotic aPL-positive patients with vs. without damage. Participants underwent carotid/femoral ultrasound for atherosclerotic plaque detection and carotid–femoral and carotid-radial pulse wave velocity (PWV). Results: We included 112 patients with an APS diagnosis, 57 (50.9%) with primary APS and 55 (49.1%) with associated SLE. Cardiovascular (CVD) risk factors and complications were significantly more frequent in the thrombotic group, as well as in patients with high damage within the thrombotic group. We did not identify any risk factors for increased damage in the non-thrombotic group. Atherosclerotic plaque presence was present in 27 (24%) of the patients in this study with the same frequency in the APS and APS/SLE groups (p = 0.5446). Pulse wave velocity (PWV) was elevated in 27–32% patients according to analyzed arteries. Elevated PWV was more frequent in the APS group in comparison to APS/SLE only between carotid and radial arteries (p = 0.0012). Both atherosclerotic plaque presence and PWV did not correlate with damage severity. Conclusions: DIAPS indicates substantial damage in APS patients in our study. High organ damage mainly affected thrombotic patients and was related to CVD complications. At the same time, screening of subclinical atherosclerosis seems not to predict higher damage in APS patients. Full article

Background: Coronavirus disease 2019 (COVID-19) involves a complex interplay of dysregulated immune responses, a pro-inflammatory cytokine storm, endothelial injury, and thrombotic complications. This study aimed to evaluate the impact of kidney function on clinical, laboratory, and outcome parameters in patients hospitalized with COVID-19. Methods: We conducted a retrospective analysis of 359 patients admitted during the first wave of COVID-19, stratified by estimated glomerular filtration rate (eGFR < 60 vs. ≥60 mL/min/1.73 m²). Data on demographics, vital signs, laboratory values, and clinical outcomes—including mortality, hemodialysis requirement, intensive care unit (ICU) admission, and mechanical ventilation (MV)—were collected. Univariate and multivariate linear regression, as well as area under the receiver operating characteristic curve (AUC-ROC) analyses, were performed. A p-value < 0.05 was considered statistically significant. Results: Patients with an eGFR < 60 were older and more likely to have systemic hypertension, chronic kidney disease, a history of solid organ transplantation, and immunosuppressive therapy. This group showed higher rates of mortality (41.6% vs. 19.2%), hemodialysis requirement (32.3% vs. 9.6%), ICU admission (50.9% vs. 37.9%), and MV (39.8% vs. 21.2%). Laboratory results revealed acidosis, anemia, lymphopenia, elevated inflammatory markers, and hyperkalemia. Conclusions: An admission eGFR < 60 mL/min/1.73 m² is associated with worse clinical outcomes in COVID-19 and may serve as a simple, early marker for risk stratification. Full article

Background: Retinal vascular occlusion (RVO) and retinal artery occlusion (RAO) have been reported as rare adverse events following COVID-19 vaccination, raising concerns about vaccine safety. This review synthesizes cohort and case–control studies assessing the association between COVID-19 vaccines and RVO/RAO, while exploring potential pathophysiological mechanisms. Methods: We analyzed large-scale population-based studies from South Korea, Europe, and the TriNetX database, focusing on odds ratios (OR), hazard ratios (HR), and relative risks (RR) across mRNA and adenoviral vector vaccines. Pathological processes were hypothesized based on molecular and clinical evidence. Results: Studies investigating the association between COVID-19 vaccination and retinal vascular occlusion show conflicting results; some studies report no association (e.g., OR 0.93, 95% CI 0.60–1.45), others suggest reduced risk (e.g., OR 0.80, 95% CI 0.64–0.99), and one indicates increased risk over two years (HR 2.19, 95% CI 2.00–2.39). Adenoviral vector vaccines, particularly ChAdOx1, show higher RAO incidence in specific cohorts. Proposed mechanisms include vaccine-induced immune thrombotic thrombocytopenia (VITT) via anti-PF4 antibodies, spike protein-mediated endothelial dysfunction, and adjuvant-driven inflammation. Conclusions: While causality remains unproven, temporal heterogeneity and vaccine type-specific risks warrant further investigation. Longitudinal studies with robust controls are needed to clarify these associations in the post-pandemic context. Full article

Background/Objectives: Immature platelet fraction (IPF) and reticulated platelets (RPs) are biomarkers reflecting the youngest and most metabolically active platelets in circulation. RPs, a subset of immature platelets, contain residual RNA and have been associated with increased thrombotic potential. Elevated IPF levels indicate enhanced platelet production, commonly observed during elevated platelet turnover, such as in autoimmune reactions, consumption, and thrombotic events. This systematic review aims to evaluate the potential role of IPF and RPs in the context of cerebrovascular events, specifically ischemic and hemorrhagic stroke, as well as transient ischemic attacks (TIAs), and to assess their clinical utility in stroke monitoring and management. Methods: A comprehensive literature search was conducted in PubMed, Scopus, Cochrane Library, and Web of Science for studies published between 2000 and 2024, which focused on IPF and RPs in human subjects with cerebrovascular events. Results: Six studies met the inclusion criteria. Findings suggest that elevated levels of IPF and RP are associated with the acute and chronic phases of ischemic stroke and TIA and may reflect increased platelet turnover and thrombotic activity. Some evidence supports their role in predicting stroke severity, recurrence, and underlying etiology, although results are not yet consistent across all studies. Conclusions: IPF and RPs are emerging biomarkers with potential applications in acute ischemic stroke and risk stratification. While current evidence is promising, further research is needed to standardize measurement techniques and validate their routine use in clinical practice. Full article