Hematology Reports最新文献

{"title":"Management of Refractory Malignancy-Associated Hemophagocytic Lymphohistiocytosis in Adolescent Patients: A Case Series of Novel Therapeutics and Treatment Challenges.","authors":"Meha Krishnareddigari, Kenny Vo, Arun Panigrahi","doi":"10.3390/hematolrep17030028","DOIUrl":"10.3390/hematolrep17030028","url":null,"abstract":"<p><strong>Background: </strong>Hemophagocytic lymphohistiocytosis (HLH) is a potentially fatal syndrome of immune dysregulation with primary (genetic) and secondary (acquired) forms, including malignancy-associated HLH (m-HLH). The condition often presents significant diagnostic and therapeutic challenges due to overlapping symptoms with underlying malignancies and the absence of standardized guidelines for refractory cases. The established standard of care is dexamethasone and etoposide, but no guidelines exist for refractory HLH or cases triggered by malignancy.</p><p><strong>Case presentations: </strong>This case series describes three adolescent patients with m-HLH, focusing on complexities in diagnosis, treatment regimens, and toxicity management. While dexamethasone and etoposide remain a standard of care, their efficacy in refractory cases is limited. We highlight the novel use of targeted therapies, including emapalumab, an interferon-gamma inhibitor, and ruxolitinib, a JAK1/2 inhibitor, which showed potential in modulating immune hyperactivation.</p><p><strong>Conclusions: </strong>Our findings emphasize the need for individualized treatment approaches in adolescent m-HLH and importance of further research to establish evidence-based therapeutic guidelines for refractory cases.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127318","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Racial Inequities Influencing Admission, Disposition and Hospital Outcomes for Sickle Cell Anemia Patients: Insights from the National Inpatient Sample Database.","authors":"Jayalekshmi Jayakumar, Nikhil Vojjala, Manasa Ginjupalli, Fiqe Khan, Meher Ayyazuddin, Davin Turku, Kalaivani Babu, Srinishant Rajarajan, Charmi Bhanushali, Tijin Ann Mathew, Poornima Ramadas, Geeta Krishnamoorty","doi":"10.3390/hematolrep17030027","DOIUrl":"10.3390/hematolrep17030027","url":null,"abstract":"<p><p><b>Background:</b> Sickle cell disease (SCD) significantly impacts diverse racial groups, particularly African American and Hispanic persons, who experience notable disparities in healthcare outcomes. Despite the extensive literature on SCD, studies focusing on in-hospital racial inequities remain limited. <b>Methods:</b> We conducted a retrospective analysis using the National Inpatient Sample (NIS) from 2016 to 2020, identifying adult hospitalizations for SCD (HbSS genotype). Hospitalizations were categorized by race-White, African American, Hispanic, and other, and analyzed for demographic variables, admission types, disposition outcomes, and complications. Statistical analyses included chi-square tests and multivariate logistic regression, adjusting for confounders. <b>Results:</b> Of the 1,089,270 identified hospitalizations, 90.31% were African American. African American and Hispanic patients exhibited significantly higher non-elective admissions compared to Whites (77.81%). In-hospital mortality was highest among Hispanics (0.82%). Multivariate regression analysis revealed that African Americans and others had higher odds of prolonged hospital stays (Adjusted Odds Ratio (AOR): 1.30 and 1.20, respectively). African Americans and Hispanics also had increased risks of in-hospital complications of SCD. <b>Conclusions:</b> This study highlights substantial racial disparities in SCD hospitalizations, with African Americans and Hispanics facing poorer outcomes compared to Whites. Hispanics also demonstrated increased mortality. These findings underscore the need for targeted healthcare interventions to address racial inequities in SCD management and improve outcomes for all affected populations.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101344/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127344","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Outcome and Molecular Profile in Patients with <i>DDX41</i> Mutation Hot-Spots.","authors":"Nadia Toumeh, Yazan Jabban, Ahmad Nanaa, Rong He, David Viswanatha, Dragan Jevremovic, James M Foran, Cecilia Y Arana Yi, Antoine N Saliba, Mehrdad Hefazi Torghabeh, William J Hogan, Mithun V Shah, Abhishek A Mangaonkar, Mrinal M Patnaik, Hassan B Alkhateeb, Aref Al-Kali","doi":"10.3390/hematolrep17030026","DOIUrl":"10.3390/hematolrep17030026","url":null,"abstract":"<p><p><b>Background/Objectives:</b><i>DDX41</i>, DEAD-box RNA helicase 41 gene located on chromosome 5q25.3, is one of the most mutated genes in patients with germline predisposition to myeloid neoplasms. Germline and somatic mutations often have different locations and patterns of mutation, with some hotspots displaying diversity based on ethnicity. We aimed to explore clinical outcomes in patients with various <i>DDX41</i> hot-spot mutations. <b>Methods</b>: This was a retrospective study of patients at Mayo Clinic with <i>DDX41</i> mutation identified through Next Generation Sequencing (NGS) between 2018 and 2024. We completed unadjusted comparisons using continuous or categorical variables, and survival rates were assessed using the Kaplan-Meier method and cox regression analysis. <b>Results</b>: Overall survival appears to be higher in those with p.M1| when compared to p.Asp140GlyFs*2 and p.Arg525His, with comparable survival between p.Arg525His and p.Asp140GlyFs*2. Among males with p.M1| who underwent bone marrow transplant, those who underwent bone marrow transplant appeared to have lower survival rates, although not statistically significant. Our study was limited by a small sample size, therefore limiting our ability to reach significance. <b>Conclusions</b>: Our findings suggest potential implications for clinical outcomes based on <i>DDX41</i> mutation hot-spots.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101365/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Severe Aplastic Anemia Complicated with Fatal Invasive Fungal Infections in a Young Patient Harboring Perforin Gene Polymorphisms.","authors":"Maria I Krithinaki, Ioannis Kokkinakis, Styliani Markatzinou, Christos Masaoutis, Elena Solomou, Ioanna Papakitsou, Nektaria Xirouchaki, Ioannis Liapis, Helen A Papadaki, Charalampos G Pontikoglou","doi":"10.3390/hematolrep17030025","DOIUrl":"10.3390/hematolrep17030025","url":null,"abstract":"<p><strong>Background: </strong>Severe aplastic anemia (SAA) is an uncommon life-threatening disorder characterized by hypocellular bone marrow and pancytopenia. It is typically associated with immune-mediated mechanisms, requiring immunosuppressive therapy (IST) or hematopoietic stem cell transplantation (HSCT). Infections, especially invasive fungal infections such as mucormycosis and aspergillosis, constitute principal causes of morbidity and mortality in patients with SAA. Genetic predispositions, including perforin (PRF1) polymorphisms, may further complicate disease outcomes by impairing immune function.</p><p><strong>Case report: </strong>We describe a case of a 36-year-old female patient diagnosed with SAA, for whom IST was considered, due to the unavailability of a matched sibling donor for HSCT. The patient presented with a feverish condition and deep neck space abscesses were revealed by imaging, caused by invasive aspergillosis. To prioritize infection control, IST was postponed and antifungal therapy with abscess drainage was initiated. However, aspergillosis progressed, despite aggressive and prompt treatment, and ultimately resulted in sepsis, multiorgan failure, and death. In addition, mucormycosis was confirmed post-mortem. Two heterozygous <i>PRF1</i> polymorphisms (c.272C>T and c.900C>T), were identified by genetic testing, which may have contributed to immune dysregulation and fungal dissemination.</p><p><strong>Conclusions: </strong>The complex interplay between managing SAA and addressing invasive fungal infections, which remain a leading cause of mortality in immunocompromised patients, is highlighted in this case. The latter emphasizes the importance of prompt diagnosis and targeted treatment to alleviate infection-related complications while maintaining care continuity for the hematologic disorder. The detection of <i>PRF1</i> polymorphisms raises questions about their implication in immune regulation and disease trajectory, emphasizing the need for further research in this field.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101316/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127357","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial Intelligence (AI) and Drug-Induced and Idiosyncratic Cytopenia: The Role of AI in Prevention, Prediction, and Patient Participation.","authors":"Emmanuel Andrès, Amir El Hassani Hajjam, Frédéric Maloisel, Maria Belén Alonso-Ortiz, Manuel Méndez-Bailón, Thierry Lavigne, Xavier Jannot, Noel Lorenzo-Villalba","doi":"10.3390/hematolrep17030024","DOIUrl":"10.3390/hematolrep17030024","url":null,"abstract":"<p><p>Drug-induced and idiosyncratic cytopenias, including anemia, neutropenia, and thrombocytopenia, present significant challenges in fields like immunohematology and internal medicine. These conditions are often unpredictable, multifactorial, and can arise from a complex interplay of drug reactions, immune abnormalities, and other poorly understood mechanisms. In many cases, the precise triggers and underlying factors remain unclear, making diagnosis and management difficult. However, advancements in artificial intelligence (AI) are offering new opportunities to address these challenges. With its ability to process vast amounts of clinical, genomic, and pharmacovigilance data, AI can identify patterns and risk factors that may be missed by traditional methods. Machine learning algorithms can refine predictive models, enabling earlier detection and more accurate risk assessments. Additionally, AI's role in enhancing patient engagement-through tailored monitoring and personalized treatment strategies-ensures more effective follow-up and improved clinical outcomes for patients at risk of these potentially life-threatening conditions. Through these innovations, AI is paving the way for a more proactive and personalized approach to managing drug-induced cytopenias.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101246/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Primary Mediastinal B-Cell Lymphoma and [18F]FDG PET/CT: What We Learned and What Is New.","authors":"Anna Giulia Nappi, Francesco Dondi, Achille Lazzarato, Lorenzo Jonghi-Lavarini, Joana Gorica, Flavia La Torre, Giulia Santo, Alberto Miceli","doi":"10.3390/hematolrep17030023","DOIUrl":"10.3390/hematolrep17030023","url":null,"abstract":"<p><p>Primary mediastinal large B-cell lymphoma (PMLBCL) is a rare and aggressive non-Hodgkin lymphoma (NHL), considered a specific entity with proper characteristics, therapies, and prognosis. First-line treatment is not unique, and subsequent strategies in case of disease persistence or relapse are the subject of debate and studies. In this scenario, [18F]FDG PET/CT plays a pivotal role both in characterizing the mediastinal mass, the main feature of PMLBCL, in staging, in restaging during therapy (interim PET), and at the end of treatment (EoT PET), to guide clinical management and give prognostic insights. The main issue with PMLBCL is distinguishing viable disease from residual fibrotic/inflammatory mass after therapy and, consequently, settling the next clinical strategy. Novel therapeutic approaches are ongoing and associated with the deepening of [18F]FDG PET/CT potentials as a principal tool in this context. In this review, we will explore PMLBCL from a Nuclear Medicine point of view to help clinicians in the management of these patients.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101282/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127341","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of Diffuse Large B-Cell Lymphoma as Post-Transplant Lymphoproliferative Disorder in a Kidney Transplant Recipient: A Case Report.","authors":"Salem Alshemmari, Abdulaziz Hamadah, Samar Ousia, Rasha Abdel Tawab Hamed, Hany Zaky","doi":"10.3390/hematolrep17030022","DOIUrl":"10.3390/hematolrep17030022","url":null,"abstract":"<p><p><b>Background and Clinical Significance:</b> Post-transplant lymphoproliferative disorder (PTLD) is a severe complication of solid organ transplantation, often associated with prolonged immunosuppression. Diffuse large B-cell lymphoma (DLBCL) is the most common subtype. Managing PTLD requires a balance between reducing immunosuppression and preventing graft rejection. <b>Case Presentation</b>: A 41-year-old female kidney transplant recipient developed PTLD eight years post-transplant, presenting with a right submandibular mass. Biopsy confirmed CD20-positive DLBCL. Initial treatment involved reducing immunosuppression and rituximab monotherapy, which failed to prevent disease progression. The patient underwent six cycles of R-CHOP chemotherapy, achieving complete metabolic remission. Relapse occurred twice, with disease progression in the cervical nodes and tonsils. Salvage therapies, including polatuzumab vedotin and rituximab, achieved remission. During a subsequent relapse, loncastuximab tesirine induced metabolic resolution. Compromised renal function limited treatment options and a second renal transplant was delayed, reducing the risk of PTLD recurrence. <b>Conclusions</b>: This case underscores the challenges of managing PTLD in transplant recipients, especially in relapsed/refractory cases. Single-agent rituximab was insufficient, but combination chemotherapy and novel agents like loncastuximab tesirine were effective. Balancing oncologic control and graft preservation remains critical. This case highlights the need for individualized approaches and novel therapies in managing PTLD while addressing the complexities of immunosuppression and organ preservation.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 3","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12101285/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144127316","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Successful Management of Acquired von Willebrand Syndrome Associated with Monoclonal Gammopathy of Undetermined Significance After Sotorasib Treatment in a Patient with Non-Small-Cell Lung Carcinoma.","authors":"Mélissa Julien, Léa Pierre, Anne-Cécile Gérout, Laurent Sattler, Olivier Feugeas, Dominique Desprez","doi":"10.3390/hematolrep17020021","DOIUrl":"https://doi.org/10.3390/hematolrep17020021","url":null,"abstract":"<p><p><b>Background:</b> This case report investigates the effects of sotorasib treatment in a patient with acquired von Willebrand syndrome (AVWS) associated with monoclonal gammopathy of undetermined significance (MGUS), who subsequently developed non-small-cell lung carcinoma (NSCLC) with a KRAS G12C mutation. <b>Case Presentation:</b> The patient, a 79-year-old male, presented with a prolonged history of recurrent lower gastrointestinal bleeding attributed to digestive angiodysplasia, which had persisted for over 30 years. AVWS was suspected based on a qualitative deficiency in von Willebrand factor (VWF), with abnormal results for factor VIII activity (FVIII:C), VWF antigen (VWF:Ag), and VWF ristocetin cofactor activity (VWF:Rco) (40%, 20%, and <2.4%, respectively). Further evaluation revealed the presence of an IgM kappa monoclonal spike, suggesting MGUS. In 2022, the patient was diagnosed with NSCLC harboring the KRAS G12C mutation and initiated second-line treatment with sotorasib. Notably, one year after the initiation of sotorasib therapy, the patient's hemostasis had normalized, accompanied by significant improvements in VWF levels. VWF multimer electrophoresis demonstrated the restoration of high-molecular-weight multimers (HMWMs), and serum protein electrophoresis no longer detected MGUS. <b>Conclusion:</b> These improvements were likely attributable to the indirect effects of sotorasib on the bone marrow microenvironment. By inhibiting KRAS in stromal cells and osteoclasts, sotorasib may have disrupted the supportive niche necessary for malignant plasma cell survival, resulting in a reduction in the monoclonal spike. Unfortunately, the patient eventually succumbed to carcinogenic pleurisy.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 2","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12027059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hemolytic Anemia Due to Gamma-Glutamylcysteine Synthetase Deficiency: A Rare Novel Case in an Arab-Muslim Israeli Child.","authors":"Motti Haimi, Jamal Mahamid","doi":"10.3390/hematolrep17020020","DOIUrl":"https://doi.org/10.3390/hematolrep17020020","url":null,"abstract":"<p><strong>Background: </strong>Gamma-glutamylcysteine synthetase catalyzes the first and rate-limiting step in the synthesis of glutathione. Gamma-glutamylcysteine synthetase deficiency is a very rare condition that has so far been detected so far in nine patients from seven families worldwide. The inheritance of this disorder is autosomal recessive.</p><p><strong>Methods: </strong>We report a case of 4.11-year-old boy, of Arab-Muslim origin, living in an Arab town in Israel who presented at the age of 2 days with severe anemia, reticulocytosis, and leukocytosis. Investigation for common causes of hemolytic anemia was negative (peripheral blood smear was normal, and he had a negative Coombs test, normal G6PD, and normal flow cytometry spherocytosis). The anemia worsened during the following days (hemoglobin (Hb): 7.2 g/dL) and he needed several blood transfusions. NGS (next-generation sequencing) gene panel analysis was performed.</p><p><strong>Results: </strong>In an NGS gene panel analysis for hereditary hemolytic anemias, we found a homozygotic change in the GCLC gene-G53.385.643c379C > T(homo)pArg127Cys-which confirms the diagnosis of gamma-glutamylcysteine synthetase deficiency. An additional rare change was found in this case in the GCLC gene, with unknown clinical significance: g.53373917, c 828 + 3A > G. Except for chronic anemia (Hb levels around 8 g/dL), the child has normal physical and neurological development.</p><p><strong>Conclusions: </strong>This study reports a rare case of gamma-glutamylcysteine synthetase deficiency in a 4.11-year-old Arab-Muslim boy from Israel who presented with severe anemia at 2 days old, aiming to document the first such case in the Middle East and contribute to the medical literature on this extremely rare condition that has only been detected in nine patients worldwide. Genetic analysis revealed a homozygotic change in the GCLC gene, confirming the diagnosis, and while the patient experiences chronic anemia, he maintains normal physical and neurological development, adding valuable insights to the understanding of this rare genetic disorder. An additional rare change was found in this case in the GCLC gene, with unknown clinical significance: g.53373917, c 828 + 3A > G.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 2","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026703/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006116","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Blood Coagulation Favors Anti-Inflammatory Immune Responses in Whole Blood.","authors":"Victor I Seledtsov, Anatoly A Pyshenko, Tatyana Ya Lyubavskaya, Irina A Seledtsova, Alexei A von Delwig","doi":"10.3390/hematolrep17020019","DOIUrl":"https://doi.org/10.3390/hematolrep17020019","url":null,"abstract":"<p><strong>Background: </strong>We studied the effects of human blood coagulation on antioxidant activity and the cellular secretion of immunoregulatory molecules in vitro.</p><p><strong>Methods: </strong>Reactive oxygen species (ROS) activity and cytokine content were determined in plasma and serum blood samples incubated with lipopolysaccharide (LPS) for 3 h or 18 h.</p><p><strong>Results: </strong>Coagulation process significantly decreased ROS activity induced by LPS in blood samples from healthy donors. Human serum was found to have significantly higher antioxidant activity than plasma. Blood coagulation markedly reduced LPS-induced secretion of TNF-α by cells, without significantly affecting the secretion of interleukin-1 (IL-1), IL-6, IL-8, or C-reactive protein (CRP). Blood clotting led to an increase in LPS-induced release of vascular endothelial growth factor (VEGF) by blood cells. A significant increase in procalcitonin levels was also observed in serum samples.</p><p><strong>Conclusions: </strong>Blood clotting enhances the antioxidant and anti-inflammatory functions of immunoreactive blood cells.</p>","PeriodicalId":12829,"journal":{"name":"Hematology Reports","volume":"17 2","pages":""},"PeriodicalIF":1.1,"publicationDate":"2025-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12026462/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144006114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}