Influence of ABO Blood Group on Fibrinogen Levels and Platelet Count in Apparently Healthy Nigerian Subjects
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Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism
International Journal of Molecular Sciences Review Factor XIII and Fibrin Clot Properties in Acute Venous Thromboembolism Michał Z ˛abczyk 1,2 , Joanna Natorska 1,2 and Anetta Undas 1,2,* 1 John Paul II Hospital, 31-202 Kraków, Poland; [email protected] (M.Z.); [email protected] (J.N.) 2 Institute of Cardiology, Jagiellonian University Medical College, 31-202 Kraków, Poland * Correspondence: [email protected]; Tel.: +48-12-614-30-04; Fax: +48-12-614-21-20 Abstract: Coagulation factor XIII (FXIII) is converted by thrombin into its active form, FXIIIa, which crosslinks fibrin fibers, rendering clots more stable and resistant to degradation. FXIII affects fibrin clot structure and function leading to a more prothrombotic phenotype with denser networks, characterizing patients at risk of venous thromboembolism (VTE). Mechanisms regulating FXIII activation and its impact on fibrin structure in patients with acute VTE encompassing pulmonary embolism (PE) or deep vein thrombosis (DVT) are poorly elucidated. Reduced circulating FXIII levels in acute PE were reported over 20 years ago. Similar observations indicating decreased FXIII plasma activity and antigen levels have been made in acute PE and DVT with their subsequent increase after several weeks since the index event. Plasma fibrin clot proteome analysis confirms that clot-bound FXIII amounts associated with plasma FXIII activity are decreased in acute VTE. Reduced FXIII activity has been associated with impaired clot permeability and hypofibrinolysis in acute PE. The current review presents available studies on the role of FXIII in the modulation of fibrin clot properties during acute PE or DVT and following these events. -
Hemolytic Disease of the Newborn
Intensive Care Nursery House Staff Manual Hemolytic Disease of the Newborn INTRODUCTION and DEFINITION: Hemolytic Disease of the Newborn (HDN), also known as erythroblastosis fetalis, isoimmunization, or blood group incompatibility, occurs when fetal red blood cells (RBCs), which possess an antigen that the mother lacks, cross the placenta into the maternal circulation, where they stimulate antibody production. The antibodies return to the fetal circulation and result in RBC destruction. DIFFERENTIAL DIAGNOSIS of hemolytic anemia in a newborn infant: -Isoimmunization -RBC enzyme disorders (e.g., G6PD, pyruvate kinase deficiency) -Hemoglobin synthesis disorders (e.g., alpha-thalassemias) -RBC membrane abnormalities (e.g., hereditary spherocytosis, elliptocytosis) -Hemangiomas (Kasabach Merritt syndrome) -Acquired conditions, such as sepsis, infections with TORCH or Parvovirus B19 (anemia due to RBC aplasia) and hemolysis secondary to drugs. ISOIMMUNIZATION A. Rh disease (Rh = Rhesus factor) (1) Genetics: Rh positive (+) denotes presence of D antigen. The number of antigenic sites on RBCs varies with genotype. Prevalence of genotype varies with the population. Rh negative (d/d) individuals comprise 15% of Caucasians, 5.5% of African Americans, and <1% of Asians. A sensitized Rh negative mother produces anti-Rh IgG antibodies that cross the placenta. Risk factors for antibody production include 2nd (or later) pregnancies*, maternal toxemia, paternal zygosity (D/D rather than D/d), feto-maternal compatibility in ABO system and antigen load. (2) Clinical presentation of HDN varies from mild jaundice and anemia to hydrops fetalis (with ascites, pleural and pericardial effusions). Because the placenta clears bilirubin, the chief risk to the fetus is anemia. Extramedullary hematopoiesis (due to anemia) results in hepatosplenomegaly. -
Association Between ABO and Duffy Blood Types and Circulating Chemokines and Cytokines
Genes & Immunity (2021) 22:161–171 https://doi.org/10.1038/s41435-021-00137-5 ARTICLE Association between ABO and Duffy blood types and circulating chemokines and cytokines 1 2 3 4 5 6 Sarah C. Van Alsten ● John G. Aversa ● Loredana Santo ● M. Constanza Camargo ● Troy Kemp ● Jia Liu ● 4 7 8 Wen-Yi Huang ● Joshua Sampson ● Charles S. Rabkin Received: 11 February 2021 / Revised: 30 April 2021 / Accepted: 17 May 2021 / Published online: 8 June 2021 This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply 2021, corrected publication 2021 Abstract Blood group antigens are inherited traits that may play a role in immune and inflammatory processes. We investigated associations between blood groups and circulating inflammation-related molecules in 3537 non-Hispanic white participants selected from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial. Whole-genome scans were used to infer blood types for 12 common antigen systems based on well-characterized single-nucleotide polymorphisms. Serum levels of 96 biomarkers were measured on multiplex fluorescent bead-based panels. We estimated marker associations with blood type using weighted linear or logistic regression models adjusted for age, sex, smoking status, and principal components of p 1234567890();,: 1234567890();,: population substructure. Bonferroni correction was used to control for multiple comparisons, with two-sided values < 0.05 considered statistically significant. Among the 1152 associations tested, 10 were statistically significant. Duffy blood type was associated with levels of CXCL6/GCP2, CXCL5/ENA78, CCL11/EOTAXIN, CXCL1/GRO, CCL2/MCP1, CCL13/ MCP4, and CCL17/TARC, whereas ABO blood type was associated with levels of sVEGFR2, sVEGFR3, and sGP130. -
Blood Product Replacement: Obstetric Hemorrhage
CMQCC OBSTETRIC HEMORRHAGE TOOLKIT Version 2.0 3/24/15 BLOOD PRODUCT REPLACEMENT: OBSTETRIC HEMORRHAGE Richard Lee, MD, Los Angeles County and University of Southern California Medical Center Laurence Shields, MD, Marian Regional Medical Center/Dignity Health Holli Mason, MD, Cedars-Sinai Medical Center Mark Rollins, MD, PhD, University of California, San Francisco Jed Gorlin, MD, Innovative Blood Resources/Memorial Blood Center, St. Paul, Minnesota Maurice Druzin, MD, Lucile Packard Children’s Hospital Stanford University Jennifer McNulty, MD, Long Beach Memorial Medical Center EXECUTIVE SUMMARY • Outcomes are improved with early and aggressive intervention. • Both emergency blood release and massive transfusion protocols should be in place. • In the setting of significant obstetric hemorrhage, resuscitation transfusion should be based on vital signs and blood loss and should not be delayed by waiting for laboratory results. • Calcium replacement will often be necessary with massive transfusion due to the citrate used for anticoagulation in blood products. • During massive transfusion resuscitation, the patient’s arterial blood gas, electrolytes, and core temperature should be monitored to guide clinical management and all transfused fluids should be warmed; direct warming of the patient should be initiated as needed to maintain euthermia and to avoid added coagulopathy. BACKGROUND AND LITERATURE REVIEW After the first several units of packed red blood cells (PRBCs) and in the face of continuing or worsening hemorrhage, aggressive transfusion therapy becomes critical. This report covers the experience with massive transfusion protocols. Lessons from military trauma units as well as civilian experience with motor vehicle accidents and massive obstetric hemorrhage have identified new principles such as earlier use of plasma (FFP/thawed plasma/plasma frozen within 24 hours/liquid plasma) and resuscitation transfusion while laboratory results are pending. -
Update on Antithrombin I (Fibrin)
©2007 Schattauer GmbH,Stuttgart AnniversaryIssueContribution Update on antithrombinI(fibrin) Michael W. Mosesson 1957–2007) The Blood Research Institute,BloodCenter of Wisconsin, Milwaukee,Wisconsin, USA y( Summary AntithrombinI(fibrin) is an important inhibitor of thrombin exosite 2.Thelatterreaction results in allostericchanges that generation that functions by sequestering thrombin in the form- down-regulate thrombin catalytic activity. AntithrombinIdefi- Anniversar ingfibrin clot,and also by reducing the catalytic activity of fibrin- ciency (afibrinogenemia), defectivethrombin binding to fibrin th boundthrombin.Thrombin binding to fibrin takesplace at two (antithrombin Idefect) found in certain dysfibrinogenemias (e.g. 50 classesofnon-substrate sites: 1) in thefibrin Edomain (two per fibrinogen Naples 1), or areduced plasma γ ’ chain content (re- molecule) throughinteractionwith thrombin exosite 1; 2) at a ducedantithrombin Iactivity),predispose to intravascular singlesite on each γ ’ chain through interaction with thrombin thrombosis. Keywords Fibrinogen,fibrin, thrombin, antithrombin I ThrombHaemost 2007; 98: 105–108 Introduction meric with respecttoits γ chains,and accounts for ~85% of human plasma fibrinogen. Thrombinbinds to its substrate, fibrinogen, through an anion- Low-affinity thrombin binding activity reflects thrombin ex- binding sitecommonlyreferred to as ‘exosite 1’ (1,2). Howell osite1bindinginEdomain of fibrin, as recentlydetailedbyana- recognized nearly acenturyago that the fibrin clot itself exhibits lysesofthrombin-fibrin -
Journal of Blood Group Serology and Molecular Genetics Volume 34, Number 1, 2018 CONTENTS
Journal of Blood Group Serology and Molecular Genetics VOLUME 34, N UMBER 1, 2018 This issue of Immunohematology is supported by a contribution from Grifols Diagnostics Solutions, Inc. Dedicated to advancement and education in molecular and serologic immunohematology Immunohematology Journal of Blood Group Serology and Molecular Genetics Volume 34, Number 1, 2018 CONTENTS S EROLOGIC M ETHOD R EVIEW 1 Warm autoadsorption using ZZAP F.M. Tsimba-Chitsva, A. Caballero, and B. Svatora R EVIEW 4 Proceedings from the International Society of Blood Transfusion Working Party on Immunohaematology Workshop on the Clinical Significance of Red Blood Cell Alloantibodies, Friday, September 2, 2016, Dubai A brief overview of clinical significance of blood group antibodies M.J. Gandhi, D.M. Strong, B.I. Whitaker, and E. Petrisli C A S E R EPORT 7 Management of pregnancy sensitized with anti-Inb with monocyte monolayer assay and maternal blood donation R. Shree, K.K. Ma, L.S. Er and M. Delaney R EVIEW 11 Proceedings from the International Society of Blood Transfusion Working Party on Immunohaematology Workshop on the Clinical Significance of Red Blood Cell Alloantibodies, Friday, September 2, 2016, Dubai A review of in vitro methods to predict the clinical significance of red blood cell alloantibodies S.J. Nance S EROLOGIC M ETHOD R EVIEW 16 Recovery of autologous sickle cells by hypotonic wash E. Wilson, K. Kezeor, and M. Crosby TO THE E DITOR 19 The devil is in the details: retention of recipient group A type 5 years after a successful allogeneic bone marrow transplant from a group O donor L.L.W. -
Apheresis Donation This Quick Reference Guide Will Help You Identify the Best Donation for Your Unique Blood Type
Apheresis Donation This quick reference guide will help you identify the best donation for your unique blood type. Donors now have the opportunity to make an apheresis (ay-fur-ee-sis) donation and donate just platelets, red cells, or plasma at blood drives. These individual components are vital for local patients in need. Platelets Control Bleeding Red Cells Deliver Oxygen Plasma transports blood cells & controls bleeding Donation Type Blood Types Requirements Donation Time A+, B+, O+ Over 75% of population has one of these blood types. Platelet Donation: Be healthy, weigh at least 114 lbs 2 hours cancer & surgery patients no aspirin for 48 hours Platelets only last five days after donation so the need is constant. O-, O+, A-, B- Special height, weight, Double Red: O-Negative is the 1 hour and hematocrit requirements. surgery, trauma patients, universal red cell donor. +25 min Please call us or see a staff member accident, & burn victims Only 17% of population has one of these negative blood types Plasma: AB+, AB- Trauma patients, burn Universal Plasma Donors 1 hour Be healthy, weigh at least 114 lbs victims, & patients with +30 min serious illness or injuries Only 4% of population How Apheresis works: Blood is drawn from the donor’s arm and the components are separated. Only the components being donated are collected while the remaining components are safely returned to the donor How to Schedule an Appointment: Please call 800-398-7888 or visit schedule.bloodworksnw.org. Walk-ins are also welcome at some blood drives, so be sure to ask our staff when you stop in. -
Blood Type and Transplantation & A2 Donor to B Recipient
Page 1 of 2 Blood Type and Transplantation Information for Kidney Transplant Patients Does blood type matter in transplantation? Everyone waiting for a transplant has their blood typed. You will have one of four blood types: O, A, B or AB. Your blood type is determined by the antigens that are present on your blood cells. These antigens are A or B. These antigens will be found both in your blood and on your organs. What antigen does each blood type have? Blood type O Blood type A Blood type B Blood type AB have no have A antigens. have B antigens. have both A O antigens. A B AB and B antigens. How does my body react to antigens? Your body will react to antigens that are different than your own by attacking with antibodies. Antibodies are proteins created by your immune system to attack anything that does not belong. Antibodies are the soldiers in your body’s army protecting you from foreign invasions such as viruses. Unfortunately, the antibodies cannot tell the difference between harmful viruses and beneficial transplanted organs. What blood type will my donor be? Transplants can occur between all blood types. However, when the donor’s blood type is different than yours and there are different antigens being transplanted on your new organ, your antibodies will be triggered and attack the transplanted organ. This is called rejection. Because of this, transplants usually happen between a donor and a recipient of the same blood type. This is called an identical transplant. Can I get an organ from a donor that has a different blood type than mine? Yes! If you do not have antibodies in your body against the antigens that come from the donor, your immune system should not attack the transplanted organ. -
In Vitro Selection for Adhesion of Plasmodium Falciparum-Infected Erythrocytes to ABO Antigens Does Not Affect Pfemp1 and RIFIN
www.nature.com/scientificreports OPEN In vitro selection for adhesion of Plasmodium falciparum‑infected erythrocytes to ABO antigens does not afect PfEMP1 and RIFIN expression William van der Puije1,2, Christian W. Wang 4, Srinidhi Sudharson 2, Casper Hempel 2, Rebecca W. Olsen 4, Nanna Dalgaard 4, Michael F. Ofori 1, Lars Hviid 3,4, Jørgen A. L. Kurtzhals 2,4 & Trine Staalsoe 2,4* Plasmodium falciparum causes the most severe form of malaria in humans. The adhesion of the infected erythrocytes (IEs) to endothelial receptors (sequestration) and to uninfected erythrocytes (rosetting) are considered major elements in the pathogenesis of the disease. Both sequestration and rosetting appear to involve particular members of several IE variant surface antigens (VSAs) as ligands, interacting with multiple vascular host receptors, including the ABO blood group antigens. In this study, we subjected genetically distinct P. falciparum parasites to in vitro selection for increased IE adhesion to ABO antigens in the absence of potentially confounding receptors. The selection resulted in IEs that adhered stronger to pure ABO antigens, to erythrocytes, and to various human cell lines than their unselected counterparts. However, selection did not result in marked qualitative changes in transcript levels of the genes encoding the best-described VSA families, PfEMP1 and RIFIN. Rather, overall transcription of both gene families tended to decline following selection. Furthermore, selection-induced increases in the adhesion to ABO occurred in the absence of marked changes in immune IgG recognition of IE surface antigens, generally assumed to target mainly VSAs. Our study sheds new light on our understanding of the processes and molecules involved in IE sequestration and rosetting. -
The Plasmin–Antiplasmin System: Structural and Functional Aspects
View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Bern Open Repository and Information System (BORIS) Cell. Mol. Life Sci. (2011) 68:785–801 DOI 10.1007/s00018-010-0566-5 Cellular and Molecular Life Sciences REVIEW The plasmin–antiplasmin system: structural and functional aspects Johann Schaller • Simon S. Gerber Received: 13 April 2010 / Revised: 3 September 2010 / Accepted: 12 October 2010 / Published online: 7 December 2010 Ó Springer Basel AG 2010 Abstract The plasmin–antiplasmin system plays a key Plasminogen activator inhibitors Á a2-Macroglobulin Á role in blood coagulation and fibrinolysis. Plasmin and Multidomain serine proteases a2-antiplasmin are primarily responsible for a controlled and regulated dissolution of the fibrin polymers into solu- Abbreviations ble fragments. However, besides plasmin(ogen) and A2PI a2-Antiplasmin, a2-Plasmin inhibitor a2-antiplasmin the system contains a series of specific CHO Carbohydrate activators and inhibitors. The main physiological activators EGF-like Epidermal growth factor-like of plasminogen are tissue-type plasminogen activator, FN1 Fibronectin type I which is mainly involved in the dissolution of the fibrin K Kringle polymers by plasmin, and urokinase-type plasminogen LBS Lysine binding site activator, which is primarily responsible for the generation LMW Low molecular weight of plasmin activity in the intercellular space. Both activa- a2M a2-Macroglobulin tors are multidomain serine proteases. Besides the main NTP N-terminal peptide of Pgn physiological inhibitor a2-antiplasmin, the plasmin–anti- PAI-1, -2 Plasminogen activator inhibitor 1, 2 plasmin system is also regulated by the general protease Pgn Plasminogen inhibitor a2-macroglobulin, a member of the protease Plm Plasmin inhibitor I39 family. -
Journal of Blood Group Serology and Molecular Genetics Volume 33, Number 3, 2017 CONTENTS
Journal of Blood Group Serology and Molecular Genetics VOLUME 33, N UMBER 3, 2017 This issue of Immunohematology is supported by a contribution from Grifols Diagnostics Solutions, Inc. Dedicated to advancement and education in molecular and serologic immunohematology Immunohematology Journal of Blood Group Serology and Molecular Genetics Volume 33, Number 3, 2017 CONTENTS C ASE R EPO R T 99 ABO serology in a case of persistent weak A in a recipient following a group O–matched unrelated bone marrow transplant D.E. Grey, E.A. Fong, C. Cole, J. Jensen, and J. Finlayson O R IGINAL R EPO R T 105 Stability guidelines for dithiothreitol-treated red blood cell reagents used for antibody detection methods in patients treated with daratumumab W.L. Disbro C ASE R EPO R T 110 A LU:−16 individual with antibodies C. Éthier, C. Parent, A.-S. Lemay, N. Baillargeon, G. Laflamme, J. Lavoie, J. Perreault, and M. St-Louis C ASE R EPO R T 114 Postpartum acute hemolytic transfusion reactions associated with anti-Lea in two pregnancies complicated by preeclampsia M. Marchese O R IGINAL R EPO R T 119 Red blood cell phenotype prevalence in blood donors who self- identify as Hispanic C.A. Sheppard, N.L. Bolen, B. Eades, G. Ochoa-Garay, and M.H. Yazer R EVIEW 125 DEL Phenotype D.H. Kwon, S.G. Sandler, and W.A. Flegel 133 138 142 144 A NNOUN C EMENTS A DVE R TISEMENTS I NST R U C TIONS S UBS cr IPTION FO R A UTHO R S I NFO R M AT I O N E DITO R - IN -C HIEF E DITO R IAL B OA R D Sandra Nance, MS, MT(ASCP)SBB Philadelphia, Pennsylvania Patricia Arndt, MT(ASCP)SBB Geralyn M. -
RIASTAP®, Fibrinogen Concentrate (Human) Lyophilized Powder for Solution for Intravenous Injection
HIGHLIGHTS OF PRESCRIBING INFORMATION -------------------------------------CONTRAINDICATIONS ------------------------------------ These highlights do not include all the information needed to use RIASTAP • Known anaphylactic or severe systemic reactions to human plasma-derived products (4). safely and effectively. See full prescribing information for RIASTAP. ---------------------------------WARNINGS AND PRECAUTIONS---------------------------- RIASTAP®, Fibrinogen Concentrate (Human) • Monitor patients for early signs of anaphylaxis or hypersensitivity reactions and if necessary, discontinue administration and institute appropriate treatment (5.1). Lyophilized Powder for Solution for Intravenous Injection • Thrombotic events have been reported in patients receiving RIASTAP. Weigh the benefits of administration versus the risks of thrombosis (5.2). Initial U.S. Approval: 2009 • Because RIASTAP is made from human blood, it may carry a risk of transmitting ------------------------------------RECENT MAJOR CHANGES--------------------------------- infectious agents, e.g., viruses, the variant Creutzfeldt-Jakob disease (vCJD) agent Indications and Usage (1) 06/2021 and, theoretically, the Creutzfeldt-Jakob disease (CJD) agent (5.3). Dosage and Administration (2.2) 07/2020 -------------------------------------ADVERSE REACTIONS-------------------------------------- ----------------------------------INDICATIONS AND USAGE----------------------------------- • The most serious adverse reactions observed are thrombotic episodes (pulmonary RIASTAP, Fibrinogen