Effect of Donor Variables on Platelet Yield Among Donor
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Unintentional Platelet Removal by Plasmapheresis
Journal of Clinical Apheresis 16:55–60 (2001) Unintentional Platelet Removal by Plasmapheresis Jedidiah J. Perdue,1 Linda K. Chandler,2 Sara K. Vesely,1 Deanna S. Duvall,2 Ronald O. Gilcher,2 James W. Smith,2 and James N. George1* 1Hematology-Oncology Section, Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 2Oklahoma Blood Institute, Oklahoma City, Oklahoma Therapeutic plasmapheresis may remove platelets as well as plasma. Unintentional platelet loss, if not recognized, may lead to inappropriate patient assessment and treatment. A patient with thrombotic thrombocytopenic purpura- hemolytic uremic syndrome (TTP-HUS) is reported in whom persistent thrombocytopenia was interpreted as continuing active disease; thrombocytopenia resolved only after plasma exchange treatments were stopped. This observation prompted a systematic study of platelet loss with plasmapheresis. Data are reported on platelet loss during 432 apheresis procedures in 71 patients with six disease categories using three different instruments. Com- paring the first procedure recorded for each patient, there was a significant difference among instrument types ,than with the COBE Spectra (1.6% (21 ס P<0.001); platelet loss was greater with the Fresenius AS 104 (17.5%, N) .With all procedures, platelet loss ranged from 0 to 71% .(24 ס or the Haemonetics LN9000 (2.6%, N (26 ס N Among disease categories, platelet loss was greater in patients with dysproteinemias who were treated for hyper- viscosity symptoms. Absolute platelet loss with the first recorded apheresis procedure, in the 34 patients who had a normal platelet count before the procedure, was also greater with the AS 104 (2.23 × 1011 platelets) than with the Spectra (0.29 × 1011 platelets) or the LN9000 (0.37 × 1011 platelets). -
Platelet-Rich Plasmapheresis: a Meta-Analysis of Clinical Outcomes and Costs
THE jOURNAL OF EXTRA-CORPOREAL TECHNOLOGY Original Article Platelet-Rich Plasmapheresis: A Meta-Analysis of Clinical Outcomes and Costs Chris Brown Mahoney , PhD Industrial Relations Center, Carlson School of Management, University of Minnesota, Minneapolis, MN Keywords: platelet-rich plasmapheresis, sequestration, cardiopulmonary bypass, outcomes, economics, meta-analysis Presented at the American Society of Extra-Corporeal Technology 35th International Conference, April 3-6, 1997, Phoenix, Arizona ABSTRACT Platelet-rich plasmapheresis (PRP) just prior to cardiopulmonary bypass (CPB) surgery is used to improve post CPB hemostasis and to minimize the risks associated with exposure to allogeneic blood and its components. Meta-analysis examines evidence ofPRP's impact on clinical outcomes by integrating the results across published research studies. Data on clinical outcomes was collected from 20 pub lished studies. These outcomes, DRG payment rates, and current national average costs were used to examine the impact of PRP on costs. This study provides evidence that the use of PRP results in improved clinical outcomes when compared to the identical control groups not receiving PRP. These improved clinical out comes result in subsequent lower costs per patient in the PRP groups. All clinical outcomes analyzed were improved: blood product usage, length of stay, intensive care stay, time to extu bation, incidence of cardiovascular accident, and incidence of reoperation. The most striking differences occur in use of all blood products, particularly packed red blood cells. This study provides an example of how initial expenditure on technology used during CPB results in overall cost savings. Estimated cost savings range from $2,505.00 to $4,209.00. -
Important Information for Female Platelet Donors
Important Information for Female Platelet Donors We are grateful for the support you provide our community blood program and especially appreciate your willingness to help save lives as a volunteer platelet donor. We also take our responsibility to provide a safe and adequate blood supply very seriously and need to share the following information regarding a change to our donor eligibility criteria for female platelet donors. We recently began performing a Human Leukocyte Antigen (HLA) antibody test on each of our current female platelet donors who have ever been pregnant. In addition, we modified our Medical History Questionnaire to ask donors whether they have been pregnant since their last donation. Platelet donors who respond yes to that question will be screened for HLA antibodies. Platelet donors will also be retested after every subsequent pregnancy. These adjustments are being made as part of our effort to reduce occurrences of Transfusion-Related Acute Lung Injury (TRALI). TRALI is a rare but serious complication of blood transfusions most commonly thought to be caused by a reaction to HLA antibodies present in the donor’s plasma. When transfused, these antibodies can sometimes cause plasma to leak into the patient’s lungs, creating fluid accumulation — a condition referred to as acute pulmonary edema. Female donors who have been pregnant are more likely than others to have these HLA antibodies in their plasma. Once the antibodies develop, they are present forever. The antibodies could be harmful if transfused into certain patients. The antibodies are present in plasma — and platelet donations contain a high volume of plasma, so our current efforts are directed at screening blood samples from female platelet donors to test for the HLA antibody. -
CD59: a Long-Known Complement Inhibitor Has Advanced to a Blood Group System
B LOOD G ROUP R EVIEW CD59: A long-known complement inhibitor has advanced to a blood group system C. Weinstock, M. Anliker, and I. von Zabern The blood group system number 35 is based on CD59, a 20-kDa by Zalman et al.1 from the group of H.J. Muller-Eberhard in La membrane glycoprotein present on a large number of different Jolla, California, and in 1988 by Schönermark et al. from the cells, including erythrocytes. The major function of CD59 is to group of G.M. Hänsch in Heidelberg (Germany).2 This inhibitor protect cells from complement attack. CD59 binds to complement components C8 and C9 and prevents the polymerization of C9, was published under the designations “HRF (homologous which is required for the formation of the membrane attack restriction factor)” and “C8bp (C8 binding protein),” complex (MAC). Other functions of CD59 in cellular immunity respectively, to describe its properties.1,2 “C8bp” indicates the are less well defined. CD59 is inserted into the membrane by a glycosylphosphatidylinositol (GPI) anchor. A defect of this anchor binding capacity for C8. The name “HRF” points to a species causes lack of this protein from the cell membrane, which leads to incompatibility of this “factor” that provides protection from an enhanced sensitivity towards complement attack. Patients with complement attack more effectively in a homologous (e.g., paroxysmal nocturnal hemoglobinuria (PNH) harbor a varying human erythrocytes as a target of human complement) than in percentage of red blood cell clones with a defect in GPI-anchored proteins, including CD59. The most characteristic symptoms of a heterologous system (e.g., human erythrocytes as a target of this disease are episodes of hemolysis and thromboses. -
Essential Thrombocythemia Facts No
Essential Thrombocythemia Facts No. 12 in a series providing the latest information for patients, caregivers and healthcare professionals www.LLS.org • Information Specialist: 800.955.4572 Introduction Highlights Essential thrombocythemia (ET) is one of several l Essential thrombocythemia (ET) is one of a related “myeloproliferative neoplasms” (MPNs), a group of closely group of blood cancers known as “myeloproliferative related blood cancers that share several features, notably the neoplasms” (MPNs) in which cells in the bone “clonal” overproduction of one or more blood cell lines. marrow that produce the blood cells develop and All clonal disorders begin with one or more changes function abnormally. (mutations) to the DNA in a single cell; the altered cells in l ET begins with one or more acquired changes the marrow and the blood are the offspring of that one (mutations) to the DNA of a single blood-forming mutant cell. Other MPNs include polycythemia vera and cell. This results in the overproduction of blood cells, myelofibrosis. especially platelets, in the bone marrow. The effects of ET result from uncontrolled blood cell l About half of individuals with ET have a mutation production, notably of platelets. Because the disease arises of the JAK2 (Janus kinase 2) gene. The role that this from a change to an early blood-forming cell that has the mutation plays in the development of the disease, capacity to form red cells, white cells and platelets, any and the potential implications for new treatments, combination of these three cell lines may be affected – and are being investigated. usually each cell line is affected to some degree. -
Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods
Guidance for Industry Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods Additional copies of this guidance document are available from: Office of Communication, Training and Manufacturers Assistance (HFM-40) 1401 Rockville Pike, Rockville, MD 20852-1448 (Tel) 1-800-835-4709 or 301-827-1800 (Internet) http://www.fda.gov/cber/guidelines.htm U.S. Department of Health and Human Services Food and Drug Administration Center for Biologics Evaluation and Research (CBER) January 2001 Technical Correction February 2001 TABLE OF CONTENTS Note: Page numbering may vary for documents distributed electronically. I. INTRODUCTION ............................................................................................................. 1 II. BACKGROUND................................................................................................................ 1 III. CHANGES FROM THE DRAFT GUIDANCE .............................................................. 2 IV. RECOMMENDED DONOR SELECTION CRITERIA FOR THE AUTOMATED RED BLOOD CELL COLLECTION PROTOCOLS ..................................................... 3 V. RECOMMENDED RED BLOOD CELL PRODUCT QUALITY CONTROL............ 5 VI. REGISTRATION AND LICENSING PROCEDURES FOR THE MANUFACTURE OF RED BLOOD CELLS COLLECTED BY AUTOMATED METHODS.................. 7 VII. ADDITIONAL REQUIREMENTS.................................................................................. 9 i GUIDANCE FOR INDUSTRY Recommendations for Collecting Red Blood Cells by Automated Apheresis Methods This -
Transfusion Reactions 7
HEMATOLOGY Immunohematology, transfusion medicine and bone marrow transplantation Institute of Pathological Physiology First Facultry of Medicine, Charles University in Prague http://patf.lf1.cuni.cz Questions and Comments: MUDr. Pavel Klener, Ph.D., [email protected] Presentation in points 1. Imunohematology 2. AB0 blood group system 3. Rh blood group system 4. Hemolytic disease of the newborn and neonatal alloimmune thrombocytopenia 5. Pre-transfusion examinations 6. Transfusion reactions 7. Transfusion medicine and hemapheresis 8. HLA system 9. Stem cell/ bone marrow transplantation Origins of immunohematology and transfusion medicine Imunohematology as a branch of medicine developed hand in hand with the origins of transfusion therapy. It focuses on concepts and questions associated with transfusion therapy, immunisation (as a result of transfusion therapy and pregnancy) and organ transplantation. In 1665, an English physiologist, Richard Lower, successfully performed the first animal- to-animal blood transfusion that kept ex-sanguinated dogs alive by transfusion of blood from other dogs. In 1667, Jean Bapiste Denys, transfused blood from the carotid artery of a lamb into the vein of a young man, which at first seemed successful. However, after the third transfusion of lamb’s blood the man suffered a reaction and died. Due to the many disastrous consequences resulting from blood transfusion, transfusions were prohibited from 1667 to 1818- when James Blundell of England successfully transfused human blood to women suffering from hemorrhage at childbirth. Revolution in 1900 In 1900 Karl Landsteiner discovered the AB0 blood groups. This landmark event initiated the era of scientific – based transfusion therapy and was the foundation of immunohematology as a science. -
Blood and Immunity
Chapter Ten BLOOD AND IMMUNITY Chapter Contents 10 Pretest Clinical Aspects of Immunity Blood Chapter Review Immunity Case Studies Word Parts Pertaining to Blood and Immunity Crossword Puzzle Clinical Aspects of Blood Objectives After study of this chapter you should be able to: 1. Describe the composition of the blood plasma. 7. Identify and use roots pertaining to blood 2. Describe and give the functions of the three types of chemistry. blood cells. 8. List and describe the major disorders of the blood. 3. Label pictures of the blood cells. 9. List and describe the major disorders of the 4. Explain the basis of blood types. immune system. 5. Define immunity and list the possible sources of 10. Describe the major tests used to study blood. immunity. 11. Interpret abbreviations used in blood studies. 6. Identify and use roots and suffixes pertaining to the 12. Analyse several case studies involving the blood. blood and immunity. Pretest 1. The scientific name for red blood cells 5. Substances produced by immune cells that is . counteract microorganisms and other foreign 2. The scientific name for white blood cells materials are called . is . 6. A deficiency of hemoglobin results in the disorder 3. Platelets, or thrombocytes, are involved in called . 7. A neoplasm involving overgrowth of white blood 4. The white blood cells active in adaptive immunity cells is called . are the . 225 226 ♦ PART THREE / Body Systems Other 1% Proteins 8% Plasma 55% Water 91% Whole blood Leukocytes and platelets Formed 0.9% elements 45% Erythrocytes 10 99.1% Figure 10-1 Composition of whole blood. -
Thrombocytopenia in Older Adults Melissa (Kah Poh) Loh, MD
URMC Division of Geriatrics & Aging March 2019 Thrombocytopenia in Older adults Melissa (Kah Poh) Loh, MD Background Thrombocytopenia (or low platelet count) is a common hematologic abnormality encountered in older adults Common causes of thrombocytopenia include (Table 1): Immune-related [e.g. immune thrombocytopenia purpura (ITP)] Drug-induced [e.g. heparin-induced thrombocytopenia (HIT)] Bone marrow failure Other: Infections (e.g. H. pylori, HIV, hepatitis), pseudothrombocytopenia (Figure 1), alcohol abuse, liver Figure 1: Peripheral smear showing clumped cirrhosis, blood transfusion, thrombotic thrombocytopenia platelets (pseudothrombocytopenia — falsely purpura (TTP), and hemolytic-uremic syndrome (HUS), low platelet count) thyroid disease Age-related changes in the organ and vasculature systems increase the risks of thrombocytopenia on hemostasis Factors that may enhance bleeding in older adults. These include: Comorbidities Medications Loss of subcutaneous tissue Age-specific factors that may prevent bleeding in older adults include enhanced platelet aggregation and increased fibrinogen, factor V, and von Willebrand factor Thrombocytopenia is often multifactorial in older adults. Table 1: Quick Facts on Thrombocytopenia PATHOPHYSIOLOGY Immune Thrombocytopenia Purpura Drug-Induced Increased platelet clearance in the reticulo-endothelial Impaired production (direct marrow toxicity or system of bone marrow, spleen, and/or liver megakaryocyte-specific inhibition) Inadequate platelet production due to megakaryocyte Increased platelet clearance (indirect immune clearance, inhibition by IgG antibodies antibody-specific immune clearance, miscellaneous immune -mediated) Often suppress other cell lines CAUSES Immune Thrombocytopenia Purpura Drug-Induced Often idiopathic See Table 2 Can be associated with underlying hematologic abnormalities (e.g. myelodysplastic syndrome, chronic lymphocytic leukemia) INCIDENCE RATES Immune Thrombocytopenia Purpura Drug-Induced 4.62 per 100,000 adults aged >60 years vs. -
Clinical Transfusion Practice
Clinical Transfusion Practice Guidelines for Medical Interns Foreword Blood transfusion is an important part of day‐to‐day clinical practice. Blood and blood products provide unique and life‐saving therapeutic benefits to patients. However, due to resource constraints, it is not always possible for the blood product to reach the patient at the right time. The major concern from the point of view of both user (recipient) and prescriber (clinician) is for safe, effective and quality blood to be available when required. Standard practices should be in place to include appropriate testing, careful selection of donors, screening of donations, compatibility testing, storage of donations for clinical use, issue of blood units for either routine or emergency use, appropriate use of blood supplied or the return of units not needed after issue, and reports of transfusion reactions – all are major aspects where standard practices need to be implemented. In order to implement guidelines for standard transfusion practices, a coordinated team effort by clinicians, blood transfusion experts, other laboratory personnel and health care providers involved in the transfusion chain, is needed. Orientation of standard practices is vital in addressing these issues to improve the quality of blood transfusion services. Bedside clinicians and medical interns are in the forefront of patient management. They are responsible for completing blood request forms, administering blood, monitoring transfusions and being vigilant for the signs and symptoms of adverse reactions. -
Platelet Pheresis It Does Matter
Neighborhood Blood Donation Centers Eastern Hills Mall Neighborhood Donation Center 4545 Transit Rd., Williamsville, 14221 WNY’s only organ, eye, tissue Monday 10am - 8pm & community blood center. Wednesday 1pm - 8pm Friday 7am - 2pm Saturday 7am - 3pm Tonawanda Neighborhood Donation Center 96 Niagara Street, Tonawanda, 14150 Monday, Tuesday & Thursday 10am-8pm EVERY other Saturday 7am-3pm Southgate Neighborhood Blood Donation Center 1000 Union Rd., West Seneca, 14224 Monday & Wednesday 10am -8pm Friday 7am - 2pm EVERY other Saturday 7am - 3pm Unyts Neighborhood Donation Center 110 Broadway, Buffalo, 14203 Tuesday 10am -3pm To make an appointment to donate please call 512.7940. Platelet Pheresis It Does Matter. Becoming a 110 Broadway • Buffalo, NY 14203 Platelet Donor www.unyts.org What is Platelet Pheresis? o Patients in a high-dose chemotherapy treatment often It is Automated Blood Collection, an increasingly need 8 units of platelets every three days common procedure. Automation is the process of o Leukemia patients may require 10-12 units of platelets removing a specific component of the blood, such as weekly platelets, and returning the remaining components, o Bone marrow transplant patients can use as many as 120 such as red blood cells and plasma, to the donor. units of platelets Platelets must be transfused within five days Life-Saving Platelets Up to 40% of platelets donated are transfused to children Your blood may be more special than you think. Platelets are essential for normal blood clotting and are used in the Platelets are often in very short supply due to their high treatment of serious illness, including cancer, leukemia demand and short shelf life. -
Red Blood Cell-Derived Semaphorin 7A Promotes Thrombo-Inflammation
ARTICLE https://doi.org/10.1038/s41467-020-14958-x OPEN Red blood cell-derived semaphorin 7A promotes thrombo-inflammation in myocardial ischemia- reperfusion injury through platelet GPIb David Köhler1, Tiago Granja1, Julia Volz2, Michael Koeppen1, Harald F. Langer3, Georg Hansmann4, Ekaterina Legchenko 4, Tobias Geisler5, Tamam Bakchoul 6, Claudia Eggstein1, Helene A. Häberle1, ✉ Bernhard Nieswandt2 & Peter Rosenberger1 1234567890():,; Myocardial ischemia is one of the leading health problems worldwide. Therapy consists of the restitution of coronary perfusion which is followed by myocardial inflammation. Platelet–neutrophil interaction is a crucial process during inflammation, yet its consequences are not fully understood. Here, we show that platelet–neutrophil complexes (PNCs) are increased in patients with acute myocardial infarction and that this is associated with increased levels of neuronal guidance protein semaphorin 7A (SEMA7A). To investigate this further, we injected WT animals with Sema7a and found increased infarct size with increased numbers of PNCs. Experiments in genetically modified animals identify Sema7a on red blood cells to be crucial for this condition. Further studies revealed that Sema7a interacts with the platelet receptor glycoprotein Ib (GPIb). Treatment with anti-Sema7a antibody protected from myocardial tissue injury. In summary, we show that Sema7a binds to platelet GPIb and enhances platelet thrombo-inflammatory activity, aggravating post-ischemic myocardial tis- sue injury. 1 Department of Anesthesiology and Intensive Care Medicine, University Hospital, Tübingen, Germany. 2 Institute of Experimental Biomedicine and Rudolf Virchow Center, Würzburg, Germany. 3 Department of Cardiology, University Hospital Lübeck, Lübeck, Germany. 4 Department of Pediatric Cardiology, Hannover Medical School, Lübeck, Germany. 5 Department of Cardiology, University Hospital, Tübingen, Germany.