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The method in use consists of a 1: Another parameter that cannot be overlooked is the formation of ABH immunocomplexes following mainly the transfusion of platelets with minor ABO-incompatibility.
Circulating portions of ABH antigens and ABH glycosylated complexes of the recipient recognize and inactivate the transfused anti-A and anti-B antibodies.
The long-term fate as well as the clinical relevance of the resulting formation of these soluble ABH immunocomplexes is not yet known, but they could be possibly harmful for the recipient.
Nowadays, many efforts could be considered as accepted practice in order to overcome the ABO barrier in platelet transfusions. As a conclusion, it seems that the most effective and safest therapeutic strategy in platelet transfusions, that carries the lowest risk for the patient, is the one from an ABO-identical donor, which is though not always feasible.
The implementation of protocols to overcome the ABO barrier in platelet transfusions is most likely to increase both the workload and the cost.
Taking into consideration all these available data, a practical costless approach to inventory management could be to:. Human platelets do not express any antigens of the rhesus system.
However, platelet concentrates contain the variable volume of contaminating RBCs, which may induce RhD alloimmunization when transfused in a RhD negative subject.
Although the risk is low especially for the majority of thrombocytopenic patients who need long-term platelet transfusions immunosuppressive therapy, malignancies , it could have a clinical impact in childbearing age women, when RhD alloimmunization can cause hemolytic disease of the fetus and newborn.
Several studies have attempted to correlate anti-D alloimmunization after platelets transfusion with the total number of the platelets units transfused.
ABO-incompatibility is reported to reduce the rate of anti-D alloimmunization in normal volunteers and pregnant women. Actually, alloimmunization rates have been reported to decrease after the implementation of universal leukoreduction.
In conclusion, nowadays, data suggest a low rate of anti-D alloimmunization related to platelet transfusion. Thus, transfusion practices could allow the transfusion of RhD positive PLT units to RhD negative patients, with the exception of females of childbearing age.
Such a treatment does not affect the survival of transfused platelets since the platelets do not express Rh antigens.
Still these molecules retain the ability to induce the development of alloantibodies. The HLA antigens of the donor are recognized by the immune system of the recipient either directly or indirectly.
Platelet refractoriness is defined as the failure to achieve an acceptable increment in platelet count following platelet transfusion at least on two occasions.
Platelet count must be measured within 1 h after transfusion. CCI of or above is considered an adequate response. The nonimmune mechanism includes, diseases of the recipient such as fever, splenomegaly, DIC, bleeding, or drugs amphotericin B, ciprofloxacin.
Most of the patients with platelet transfusion refractoriness are sensitized against HLA antigens, but anti-HPA antibodies have also been documented.
High titers of natural ABO antibodies, as it has been already described, can also underlie platelet refractoriness. Patients confirmed with immune platelet transfusion refractoriness could be investigated for the presence of HLA specific antibodies.
Most common methods used for this identification are the panel reactive antibody, an assay based on lymphocytotoxicity or the enzyme-immunoassay-based method and the antigen specificity prediction method ASP.
Two main transfusion approaches are currently implemented for patients with platelet refractoriness due to HLA alloimmunization: Either transfusion with cross-matched platelets or transfusion with HLA-matched platelets.
Recently, transfusion of platelets treated with specific acid dilutions to an alloimmunized patient had encouraging results. Platelet cross-match transfusion practice is mainly carried out by solid phase technique the solid-phase red cell adherence test.
Given the genetic variability of the HLA system, it soon became obvious that we should have a very large pool of platelet donors in order to meet the need for every patient with resistance to platelet transfusion.
The main drawbacks of the methods available are that HLA-matched platelets are an expensive approach and frequently unavailable and on the other hand since platelets have a shelf life of 5 days, platelet cross-match, although less expensive has to be frequently repeated.
It is quite clear that selecting the method with which we approach and manage platelet refractoriness depends on the available techniques and their cost and thus practices vary considerably among institutions and countries.
Although in the literature, there are studies describing the effectiveness of each transfusion practice alone, there are not many studies directly comparing these two approaches.
One study concluded that although HLA-compatible platelets provide the optimal support for refractory patients, cross-match-selected platelets can serve as an acceptable alternative approach,[ 74 ] while another recent study[ 75 ] has shown that the use of cross-match-compatible or HLA-matched units did not provide better increments in PLT count when compared to random nonselected units.
The other parameter that should be taken into account is the cost effectiveness of these approaches. Only one study with economic analysis showed that the HLA-matched single-donor platelets were relatively cost-inefficient in comparison to the crossmatch-compatible platelets.
What is more important in determining the superiority of the available methods is accessing not only the laboratory outcome reduction in HLA alloimmunization, improvement in PLT count increment but also the clinical outcome i.
Two recent reviews have tried to answer the question of the efficacy of a cross-matched platelets and b HLA-matched platelet transfusions.
Both reviews concluded that data on the clinical outcome are scarce and that fact warrants the need of future prospective studies addressing the impact of both approaches on clinical outcomes.
In terms of prevention, it has become clear over the past years that the basis of HLA alloimmunization after platelet transfusion is not the HLA I that platelets harbor but rather the HLA II expressed on the white cells that circulate in the transfused product.
ABO-identical platelet transfusion seems to be the best, safest, and most effective approach in platelet transfusion practice and should be implemented when possible.
The identification of high-risk patients i. In this case, prophylactic administration of anti-D globulin should be applied.
The development of anti-HLA antibodies is the most frequent reason of immune platelet refractoriness. The choice of leukoreduced products for thrombocytopenic patients requiring long-term platelet support can be an effective measure of reducing the incidence of both anti-D and anti-HLA alloimmunization.
Administration of cross-matched platelets or HLA-matched depends on the accessibility to such methods by individual blood bank services, but data are still lacking for the efficacy of both practices in terms of clinical outcome.
National Center for Biotechnology Information , U. Asian J Transfus Sci. Author information Copyright and License information Disclaimer.
Sofias 76, , Athens, Greece. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.
This article has been cited by other articles in PMC. Abstract Platelet transfusions have contributed to the revolutionary modern treatment of hypoproliferative thrombocytopenia.
ABO-incompatibility, human leukocyte antigen-platelet refractoriness, platelet transfusion, RhD. Introduction Platelet transfusions have contributed to the revolutionary modern treatment of thrombocytopenia in patients with cancer and hematological malignancies receiving chemotherapy over the past 50 years.
Transfusions of Platelets with Minor ABO-incompatibility Transfusion of platelets with minor ABO-incompatibility incompatible plasma has also been associated with poorer platelet count increments, but the main concern is the subsequent development of hemolytic transfusion reaction HTR of the recipient.
Encourage instrument manufacturers to develop and validate automated anti-A and anti-B titer screening,[ 34 ].
Wash and resuspend platelets in saline,[ 15 ]. Reduce plasma volume of group O apheresis PLTs concentrates to 50 ml,[ 38 ] and. Replace plasma with additive solutions or AB plasma after washing, with the limitations described for the existing soluble A and B circulating antigens in AB plasma.
Evaluate the patient and identify high-risk cases i. With the development of DNA sequencing , it has been possible to identify a much larger number of alleles at the ABO locus, each of which can be categorized as A, B, or O in terms of the reaction to transfusion, but which can be distinguished by variations in the DNA sequence.
The same study also identified 18 rare alleles, which generally have a weaker glycosylation activity. People with weak alleles of A can sometimes express anti-A antibodies, though these are usually not clinically significant as they do not stably interact with the antigen at body temperature.
Cis AB is another rare variant, in which A and B genes are transmitted together from a single parent. The distribution of the blood groups A, B, O and AB varies across the world according to the population.
There are also variations in blood type distribution within human subpopulations. In the UK, the distribution of blood type frequencies through the population still shows some correlation to the distribution of placenames and to the successive invasions and migrations including Norsemen , Danes , Saxons , Celts , and Normans who contributed the morphemes to the placenames and the genes to the population.
The two common O alleles, O01 and O02, share their first nucleotides with the group A allele A A premature stop codon results from this frame-shift mutation.
This variant is found worldwide, and likely predates human migration from Africa. The O01 allele is considered to predate the O02 allele.
Some evolutionary biologists theorize that there are four main lineages of the ABO gene and that mutations creating type O have occurred at least three times in humans.
The continued presence of the O alleles is hypothesized to be the result of balancing selection. It is possible that food and environmental antigens bacterial, viral, or plant antigens have epitopes similar enough to A and B glycoprotein antigens.
The antibodies created against these environmental antigens in the first years of life can cross-react with ABO-incompatible red blood cells that it comes in contact with during blood transfusion later in life.
Anti-B antibodies are hypothesized to originate from antibodies produced against Gram-negative bacteria , such as E.
However, it is more likely that the force driving evolution of allele diversity is simply negative frequency-dependent selection; cells with rare variants of membrane antigens are more easily distinguished by the immune system from pathogens carrying antigens from other hosts.
Thus, individuals possessing rare types are better equipped to detect pathogens. The high within-population diversity observed in human populations would, then, be a consequence of natural selection on individuals.
HIV can be neutralized in in vitro experiments using antibodies against blood group antigens specifically expressed on the HIV-producing cell lines.
The carbohydrate molecules on the surfaces of red blood cells have roles in cell membrane integrity, cell adhesion , membrane transportation of molecules, and acting as receptors for extracellular ligands, and enzymes.
ABO antigens are found having similar roles on epithelial cells as well as red blood cells. The ABO antigen is also expressed on the von Willebrand factor vWF glycoprotein ,  which participates in hemostasis control of bleeding.
Higher levels of vWF are more common amongst people who have had ischemic stroke from blood clotting for the first time.
According to Glass, Holmgren, et al. The mechanisms behind this association with cholera are unclear in the literature.
ABO blood group incompatibilities between the mother and child does not usually cause hemolytic disease of the newborn HDN because antibodies to the ABO blood groups are usually of the IgM type, which do not cross the placenta.
In human cells, the ABO alleles and their encoded glycosyltransferases have been described in several oncologic conditions.
In most human carcinomas, including oral carcinoma, a significant event as part of the underlying mechanism is decreased expression of the A and B antigens.
A multi-locus genetic risk score study based on a combination of 27 loci, including the ABO gene, identified individuals at increased risk for both incident and recurrent coronary artery disease events, as well as an enhanced clinical benefit from statin therapy.
In April , an international team of researchers announced in the journal Nature Biotechnology an inexpensive and efficient way to convert types A, B, and AB blood into type O.
The removal of A and B antigens still does not address the problem of the Rh blood group antigen on the blood cells of Rh positive individuals, and so blood from Rh negative donors must be used.
Patient trials will be conducted before the method can be relied on in live situations. Another approach to the blood antigen problem is the manufacture of artificial blood , which could act as a substitute in emergencies.
During the s, connecting blood groups to personality types became popular in Japan and other areas of the world.
Other popular but unsupported ideas include the use of a blood type diet , claims that group A causes severe hangovers , group O is associated with perfect teeth, and those with blood group A2 have the highest IQs.
Scientific evidence in support of these concepts is nonexistent. From Wikipedia, the free encyclopedia.
Your quality assurance QA departments can have full system access to review activity, identify possible user errors, and implement corrections.
Additionally, quality assurance mechanisms are built into each processing group. ABO Express includes a full complement of recruitment tools.
Your nursing staff can efficiently document and review donor medical history and phlebotomy results, and perform corrective actions on uploaded units.
Database inquiry and reporting functionality includes daily reporting of first-time donors, and managing changes to critical donor demographic information.
ABO Express includes management controls for the creation and maintenance of user-modifiable table files that empower your facility to dictate most of the system decision algorithms.
Additionally, ABO Express includes a complete range of Information Services management tools such as security administration, database management, and file maintenance to support smooth operation of the system.
It also includes Billing features to support your accounts receivable processing in an online, fully automated environment. Each function in the ABO Express system that deals with the distribution of products, the donation of specially processed units, or the testing and processing of requested products may create an automatic accounts receivable record.
However, ABO Express has been designed and built to provide a whole new level of ease, offer exciting and innovative functionality, and exhibit robust performance.
The integration, automation, platform diversity, and integration capabilities of this next generation product will support your risk management, operations, and data management like never before.