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Are antibodies removed before blood transfusion

Are antibodies removed before blood transfusion


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I am an O blood group person meaning, I can donate my blood to all as I don't have any Antigen A and B. But my body does contain antibodies A and B right?

If they were along with the donor blood, wouldn't they cause clotting with the recipients blood?

We spent a whole period over this. My teacher said they probably remove the antibody before transfusion, but I couldn't find much info on that. I postulated that these antibodies can not work outside the donor body for some reason.

Thanks for the help


I quote from the below.

Groups and Red Cell Antigens

by

Laura Dean (page 7). Available at:

http://www.ncbi.nlm.nih.gov/books/NBK2265/

"Red blood cell incompatibility may also occur when the patient's RBC antigens are attacked by antibodies from the donor's plasma. This tends to be a minor problem because of the small amount of antibody present in the donated plasma, which is further diluted on transfusion into the recipient's circulation."

I dont think the antibodies are removed, but in countries with a good medical system I believe the matching blood type is always used.

http://en.wikipedia.org/wiki/Acute_hemolytic_transfusion_reaction


It important to know a person’s rhesus factor before a blood transfusion? A patient who is Rh+ can receive only Rh– blood. A patient who is Rh– can receive only Rh+ blood. A patient who is Rh+ can receive only Rh+ blood. A patient who is Rh– can receive only Rh– blood.

The right answer is A patient who is Rh– can receive only Rh– blood.The blood group is not the only thing that matters, it adds a category: rhesus. Rhesus refers to a red blood cell antigen that is on their wall. There are two blood group systems: Rh positive (Rh +) and Rh negative (Rh-).Rhesus is positive in people who have this antigen. It concerns the majority of the population. Negative rhesus refers to people without the antigen. This rhesus factor is especially useful to know if a blood transfusion is feasible between two people.The blood transfusions can be “iso-rhesus”, that is to say between Rh + and Rh- but only in one sense: Rh- can give to Rh + but Rh + can not give to Rh-. Again because of the presence of antibodies directed against the antigen in Rh- people.


[Immune hemolytic diseases caused by irregular antibodies and its research advance in clinic]

The irregular antibodies are other than antibodies from ABO blood group system because of pregnancies and blood transfusions, clinical autoimmune, drug-induced etc. The irregular IgG and/or IgM antibodies emerge and lead to the difficult identification of clinical blood type, difficult matching of blood, hemolytic disease of newborn, hemolytic transfusion reaction, and so on. It is very necessary to screen and identify the irregular antibodies before blood transfusion or antepartum. For some difficult identifying samples, some detections on serological level should be done firstly, combining with flow cytometry analysis, the difficult-matching patients' genotypes and fetal genotypes were detected by molecular biology techniques such as PCR and PCR-SSP in order to further predict fetal hemolytic disease of newborn and to provide the right blood to difficult-matching patients, and free fetal DNA extracted from maternal plasma. So that some measures must early be taken for clinical prevention and treatment to reduce immune hemolytic reactions. In this paper, the emergence of irregular antibodies, species, laboratory testing, pathogenesis, clinical symptoms and the current research are reviewed.


Human Biology Chapter 6 (Blood)

*SCID, severe combined immunodeficiency disease, results from the lack of adenosine deaminase.

*Leukemia is the uncontrolled growth of white blood cells. Infectious mononucleosis is when the lymphocytes are mononuclear. Thrombocytopenia is an insufficient number of platelets. Hemophilia is an inherited clotting disorder. A thromboembolism is when a blood clot prevents blood from reaching certain tissues.

It is caused by an Epstein-Barr virus.

Symptoms include fever, sore throat, and swollen lymph glands.

There is uncontrolled white blood cell proliferation.

Active EBV can be passed in saliva.

*Mononucleosis is caused by the Epstein-Barr virus, which does not involve uncontrollable white blood cell proliferation.

Nosebleeds and gastrointestinal bleeding due to increased breakdown of platelets outside the marrow is a condition called thrombocytopenia.

*Blood clotting requires at least 12 clotting factors along with calcium ions (Ca2+) to ensure that plasma and the formed elements remain in the blood vessels.

*Blood clotting requires 12 clotting factors and calcium ions (Ca2+) to ensure that plasma and the formed elements remain in the blood vessels.

*After blood clots, the yellowish fluid that escapes from the clot is called serum.

Formed elements and plasma would not remain in the blood.

Red blood cells would increase in concentration.

The Ca2+ concentration in the blood would increase.

The blood pressure of the individuals would increase.

*If blood clotting doesn't occur correctly the formed elements and plasma would not remain in the blood. The concentration of red blood cells would decrease due to the loss of cells. The Ca2+ concentration in the blood would decrease. The blood pressure of the individuals would decrease due to the loss of blood. Fluid would not accumulate in the body.


Antibodies in blood after transfusion

I have had three transfusions since the end of Nov. My hct dropped to 19 so I am getting ready for a fourth, however, they tell me I have antibodies in my blood and the transfusion has to be postponed until further lab work is completed. Can anyone tell me anything about this situation?

Laurie,
My simple version is that when you get transfusions, if the the transfused blood is not treated properly – irradiated to remove those anti-bodies – they remain in your system. Then all subsequent blood for transfusions must match/or not upset the antibody so as not to cause your body to reject the blood infusion. This is a very crude non-medical explanation. From my understanding, once you pick up an anti-body it is takes longer and is harder to match your blood.

I have been receiving tx’s since 2005. All my blood transfusions except my very 1st one prior to my MDS diagnosis, are from irradiated, leuko-depleted blood. Everything but pure red blood cells are removed and then radiated prior to my receiving. This does take some time.

Best wishes and speak with your doctor about pre-treatment of your blood. Also notced you are 5q-, have you tried Revlimid?
–cheryl

Excuse me…but I disagree with you.
I have always received Leuko-reduced, irradiated blood and have 5 antibodies.

Guess my crude explanation was incorrect. Maybe I should have stated that pre-treatment "reduces" the chances of anti-bodies, but does not guarantee it.

Promise to keep my medical explanations to a minimum in the future.

Best wishes to both of you.

I am not yet on Revlimid—trying to get to that point. I have had unstable HCT since last June with HCT at or around 25 sometimes lower and sometimes but rarely higher—usually after tx. I am having trouble with being winded all of the time—can’t walk far and now they tell me it may have had some impact on my heart. I would guess that they will be holding off on the Revlimid until they find out the condition of my heart.


What types of transfusion reactions can jeopardize the safety of blood transfusions?

Transfusions are generally safe and there are more successful red blood cell (RBC) transfusions than those that produce severe adverse effects. 2 However, blood transfusions can induce immunosuppression by eliciting antibodies for human leukocyte antigen (HLA) or transmit viruses such as cytomegalovirus (CMV). Transfusion reactions, such as febrile non-hemolytic transfusion reaction (FNHTR) or platelet transfusion refractoriness, can be induced by leukocyte (or white blood cell, WBC) antibodies. 3 The presence of WBCs in blood and platelet products is associated with an increased incidence of FNHTR, transmission of CMV and alloimmunization to HLA antigens in transfusion recipients. 3 Depletion of leukocytes below a specific level can prevent HLA alloimmunization. 4 Removal of >99.9% of leukocytes in platelets and red cell units can also reduce potential transmission of CMV. 5


Blood Transfusion

what is the percent yield of factor VIII in the final cryoprecipitate?

what is the % yield of plts in the PRP from this unit?

does this product meet AABB standards for plt concentrate production?

-patients with warm autoimmune hemolytic anemia?

if the patients RBC were tested against anti-H lctin and did not react, this person would be identified as a(an)?

the tech suspects that this is a case of an acquired B antigen. which of the following would support this suggestion?

what % of this couples offspring can be expected to be D-neg

which of the following conclusions regarding the family typing is most likely?

which, if any, of these three individuals can make anti-D?

which of the following statements is true? the alleged father

found primarily in whites

associated with weak Kell sys. antigenic expression

associated with the presence of chronic granulomatous disease (WBC cant produce superoxide radical used to kill certain pathogens-->immunocomprimised)

what is the most likely cause of the discrepancy?

how many bags should be thawed and pooled to provide 2g of fibrinogen?

the patient is group A. which cryo units would most appropriately be used to treat this patient?

the resident says the victim has a donor card in his wallet indicating that he is type B+. what should be done immediately?

what should be the next step in the work up of this ER patient?

you tell the nurse immediately to

which of the following directives would NOT be included in the additional activities you would request the nurse to do?

all paper work checks on this transfusion reaction are OK. the pretransfusion sample has straw colored plasma. the posttransfusion sample has a red-tinged plasma. this is indicative of..


Future directions

Significant progress has been made in both the understanding of TRALI and its mitigation. Future strategies for the prevention of TRALI may include immune-based strategies to block donor antibodies or the immune response to transfused antibodies. Human investigations have found increased plasma levels of the inflammatory cytokine IL-8 but lower levels of the anti-inflammatory cytokine IL-10 in both antibody- and nonantibody-mediated cases of TRALI compared with those of possible TRALI. 1,20,126 Recently, it was shown that regulatory T cells and dendritic cells were protective in a murine model of antibody-mediated TRALI, and this protection was associated with increased plasma levels of IL-10. 127 In addition, there was evidence of a benefit of IL-10 administration in the prevention of murine TRALI as well as treatment after its induction with HLA antibodies (Figure 2). These findings may indicate a distinct mechanism of pathogenesis in TRALI compared with other forms of lung injury as well as opportunities for prevention and treatment.

TRALI suppression in CD4+ T cell–depleted mice with murine IL-10 administration. (A) Decreased lung wet/dry (W/D) weight ratios of CD4+ T cell–depleted C57BL/6 mice infused with 34-1-2s/AF6-88.5.5.3 and treated prophylactically with murine IL-10 administration (45 mg/kg intravenously). (B) Lung W/D weight ratios of CD4+ T cell–depleted C57BL/6 mice infused with 34-1-2s/AF6-88.5.5.3 and treated therapeutically 15 minutes later with or without murine IL-10 administration (45 mg/kg intravenously) after onset of TRALI (at least a 2° drop in rectal temperature 10 minutes after TRALI antibody injection). Comparisons in both panels were analyzed with one-tailed unpaired t test. Each dot represents 1 mouse, and error bars represent standard deviation. *P < .05 ****P <. 0001. PBS, phosphate-buffered saline. Reprinted from Kapur et al 127 with permission.

TRALI suppression in CD4+ T cell–depleted mice with murine IL-10 administration. (A) Decreased lung wet/dry (W/D) weight ratios of CD4+ T cell–depleted C57BL/6 mice infused with 34-1-2s/AF6-88.5.5.3 and treated prophylactically with murine IL-10 administration (45 mg/kg intravenously). (B) Lung W/D weight ratios of CD4+ T cell–depleted C57BL/6 mice infused with 34-1-2s/AF6-88.5.5.3 and treated therapeutically 15 minutes later with or without murine IL-10 administration (45 mg/kg intravenously) after onset of TRALI (at least a 2° drop in rectal temperature 10 minutes after TRALI antibody injection). Comparisons in both panels were analyzed with one-tailed unpaired t test. Each dot represents 1 mouse, and error bars represent standard deviation. *P < .05 ****P <. 0001. PBS, phosphate-buffered saline. Reprinted from Kapur et al 127 with permission.

Prior studies have suggested a lack of benefit of the anti-inflammatory effects of systemic corticosteroids in ARDS and a lipopolysaccharide-stimulated murine model of TRALI. 60,128 Differences in murine TRALI models or the timing of corticosteroid administration may explain these disparate effects. Other anti-inflammatory modalities to prevent or treat TRALI have also been proposed, including the targeting of C-reactive protein, IL-8, reactive oxidative species, neutrophil extracellular traps, or Fc receptors. 129 Additional investigations are needed to confirm that these murine model findings parallel human pathophysiology before embarking on clinical studies of TRALI prevention or treatment. The recognition that any immunomodulatory therapy could increase the risk of infection is especially relevant in immunocompromised patients (eg, those with hematologic malignancies). In contrast to TRALI, few in vitro or in vivo investigations have been conducted to further understand the pathogenesis of TACO. In vivo models of TACO are needed to study the effect of individual blood components relative to other intravenous fluids on pulmonary capillary pressures, specific rates of blood administration, and the benefit of prophylactic diuretics as well as the role of systemic inflammation.

Work to improve blood collection and storage may also provide the opportunity to prevent TACO and TRALI. Modifications to blood components include the development of novel filters, apheresis collection systems, pathogen reduction, extended storage of platelets, and new methods of leukodepletion or irradiation. A novel prestorage filter absorbed HLA antibodies and lipids in addition to leukocytes and platelets, and it was associated with reduced neutrophil activation and TRALI incidence in an animal model. 130 Translation of an effective filter to clinical practice could obviate the need for specific donor mitigation strategies. Continued research to develop RBC and platelet storage solutions that preserve blood product quality but also mitigate TRALI also hold promise. 131-134 In addition, an ongoing randomized clinical trial is revisiting the potential benefit of washing allogeneic RBCs in reducing the incidence of TACO and TRALI. 92,135

At a systems level, prevention of TACO and TRALI requires implementation science research to harness the ever-expanding role of EHRs in medical care. The application of natural language processing or machine learning methods to EHR data of transfusion recipients would allow for more widespread surveillance and sophisticated approaches to adverse event reporting for blood and blood-derived products. Automated identification of adverse events utilizing large sources of blood donor, component, and transfusion recipient data would allow assessment of the safety of blood component modifications (eg, pathogen-reduced products or extended storage of platelets) in addition to additional mitigation strategies. Expanded active surveillance of pulmonary transfusion reactions would also serve to aid in the refinement of current diagnostic criteria for TACO and TRALI, allowing better discrimination of individual reactions from other causes of pulmonary edema.

Predictive algorithms could also be embedded within the EHR to allow for real-time identification of patients at increased risk of an adverse pulmonary transfusion event. For example, clinical decision support systems incorporating hemodynamic parameters or creatinine clearance could trigger recommendations for diuretic administration or alternatives to transfusion in patients at risk for TACO. Evidence of a systemic inflammatory response or other recipient risk factors could trigger allocation of lower-risk platelet or plasma units to hospitalized patients at increased risk for TRALI. Real-time identification of at-risk individuals could also be coupled to clinical trials of immune-based therapies for TRALI. Continued collaboration by bench and clinical researchers, clinicians, epidemiologists, and blood donor centers will be required to further understand and minimize these severe complications of blood transfusion.


Contents

Immediate-spin cross-matching Edit

Immediate-spin cross-matching (ISCM) is an abbreviated form of cross-matching that is faster, but less sensitive its primary use is to detect a mismatch between ABO blood types. It is an immediate test that involves combining the patient's serum and donor's red blood cells at room temperature, then centrifuging the sample and observing for agglutination or hemolysis. A lack of agglutination or hemolysis indicates a negative test reaction, or compatible match. [1] : 603 ISCM is not appropriate in all circumstances if the recipient's antibody screen is positive, or if they have had a positive antibody screen in the past, a full crossmatch is performed instead. [2] : 261

Anti-human globulin cross-matching Edit

The AHG crossmatch is done by incubating the recipient serum/plasma with the donor's red blood cells and adding anti-human globulin. It is essentially an indirect Coomb's test. It is also called "full cross-matching", "IAT cross-matching" and "Coomb's cross-matching". [4]

Electronic cross-matching Edit

Electronic cross-matching is a computer-assisted analysis using data, from the donor unit (where a donor's blood is tested prior to donation) and testing done on blood samples from the intended recipient. This includes ABO/Rh typing of the unit and of the recipient, and an antibody screen of the recipient. Electronic cross-matching can only be used if a patient has a negative antibody screen, which means that they do not have any active red blood cell atypical antibodies, or they are below the detectable level of current testing methods. If all of the data entered is compatible, the computer will print a compatibility label stating that the unit is safe to transfuse.

Major versus minor Edit

  • Major cross-match: Here the Recipient serum is tested against donor packed cells to determine if the recipient has preformed antibodies against any antigens on the donor's cells. This is the required cross-match prior to release of a unit of packed cell from blood bank.
  • Minor cross-match: Here the Recipient red cells are tested against donor serum to detect donor antibodies directed against a patient's antigens. This is no longer required. It is assumed that the small amount of donor serum and antibodies left in a unit of packed cells will be diluted in a recipient.

As the complete cross-matching process takes approximately 1 hour, it is not always used in emergencies.

In the case of an emergency, a type-specific blood to which the recipient has no antibodies, can be requested. It is thought that this lifesaving measure is of more benefit than any risk of an antibody-mediated transfusion reaction. This type of blood has less risk of a serious transfusion reaction because it is both ABO compatible and Rhesus (Rh)-compatible.

Universal donor blood, which is both type O and Rh negative, can be given if the recipient's blood group is not known, as may happen in an emergency. It is the policy of some institutions to reserve the releasing of O- blood only for female patients of childbearing age. This serves two purposes. First, it preserves the lower stock of O- blood and secondly, this eliminates the risk of O- negative mothers forming anti-D (Rh) antibodies from exposure to O+ blood. Anti-D (Rh) can cross the placenta during pregnancy and attack an unborn child's RBCs if they are D (Rh) positive causing haemolytic disease of the newborn.

In an emergency, blood grouping can be done easily and quickly in 2 or 3 minutes in the laboratory on glass slides with appropriate reagents, by trained technical staff. This method depends on the presence or absence of agglutination (clumping of red blood cells), which can usually be visualized directly. Presence of agglutination indicates incompatibility. Occasionally a light microscope may be needed. If laboratory services are not available, the bedside card method of blood grouping may be used, where a drop of the intended recipients blood is added to dried reagents on a prepared card. This method may not be as reliable as laboratory methods, which are preferable.



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