One month later, anti-Swain-Langley Sl a was identified Figure 1. Sl a is an antigen in the Knops blood group system and is destroyed by 0. This technique was used, and the chemically-treated cells were used to rule out additional antibodies. Care must be taken when performing rule outs using 0. Approximately 3 years later, an antibody screen was performed Figure 2 , and anti-S was suspected. Additional testing confirmed the new antibody.
Temperature was Normocephalic, pupils equal, round and reactive to light, extraocular movements intact, mouth without erythema, lesions, or exudates, no jugular venous distention, and no carotid bruits. Clear to auscultation bilaterally, no rales, rhonchi, or wheezing, good aeration. Patient continued to receive phenotypically matched RBC units. The most recent sample indicates a third antibody is present.
Anti-Jsa was suspected and confirmed. What are the serological findings indicating an antibody to a high incidence antigen may be present in plasma? What is the primary concern when a patient sample contains a clinically insignificant antibody to a high-prevalence antigen? How are clinically significant antibodies distinguished from clinically insignificant antibodies?
What is an approach for follow-up testing on a patient with a history of an alloantibody? What is 1 serologic picture of a sample with an antibody to a low prevalence antigen? What are some medical alternatives used in lieu of allogeneic blood transfusion for a patient with either multiple antibodies or a clinically significant antibody to a high-prevalence antigen when no compatible RBCs can be found? Numerous institutions have distinct policies and procedures regarding transfusing patients with SCD.
Chronically transfused patients are more likely to develop clinically significant alloantibodies with each additional blood infusion.
In a study performed by Heddle and colleagues, 4 the frequency of alloimmunization after blood transfusion was about 2. Furthermore, they postulated that patients with hematological disorders had a higher percentage 5.
Transfusing partially phenotypically similar RBCs limits the chances of developing clinically significant antibodies. However, in a study by Higgins and Sloan, 5 the increased frequency of alloimmunization by SCD patients could not be substantiated.
In fact, the study concluded that whether a patient becomes alloimmunized was almost independent to the number of transfusions he or she has received. Furthermore, the study did find some collaborating evidence supporting the idea that a small group in the population does have a greater risk of alloimmunization independent of disease state or age. All or a majority of initial reagent panel cells tested are reactive in a uniform pattern in terms of both strength and test phase with negative auto control as shown in Figure 1.
The only cell that is negative is number 7, and this cell lacks the Swain-Langley Sl a antigen. Anti-Sl a is usually associated with African ethnicity because the antigen prevalence in African-American persons is much lower than in Caucasians. The primary concern is missing the detection of underlying clinically significant alloantibodies that may be masked.
A cell that is Sl a positive may also be positive for an antigen the patient lacks, and an underlying alloantibody may be missed if reactivity is accounted for by the anti-Sl a. Since the Sl a antigen is destroyed by 0.
Using this technique, anti-S was identified Figure 2. Knowing that some antigens other than Sl a are destroyed by 0. In this case, 2 reagent cells negative for Sl a and S but positive for Js a were included in the selected panel Figure 3. This allowed for the detection and identification of anti-Js a.
Applying this strategy to a person with the phenotype Ro [C- E- K- S- Jk b- Fy a- ] would mean that the same problem we would be trying to prevent—locating such difficult-to-find units because the patient has anti-C, -E, -K, -S, -Jk b and -Fy a —would be the exact problem the transfusion service would have every time the patient needs a transfusion.
A survey of 1, hospital transfusion services in North America revealed that most match transfusions for non-alloimmunized patients with sickle cell disease for ABO and D, only. In this situation, The C-, E-, K- phenotype is present in Before closing, I would like to share an additional observation on this subject.
On occasion in our hospital, we have had to transfuse Rh D -positive red blood cells to an Rh D -negative patient undergoing a liver or multi-organ transplant. I have had the opportunity to perform an antibody screen on approximately 15 of these patients months-to-years later when they returned to the clinic or the hospital. Not one has formed anti-D. Presumably, the immunosuppressive regimens for preventing rejection of organ transplants are also highly effective for preventing primary alloimmunization to the highly immunogenic Rh D blood group antigen.
There is a certain logic to support this observation. This observation raises the possibility of preventing antibody formation in chronically transfused patients by simultaneous immunosuppression. Perhaps there is a resident or fellow in training who is reading this interview and will pursue this observation in his or her medical center.
Prospective phenotype matching in a stroke-prevention trial in sickle cell anemia: a multicenter transfusion trial.
Ballas SK. Iron overload is a determinant of morbidity and mortality in adult patients with sickle cell disease. Semin Hematol. Transfusion and alloimmunization in sickle cell disease. Antibody screens are performed as part of routine pretransfusion testing for blood recipients. In this test, serum or plasma is added to RBCs from between two and four group O persons specifically chosen by the manufacturer to carry antigens that could be the target of significant RBC antibodies.
The test can be done using one of several platforms, primarily either tubes , gel testing , or solid-phase testing. If the antibody screen is positive, in most cases the next step would be to perform antibody identification.
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