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D Mallory

Publications and source records attributed to D Mallory.

10 recordsLinked to original sources

Screening with monoclonal anti-Fy3 to provide blood for phenotype-matched transfusions for patients with sickle cell disease.

BACKGROUND: In the United States, there is a shortage of blood group phenotype-matched red cells (RBCs) for patients with sickle cell disease (SCD). A protocol designed to supply phenotype-matched RBCs for these patients by combining the recruitment of African American blood donors and automated testing of RBCs for these patients for the presumptive Fy(a-b-) phenotype using monoclonal anti-Fy3 was evaluated. STUDY DESIGN AND METHODS: African American donors were recruited, to increase the likelihood of phenotype matches in the donor population. Samples of RBCs were tested for the presumptive Fy(a-b-) phenotype by using monoclonal anti-Fy3 and an automated blood typing analyzer. RBCs confirmed to be Fy(a-b-) were retyped for selected Rh, MNS, Kell, Duffy, and Kidd blood system antigens. The extended phenotypes were matched with those of 41 SCD patients requiring transfusions. RESULTS: Of 8323 blood donations during the study, approximately 40 percent (3329) were made by African Americans. Approximately 22 percent (737) of African Americans were identified as Fy(a-b-) by this protocol and 12 percent (410) were phenotype matches for the 41 SCD patients. CONCLUSION: Combining the recruitment of African American blood donors and automated phenotyping using monoclonal anti-Fy3 offers a practical, relatively low-cost strategy for supplying phenotype-matched RBCs for SCD patients. This protocol increases the options for addressing the shortage of phenotype-matched RBCs for SCD patients.

Anemia, Sickle Cell

IgA anaphylactic transfusion reactions.

IgA anaphylactic transfusion reactions are rare events, estimated to occur in 1 in 20,000 to 47,000 transfusions. The signs and symptoms of these reactions do not differentiate them from other causes of anaphylaxis. The diagnosis of an anaphylactic transfusion reaction is established by showing an IgA-antibody in the patient's serum. Most laboratories that test for IgA antibodies rely on the PHA method, which uses red blood cells that are coated with serologically defined IgA multiple myeloma proteins. We tested sera referred from Red Cross regional blood centers and hospitals from patients with suspected IgA anaphylactic reactions and found an IgA antibody in 76.3% of IgA-deficient patients. However, only 17.5% of all samples referred contained an IgA antibody, indicating that most persons with suspected IgA anaphylactic reactions had experienced acute generalized reactions that were from causes other than anti-IgA transfusion. Using PHIA to measure serum concentrations of IgA and PHA to detect IgA antibodies, we found the frequency of IgA deficiency (< 0.05 mg/dL) and class-specific anti-IgA in random blood donors to be approximately 1 in 1,200. Titers of anti-IgA did not distinguish these seemingly healthy blood donors from patients with a history of an anaphylactic transfusion reaction. Because the frequency of 1 in 1,200 greatly exceeds the observed frequency of anaphylactic reactions in transfused persons, we conclude that using PHA for anti-IgA does not reliably predict risk for an anaphylactic transfusion reaction. Additional research is needed to define a more specific marker to identify those persons who are truly at risk for these serious, but rare, complications of blood transfusion.

Anaphylaxis

Hemagglutination assays for the diagnosis and prevention of IgA anaphylactic transfusion reactions.

Passive hemagglutination assays (PHA) may be used to detect IgA antibodies to confirm clinical diagnoses of suspected IgA anaphylactic transfusion reactions. Passive hemagglutination inhibition assays (PHIA) may be used to identify IgA-deficient blood donors whose plasma-containing components are transfused to prevent anaphylactic transfusion reactions in prospective recipients at risk because of the presence of IgA antibodies. Using a standard PHA, we detected class-specific anti-IgA in 76.3% of 80 IgA-deficient patients with a history of an anaphylactic transfusion reaction, and in 21.7% of 97 asymptomatic IgA-deficient blood donors or their IgA-deficient family members. Using PHIA, we confirmed IgA deficiency (< 0.05 mg/dL) for the donors of 525 plasma-containing blood components that were transfused without acute clinical reactions to 48 IgA-deficient recipients with anti-IgA and/or a history of an anaphylactic transfusion reaction. The frequency of IgA-deficiency with class-specific anti-IgA among 32,376 random blood donors was 0.08% (1/1,200). The combined use of PHA for detecting anti-IgA and PHIA for measuring IgA concentration provides an effective and safe strategy for the diagnosis and prevention of IgA anaphylactic transfusion reactions. However, PHA for anti-IgA lacks specificity for identifying persons who are truly at risk for significant anaphylactic transfusion reactions. The consequence is an overdiagnosis of IgA anaphylactic transfusion reactions and an overestimation of the number of persons at risk for IgA anaphylactic transfusion reactions because of the detection of an IgA antibody in their serum.

Anaphylaxis

A decade of rare donor services in the United States. Report of the American Red Cross Rare Donor Registry (1981-1990).

Between 1981 and 1990, the American Red Cross Rare Donor Registry supplied 9,872 units of red cell components with rare phenotypes to blood centers in the United States and abroad. Approximately 51% were from donors with high-frequency antigen-negative phenotypes and 49% were from donors with multiple antigen-negative phenotypes. Since 1989, the disease category requiring the largest number of units has been sickle cell disease. Strategies to ensure that the Registry will have adequate resources to meet future requirements include testing selected donors for rare phenotypes and blood conservation programs, such as intraoperative salvage and the treatment of anemia of chronic renal failure with recombinant erythropoietin.

Anemia, Sickle Cell

Lewis incompatibility.

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Blood Group Incompatibility