Literature DB >> 9111274

Delayed hemolytic transfusion reactions in sickle cell disease: simultaneous destruction of recipients' red cells.

K E King1, R S Shirey, M W Lankiewicz, J Young-Ramsaran, P M Ness.   

Abstract

BACKGROUND: Bystander hemolysis may be defined as the destruction of antigen-negative red cells during immune hemolysis, such as delayed hemolytic transfusion reaction (DHTR). Although many have suspected that bystander hemolysis does occur, that phenomenon is very difficult to document. STUDY DESIGN AND METHODS: Five patients with sickle cell disease (SCD) who underwent exchange transfusion and subsequently experienced a DHTR were retrospectively evaluated. Serial samples were examined for complete blood counts, the percentage of hemoglobin A and S, and the percentage of reticulocytes. The total red cell count and the percentage of hemoglobin S were used to calculate the hemoglobin S red cell count. The patients' profiles were compared to proposed models.
RESULTS: DHTRs due to anti-E, -S, -Fy(a), or -Jk(a) or serologically undetectable antibodies were identified 7 to 19 days after exchange transfusion. All patients had a significant decrease in hemoglobin A red cells; 56.4 to 94.7 percent of hemoglobin A red cells were hemolyzed. Patients 4 and 5 had a decrease in hemoglobin S red cells which indicated the destruction of autologous red cells during DHTR. The evidence for bystander hemolysis was particularly convincing in Patient 5, because there was a substantial decrease in hemoglobin S red cells despite a reticulocyte production index of 2.2 percent at the nadir of the DHTR.
CONCLUSION: Hemoglobin S provides a biologic marker for monitoring autologous red cell loss in sickle cell patients. We have shown one patient with clinical evidence of bystander hemolysis complicating a DHTR.

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Year:  1997        PMID: 9111274     DOI: 10.1046/j.1537-2995.1997.37497265337.x

Source DB:  PubMed          Journal:  Transfusion        ISSN: 0041-1132            Impact factor:   3.157


  21 in total

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3.  Antigen density dictates RBC clearance, but not antigen modulation, following incompatible RBC transfusion in mice.

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4.  Transfusion of murine red blood cells expressing the human KEL glycoprotein induces clinically significant alloantibodies.

Authors:  Sean R Stowell; Kathryn R Girard-Pierce; Nicole H Smith; Kate L Henry; C Maridith Arthur; James C Zimring; Jeanne E Hendrickson
Journal:  Transfusion       Date:  2013-04-29       Impact factor: 3.157

5.  Alloimmunization in sickle cell disease: changing antibody specificities and association with chronic pain and decreased survival.

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Review 7.  Delayed hemolytic transfusion reaction in sickle cell disease.

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Review 8.  Red blood cell alloimmunization in sickle cell disease: pathophysiology, risk factors, and transfusion management.

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9.  Hyperhemolysis in a patient with beta-thalassemia major.

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10.  Whole-exome sequencing of sickle cell disease patients with hyperhemolysis syndrome suggests a role for rare variation in disease predisposition.

Authors:  Savannah Mwesigwa; Joann M Moulds; Alice Chen; Jonathan Flanagan; Vivien A Sheehan; Alex George; Neil A Hanchard
Journal:  Transfusion       Date:  2017-12-06       Impact factor: 3.157

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