Abstract
Introduction/Objective
H antigen is a precursor for A and B antigens and is mostly converted except for the O blood group, which has the highest amount of H antigen. I is present on all adult RBCs. Anti-IH is usually an IgM antibody active at cold temperatures, and rarely demonstrates a wide thermal amplitude and can cause a significant hemolytic transfusion reaction.
Methods
Data was collected from patient information and transfusion management systems.
Results
38 year old female with sickle cell disease presented to the emergency room with dizziness, tachypnea and Hgb: 5.9 g/dl Hct:19.1%. Upon further review, patient chart showed that she had received an emergency RBC exchange transfusion 21 days prior to this admission for acute chest syndrome. She was B positive. The units for RBC exchange consisted of 5 group B and 1 group O units and an additional 1 group O unit later. All RBC units were matched for her phenotype; Rh, K, Duffy & Kidd, except anti-S which was ruled out. At the time of discharge, Hgb was 9.3 g/dl and Hct was 27.7%. The drop in Hgb between discharge and the present admission prompted a suspicion for delayed hemolytic reaction/hyperhemolysis. The sample sent to the local Reference Laboratory came back as follows: DAT/Coombs Positive, DAT C3 positive; positive for cold auto-anti-IH antibody. A thermal amplitude test indicated that the anti-IH was reactive at 30 C and therefore had the potential to be of clinical significance. Her Hgb continued to drop and 3 days later Hb=3.7 g/dl with instructions not to transfuse unless clinically emergent. With treatment of IVIG and steroids, reducing further blood draws and monitoring the patient for clinical symptoms only, her Hgb/Hct started to rise and the patient was discharged 4 days later with Hgb: 6.4 g/dl, and no symptoms of anemia.
Conclusion
Our case study is important in two ways: Firstly, it raises awareness of the severity of a cold autoantibody, i.e. anti-IH, with a wide thermal amplitude. Specifically, in this case, our attempt to provide phenotypically similar RBCs resulted in the destruction of all the type O donor cells as well as some of the B donor cells. Secondly, even with Hgb counts as low as 3.7, treating the patient and not the number proved to be better clinical practice. In conclusion, a good monitoring protocol for sickle cell patients is required to transfuse less and avoid serious complications.
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