{"title":"Detection of anti-IH and transient adult anti-i in infectious mononucleosis potentially masking other red blood cell alloantibodies.","authors":"Johanna Bustillos, Niki Lee","doi":"10.1093/labmed/lmaf052","DOIUrl":null,"url":null,"abstract":"<p><strong>Introduction: </strong>A 29-year-old man with multiple co-morbidities, including alcoholic cirrhosis, was admitted for severe alcohol-related hepatitis, epistaxis, and fever of unknown cause. With no history of transfusions, the patient's hemoglobin level had dropped from 100 g/L to 81 g/L, with a platelet count of 46 × 109/L. Pretransfusion testing was ordered for potential transfusion.</p><p><strong>Methods: </strong>Automated group and antibody screen performed on the Quidel Ortho Clinical Diagnostics Vision platform and all complex investigation performed by the conventional manual tube method.</p><p><strong>Results: </strong>Pretransfusion tests showed that the patient was A RhD positive on forward grouping, while the reverse grouping showed an unexpected agglutination in A1 and A2 cells. Stronger agglutination reactions were noted at room temperature. The routine 3-cell antibody screen was negative but showed panreactivity on the saline room-temperature 11-cell panel and nonreactive at 37°C and on the indirect antiglobulin test (IAT). A stronger reaction was observed when the patient's plasma was tested against cord (i) cells than with adult (I) cells. It was concluded that a compound cold antibody anti-IH was present. A compatible O RhD positive red blood cell (RBC) unit was transfused to the patient which was noted to be M positive in addition to 2 A RhD positive platelet units. In the subsequent episode, viral serology returned a positive high avidity index with Epstein-Barr virus and cytomegalovirus mononucleosis assays implying a reinfection or reactivation of both infectious mononucleosis and cytomegalovirus mononucleosis. Therefore, transient anti-i was not ruled out. A new group and screen sample was obtained that demonstrated the same discrepancy in the reverse grouping, but the antibody screen revealed an anti-M alloantibody. An additional 3 crossmatch compatible group O RhD positive, M negative RBC units was transfused, but no clinically significant increment in hemoglobin was observed. A further 3 crossmatch compatible group A RhD positive, M negative RBC units were transfused, finally producing an increment increase in hemoglobin level.</p><p><strong>Discussion: </strong>This report highlights that benign cold antibodies can often be a nuisance in the investigation of RBC alloantibodies. Prewarming techniques must be used to eliminate these interferences and discrepancies, while titration of these cold agglutinins at different temperatures can help differentiate them.</p>","PeriodicalId":94124,"journal":{"name":"Laboratory medicine","volume":" ","pages":""},"PeriodicalIF":1.0000,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Laboratory medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1093/labmed/lmaf052","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Introduction: A 29-year-old man with multiple co-morbidities, including alcoholic cirrhosis, was admitted for severe alcohol-related hepatitis, epistaxis, and fever of unknown cause. With no history of transfusions, the patient's hemoglobin level had dropped from 100 g/L to 81 g/L, with a platelet count of 46 × 109/L. Pretransfusion testing was ordered for potential transfusion.
Methods: Automated group and antibody screen performed on the Quidel Ortho Clinical Diagnostics Vision platform and all complex investigation performed by the conventional manual tube method.
Results: Pretransfusion tests showed that the patient was A RhD positive on forward grouping, while the reverse grouping showed an unexpected agglutination in A1 and A2 cells. Stronger agglutination reactions were noted at room temperature. The routine 3-cell antibody screen was negative but showed panreactivity on the saline room-temperature 11-cell panel and nonreactive at 37°C and on the indirect antiglobulin test (IAT). A stronger reaction was observed when the patient's plasma was tested against cord (i) cells than with adult (I) cells. It was concluded that a compound cold antibody anti-IH was present. A compatible O RhD positive red blood cell (RBC) unit was transfused to the patient which was noted to be M positive in addition to 2 A RhD positive platelet units. In the subsequent episode, viral serology returned a positive high avidity index with Epstein-Barr virus and cytomegalovirus mononucleosis assays implying a reinfection or reactivation of both infectious mononucleosis and cytomegalovirus mononucleosis. Therefore, transient anti-i was not ruled out. A new group and screen sample was obtained that demonstrated the same discrepancy in the reverse grouping, but the antibody screen revealed an anti-M alloantibody. An additional 3 crossmatch compatible group O RhD positive, M negative RBC units was transfused, but no clinically significant increment in hemoglobin was observed. A further 3 crossmatch compatible group A RhD positive, M negative RBC units were transfused, finally producing an increment increase in hemoglobin level.
Discussion: This report highlights that benign cold antibodies can often be a nuisance in the investigation of RBC alloantibodies. Prewarming techniques must be used to eliminate these interferences and discrepancies, while titration of these cold agglutinins at different temperatures can help differentiate them.