<abstract xmlns="http://www.w3.org/1999/xhtml"><p>Anti-Ge2 may be immune or naturally occurring, and it reacts with an antigen on glycophorin D. Ge2 is encoded by a gene, <italic>GYPC,</italic> which is located on the long arm of chromosome 2. Anti-Ge2 is usually an immunoglobulin G (IgG) antibody. In the available literature, we have not been able to find any reported cases of proven acute hemolytic transfusion reactions caused by anti-Ge2. We present the case of a 67-year-old man with metastatic pancreatic carcinoma who had symptomatic anemia and a hemoglobin concentration of 6.3 g/dL. During pretransfusion testing, anti-Ge2 was identified in his serum. Only a single unit of compatible, Ge:–2 frozen red blood cells (RBCs) could be provided by the blood supplier. A second unit of crossmatched, least-incompatible, leukocyte-reduced RBCs, presumably Ge:2, was also transfused. The transfusion was completed without incident, and the patient’s hemoglobin concentration rose appropriately. Posttransfusion values for haptoglobin, lactate dehydrogenase, and urine hemoglobin were within normal limits. A monocyte monolayer assay performed on this anti-Ge2 supports the data that antibodies of this specificity do not cause hemolysis. The clinical and laboratory data obtained in our patient clearly indicated that no hemolysis of transfused RBCs occurred during and for 24 hours after transfusion. We believe that this report adds to a limited experience with anti-Ge2 and provides further evidence for concluding that, in all likelihood, this is not a clinically important RBC antibody. The risk of transfusing apparently “incompatible” (Ge:2) RBCs seems remote and should allow for timely administration of RBCs when treating patients with serious anemia. <italic><bold>Immunohematology</bold></italic><bold>2014;30:156–157.</bold></p></abstract>

Anti-Ge2 may be immune or naturally occurring, and it reacts with an antigen on glycophorin D. Ge2 is encoded by a gene, GYPC, which is located on the long arm of chromosome 2. Anti-Ge2 is usually an immunoglobulin G (IgG) antibody. In the available literature, we have not been able to find any reported cases of proven acute hemolytic transfusion reactions caused by anti-Ge2. We present the case of a 67-year-old man with metastatic pancreatic carcinoma who had symptomatic anemia and a hemoglobin concentration of 6.3 g/dL. During pretransfusion testing, anti-Ge2 was identified in his serum. Only a single unit of compatible, Ge:–2 frozen red blood cells (RBCs) could be provided by the blood supplier. A second unit of crossmatched, least-incompatible, leukocyte-reduced RBCs, presumably Ge:2, was also transfused. The transfusion was completed without incident, and the patient’s hemoglobin concentration rose appropriately. Posttransfusion values for haptoglobin, lactate dehydrogenase, and urine hemoglobin were within normal limits. A monocyte monolayer assay performed on this anti-Ge2 supports the data that antibodies of this specificity do not cause hemolysis. The clinical and laboratory data obtained in our patient clearly indicated that no hemolysis of transfused RBCs occurred during and for 24 hours after transfusion. We believe that this report adds to a limited experience with anti-Ge2 and provides further evidence for concluding that, in all likelihood, this is not a clinically important RBC antibody. The risk of transfusing apparently “incompatible” (Ge:2) RBCs seems remote and should allow for timely administration of RBCs when treating patients with serious anemia. Immunohematology2014;30:156–157.

Anti-Ge2: further evidence for lack of clinical significance

Department of Pathology and Laboratory Medicine

Immunohematology

{"article-title":"Anti-Ge2: further evidence for lack of clinical significance"}

Anti-Ge2 may be immune or naturally occurring, and it reacts with an antigen on glycophorin D. Ge2 is encoded by a gene, GYPC, which is located on the long arm...

Anti-Ge2: further evidence for lack of clinical significance

Article Category: Case Report

Publié en ligne: 01 déc. 2019

Pages: 156 - 157

DOI: https://doi.org/10.21307/immunohematology-2019-112

© 2014 D. Karunasiri et al., published by Sciendo