Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Matthes, T. et al.

Matthes, Tullen, Poole, Banks, Nagy, Stelling, Boehlen, Michel, Beris, Hustinx, Crew, Daniels,

Acquired and transient RBC CD55 deficiency (Inab phenotype) and anti-IFC.

BACKGROUND: Antigens of the Cromer blood group system reside on the glycoprotein CD55 (decay-accelerating factor). The Inab phenotype is the null phenotype of this system. So far, only five propositi have been described who exhibit this phenotype, and single-nucleotide substitutions in the CD55 gene have been found in three of them. This report describes the first example of a patient with an acquired and transient form of the Inab phenotype. CASE REPORT: A 54-year-old black patient was admitted to the hospital because of abdominal pain. Multiple splenic infarctions were visualized in the abdominal computerized tomography scan, and a prophylactic splenectomy was performed. The patient's serum reacted by an IAT with all donor RBCs tested. RESULTS: Serologic analysis showed that the patient had the rare Inab phenotype and that his serum contained anti-IFC. Flow cytometry demonstrated the absence of CD55 on his RBCs, whereas lymphocytes, monocytes, granulocytes, and platelets expressed CD55, albeit at a weaker level than cells of common phenotypes. cDNA revealed no differences from the published sequences. Flow cytometry performed 12 months after splenectomy showed reappearance of the CD55 antigen; serologic tests performed after 17 months revealed that the anti-IFC had almost disappeared and that the RBCs were again agglutinated by various Cromer antibodies. CONCLUSION: A patient with an acquired and transient form of the Inab phenotype is described, in whom the CD55 deficiency is limited to the RBCs and is associated with splenic infarctions.[1]

References

Acquired and transient RBC CD55 deficiency (Inab phenotype) and anti-IFC. Matthes, T., Tullen, E., Poole, J., Banks, J., Nagy, M., Stelling, M.J., Boehlen, F., Michel, M., Beris, P., Hustinx, H., Crew, V., Daniels, G. Transfusion (2002) [Pubmed]

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