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Rhmod, a second kindred (Craig)

D McGuire, R E Rosenfield, K Y Wong

    Vox Sanguinis
    |January 1, 1976
    PubMed
    Summary
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    Three siblings with stomatocytic hemolytic anemia exhibited identical Rh phenotypes with varying degrees of Rh antigen depression. This suggests complex genetic factors influencing Rh antigen expression beyond a single suppressor gene.

    Area of Science:

    • Hematology
    • Genetics
    • Immunology

    Background:

    • The Rh blood group system is crucial for transfusion compatibility and understanding hemolytic disease of the newborn.
    • Rh antigen expression is genetically determined and can be subject to variations and deficiencies.

    Observation:

    • Three siblings presented with identical Rh phenotypes (w1, w2, -3, -4, w5) and stomatocytic hemolytic anemia.
    • Quantitative hemagglutination studies revealed differential depression of Rh antigens, with some antigens (Rh17, Rh29) normal, others (Rh5, Rh25) showing partial depression, and several severely depressed (Rh1, Rh13, Rh14, Rh15, Rh16).
    • Specific antigens like Rh2 (C) were depressed, Rh7 (Ce) was absent, and Rh12 (G) was significantly depressed.

    Findings:

    • The pattern of Rh antigen depression was inconsistent across affected family members, including parents and offspring, suggesting complex genetic influences rather than a single suppressor gene.

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  • A common observation was the depression of Rh14 (RhB), Rh15 (RhC), and Rh16 (RhD) without affecting Rh1 (D) or Rh13 (RhA).

    • Implications:

    • The findings highlight the complex genetic regulation of Rh antigen expression and its potential impact on red blood cell phenotypes.
    • Understanding these complex patterns is vital for accurate blood typing, transfusion practices, and managing Rh-related hemolytic conditions.