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MikeB

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About MikeB

  • Birthday 03/29/1981

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  1. I wonder if maternal Anti-A has somewhat of a protective influence on twin 1 (Group A) and not on twin 2 (Group O). If I recall correctly, this was the assumption that led to the development of Rh immunoglobulin. Baby's born to mothes with ABO incompatabilities generally demonstrated less severe Rh(D) HDN than those that were ABO compatible. Just my 2 cents.
  2. Some further questions: 1. How often are titers being performed and what cell(s) are selected? 2. Once Anti-G is identified, is the presence of Anti-D/Anti-C ruled out on each subsequent sample submitted (eg, samples for titers?)
  3. MikeB

    Unusual ABO

    Alloantiboies (-M, -P1) are a likely possiblity, however we tested two seperate ABID panels and observed no reactivity at IS or 15' RT. It wasn't until 18C that the cold autoantibody was apparent. I origianlly thought IH, but would have expected the Group O cells to react stronger than the A2.
  4. MikeB

    Unusual ABO

    Female Orthopedic pre-op patient. No history of transfusion. Cold reactive antibody identified only reacting at 18C (1+) and 4C (3+) including autocontrol. No reactivity at IS or 15' RT with panel cells. DAT (w+) with Poly and C3b/C3d. No reactivity at 37C or IgG. Anti-A: 1+ Anti-B: 0 Anti-D: 4+ A1 Cells: w+ B cells: 4+ Appears to be an A subgroup with an Anti-A1, however......... Anti-A,B: 3+ Anti-A1: 0 A2 Cell 'A' : 3+ (Expired 3/29/13) A2 Cell 'B' : 3+ (Expired 4/26/13) A2 Cell 'C' : 1+ (In date) O PoolCells: 0 Autocontrol: 0 Any thoughts on why are the A2 cells reacting so strong at immediate spin compared to the A1 cells?
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