username456789

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Why does an Rh reaction (second child) cause much more severe anemia than ABO (per RR Path)? From what I can tell from reading, both involve fetal splenic macrophage destruction of the IgG-coated RBCs. It does appear that he suggests that in ABO the macros don't phagocytose them completely (resulting in spherocytes) whereas there's no mention of such thing for Rh. I suppose that would explain things (some RBCs are simply deformed rather than destroyed) . . . assuming that's the reason. But does anyone have a clue why?
 

username456789

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Isn't ABO via IgM native antibodies?

RR Path says most people have both IgM and IgG against the A and/or B antigens (appropriate for their blood type), and that in HDN involving the ABO antigens, the IgG crosses the placenta and causes extravascular hemolytic anemia in the fetus.

As I understand it (which admittedly is poorly), if it involved IgM (which by definition would have to be in the mother's circulation since they don't cross), that would likely lead to INTRAVASCULAR hemolytic anemia in the mother, right? Or maybe I'm way off there.
 

bergwood

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Dec 10, 2009
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This is from my own reasoning and immunology background, though I have no source to quote.

The Rh factor (D antigen) is a foreign antigen, and one of the most antigenic molecules (I believe). Therefore the immune response undergoes affinity maturation (higher specificity). As such, it creates a very strong immune response and any RBC with an attached antibody from the mother will undergo destruction.

The A/B antibodies are native (always present, not derived from exposure to the antigen) and therefore do not undergo affinity maturation and are not as specific for the RBC as anti-Rh antibodies are. The antibodies are less strongly bound to the RBCs, and not every RBC with an attached antibody will undergo destruction.

This explains why Rhogam is needed for Rh incompatibility, but no Rhogam-like medication is needed for ABO mismatching.