Anti-M antibodies are generally "naturally occurring" which means that they develop as the result of exposure to M-antigens found in the environment - usually expressed on bacteria or viruses.
In most cases the only type of antibodies that individuals develop to these types of antigens are of the IgM subclass. IgM antibodies are very large and cannot cross the placenta and cause any problems for the baby. Occasionally (as can also occur with the A and B major blood group antigens), an individual will develop IgG antibodies to the M-antigen. IgG antibodies CAN cross the placenta and, indeed, are actively concentrated on the fetal side. Usually, these IgG antibodies are antibodies to a wide variety of things that are “foreign” to our bodies that we have been exposed to during our lifetimes and they provide protection for the baby against common environmental pathogens (e.g., viruses and bacteria) for the first 4-6 months of the baby's life following birth.
However, if a pregnant woman has IgG anti-M antibodies and the baby happens to have M antigens on its red blood cells, the antibodies can attach to the red blood cells and mediate their destruction by the baby's own immune system, ultimately resulting in fetal anemia and, in the worst case scenario, fetal hydrops and even death (as can occur with "Rh-disease"). This is uncommon with anti-M antibodies, but has been described on numerous occasions in published literature. As with "Rh-disease", the risk for fetal complications generally increases with the level of the IgG anti-M antibody titers the pregnant woman has.
The first steps are to find out if the pregnant woman has IgG antibodies and if her partner is M-antigen positive on his red blood cells. If he is not, then their babies cannot be affected. If he is M-antigen positive, and the pregnant woman has IgG antibodies, then her antibody levels (titers) should be ascertained and followed serially during the pregnancy. Severe fetal anemia usually is a risk when high titer anti-M is present as IgG antibodies. High/increasing titers would make this a referral/transfer of pregnant pt to high risk OB for further management.
If the IgG anti-M titers are 32 or higher, then the baby should be monitored serially for evidence of significant fetal anemia (just like we do with Rh-isoimmunization) by performing peak systolic velocity (PSV) measurements on the baby's middle cerebral artery using Doppler Flow Velocimetry. Bilirubin studies are also performed through amniocentesis or PUBS (percutaneous umbilical blood sampling), to detect increased bilirubin levels. These levels are plotted on a Lily Curve to determine severity of disease and a plan of action. EGA less than 28 weeks with NO sign of fetal hydrops-can give IVIG for 5 days and repeat in 15-21 days. For MILD/No disease evidence-baby goes to term and induction is performed. For INTERMEDIATE disease-baby goes to 36-38 weeks and induction is performed. For SEVERE disease-depending on EGA, baby is transfused OR delivered ASAP.
If the baby does develop significant anemia, then it should be either transfused with M-negative blood or delivered, depending on the severity of the anemia and the gestational age at which the baby gets in trouble. It would be a good idea for the couple to discuss their situation with a specialist in Maternal-Fetal Medicine before they conceive again. Future subsequent children can be increasingly affected by hemolytic disease of the newborn.
My/our pt was counseled on the above information and educated about the need to follow serial IgG ant-M titers through her pregnancy.
link more Info here about anti-M at p. 556...
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