Hemolytic disease in fetuses and newborns due to antibodies against the M-antigen
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Published on: June 24, 2020
Marco Páez1, María Jiménez2, Ana Corredor3
1Departamento de Patología y Laboratorio Clínico, Fundación Santa Fe de Bogotá, Bogotá, D.C., Colombia. marco.paez@fsfb.org.co.
There are few case reports of hemolytic disease in fetuses and newborns (HDFN) caused by alloantibodies against the MNS blood group system. The reason for this dearth is that antibodies toward these antigens are usually IgM, which not only cannot cross the placental circulation but also react at temperatures below 37°C. They are, therefore, of minimal clinical importance. Nevertheless, cases have been reported in which the presence of anti-M IgG antibodies caused severe HDFN and even intrauterine death in the presence of maternal-fetal MNS incompatibility indicating that they could have a high clinical impact. The hemolytic pattern observed in these cases is similar to that caused by anti-Kell antibodies. Progressive anemia is mediated and developed through hematopoietic suppression inducing the destruction of bone marrow precursor cells with the resulting absence of reticulocytes in peripheral blood. This occurred in the case of a woman at 38.5 weeks of gestation who showed a discrepancy between direct and reverse blood type determination. A direct Coombs test was performed on the newborn’s blood, which was positive in the absence of maternal-fetal ABO incompatibility. Further tests were performed and anti-M antibodies were found in the maternal serum screening. Our final diagnosis was largely due to discrepancy issues in maternal blood. Although anti-M antibodies do not usually play a significant role in HDFN, this case stresses the importance of identifying the presence of antibodies that can be crucial in preventing HDFN and lead to new recommendations for the screening and prompt treatment of hemolysis in newborns.
There are few case reports of hemolytic disease in fetuses and newborns (HDFN) caused by alloantibodies against the MNS blood group system. The reason for this dearth is that antibodies toward these antigens are usually IgM, which not only cannot cross the placental circulation but also react at temperatures below 37°C. They are, therefore, of minimal clinical importance. Nevertheless, cases have been reported in which the presence of anti-M IgG antibodies caused severe HDFN and even intrauterine death in the presence of maternal-fetal MNS incompatibility indicating that they could have a high clinical impact. The hemolytic pattern observed in these cases is similar to that caused by anti-Kell antibodies. Progressive anemia is mediated and developed through hematopoietic suppression inducing the destruction of bone marrow precursor cells with the resulting absence of reticulocytes in peripheral blood. This occurred in the case of a woman at 38.5 weeks of gestation who showed a discrepancy between direct and reverse blood type determination. A direct Coombs test was performed on the newborn’s blood, which was positive in the absence of maternal-fetal ABO incompatibility. Further tests were performed and anti-M antibodies were found in the maternal serum screening. Our final diagnosis was largely due to discrepancy issues in maternal blood. Although anti-M antibodies do not usually play a significant role in HDFN, this case stresses the importance of identifying the presence of antibodies that can be crucial in preventing HDFN and lead to new recommendations for the screening and prompt treatment of hemolysis in newborns.
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