A case of severe foetal anaemia due to anti-M isoimmunisation salvaged by intrauterine transfusions.

Abstract

Haemolytic disease of the foetus and newborn (HDFN) is caused by transplacental passage of maternal IgG antibodies directed against an antigen of paternal origin present on the foetal red blood cells. IgG antibodies coat foetal antigens and cause decreased red blood cell survival leading to fetal anaemia. The antibodies causing severe forms of HDFN are anti-D, anti-c and anti-K1. However, more than 50 different red-cell antigens have been reported to be associated with HDFN and no prophylactic immune globulins are available to prevent the formation of these antibodies1. Anti-RhD was once the major aetiology of HDFN, but with routine antenatal administration of anti-D to all vulnerable women, maternal allo-immunisation to other red cell antigens as a cause of HDFN is becoming a greater concern. Anti-M is typically a naturally occurring immunoglobulin M (IgM) antibody, optimally reactive at 4 °C and considered clinically insignificant. This saline agglutinin was first identified by Wolff and Johnsson in 19332. Anti-M rarely causes agglutination of red cells at 37 °C or in the antiglobulin phase of testing. Rarely, the alloanti-M can be of IgG type or a combination of both IgG and IgM. These have a potential to cause haemolytic transfusion reactions and HDFN but have been very rarely implicated as the cause of severe HDFN requiring intrauterine transfusion (IUT). The MN determinants are carried on the transmembrane protein glycophorin A, are fully developed on foetal red cells, and can be detected as early as 9 weeks’ gestation3. This case report describes a woman with a history of six intrauterine deaths, all between 11 to 32 weeks of gestation. Her seventh affected pregnancy was salvaged by intrauterine administration of packed red blood cell transfusions at 29 weeks of gestation, after she was found to be allo-immunised against M antigen.