The white blood cell DNA of 36 cord blood samples with Hb Bart's in the red blood cells was studied for alpha-globin gene deletions by hybridization of DNA fragments digested by the restriction endonucleases Eco RI, Hpa I, Bam HI, and Bgl II. All 16 DNA samples from cord blood with Hb Bart's below 3% and no other abnormal hemoglobin had one alpha-globin gene deletion (alpha thal2), except one which had two alpha-globin gene deletions (alpha thal1). Most of the alpha thal2 were of the rightward deletion alpha thal2 genotype. Two new types of alpha thal2 variation was found, probably due to a polymorphism somewhere in an area outside the alpha-globin gene. All 14 cases with Hb Bart's between 3.5% and 8.5% and no other abnormal hemoglobin had two alpha-globin gene deletions (alpha thal1), except one that did not have any alpha-globin gene deletion and one that had one alpha-globin gene deletion. Three DNA samples of cord blood with Hb Bart's accompanied by Hb CoSp did not have any alpha-globin gene deletion. Sixty-five DNA samples from cord blood without Hb Bart's or other abnormal hemoglobin had no alpha-globin gene deletions, except one that had one alpha-globin gene deletion (alpha thal2). Two of the 65 DNA samples were found to have triplicated alpha-globin gene loci.
Haemolytic disease of the foetus and newborn (HDFN) is caused by maternal red blood cells (RBC) alloimmunisation resulted from incompatibility of maternal and foetal RBCs. However, only a few HDFN attributed to anti-M were reported, varying from asymptomatic to severe anaemia with hydrops foetalis and even intrauterine death. A case of severe HDFN due to anti-M alloantibody from an alloimmunized grandmultiparous Malay woman with recurrent pregnancy loss is reported here. The newborn was delivered with severe and prolonged anaemia which required frequent RBC transfusions, intensive phototherapy and intravenous immunoglobulin administration. Although anti-M is rarely known to cause severe HDFN, a careful serological work-up and close assessment of foetal well-being is important, similar to the management of RhD HDFN. Alloimmunisation with anti-M type can lead to severe HDFN and even foetal loss.