The weak D phenotype is caused by many different RHD alleles encoding aberr
ant RhD proteins, raising the possibility of distinct serologic phenotypes
and of anti-D immunizations in weak D. We reported 6 new RHD alleles, D cat
egory III type IV, DIM, and the weak D types 4.1, 4.2.1, 4.2.2, and 17. The
immunohematologic features of 18 weak D types were examined by agglutinati
on and flow cytometry with more than 50 monoclonal anti-D. The agglutinatio
n patterns of the partial D phenotypes DIM, D-III type IV, and D-IV type II
I correlated well with the D epitope models, those of the weak D types show
ed no correlation. In flow cytometry, the weak D types displayed type-speci
fic antigen densities between 70 and 4000 RhD antigens per cell and qualita
tively distinct D antigens, A Rhesus D similarity index was devised to char
acterize the extent of qualitative changes in aberrant D antigens and discr
iminated normal D from all tested partial D, including D category III. In s
ome rare weak D types, the extent of the alterations was comparable to that
found in partial Ds that were prone to anti-D immunization. Four of 6 case
reports with anti-D in weak D represented auto-anti-D. We concluded that,
in contrast to previous assumptions, most weak D types, including prevalent
ones, carry altered D antigens, These observations are suggestive of a cli
nically relevant potential for anti-D immunizations in some, but not in the
prevalent weak D types, and were used to derive an improved transfusion st
rategy in weak D patients. (Blood, 2000;95:2699-2708) (C) 2000 by The Ameri
can Society of Hematology.