Dot Stern, Blood Bank, POW.

Mrs LT (1)

33 y.o. female, G2P0.

Group A Rh(D) negative, cde (rr).

Had a termination in 2001 @ 15/40. No anti-D

prophylaxis was administered.

Anti-D and anti-C identified in November ’13.

The anti-D quantitation was 23IU/mL.

Mrs LT (2)

A sample sent to Sydney ARCBS in Dec ’13

reacted with 2 r”G cells thus confirming the

presence of anti-G.

The antibody quantitation was 12.8IU/mL and

the previous sample run in parallel measured

15.2IU/mL.

LT’s partner typed as cDEe (probable R2r).

LT (3)

Maternal samples were sent to Brisbane ARCBS

on two occasions. Foetal DNA was isolated and

testing showed that the baby was rr.

The pregnancy was followed with monthly antibody

identifications and quantitations.

A healthy baby boy was born in June, Hb 176g/L,

blood group A Rh(D)neg, DAT negative.

Rh genes

There are 2 homologous, closely linked genes

found on the short arm of chromosome 1 :

RHD codes for D and RHCE codes for Cc and Ee.

These genes produce proteins which span the

red cell membrane 12 times.

The G antigen (RH12)

Ser103 encoded by RHD or RHCE*C is

essential for G reactivity.

Very rarely are D+ or C+ cells G negative.

DcE expressing normal D but no G was found in 3

generations of a Caucasian family.

DIIIb are G negative and patients of this phenotype

may produce separable anti-G.

rG phenotype

rG : D-, C-, E-, ?c+w, ?e+w, G+ may arise as the result

of RHCE encoding Trp16 in exon 1 and Ile60, Ser68

and Ser103 in exon 2. This gene could represent

RHCE*ce in which exon2 is substituted by exon 2

from RHD or RHCE*C.

r”G : ?D+w , ?C+w , E+, c-, e+, G+ arises as the

result of RHD-CE-D with exons 4-8 derived from

RHCE*C. This encodes Ser103.

r”G haplotype

r”G : ?D+w , ?C+w , E+, c-, e+, G+ arises as the

result of RHD-CE-D with exons 4-8 derived from

RHCE*C. This encodes Ser103 and Trp16.

rG

This gene produces G, very weak C, weak e and

the low frequency antigen JAHK (RH53).

The gene is RHCE*Ce with 365C>T in exon 3

encoding Ser122Leu in the membrane spanning

loop next to the extracellular loop containing

Ser103. It is likely that conformational changes

are responsible for the weak C and e and JAHK

expression as well as the strong G expression.

Anti-G

Originally found in the sera of rr people together

with anti-D and/or -C.

Can be isolated using a double absorption/elution

technique.

How do I prove it’s there (or not)? Patient’s plasma +

papainised Ror

cells. Adsorb for 30

minutes @37oC elution

?Anti-C in supernate

Eluate: anti-D and/or anti-G

Papainised r’r

Adsorb 30 mins

@37oC

elution

? Anti-D in supernate

?anti-G in eluate

Discussion

It is important to prove/disprove the presence of

anti-G in a sample said to contain anti-D+C. If anti-D

is not present i.e. the antibody is actually anti-C+G,

anti-D prophylaxis should be administered.

In a 2001 (1) report of 27 women said to have

anti-D+C, anti-C+G was identified in 4 samples

(14.8%) and anti-G was present in 88.9% of cases.

Discussion (cont)

The finding of “anti-C+D” when the spouse is

Rh(D) negative may lead to paternity testing.

The use of foetal DNA to confirm genotype can

help allay parental fears as well as save precious

anti-D gammaglobulin, an approach used in many

European countries.

References (1) The frequency of anti-C + anti-G in the absence of

anti-D in alloimmunised pregnancies. Palfi M,

Gunnarsson C. Trans. Med. 11(3) June 2001.

Diagram reproduced from Daniels, G. Human Blood

Groups 3rd ed. with permission of the author.