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Donor-Derived
Red Blood
Allogeneic
Keith
By Jill Hows,
Beddow,
Irena
cases
Six
of
donor-derived
marrow
immune
hemolytic
anemia
antibodies
after
transplantation
severe
increased
plasma
rine
to prevent
that
in each
graft-v-host
case,
present
positive
antigens
test was
four
(BMT)
are
intravascular
hemolysis
red cell transfusion,
exchange.
All recipients
cases;
disease.
one
to
bone
In 2/6
Investigations
case;
cases,
showed
ABO or Rho(D) red cell
The direct
antiglobulin
serum
antibody
(anti-A,
anti-D,
one
case)
was
first
detected
one to three
weeks
after BMT. Eluates made from
recipient
red cells showed
the same
specificity
as serum
antibody.
Maximum
hemolysis
occurred
nine
to 1 6 days
after BMT, suggesting
that active
production
of antibody
by “passenger”
donor
lymphocytes
was the likely
mechanism of hemolysis,
rather
than passive
transfer
of antibody
A
LLOGENEIC
cytes
humans
to the
bone
involves
recipient.
marrow
If this
occurs,
hemolysis.
report
six bone
in
to produce
antibodies
specific
that are lacking
on the donor’s
it could
hemolysis
in the posttransplant
cations
such as renal failure
severe
We
(BMT)
the transfer
of mature
donor
lymphoIt is theoretically
possible
for trans-
ferred
donor
lymphocytes
recipient
red cell antigens
red cells.
transplantation
present
clinically
for
own
as immune
period.
Conceivably,
complicould occur in association
with
marrow
transplantation
(BMT)
cases
in which the appearance
of red cell antibodies
was associated
with clinical
and laboratory
evidence
of immune
hemolysis.
The peak
time
BMT,
making
marrow
for hemolysis
passive
transfer
infusion
we suggest
lymphocytes
cause
of
hemolysis
an unlikely
that
active
stimulated
the
hemolysis.
due
to this
analyzed
97 consecutive
from one
cyclosponine
center
and
was one to two weeks
of plasma
antibody
cause.
From
production
by recipient
To
of
the data
determine
mechanism,
we
the
have
cyclosporine-treated
(Hammersmith).
this phenomenon
after
in the
presented,
antibody
by
RBC
antigens
The
was
donor
is the
frequency
of
retrospectively
BMT
association
strengthened
patients
between
by our
failure
to find, on retrospective
analysis,
a single
case of
immune
hemolysis
or donor-derived
antibody
production
in 1 3 patients
treated
with methotrexate
in the postgraft
period.
MATERIALS
AND
and
in the
1986:
Spruce,
D. Petz
infusion.
Retrospective
analysis
of 21 conBMT patients
receiving
marrow
lacking
ABO or D antigens
present
in the recipient
showed
that
(1 ) 1 5/18
patients
tested
had red cell antibody
production
against
recipient
red cell antigens;
(2)
despite
the frequent
presence
of antibody
specific
for
recipient
red cell antigens,
only 3/21
patients
developed
clinically
significant
hemolysis;
(3) clinical
hemolysis
could
not be predicted
by donor
or recipient
red cell antibody
titers.
We conclude
that although
red cell antibody
against
recipient
antigens
is frequently
produced
after
minor
ABO
and D mismatched
BMT in cyclosporine-treated
recipients,
marrow
cyclosporine-treated
only
1 0%
immune
likely
to
1 5%
cells.
a 1986
of
hemolysis.
The
of
antibody
source
by Grune
Rho(D)
positive
serum contained
patients
received
cases
develop
clinically
data
presented
show
is “passenger”
& Stratton,
significant
that the
donor
most
lymphoid
Inc.
and the donor A Rho(D)
negative;
the donor’s
weak anti-D
at the time of the transplant.
All
cyclosponine
after BMT to prevent
graft-v-host
disease (GVHD).
Group
2.
To assess the frequency
of immune
hemolysis,
a
retrospective
analysis of 97 consecutive
BMT patients
transplanted
at one center (Hammersmith)
was carried out. All patients
received
cyclosporine
in the postgraft
period for the prevention
of GVHD.
Twenty-one
patients received minor ABO or D mismatched
marrow
(ie, donor lacking ABO or Rh antigens
present in the recipient)
and
were designated
“group
2” patients.
Within
group 2, 14 patients
received marrow from donors lacking recipient
A or B antigens;
this
included
cases 1 and 2 from group 1 . Seven D-positive
recipients
received marrow from D-negative
donors and included case 6 from
group
1 . Two patients
were ABO and D mismatched.
Group
2
patient
charts were reviewed
for evidence
of immune
hemolysis.
Weekly
blood bank records
from the post-BMT
period
were
searched
for the occurrence
of any positive direct antiglobulin
tests
(DAT).
Sera from group 2 patients
receiving
minor ABO mismatched
marrow, stored at - 20 #{176}C
for up to 36 months, were tested
for donor type IgG and 1gM anti-A and anti-B at one and three
months after BMT.
Serology
Standard
serological
methods
were used. The DAT was performed using polyspecific
antihuman
globulin
(AHG)
reagents.
In
DAT-positive
cases, testing with anti-C3 and anti-IgG
reagents
was
carried
out. Eluates
were made
by the chloroform’
or ether2
technique.
Anti-A and anti-B were estimated
by titrating
the stoned
From
1 (January),
Wayne
After
METHODS
Group 1. Six patients
from three transplant
centers
who presented clinically
with immune
hemolysis
after BMT were investigated. Informed
consent to investigations
was obtained
according
to
each of the transplant
center’s ethical committee
guidelines.
Clinical
and laboratory
data are shown
in Table
1 . Hematologic
and
biochemical
data illustrating
a typical case are shown in Fig 1.
Patients
1 through
5 were transplanted
from HLA-identical
sibling
donors and patient 6, from an HLA phenotypically
matched
unrelated donor. In cases 1 through 5, the donors lacked A on B antigens
present
on the recipients’
red cells. In case 6, the patient
was A
Vol 67, No
Hemolysis
R. Branch,
Lawrence
secutive
Patients
Blood,
Donald
A. Krance,
attributed
allogeneic
reported.
and Immune
Transplantation
Gordon-Smith,
Robert
was
seen,
6/6
required
and 1 /6 was treated
by
were receiving
cyclospo-
the donor
lacked
in the recipient.
in 6/6.
Relevant
anti-B,
Antibodies
Marrow
Edward
Sniecinski,
red
cell
Cell
Bone
pp
177-18
1
the
Hospital,
Duarte,
Royal
London;
Calif
and
Supported
CA
33572
Medical
W12
©
Health
reprint
1 986
by the
18,
Medical
of
by Public
School,
OHS
City
Childrens
March
Address
the
the
awarded
Submitted
Postgraduate
Hope
Hospital.
Service
National
1985;
requests
Hammersmith
School,
San
Grants
Cancer
accepted
to Dr J.M.
Hospital,
Hammersmith
National
July
Medical
Center,
Diego.
No.
CA
30206
and
Institute.
18. 1985.
Hows,
Royal
Du
Cane
Postgraduate
Rd.
London
England.
by
Grune
& Stratton,
Inc.
0006-4971/86/6701-0027$03.00/0
177
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178
HOWS
Table
1 . Cli nical
and
La boratory
Data-Patients
Presenting
With
Group
Case
No.
D,agnosis
1
D
CGL
R
1 7/M
D
1 5/F
Immunosuppressive
A
Therapy
Pre-BMT
R
0 +
1
Transfusions
and
Rh Type
Age/Sex
He molysis-Group
Cy 60
-
60
TBI
200
Plate-
RBC5
lets
Post-BMT
mg/kg
DN
Packed
x 2
mg/m2
x
1
CyA
A
HDMP
0-
A
-
.
Details
CGL
3
1 3/M
SAA
1 1 /F
24/M
0 +
1 6/F
A +
0 +
B +
Cv 60
Severe
-
IVH.
mum
60
TBI
200
Cy 50
TNI
x 2
mg/m2
x
A +
CyA
1
mg/kg
750
x 4
CyA
0 +
B+
MP
AML
1 1 /F
1 4/M
0 +
A +
1 20
TBI
VP-16
x
1 1 cGy
40
mg/kg
x
1
CyA
A +
MP
0+
ALL
26/M
22/M
B+
AB+
Cy
120
TBI
mg/kg
1 20
x
x
1
CyA
0+
1 1 cGy
MP
B+
6
SAA
32/F
A
1 7/F
A +
-
50
Cy
ALG
mg/kg
1 2.5
x 4
mg/kg
CyA
x 4
HDMP
A
+9
Platelets
total
were
nodal
washed
and
irradiation;
resuspended
CyA,
in AB
cyclosporine;
plasma.
HDMP,
D, donor;
high-dose
A +
-
Azathiaprine
R,
recipient;
A
sera against suitable test red cells. The agglutination
titer at 20 #{176}C
was measured
as well as the titer at 37 #{176}C
using anti-IgG
AHG in
the indirect
antiglobulin
test. Appropriate
saline controls
were
performed.
The lgG and 1gM components
of the antibodies
were
estimated
by testing
the sera before and after treatment
with
2-mercaptoethanol3
or dithiothreitol.4
The IgM titers were measured
by agglutination
at 20 #{176}C,
and the lgG titers were estimated
by the
indirect antiglobulin
test at 37 #{176}C.
MP,
DN,
methylprednisone;
(median,
red cell
12) after
antigens
(median,
13)
BMT.
were
after
Group
I.
hemolysis
Group
between
1 patients
days
presented
9 and
10). The results
of serological
Table
2. The DAT
first became
mc
Transfused
(O+woshed)
2 2 1
$$$$$
2 2
2
clinically
16 post-BMT
(median,
with
antibodies
case
level
day
investigations
are shown
in
positive
at four to 22 days
3
$
were
Six
(including
YS
20
POST
25
30
BMT
Fig 1 .
Case 3 from group
1 . Minor
ABO
mismatched
BMT
(donor
0 + , recipient
B + ). Flow chart
shows
hematologic
and
biochemical
evidence
for hemolysis.
Fourteen
units of packed
0 +
cells were
required
to maintain
the hemoglobin
between
day 10
and day 1 9 post-BMT.
Note
that
the hemoglobin.
the lactic
dehydrogenase.
and the total bilirubin
were normal
for the first
five
days post-BMT.
During the hemolytic
episode.
no incompatible isohemagglutinins
were
infused;
RBCs
transfused
were
washed
group
0. platelets
were
group
B or 0 washed
and
resuspended
in fresh AB plasma.
day
required
day
to
+
maximum
units
RBCs
day
required
day
16.
TBI,
total
anti-lymphocyte
body
irradiation;
globulin.
cases
3 through
6 inclusive
only
transiently
cases.
present
However,
in the
in the
cases
serological
receiving
I and
2 from
to rise,
data
ABO
group
sera
of the
D-incompatible
reaching
is shown
mismatched
a
in Table
3.
marrow
1) developed
a positive
DAT after BMT.
1 ) showed
clinical
anti-A
and anti-B
However,
only 2/6 (cases
1 and 2 in group
evidence
for immune
hemolysis.
Donor
titers
pre-BMT
and recipient
anti-A
and
anti-B
and
Three
15
hemolysis,
1 3. Five
In
titers
one
three
cases
by either
and
out
D-incompatible
donor
of the
seven
marrow
developed
a.positive
DAT-positive
cases,
BMT.
In one case
months
6 in group
BMT
hemolysis
or recipient
patients
present.
for IgG
in group
(including
patient
are
could
antibody
antibody
specific
titers
shown.
not
be
or the
The antibodies
subclasses.
2 who
6 from
received
group
I)
DAT after
BMT (Table
3). In all three
anti-D
was detected
in the serum
after
(AG),
anti-C
and
anti-E
were
also
detected.
Only one patient
(AR)
rhesus
antibodies
(AR)
showed
sis (case
after
clinical
proportion
of IgG and 1gM
were not tested
with antisera
10
maximum
RBCs
Antibodies
against
the recipient’s
first
detectable
nine
to I 5 days
BMT.
Group
2.
Relevant
out of 16 patients
predicted
5
day
required
+ 18.
(case 6), the anti-D
titer continued
of 256 on day 70 after BMT.
DAT-positive
0
maximum
eluates
prepared
from recipient
RBCs contained
antibody
to
antigens
present
on recipient
red cells of the same specificity
found
in the serum.
Table
2 also shows
that
the red cell
ABO-incompatible
RESULTS
to
daunorubicin;
ALG.
units
+ 19
to + 14.
11
+
Fourteen
+ 10 to
RBCs
hemolysis,
Moderate
-
Cy, cyclophosphamide;
methylprednisone;
units
+ 1 2. Six units
+9
TNI,
Seven
Moderate
+
day
1).
+ 10.
B+
day
hemolysis,
day
5
day
required
+ 10.
required
Moderate
A +
maximum
Hemoglobinuria.
day
(seeFig
4
units
+ 10 to + 15.
RBCs
hemolysis.
RBCs
Treated
Nine
+22.
Maximum
#{149}
day
hemolysis.
Severe
0+
Maxi+ 15.
exchange.
Six units
+ 16 to
cGy
day
required
+ 16.
x 5 cGy
Hemoglobinuria.
plasma
Moderate
A +
HDMP
and RBC
Requirement
hemolysis
with
x 5 cGy
mg/kg
DN
of Hemolysis
Transfusion
RBCs
2
AL
ABO Group and
Rh Type of
.
ABO
Immune
ET
with a positive
clinical
evidence
I; see Tables
I and
DAT due to
of hemoly-
2).
DISCUSSION
Anti-A
residual
and
recipient
anti-B
plasma
production
cells
against
after
major
donor
red
ABO
mismatched
cells
by
From www.bloodjournal.org by guest on June 17, 2017. For personal use only.
DONOR-DERIVED
RBC
ANTIBODIES
Table
2.
AND
Serological
Maximum
No.
Day
Post-BMT
Investig
ation
of Patients
ABOGroup
Hemolysis
Case
179
BMT
D
A
With
I mmune
sis-Group
Hemoly
1
Day
Post-BMT
DAT
Positive
#{176}
Presenting
DAT
First
for
Antibody
Antibody
in Eluate
in Serum
Day Post-BMT
Serum Antibody
Last Detected
Positive
1
+15
0+
A-
C3
+18
ND
Anti-A
+38
2
+16
0+
A+
C3
+15
ND
Anti-A
+24
3
+ 10
0+
B+
lgG + C3
+ 10
Anti-B
Anti-B
+42
4
+ 10
0 +
A +
C3
+ 4
Anti-A
Anti-A
+ 30
5
+ 12
B+
AB+
C3
+9
Anti-A
Anti-A
+42
6
+ 13
A-
A+
IgG
+ 13
Anti-D
Anti-D
+70t
DAT,
direct
Serum
antiglobulin
antibody
titer
tAnti-D
BMT
not
256;
is well
test;
D, donor;
detectable
later samples
documented.5
R, recipient;
in subsequent
Hemolysis
of donor
the time
of the transplant
can
of recipient
antibodies
by plasma
removal
of donor
cells
not done.
not tested.
cells at
removal
red
ND,
follow-up.
from
the
red
be prevented
exchange6
marrow
blood
cally
by
or by
with hemoglobinuria
hemolysis
occurring
before
infu-
More
recently,
cases
of immune
recipients
of minor
ABO
reported.9”#{176} Some reported
Table
3.
ABO
Minor
Antibody
hemolysis
occurring
mismatched
marrow
episodes
of hemolysis
and Rhesus
(D) Mismatch
Recipient
Antibody
Titer 1 mo
Post-BMT
IgG/IgM
Donor
Antibody
Ther
IgG/lgM
Relevant
Patient
BMT
been
clini-
centers
2)
nism.
BMT,
(Group
Recipient
Antibody
Titer
DAT
Day Positive
Post-BMT
3 mo
Post-BMT
IgG/lgM
Anti-B
64/2
4/2
<2/<2
JC
Anti-B
32/16
4/2
<2/.cz2
CW
Anti-B
32/8
4/2
<2/<2
CR
Anti-A
32/32
2/2
<2/<2
+4
AK
Anti-A
32/64
8/2
<2/<2
+ 22
64/128
<2/<2
<2/<2
+ 28
0
+7
liver”
two
cases
of acute
renal
failure
were documented.9
in patients
receiving
and
kidney’2
associated
Cases
minor
transplants
have
of immune
ABO
mis-
also
appeared
+8
Anti-B
Anti-A
128/32
8/4
ND
KS
Anti-A
ND
ND
ND
0
55
Anti-B
ND
ND
ND
0
GB
Anti-A
64/16
8/2
<2/<2
JW
Anti-A
16/4
8/2
NW
Anti-A
16/32
4/4
<2/<2
0
KR
Anti-B
16/2
8/2
<2/<2
0
<2/’z2
0
+22t
0
19t
SR
Anti-A
16/8
2/<2
MTh
Anti-A
64/64
4/4
4/<2
0
ND
ND
ND
0
Anti-D
Anti-B
JR
Anti-D
ARII
Anti-D
CJ
Anti-D
0
AG
Anti-D
0
Anti-Dil
4
256
+13t
Anti-DIl
Anti-Dl!
Anti-Dil
Anti-Dl!
Anti-Cl!
Anti-Cl!
Anti-El!
Anti-El!
+22
Ant-D
0
0
0
0
Anti-D
0
0
0
0
Case
1 from
§Minor
ABO
group
and
plasma
transplant
after
minor
our data, active production
is the most likely mecha-
hemolysis
occurred
one to three weeks after
that passive
transfer
of antibody
at the
in blood
products
(Table
cause.
None
of the
ABO-incompatible
1); therefore,
transfusion
of
incompatible
plasma
does not account
for the phenomenon.
Retrospective
analysis
of minor
ABO
mismatched
BMT
patients
showed
that
only
a minority
(2/16)
developed
significant
hemolysis,
despite
the
production
of
occurs
Table
without
signs of overt
3, it can be seen that
cannot
anti-B
be predicted
titers.
Most
from
minor
hemolysis.
the onset
From data shown
in
of immune
hemolysis
either
donor or recipient
anti-A
or
ABO
mismatched
patients
were
transfused
with packed
group 0 cells. However,
the
sion of group
A or B red cells may have contributed
severity
of hemolytic
group
1 (Table
1).
episodes
seen
transfuto the
I , 2, 4, and
in patients
5 in
We have shown that production
of donor-derived
antibody
specific
for recipient
ABO
antigens
is transient,
with
the
relevant
antibody
being
virtually
undetectable
by three
months
post-BMT
(Table
3). These
data are consistent
with
after
.
by Buckner
recipient
BMT.
et al6 in which
ABO
The
. .
antigens
transient
nature
.
donor-derived
was
absent
or weak
of donor-derived
antibody
one year
antibody
was
rhesus
(D)
mismatch.
No
anti-D
detected
1.
detected
Maximum
suggesting
three
hemolysis.
1.
#{182}Titer
not estimated.
last
from
hemolysis
1.
ients.
IlCase6fromgroup
patients
immune
against
recipient
ABO antigens
is not understood
and contrasts with the more persistent
donor-derived
rhesus
antibodies detected.
Possible
mechanisms
are discussed
below.
The probable
cause of immune
hemolysis
in case 6 group
I
not done.
significant
with
time of the transplant
is an unlikely
patients
in group
1 received
significant
against
TP
tClinically
six
presented
ABO or D mismatch
BMT.
From
of donor-derived
red cell antibody
a report
+21
CH
Case 2 from group
investigated
who
antibody
against
recipient
red cell antigens
in the majority
of
cases (Table
3). Six out of 16 patients
developed
a positive
DAT,
suggesting
that
in vivo red cell sensitization
often
DD
+
have
clinically
PG
2/<2
We
in
have
were
AG
Anti-D
matched
and
in the literature.
sion.7’t
ND,
severe,
on day
+98
(CJ)
and
+365
(AG).
in recip-
donor-derived
.
.
anti-D.
recipients
serum
until
of 256 on day 70 after
Anti-D.
was
not detectable
in the
1 3 days after BMT and rose to a titer
BMT. On retrospective
analysis
of 97
cases,
seven
D-positive
patients
received
marrow
from
Dnegative
donors.
Three
out of seven
patients
(including
patient
6 in group
1) produced
donor-derived
anti-D
(Table
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HOWS
180
3).
In contrast
ABO
to the
cases,
the
tinued
to produce
year after
BMT.
antibodies
tolerance
lymphocytes
antibody
production
of D-incompatible
anti-D
for prolonged
The early disappearance
in the
marrow
con-
periods
of up to one
of donor-derived
in the ABO
cases
may
be due to high
zone
brought
about
by continued
exposure
of donor
to A or B antigens
in the recipients’
plasma
and
In
tissues.
contrast,
the rhesus
mismatched
are only exposed
to recipient
lymphocytes
transiently
from
the
rhesus
enough
antibody
BMT
donor
rhesus
antigens
until residual
recipient
red cells are
circulation.
The
antigenic
stimulus
derived
antibody
to induce
production.
The
transient
recipients
role
of
production
tolerance,
but
cyclosponine
in
may
instead
facilitating
be
reported
have
pressed
with
observation.
transplanted
was used
We have
hemolysis
of
confirm
is
now
retrospective
by blocking
to antigen
proliferation
case
not
of
This
prospectively
agent
to
that
of T lymphocytes
However,
T lymphocyte
presensitized
lymphocytes
in
production
mismatched
is a secondary
case (AR),
immune
we have
shown
anti-D
that the donor was presensitized
to the D antigen,
with
present
in the donor’s
serum.
The
donor-derived
anti-D
produced
a secondary
in this
immune
recipient
response
was,
to the
therefore,
D antigen
the result
of
by the donor
lymphocytes,
analogous
to
anti-B
in the ABO-incompatible
the
definite
evidence
gens in the other
presensitization
to rhesus
antiin which
donor-derived
rhesus
antibodies
were
was a I 5-year-old
for donor
two cases
produced.
boy who
production
of
cases described.
antibodies
were
detected
(Ci),
the
by the patient’s
sister.
Her serum
did
rhesus
antibodies
at the time of the
she
I 7 years.
has
two
rhesus
It is therefore
the
frequency
patients
had
anti-A
and
We have no
Indeed,
the donor
for patient
AG
had not been transfused,
suggest-
D-positive
possible
evidence
for
children
that
during
anti-D
of clinical
mismatched
required
the donor
pregnancy
and
in the recipient
hemolysis
BMT,
increased
is low
in
it can be severe.
red cell support,
intravascular
hemolysis,
and
one patient
required
plasma
exchange.
Renal
failure
was not
apparent
in our patients;
however,
this remains
a potential
It is not possible
hemolyze
from monitoring
anti-B
titers
(Table
3).
hemolysis
receiving
occurs
minor
to predict
in approximately
10%
ABO
or D mismatched
prevent
exacerbation
of hemolysis,
mismatched
transplants
should
or
washed
given.
BMT
group
0
red cells
Platelet
patients
red
to
recipients
be transfused
cells.
In
D
of the appropriate
concentrates
given
should
be recipient
concentrated
which
patients
donor
and recipient
Our data
suggest
that
0 platelets
are used, transfusion
patible
plasma
can be avoided
in the presence
ofcyclosporine.’6
In
BMT,
the donor
lymphocytes
are
transfer
to the recipient,
so donor-
cell antibody
In one D minor
the
however,
I 5 and
complication.
immunosup-
immunosuppressive
when
transplant;
two
all
so
confirms
this
I 3 patients
a single
antibody.
case,
donor-derived
rhesus
marrow
was donated
not contain
detectable
D-negative
proliferation
is not impaired
red
studied
or mitogens.’4”5
are reexposed
to antigen
minor
ABO
mismatched
sensitized
in vivo before
derived
response.
being
antiimmune
in which
Although
observations.
is a powerful
primarily
response
recipients
experience
reviewed
in this
minor
ABO and rhesus
All six group
1 patients
donor-derived
been unable
to identify
due
to donor-derived
patients
our
Cyclosporine
acts
in transplant
of donor-derived
due to a primary
In the third case
strong
in one center
(Duarte)
in whom
methotrexate
in the postgraft
period
to prevent
GVHD
(data
shown).
immune
group
been
cyclosponine.
Our own
We have retrospectively
that
became
sensitized
to the D antigen
that the production
of donor-derived
was a secondary
response.
to prolonged
antibody
production
is uncertain.
It is of interest
that
cases of immune
hemolysis
due to donor-derived
antibody
far
production
D, -C, and -E in the recipient
was
response
by the donor lymphocytes.
aged
eliminated
for donor-
not
leads
ing
ET AL
will
anti-A
and
significant
15% of cases
transplants.
To
of minor
ABO
with packed
mismatched
ABO
group
cases,
should
be
to minor ABO mismatched
group or group 0. If group
of significant
by using platelet
by centrifugation.’7
These
ABO-incompreparations
measures
will,
how-
ever, not completely
prevent
hemolytic
episodes.
In summary,
we have
documented
the occurrence
of
immune
hemolysis
in approximately
10% to 15% of marrow
transplant
recipients
who received
minor
ABO
or D mismatched
marrow
and
were
treated
with
cyclosporine.
We
believe
antibody
that hemolysis
is due to active
production
of red cell
by donor
lymphoid
cells in the early posttransplant
period.
sponine
Antibody
production
immunosuppression.
evaluate
the
syndrome.
have
minor
role
When
of cyclosporine
hemolysis
suggested
a transfusion
mismatched
transplants
exacerbation
may be associated
with cycloFurther
work is in progress
to
in the
occurs,
policy
that
pathogenesis
it may
for
we
be severe,
of this
and
we
patients
receiving
hope
will prevent
of the hemolysis.
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1986 67: 177-181
Donor-derived red blood cell antibodies and immune hemolysis after
allogeneic bone marrow transplantation
J Hows, K Beddow, E Gordon-Smith, DR Branch, W Spruce, I Sniecinski, RA Krance and LD Petz
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