CONTENTS
Immunohematology
Volume 11, Number 4, 1995
ABSTRACT
Review: antibodies and antigens in immune neutropenias
G.F. Lucas
Flow cytometric phenotyping of platelet HPA-1a antigen: donor
screening for a case of neonatal alloimmune thrombocytopenia due
to anti-HPA-1a antibodies
J.J.M.L. Hoffman, W.C.M. Janssen, and H.Y. von
Hegedus
Trimeresurus venom
inhibition of anti-HPA-1a and anti-HPA-1b antibody binding to
human platelets
S.J. Wlodar, D.L. Stone, and L.T. Sinor
Review: comparing platelet compatibility to red cell
compatibility protocols
S. Rolih
Application of the proteolytic enzyme papain in routine platelet
serology
J.A.G. Lown and B.J. Dale
Detection of drug-dependent platelet antibodies by use of
solid-phase red cell adherence techniques
M.F. Leach, L.K. Cooper, and J.P. AuBuchon
Case report: solid-phase platelet crossmatching to support the
alloimmunized patient
B.A. O'Connell
Case report: a pregnant woman with immune thrombocytopenic
purpura and unusual red cell antibodies
C.R. Nanton, S.M. Martin, L.O. Cook, and P.J.
Larison
G.F. LUCAS
In the 1960s and 1970s,
the role of granulocyte-specific allo-, auto-, and drug-dependent
antibodies in certain neutropenic conditions became established.
In some of these conditions, neutropenia is associated with an
increased risk of life-threatening infections or unexpected
mortality during routine blood transfusion but, in the majority
of conditions involving granulocyte antibodies, the clinical
course tends to be benign. Consequently, because the detection
and identification of granulocyte antibodies is time consuming
and labor intensive, there has been little impetus for further
development in this area. However, in the last few years,
immunochemistry and molecular biology have provided advances in
granulocyte immunology. The purpose of this review is to describe
current knowledge about the antibodies and antigens implicated in
immune neutropenias.
Geoff F. Lucas, PhD, Immunohaematology Section
Manager, International Blood Group Reference Laboratory,
Southmead Road, Bristol, BS10 5ND, UK
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J.J.M.L. HOFFMANN, W.C.M. JANSSEN, AND H.Y. von
HEGEDUS
Neonatal alloimmune thrombocytopenia can
effectively be treated by transfusing compatible platelets to the
affected newborn, but typed, compatible platelets are not
generally available. For a case of probable neonatal alloimmune
thrombocytopenia due to anti-HPA-1a, part of the donor population
of the regional blood bank was phenotyped to find HPA-1a-negative
platelets. A flow cytometric technique was used, which is
reliable, rapid, and relatively simple and therefore well-suited
for large-scale screening. Using this method, several
HPA-1a-negative donors were identified, and one of them donated
platelets that were successfully transfused to the
thrombocytopenic newborn. Immunohematology
1995;11:4
Johannes J.M.L. Hoffmann, PhD, Director,
Department of Clinical Laboratories, Catharina Hospital, P.O. Box
1350, 5602 ZA Eindhoven, The Netherlands; Willy C.M. Janssen, MT,
Research Assistant, Department of Clinical Laboratories,
Catharina Hospital, The Netherlands; Harry Y. von Hegedus, MT,
Head of Laboratory, Red Cross Blood Bank Eindhoven, Eindhoven.
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S.J. WLODAR, D.L. STONE, AND L.T. SINOR
A solid-phase red cell adherence assay was used
to demonstrate the specific inhibitory effect of seven species of Trimeresurus
snake venom on the binding of HPA-1a- and HPA-1b-specific
platelet antibodies. Trimeresurus venom did not inhibit
the binding of HLA, HPA-3a, HPA-3b, HPA-4a, HPA-5a, and HPA-5b
specific platelet antibodies. Venom from other genera of snakes,
including representatives from Agkistrodon, Ancistrodon,
Bitis, Bothrops, Bungarus, Causus, Crotalus, Dendroaspis, Ecis,
Micrurus, Naja, Notechis, Ophiophagus, Pseudechis, Sepedon
(Hemachatus), and Vipera, all failed to specifically
inhibit anti-HPA-1a and HPA-1b binding. These results may
indicate that the component in Trimeresurus snake venom
previously reported to bind to the platelet GPIIb-IIIa complex,
inhibiting fibrinogen binding, binds close to the HPA-1a and
HPA-1b epitopes. Immunohematology 1995;11:4
Steve J. Wlodar, Immucor, Inc., 3130 Gateway
Drive, Norcross, GA 30071; Darryl L. Stone, PhD, Immucor, Inc.,
Norcross, GA; Lyle T. Sinor, PhD, MAIC (to whom reprint requests
should be sent), Immucor, Inc., Norcross, GA.
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S. ROLIH
Between 1971 and 1980,
the number of platelet concentrates transfused in the United
States increased from 0.4 to 2.8 million units.1 That number increased to nearly 5 million
in 1987 and continues to increase in the 1990s. The increase in
platelet transfusions has led to a concomitant rise in the
incidence of platelet alloimmunization. As a consequence, many
transfusion services or blood products providers have developed
platelet compatibility protocols to select platelet components
that will have acceptable survival when transfused to
alloimmunized patients. Most serologists are familiar with
compatibility tests used to select red blood cells (RBCs) for
transfusion. These tests are performed before transfusion,
whether or not alloimmunization has occurred. Platelet
compatibility tests, in contrast, are implemented only after
alloimmunization and development of the refractory state.
Susan Rolih, MS, MT(ASCP)SBB, Vice President,
Technical Services, Immucor, Inc., 3130 Gateway Drive, Norcross,
GA 30091-5625.
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J.A.G. LOWN AND B.J. DALE
The use of proteolytic enzymes is well
established in red cell serology. These enzymes modify some
antigen structures and remove sialic acid from the red cell
membrane. Enzyme-sensitive structures have also been identified
on the platelet membrane. The effect of papain, a proteolytic
enzyme, used widely in red cell serology, on the detection of
various platelet alloantibodies was examined to determine its
usefulness in platelet serology. Antisera with the specificities
anti-HPA-la, -2b, -3a, -4a, -5a, -5b, and -Naka
were examined. HLA antibodies were also included. All sera were
tested by a solid-phase red cell adherence technique in parallel
with untreated platelets (UP) and papain-treated platelets (PP)
for 15 minutes at 37oC. The
reactivity of anti-HPA-2b was eliminated and that of anti- HPA-3a
was either eliminated or almost eliminated with PP. Antisera
specific for the other alloantigens tested reacted similarly or
more strongly with PP compared with UP. These findings were
confirmed by flow cytometry. The reactivity of HLA antibodies
with PP was generally enhanced. Inactivation by papain of
platelet alloantigens in the HPA-2 and HPA-3 systems, but not in
other systems, may assist in resolving mixtures of platelet
alloantibodies. Also, detection of weak antibodies of other
specificities may be enhanced. The use of PP may be a simple and
useful serologic tool for investigating platelet alloantibodies. Immunohematology
1995;11:4
John A.G. Lown, FAIMS, Transfusion Medicine
Unit, Royal Perth Hospital, Wellington St., Perth, Western
Australia, 6000; Brian J. Dale, BAppSci, Department of
Haematology, Royal Perth Hospital, Perth, Western Australia.
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M.F. LEACH, L.K. COOPER, AND J.P. AUBUCHON
Many drugs have been reported to cause
drug-dependent thrombocytopenia, either by the immune complex or
by hapten mechanisms. Testing for the presence of these platelet
antibodies has not been considered feasible for transfusion
services because their presence was thought to be rare, and their
detection involved complex and costly methods. We have developed
a new technique for detection of these antibodies which can be
performed without the need for specialized and expensive
instrumentation. A solid-phase red cell adherence assay was used
to detect drug-dependent platelet antibodies active by either the
immune complex or the hapten mechanism. Three cases were
evaluated for the presence of drug-dependent platelet antibodies.
Two patients presented with thrombocytopenia that could not be
attributed to other causes. The third case was evaluated for the
presence of drug-dependent antibodies after poor responses to
platelet transfusions. In these three cases, discontinuation of
the implicated drugs, i.e., porcine heparin, quinine sulfate,
amoxicillin, Bactrim™, and
albuterol, was followed by a correction of thrombocytopenia or
improved platelet transfusion response within 72 hours. This test
methodology and protocol has proven very useful in avoiding
transfusions with little likelihood of benefit, and in
identifying drugs interfering with platelet recovery or survival.
Further investigations with this technique may expand our
knowledge of the capability of this technique and of the observed
frequency of drug-related immunologic platelet destruction. Immunohematology
1995;11:4
Miriam F. Leach, MT(ASCP)SBB, Transfusion
Service, Dartmouth- Hitchcock Medical Center, One Medical Center
Drive, Lebanon, NH 03756; Linda K. Cooper, MT(ASCP), Transfusion
Service, and James P. AuBuchon, MD, Professor of Pathology,
Dartmouth-Hitchock Medical Center, Lebanon, NH.
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B.A. O'CONNELL
Platelet crossmatching by a solid-phase red cell
adherence assay was used to provide compatible platelets for two
alloimmunized patients with leukemia. In this study, a successful
platelet transfusion was defined as giving a corrected count
increment (CCI) of >7,500 in a posttransfusion sample. For
patient A, a total of 205 random platelet concentrates (PCs) were
crossmatched. Eleven were considered compatible. These 11 PCs
were transfused during five transfusion episodes. Four of the
five transfusions produced CCIs of >7,500 and were considered
successful. Individually, eight of the eleven units were
considered in vivo compatible, and five of the eight donors of
these units agreed to become apheresis donors. Platelets from
three of these five apheresis donors gave CCIs of >7,500. For
patient B, 1,074 random PCs were crossmatched, and 332 were
considered compatible. These units were administered during 78
different transfusions. Seventy-one of these transfusion episodes
resulted in CCIs of >7,500. In addition, 19 apheresis donors
were identified by platelet crossmatching, and they provided
platelets for 38 of 39 successful transfusions for Patient B.
Platelet crossmatching should therefore be considered when a
blood bank is called upon to support a refractory
thrombocytopenic patient. Immunohematology
1995;11:4
Bernadette A. O'Connell, MT(ASCP)SBB, Cell
Component Specialist, University of Maryland Cancer Center, 22
South Greene Street, Baltimore, MD 21201.
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C.R. NANTON, S.M. MARTIN, L.O. COOK, AND P.J.
LARISON
Maternal immune thrombocytopenia purpura (ITP)
may lead to fetal platelet destruction. This process is mediated
by IgG platelet autoantibodies that cross the placenta. In this
case, not only were platelet autoantibodies present, but red cell
alloantibodies anti-E, anti-M, and anti-He were also present.
Anti-E, present as an IgG antibody, crossed the placenta, but did
not cause clinical problems in the E+ newborn, other than
possible hyperbilirubinemia that was treated by phototherapy.
Carmela R. Nanton, SBB (ASCP), Blood Bank,
West Palm Beach VA Medical Center, 7305 N. Military Trail, Palm
Beach Gardens, FL 33410; Sharon M. Martin, Ed.D., MT(ASCP), Lloyd
O. Cook, MD, and Patricia J. Larison, MT(ASCP)SBB, Medical
College of Georgia, Augusta, GA.
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