Official Journal of
the British Blood Transfusion Society
Transfusion Medicine | ORIGINAL ARTICLE
Retrospective analysis of forward and reverse ABO typing
discrepancies among patients and blood donors in a tertiary
care hospital
R. N. Makroo, B. Kakkar, S. Agrawal, M. Chowdhry, B. Prakash & P. Karna
Department of Transfusion Medicine, Indraprastha Apollo Hospital, Delhi, India
Received 5 May 2017; accepted for publication 17 December 2017
SUMMARY
Objective: The aim of our study was to determine the incidence
and causes of ABO typing discrepancies among patients and
blood donors at our centre.
Background: An accurate interpretation of the ABO blood
group of an individual is of utmost importance to ensure patient
safety and good transfusion practices.
Methods: A retrospective observational study was carried out
in the Department of Transfusion Medicine in our hospital from
March 2013 to December 2015. Records of all patient and blood
donor samples were retrieved and analysed for ABO typing
discrepancies.
Results: In total, 135 853 patient and 62 080 donor samples were
analysed for ABO typing discrepancies. The incidence among
patients and blood donors was found to be 0·1% (138/135853)
and 0·02% (14/62080), respectively. The mean age for patients
and blood donors was 48·4 and 29·2 years, respectively. The
most common cause of ABO typing discrepancies was due
to cold autoantibodies among the patients (50·7%) and blood
donors (57%) causing discrepant results in reverse typing. The
various other causes of reverse typing discrepancies among
patients were weak/missing antibody (25·4%), cold-reacting
alloantibody (4·3%), warm autoantibody (2·2%), anti-A1 anti-
body (2·2%), Bombay phenotype (1·5%), transplantation (0·7%)
and rouleaux (0·7%), whereas in blood donors, the causes were
cold-reacting antibody (7%) and weak antibody (7%). The major
cause of forward typing discrepancies among patients (12·3%)
and blood donors (29%) was ABO subgroups.
Conclusion: The resolution of ABO typing discrepancy is essen-
tial to minimise the chance of transfusion of ABO-incompatible
blood.
Correspondence: Brinda Kakkar, Post Graduate Trainee, Department
of Transfusion Medicine, Indraprastha Apollo Hospital, Delhi 110 076,
India.
Tel.: +91 11 29872011; fax: +91 11 26825563; e-mail:
docbrindakakkar@gmail.com
© 2018 British Blood Transfusion Society
Key words: ABO blood group, ABO discrepancy, cold autoan-
tibody, forward typing discrepancy, reverse typing discrepancy.
The discovery of the ABO blood group system by Karl Land-
steiner marked the beginning of modern blood banking and
transfusion medicine. ABO typing is one of the simplest tests
performed to determine an individual’s blood group and
involves two basic steps: cell grouping (to determine A and B
antigens by testing with anti-A, anti-B and anti-AB) and serum
grouping (to determine ABO antibodies by testing with reagent
red blood cells with a known ABO phenotype) (Kaur et al.,
2014). The risk of haemolytic transfusion reaction (HTR) due
to transfusion of ABO-incompatible blood is 100–1000 times
higher than the risk of transfusion-transmitted infections, and
such a transfusion may lead to serious consequences in the
recipient (Chiaroni et al., 2004; Sharma et al., 2014).
ABO typing discrepancies are described as the mismatch
between cell (forward) grouping and serum (reverse) group-
ing. The cause of ABO typing discrepancies are clerical errors,
problems related to red cells and/or serum- or procedure-related
problems (Chiaroni et al., 2004; Kaur et al., 2014; Sharma et al.,
2014). Until and unless the discrepancy is resolved, the ABO
group of such cases should not be reported. This study was per-
formed with the aim of determining the incidence and cause of
forward and reverse ABO typing discrepancies among patients
and blood donors in our institute.
MATERIALS AND METHODS
This retrospective observational study was conducted in the
Department of Transfusion Medicine in a large tertiary care
centre located in New Delhi from March 2013 to December
2015 after approval from the institutional ethical committee. All
patient and blood donor samples received during the period
were analysed. The exclusion criteria were deferred/rejected
donors and neonatal and haemolysed samples.
As per the departmental protocol, all patient and donor sam-
ples were subjected to ABO typing using the fully automated sys-
tem Neo (Immucor Inc., Norcross, GA, USA). Immucor anti-A
doi: 10.1111/tme.12506
2 R. N. Makroo et al.
(murine monoclonal), Immucor anti-B (murine monoclonal),
Immucor anti-AB (murine monoclonal blend) and Immucor
Referencells-4 (group A1, A2, B and O pooled reagent red blood
cells) were used for forward and reverse grouping, respectively.
The tests were performed as per the manufacturer’s instructions.
ABO discrepancy was considered whenever there was a
mismatch between the forward and reverse ABO typing and/or
the strength of reaction was less than or equal to 2+ reac-
tion in either forward and/or reverse typing. In all discrepant
cases, technical/clerical errors were ruled out first. Patient and
donor details, including name, age, gender, medical history,
prior history of transfusion or transplantation or pregnancy,
and medication history were analysed. Repeat ABO typing
was performed using a fresh blood (if available) sample by
the conventional tube technique. Eryclone anti-A (mono-
clonal, clone 11H5, Tulip Diagnostics, Goa, India), Eryclone
anti-B (monoclonal, clone 6F9, Tulip Diagnostics), Eryclone
anti-AB (monoclonal, clone 11H5 + 6F9, Tulip Diagnostics) and
in-house pooled donor red blood cells (A1 cell, B cell and O cell;
a pool of 3–5 donor cells) were used for forward and reverse
grouping. Supplementary reagents used included Erybank®
anti-A1 lectin (purified extract of Dolichos biflorus seeds, Tulip
Diagnostics) and Erybank® anti-H lectin (purified extract of
Ulex europaeus seeds, Tulip Diagnostics) along with in-house
pooled A2 cells wherever required. Monoclonal antisera (anti-A,
anti-B and anti-AB) and in-house pooled cells utilised for testing
by the tube technique underwent daily quality control as per the
department protocol before use.
Resolution of ABO discrepancies and grading of the aggluti-
nation reaction were performed as per the American Association
of Blood Banks (AABB) Technical Manual, 18th edition (Fung
et al., 2014). Figs. 1–3 show the algorithm followed in our centre
for resolving ABO discrepancies. Immucor Panocell-10 was used
for antibody identification by conventional tube technique, and
the testing was performed as per the manufacturer’s instruction.
The data were entered in Microsoft Excel software (Redmond,
WA, USA). Percentages and mean values were calculated using
statistical analysis software (SAS Institute Inc., Cary, NC, USA)
9.1.3.
RESULTS
In total, 62 080 (56 440 males, 91%; 5640 females, 9%) blood
donor samples were analysed for ABO typing discrepancy, of
which 14 (0·02%) had discrepant results. The overall mean age
for blood donors with ABO typing discrepancy was 29·2 years
(19–39 years). All 14 blood donors with discrepant results were
male donors. The majority of discrepant results was noted with
the reverse typing (10; 71%) followed by forward typing (4; 29%).
The mean age of blood donors with reverse typing discrepancy
was 33 years, whereas 27·8 years was noted for blood donors with
forward typing discrepancy.
In total, 135 853 patient samples were analysed for ABO typ-
ing discrepancies, of which 138 (0·1%) had discrepant results.
Of the 138 discrepant cases, 82 (59%) were males, and 56 (41%)
Transfusion Medicine, 2018
were females. The overall mean age for patients with ABO
typing discrepancy was 48·4 years (7–87 years). The majority of
discrepant results were noted with the reverse typing (87·7%)
followed by forward typing (12·3%). Table 1 summarises the
forward and reverse typing discrepancies in blood donors vs
patients. Table 2 shows the demographic details of the patients
with ABO typing discrepancies.
Of the 35 patient samples with weak antibody reactivity, 27
had age more than 65 years, 6 were post-renal transplant recip-
ients on immunosuppressive drugs, and 2 had weak antibody
reactivity; however, the cause for the same could not be deter-
mined. Of three patient samples with warm-reacting autoanti-
body reactivity, two patients were diagnosed with warm autoim-
mune haemolytic anaemia, and the other was diagnosed with
relapsed non-Hodgkin lymphoma. One patient sample with
rouleaux was a diagnosed case of multiple myeloma.
Table 3 shows the details regarding the different strength of
reactions in blood donors and patients, and Table 4 shows the
ABO blood group distribution of blood donors and patients
presenting with ABO typing discrepancy. All the samples were
resolved on the basis of serological testing; thus, there were
no unresolved samples that required molecular typing. During
the study period, we did not encounter any near-miss events
or wrong blood transfusions resulting in adverse outcomes in
patients.
DISCUSSION
Accurate ABO typing is essential in reducing the risk of transfu-
sion of incompatible blood, which can result in serious compli-
cations in transfusion recipients (Chiaroni et al., 2004; Sharma
et al., 2014). Therefore, this study was conducted with the aim
of assessing the incidence and cause of ABO typing discrepancy
among patients and blood donors in our centre.
The incidence of ABO typing discrepancies among blood
donors in our study was 0·02%. Similar results have been
reported by Sharma et al. (2014; 0·06%) and Kaur et al. (2014;
0·04%). The most common cause of ABO typing discrepancies
in our blood donors was observed with reverse typing due to the
presence of cold-reacting autoantibody (57%). However, Sharma
et al. (2014) have reported the most common cause of ABO dis-
crepancy to be weak or missing antibody in their study, whereas
Kaur et al. (2014) found ABO subgroups to be the most common
cause.
We observed that only one (7%) of our donors had
cold-reacting alloantibody, which was of IgM type with the
specificity of anti-M, and similar results have been reported in
the published literature (Khalid et al., 2011; Kaur et al., 2014;
Sharma et al., 2014). Anti-M antibodies are naturally occurring
saline agglutinins showing optimal reactivity at room temper-
ature or below, thus not considered to be clinically significant.
ABO discrepancies resulting from such an antibody can be
resolved by performing tests at warm temperatures. They are
considered clinically significant only when they show reactivity
at 37 ∘ C and/or in the antihuman globulin phase and cannot be
© 2018 British Blood Transfusion Society
 ABO typing discrepancies among patients and blood donors 3

ABO typing discrepancy

Mismatch between the forward and reverse typing

(Strength of agglutination reaction ≤ 2+)

Rule out technical/clerical errors

Technical/clerical error identified No technical/clerical error identified

Repeat ABO typing with new sample Repeat testing with same sample

Discrepancy resolved Discrepancy not resolved Discrepancy resolved

ABO blood group reported Review records: age, diagnosis, ABO blood group reported
history of transfusion, pregnancy,
transplantation and medications

Repeat testing with fresh sample using

washed patients/donors red blood cells

Discrepancy resolved Discrepancy not resolved

ABO blood group reported Categorize the type of discrepancy

Forward typing discrepancy identified Reverse typing discrepancy identified

Fig. 1. Algorithm to resolve ABO typing discrepancies in our centre.

ignored as they have potential to cause HTRs and haemolytic
disease of the newborn (Fung et al., 2014). However, we did not
find it to be clinically significant in our study, and M negative
in-house pooled red blood cells were utilised for reverse typing.
We also observed that one (7%) of our donors had a reverse
typing discrepancy due to weak antibody. The various conditions
associated with weak or missing antibodies are patients with
extremes of age; antibody dilution due to plasma or exchange
transfusion; and immunosuppressive states such as malignan-
cies, patients under immunosuppressant treatment, congenital
or acquired agammaglobinemia and bone marrow or stem cell
transplant recipients (Fung et al., 2014). Donors might not be
completely sincere in the pre-donation interview about the drugs
they take; as a result, the immunosuppression due to drug intake
could not be formally ruled out.
Four (29%) of our donors had forward typing discrepancy
due to weak antigen reactivity detected by serological testing,
and further confirmation of such samples involves performing
molecular typing; however, we did not perform molecular typ-
ing as it was resolved by the tube technique, utilising adsorption

© 2018 British Blood Transfusion Society Transfusion Medicine, 2018

4 R. N. Makroo et al.

Forward typing discrepancy identified

Weak/missing reactivity Mixed field reactivity Unexpected or extra reactivity

? ABO subgroups ? Recent transfusion (out of group)

? Cold agglutinin
? Mismatched ABO BM/HSCT
? Exchange transfusion (SCD; HDFN) ? Rouleaux
Incubate for prolonged incubation
? ABO subgroups (A3; B3)
at different temperatures (RT,
4°C, 37°C)
Use pre-warmed sample

Washing several times with

Yes No
Resolved Not resolved saline

ABO Blood Group Perform adsorption Incubate at 37 °C for 5-10

Reported and elution minutes
Perform clerical check
and report the ABO group

Resolved Not resolved

Confirmation

Perform molecular typing or send sample to Not resolved Resolved

Immunohematology Reference Laboratory

ABO Blood Group

Reported

*Run auto-control and DAT at all the steps

*RT: room temperature; DAT: direct antiglobulin test;
BM/HSCT: bone marrow/hematopoietic stem cell transplantation

Fig. 2. Algorithm for resolving forward ABO typing discrepancies in our centre.

elution technique in our case. ABO discrepancies due to ABO
subgroups have been reported in the previously published lit-
erature (Kaur et al., 2014; Sharma et al., 2014). As a majority
of blood donation during the study period was by male donors
(91%), we did not observe any ABO typing discrepancy in female
blood donors (9%).
In our study, the incidence of ABO typing discrepancies
among patients was found to be 0·1%, with the most common
cause being reverse typing discrepancy due to cold-reacting
autoantibodies (50·7%). In our study, 35 patient samples
had reverse typing discrepancies due to weak/missing anti-
body. Of these 35 (25·4%) samples, 27 were age-related
weak/missing antibody, 6 were post-renal transplant recipients
on immunosuppressive drugs, and the other 2 remained unre-
solved as history was not available to rule in weak/missing
reactivity due to immunosuppressive drugs or hypogamma-
globinemic state.
Six (4·3%) patients had reverse typing discrepancy due to
cold-reacting alloantibody (three anti-M, two anti-N and one
anti-Leb ), which were found to be clinically significant as prior
transfusion history was noted in all these six patients. We also
observed reverse typing discrepancies due to warm autoantibod-
ies (2·2%) in our study, and further evaluation revealed that two
patients were diagnosed with autoimmune haemolytic anaemia,

Transfusion Medicine, 2018 © 2018 British Blood Transfusion Society

 ABO typing discrepancies among patients and blood donors 5

Reverse typing discrepancy

Weak/missing reactivity Unexpected or extra reactivity

Incubate for prolonged incubation ? Cold agglutinin ? anti-A1 antibody ? Rouleaux

at different temperatures (RT, 4°C,
37°C) and run auto-control (AC)

Perform saline
Negative with
replacement technique
A1 lectin
Reactivity with No reactivity Reactivity with
negative AC positive AC
ABO subgroup with No false
anti-A1 antibody agglutination

ABO group reported

? anti-H antibody
? Other cold
? weak antigenic reactivity due ABO group reported
agglutinins (anti-I, -
to weak ABO subgroups a/b
Test with anti-H lectin IH, -M, -N, -P, -Le )
Perform adsorption
and elution
Negative
Use pre-warm sample for testing
Reactivity No reactivity Run antibody screen, use cord cells
Bombay phenotype (Oh)

ABO group reported Look for other causes

? Extremes of age
Resolved Not resolved
? Immunosuppressive drugs
Screen negative Screen positive
? Hypogammaglobinemic states
? Transplantation

ABO group reported Antibody identification

Identify the antibody and use

antigen negative cells for reverse
typing

Resolved

*RT- room temperature

ABO group reported

Fig. 3. Algorithm to resolve reverse typing discrepancy in our centre.

© 2018 British Blood Transfusion Society Transfusion Medicine, 2018

6 R. N. Makroo et al.
Table 1. Forward and reverse ABO typing in blood donors vs patients
Blood donors
Forward typing discrepancy
Discrepant samples (n; %) 4 (29%)
Cause of discrepancy Weak antigen reactivity (subgroup of A1)
Reverse typing discrepancy
Discrepant samples (n, %) 10 (71%)
Cause of discrepancy Cold-reacting autoantibody (8; 57%)
Weak antibody (1; 7%)
Cold-reacting alloantibody (1; 7%, anti-M)
1 Subgroup of A – were A2 type.
Table 2. Demographic details of patients with ABO typing discrepancies
Type of discrepancy Overall mean age (years)
Forward typing 36·6
Reverse typing 51
and one patient was a diagnosed case of relapsed non-Hodgkin
lymphoma. Grouping discrepancies due to warm autoantibodies
is not uncommon, and such cases have been reported previously
(Garratty, 1993; Inaba et al., 2005).
ABO discrepancies due to rouleaux formation are seen when
there are elevated levels of proteins from certain diseases, such
as multiple myeloma, Waldenstrom’s macroglobinemia and
advanced cases of Hodgkin’s lymphoma, on administration of
plasma expanders like dextran and cord blood samples contain-
ing Wharton’s jelly (Fung et al., 2014). In our study, one (0·7%)
patient had reverse typing discrepancy due to rouleaux, which
was resolved by saline replacement technique, and further
history taking revealed that the patient was a diagnosed case of
multiple myeloma. Similar cases of grouping discrepancy due to
rouleaux formation have been reported by Shastry et al. (2015).
One (0·7%) of our patients had reverse typing discrepancy,
where forward typing was group O and reverse typing was
group A (missing expected anti-A) and was resolved by history
taking, which revealed that patient had undergone a minor
ABO-incompatible haematopoietic stem cell transplantation
(patient group A, donor group O). Blood group chimersim is an
essential feature of haematopoietic stem cell transplantation and
can present as a challenge to transfusion services as they can
lead to ABO blood group discrepancies (Gajewski et al., 2008).
In our patient, we observed that the forward typing was group
O as the donor cells had already engrafted, and the expected
Transfusion Medicine, 2018
Patients
17 (12·3%)
Weak antigen reactivity (13 subgroup of A1; 3 subgroup of AB; 1
subgroup of B)
118 (87·7%)
Cold-reacting autoantibody (70; 50·7%)
Weak antibody (35; 25·4%)
Cold-reacting alloantibody (6; 4·3%; 3 anti-M; 2 anti-N; 1 anti-Leb )
Warm-reacting autoantibody (3; 2·2%)
anti-A1 antibody (3; 2·2%; 2 subgroup of AB; 1 subgroup of A)
Bombay group (2; 1·5%)
Rouleaux (1; 0·7)
Post-minor ABO-incompatible stem cell transplant recipient (1; 0·7%;
patient group A; donor group O)
Total number Mean age (years)
Male Female Male Female
12 10 37·9 35·1
67 44 52·4 48·9
anti-A was absent probably due to immune tolerance developed
along with the transplantation.
We observed that three of our patients had unexpected reac-
tivity in reverse typing due to anti-A1 antibody, and further test-
ing of the patients’ red blood cells with anti-A1 lectin was found
to be negative, thus revealing that two of the patients belonged
to a subgroup of AB and the other belonged to a subgroup of A.
In-house pooled A2 red blood cells were also used. Anti-A1 anti-
body has been reported in around 1–8% of A2 and 22–35% of
A2B individuals, and if found to be reactive at 37 ∘ C, it can result
in HTR. Thus, the determination of the clinical significance of
this antibody is of prime importance to prevent any mismatched
blood transfusions in these patients (Fung et al., 2014).
Two (1·5%) of our patients were identified with the Bom-
bay phenotype, which is considered a rare entity in Caucasians;
however, in India, it has a prevalence of 1 in 10 000 individuals
(Shahshahani et al., 2013). These individuals can be easily misdi-
agnosed as blood group O in forward typing; therefore, inclusion
of group O cells in reverse typing and testing with anti-H lectin
are extremely important steps to be performed to correctly iden-
tify these individuals to eliminate the risk of HTRs (Shahshahani
et al., 2013).
All of the 20 (14·5%) forward typing discrepancies in patients
were related to the weak antigen reactivity due to ABO sub-
groups. Alteration or loss of ABO antigens from the surface of
red blood cells secondary to an underlying malignancy have
© 2018 British Blood Transfusion Society
 ABO typing discrepancies among patients and blood donors 7

Table 3. Details regarding the different strength of reactions in blood donors and patients (mean ± standard deviation)

Forward typing Reverse typing

Anti-A Anti-B Anti-AB Anti-A1 lectin1 Anti-H lectin2 A1 cell B cell O cell

Blood donors 1·71 ± 1·72 1·21 ± 1·71 2·5 ± 1·74 - - 1·42 ± 1·34 1·5 ± 1·45 0·28 ± 0·61
Patients 1·52 ± 1·68 1·47 ± 1·71 2·5 ± 1·4 0·78 ± 1·34 2·42 ± 1·26 1·68 ± 1·48 1·61 ± 1·54 0·86 ± 1·28

1 Testing performed in 23 patient samples.

2 Testing performed in 19 patient samples.

Table 4. ABO blood group distribution of blood donors and patients were unable to perform molecular typing to help clarify samples
with ABO typing discrepancy (n = number; percentage) with weak antigen reactivity in forward ABO typing in patients
as well as blood donors. Thirdly, we were also not able to perform
Blood group Blood donors (n = 14) Patients (n = 138)
saliva testing in two of our patients of the Bombay phenotype
Group A 6 (42·9%) 51 (37%) as the samples were received on an outpatient basis, and further
Group B 2 (14·3%) 45 (32·6%) contact with the patients revealed they do not belong to the same
Group AB 3 (21·4%) 18 (13%) city as the hospital location.
Group O 3 (21·4%) 24 (17·4) In case of any discrepancy between forward and reverse ABO
typing, no ABO type should be concluded, and the use of group
O packed red blood cell (PRBC) units is required in case of emer-
gency transfusion as long as the discrepancy is not resolved by
been reported as a rare cause of ABO discrepancy (Salmon et al.,
the laboratory or by the immunohematology reference labora-
1984); however, none of our patients were diagnosed with malig-
tory.
nancy.
Our study was not without limitations; firstly, we did not
collect the data of samples tested by neo initially, i.e. error ACKNOWLEDGMENTS
messages, samples resolved by testing in duplicate, weak/missing
All the authors have contributed equally towards data analysis
red cell reactivity and weak/extra serum reaction; thus, we were
and preparation of the manuscript.
not able to compare the results of Neo with the tube testing
performed for the final ABO group reporting. Therefore, we
cannot comment on the difference in the strength of reactions in CONFLICT OF INTEREST
the conventional tube technique vs the Neo results. Secondly, we The authors have no competing interests.

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© 2018 British Blood Transfusion Society Transfusion Medicine, 2018