International Journal of Laboratory Hematology

The Official journal of the International Society for Laboratory Hematology

REVIEW INTERNAT IONAL JOURNAL OF LABORATO RY HEMATO LOGY

Red blood cell morphology

J. FORD

Division of Hematopathology,
BC Children’s Hospital, Faculty
of Medicine, University of
British Columbia, Vancouver,
BC, Canada
Correspondence:
Jason Ford, BC Children’s
Hospital, 4500 Oak St,
Vancouver V6H 3N1, BC,
Canada. Tel.:604-875-2044;
Fax: 604-875-2815;
E-mail: jford@cw.bc.ca
doi:10.1111/ijlh.12082
Received 31 December 2012;
accepted for publication 21
January 2013
Keywords
Anemia, morphology, red blood
cell, poikilocytosis, peripheral
smear
S U M M A RY
The foundation of laboratory hematologic diagnosis is the complete
blood count and review of the peripheral smear. In patients with
anemia, the peripheral smear permits interpretation of diagnostically
significant red blood cell (RBC) findings. These include assessment
of RBC shape, size, color, inclusions, and arrangement. Abnormali-
ties of RBC shape and other RBC features can provide key informa-
tion in establishing a differential diagnosis. In patients with
microcytic anemia, RBC morphology can increase or decrease the
diagnostic likelihood of thalassemia. In normocytic anemias, mor-
phology can assist in differentiating among blood loss, marrow fail-
ure, and hemolysis—and in hemolysis, RBC findings can suggest
specific etiologies. In macrocytic anemias, RBC morphology can help
guide the diagnostic considerations to either megaloblastic or non-
megaloblastic causes. Like all laboratory tests, RBC morphologies
must be interpreted with caution, particularly in infants and chil-
dren. When used properly, RBC morphology can be a key tool for
laboratory hematology professionals to recommend appropriate
clinical and laboratory follow-up and to select the best tests for
definitive diagnosis.

molecular analysis, review of a patient’s CBC and

INTRODUCTION
Medical school educators around the world emphasize
the importance of teaching future physicians the
correct approach to the history and physical examina-
tion. These basic skills are widely understood to be
the foundation of medical practice, even in the face of
technological change.
For laboratory hematology professionals, the com-
plete blood count (CBC) and the peripheral smear are,
respectively, our history and physical examination.
Despite quantum leaps in technological development
in the clinical laboratory, with evolutions and revolu-
tions in flow cytometry and point of care testing and
peripheral smear morphology is still the mainstay of
hematologic diagnosis.
For patients with anemia, the peripheral smear
morphology provides key information to create the
differential diagnosis. Review of the peripheral smear
has three main components:
• To confirm the CBC findings. It is unusual for labo-
ratory error to affect any of the measurements in the
CBC, but spurious findings may include the following
[1, 2]:
(i) low counts due to faulty aspiration of whole
blood by the automated counter;

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352 J. FORD | RED BLOOD CELL MORPHOLOGY
(ii) macrocytosis due to RBC agglutination or
rouleaux, hyperleukocytosis, or severe hyperglyce-
mia;
(iii) microcytosis due to the blood counter’s mis-
identification of giant platelets as RBCs.
• To review relevant white blood cell (WBC) and
platelet (PLT) findings. For example, a high platelet
count is expected in anemia due to iron deficiency
and a low platelet count is expected in anemia due to
microangiopathic hemolysis.
• To review RBC morphology. There are five impor-
tant aspects:
(i) Shape. What is/are the dominant poikilocyte(s)?
(ii) Size. Is there anisocytosis or a dual population?
(iii) Color. Is there hypo- or hyperchromasia? Is
there anisochromia or polychromasia?
(iv) Inclusions. Are there Howell–Jolly bodies,
malaria parasites, nucleated RBCs, etc.?
(v) Arrangement. Is there agglutination or rou-
leaux?
A list of RBC morphologies, their definitions, and
their associated clinical states is shown in Table 1 [3].
Poikilocytosis must be interpreted in its appropriate
context: finding a rare poikilocyte in an otherwise
normal smear is likely clinically insignificant, while
finding extensive poikilocytosis in a normocytic
anemia may indicate specific causes of hemolysis. In
the neonatal period and in patients on chemotherapy,
poikilocytosis must be interpreted with special
caution: these patients may be expected to have a
background level of mild or moderate nonspecific
poikilocytosis, and only the finding of a dominant or
extensive poikilocytosis in combination with anemia
is likely clinically relevant.
Most clinicians and laboratory professionals use an
approach to anemia centering on the mean cell
volume (MCV). This review of RBC morphology will
follow the MCV approach.
Morphology in the assessment of microcytic anemia
Medical students often learn that there are five main
causes of microcytic anemia, which together form the
easily remembered acronym TAILS:
T = Thalassemia.
A = Anemia of chronic disease.
I = Iron deficiency.
L = Lead poisoning.
S = congenital Sideroblastic anemia.
Only three of these are common in most parts of
the world, namely iron deficiency, anemia of chronic
disease (ACD), and thalassemia. Lead poisoning is not
usually considered a common cause of anemia, but it
may be seen in pediatrics particularly in areas where
paint, toys, or jewelry containing lead can be eaten by
small children. Lead can also be consumed by infants
in formula made with contaminated water [4] and
may rarely cause anemia in adults with extensive
industrial exposure. Congenital sideroblastic anemia is
vanishingly rare.
In classic cases, the morphological differentiation of
the three common microcytic anemias is straightfor-
ward. The classic morphology in ACD is of unremark-
able RBCs, while iron deficiency shows anisocytosis,
anisochromia, and elliptocytosis, and thalassemia trait
demonstrates target cells and coarse basophilic
stippling.
Regrettably, these so-called classic presentations
are unreliable in practice. Elliptocytes and anisocyto-
sis are often seen in thalassemia, target cells may
occur in iron deficiency, and both iron deficiency
and thalassemia may appear as ‘unremarkable’ as
ACD. The red blood cell distribution width (RDW),
classically taught as a key differentiator of iron
deficiency from thalassemia, is also unreliable [5];
far better than the RDW is the RBC count [5, 6],
although even a high RBC count is not proof of
thalassemia.
The only ‘reliable’ classic morphologic finding that
can separate these three conditions is the presence of
coarse basophilic stippling. Coarse stippling is seen in
some cases of thalassemia and is never seen in
uncomplicated iron deficiency or ACD. A microcytic
patient with coarse basophilic stippling likely has
thalassemia—although the patient should be in an
ethnically at-risk group, and there should not be
another reasonably likely cause of basophilic stippling.
Even a likely diagnosis of thalassemia must still be
confirmed by hemoglobin HPLC, H body staining,
molecular testing, or some other reliable method.
Morphology is essentially never diagnostic of thalasse-
mia: it can only suggest whether thalassemia is more
or less likely.
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Table 1. Common RBC morphological findings

RBC morphology Morphological definition Clinical associations

Acanthocyte RBC has irregularly distributed, variably Advanced liver disease, hyposplenism, some
(spur cell) sized, pointy projections off its surface dyslipidemias, pyruvate kinase deficiency,
McLeod phenotype
Anisochromia Variation in the amount of central pallor Iron deficiency, myelodysplasia, hypochromic
among a population of RBCs anemia post transfusion
Anisocytosis Variation in size among a population of Common nonspecific finding. Seen in iron
RBCs deficiency, moderate or severe thalassemia,
megaloblastic anemia, partially treated anemia
of several causes, post transfusion
Basophilic RBC has variably sized (up to large) Thalassemia, lead poisoning, myelodysplasia,
stippling: coarse basophilic ‘granular’ discolorations pyrimidine 5′ nucleotidase deficiency,
across its entire cytoplasm, on a post chemotherapy
Wright-stained film
Basophilic RBC has small, uniform, punctate Reticulocytosis, normal finding
stippling: fine basophilic dots across its entire
cytoplasm, on a Wright-stained film
Bite cell/blister RBC has a semi-circular indentation in Oxidative hemolysis
cell its outer cytoplasmic border. There may
be a ‘roof’ to this indentation
(blister cell) or no roof (bite cell)
Dimorphism Two distinct populations of RBC are Myelodysplasia, post transfusion,
present, for example, microcytic and partially treated iron deficiency
normocytic, or hypochromic and
normochromic
Echinocyte (burr cell) RBC has regularly distributed, equally Artifact, renal failure, post transfusion,
sized, rounded projections off its surface phosphate deficiency, burns
Elliptocyte RBC is oval shaped Iron deficiency, megaloblastic anemia,
hereditary elliptocytosis, post chemotherapy
Heinz body RBC has a submembranous or Oxidative hemolysis, hyposplenism
epimembranous small round mass, which
can only be seen by supravital or
specialized Heinz body stains. This body is
not visible on a routine Wright-stained
film
Howell–Jolly Solitary round mass, relatively large Hyposplenism, erythroblastosis, myelodysplasia,
body (e.g., approximately 10–20% of the megaloblastic anemia, post chemotherapy
diameter of the RBC), within the
hemoglobinized portion of the RBC.
Appears dark blue or purple on a
Wright-stained film
Hypochromia The zone of central pallor is > 1/3 the Iron deficiency, thalassemia, anemia of chronic
diameter of the RBC disease
Irregularly The RBC is small, dark, and lacks a Nonspecific finding seen in a variety of conditions
contracted cell zone of central pallor. Its outer including G6PD deficiency, hemoglobinopathies,
margin is not spherical: it may appear and normal neonates
dented, compressed, or otherwise
‘contracted’
Pappenheimer Usually multiple small dark blue or purple Iron overload, hyposplenism, myelodysplasia
body granular inclusions, all within the
hemoglobinized portion of the RBC.
These occupy only one portion or region
of the RBC, unlike basophilic stippling
which is more ‘global’ throughout the
entire RBC

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354 J. FORD | RED BLOOD CELL MORPHOLOGY
Table 1. (Continued)
RBC morphology Morphological definition
Polychromasia RBCs show color variability as a
population: some (usually the
majority) are the usual red color,
while others are bluish
RBC Some RBCs aggregate into
agglutination multicellular masses resembling
a bunch of grapes
Rouleaux Some RBCs aggregate into linear
patterns, said to resemble a stack
of coins
Schistocyte The RBC appears to have been
fragmented: it lacks the usual
circular shape, instead showing a
triangular or other angulated
morphology. The zone of central
pallor is often missing
Sickle cell There are several sickle RBC
morphologies, including the classic
sickle (crescentic with two sharply
pointed ends) or boats (linear with
two tapered if somewhat rounded
ends)
Spherocyte The RBC is smaller and darker than
normal. There is no zone of central
pallor. The outer edge must be almost
perfectly round (to differentiate this
cell from irregularly contracted cells)
Stomatocyte The zone of central pallor is linear,
rather than circular. Usually the
‘line of pallor’ runs parallel to the
long axis of the RBC, if the latter is
ovoid, but in certain variants (e.g.,
South East Asian ovalocytosis), the
line may run across the long axis or
may be nonlinear, for example,
bifurcated or trifurcated
Target cell The RBC has a central red area within
the zone of central pallor
Teardrop cell The RBC is tapered to a point at
one end, resembling the classic
artist’s rendition of a drop of water
The ethnicities that are not at high risk of thalasse-
mia include northern Europeans, American Indians,
Canadian First Nations, Inuit, and patients from Japan
[7]. Everyone else should be considered at risk.
Coarse basophilic stippling is not pathognomonic
for thalassemia: it can also be seen in lead poisoning,
myelodysplastic syndrome, post chemotherapy, and in
rare other conditions (see Table 1). Coarse stippling
does not help differentiate a- from b-thalassemia, as it
Clinical associations
Reticulocytosis, normal neonate
Cold agglutinin, cold autoimmune hemolytic
anemia
Normal finding in the thick part of the blood
smear, hypergammaglobulinemia (monoclonal
or polyclonal)
RBC fragmentation syndromes, for example,
microangiopathic hemolytic anemia and
hemolysis secondary to cardiac valve
Severe sickling syndrome, for example, SS,
SC and SD
Autoimmune hemolytic anemia, alloimmune
hemolytic anemia (e.g., hemolytic disease of
the newborn), hereditary spherocytosis
Artifact, obstructive liver disease, hereditary
stomatocytosis, South East Asian ovalocytosis,
Rh null syndrome
Thalassemia, liver disease, hyposplenism, Hgb
C disease or SC disease, hereditary xerocytosis.
May be seen in iron deficiency
Nonspecific finding seen in several conditions
including myelofibrosis
may be seen in either condition. It must not be con-
fused with fine basophilic stippling, which is a normal
finding.
The morphology of H bodies [8], which are consis-
tent with (if not pathognomonic for) a-thalassemia, is
well known: using supravital stains, these precipitates
of b-globin tetramers appear as innumerable dark
spots distributed in a geometric fashion across the
entire cytoplasm of the RBC like the pits on the
© 2013 Blackwell Publishing Ltd, Int. Jnl. Lab. Hem. 2013, 35, 351–357

surface of a golf ball. Patients with a single or double
a-gene deletion may show a single H body RBC in
many high-power fields, while patients with hemo-
globin H disease (a-/-) demonstrate H bodies in the
majority of their RBCs. Unfortunately, the sensitivity
of H body staining is variable, ranging from approxi-
mately 40% up to approximately 90% depending on
the pattern of a-deletions [8] and the laboratory’s
technical expertise. H bodies also usually require the
presence of exclusively normal b-globin chains (i.e.,
bA-chains): if a patient has both a-thalassemia and a
simultaneous b-variant, such as hemoglobin E, it may
be much more difficult to find H bodies. This variable
sensitivity means that although the presence of H
bodies can indicate a-thalassemia, their absence does
not rule this diagnosis out.
In the right context (e.g., microcytic anemia with
a high RBC count, in a patient from a high-risk
ethnicity such as South East Asian), H bodies are in
general considered diagnostic of a-thalassemia. How-
ever, even in this context, H bodies are not ‘proof’ of
a-thalassemia: H-like bodies can be formed by other
unstable hemoglobins besides b4, such as Hemoglobin
J-New York.
The analogous RBC inclusion in b-thalassemia,
consisting of precipitates of a4, may be designated
‘Fessas bodies’ [9]. These are solitary large round
deposits within the cytoplasm of an RBC: like the
surrounding soluble hemoglobin, the precipitated
a-chains are red on a Wright stain, so Fessas bodies
are generally not visible in routine peripheral smears.
They can sometimes be seen as red cytoplasmic inclu-
sions in polychromatophilic RBCs or in nucleated
RBCs in the peripheral blood, and in RBC precursors
in marrow aspirate specimens.
One helpful morphological clue in microcytic ane-
mias is the broad range of poikilocytosis seen in many
cases of thalassemia, compared to iron deficiency. In
some patients with thalassemia, there are not only
target cells but also numerous teardrop cells and schis-
tocytes. Among the poikilocytes seen in thalassemia
are the ‘fish cells’ described by Barbara Bain [Bain,
personal communication]. These are generally not
seen in patients with iron deficiency or ACD. Fish
cells resemble teardrop cells, with one rounded end
and one tapered end: unlike teardrops, the tapered
end flares out into two buds resembling a fish’s tail.
One fish cell is seen at the center of Figure 1. This
© 2013 Blackwell Publishing Ltd, Int. Jnl. Lab. Hem. 2013, 35, 351–357
J. FORD | RED BLOOD CELL MORPHOLOGY 355
image also shows examples of the teardrops and schis-
tocytes which can be seen in thalassemia trait.
Morphology in the assessment of normocytic anemia
Most cases of normocytic anemia are caused by blood
loss, suppressed production of RBCs, or hemolysis. In
hemorrhage the RBC morphology is entirely unre-
markable, except for the polychromasia that typically
arises after the first twelve to 24 h. In patients with
reduced RBC production, red cell morphology may be
normal where the cause is extrinsic to the red cell
itself: for example, because of low erythropoietin in a
patient with renal failure. But where erythropoiesis is
intrinsically disordered (e.g., myelodysplasia) and in
cases of hemolysis, RBC morphology may be diagnos-
tically significant.
Patients with disordered RBC production (such as
myelodysplastic syndrome, MDS, or congenital dysery-
thropoietic anemia, CDA) may have a dual population,
elliptocytes, teardrop cells, or other poikilocytes. There
may also be circulating nucleated RBCs (nRBCs), show-
ing dysplastic features including asymmetric nuclear
budding, multinuclearity, megaloblastoid changes, or
karyorrhexis. In children, particularly infants, ‘reactive’
(transient) dysplastic nRBCs are frequently seen in
many patients with brisk reticulocytosis following
hemorrhage or hemolysis. ‘Reactive’ dysplasia in chil-
dren will abate after correction of the patient’s anemia.
The most common role of RBC morphology in
patients with normocytic anemia is in the assessment
Figure 1. A ‘fish cell’ and other poikilocytes in a case
of thalassemia trait. Wright stain, 9100.
356 J. FORD | RED BLOOD CELL MORPHOLOGY
of patients with hemolysis. Poikilocytosis will often
suggest a specific cause or mechanism of hemolysis
(Table 1):
• Bite and blister cells, as well as irregularly contracted
cells, are the classic findings in oxidative hemolysis: for
example, because of G6PD deficiency. Oxidative
hemolysis may also lead to (less prominent) schisto-
cytosis and spherocytosis.
• Acanthocytes are rarely the dominant finding in a
hemolytic patient, but may suggest pyruvate kinase
deficiency (where they will be accompanied by irregu-
larly contracted cells) or the McLeod phenotype.
Acanthocytes are more commonly observed in
patients with hyposplenism, liver disease, a variety of
dyslipidemias, and even anorexia nervosa.
• Sickle cells will suggest a diagnosis of sickle cell anemia
or any of the severe sickling syndromes (including
Sb0, SD and SO-Arab). In essentially every patient
with sickle cell anemia by the age of 2 years, there
will also be evidence of hyposplenism including tar-
gets, acanthocytes, and Howell–Jolly bodies. Patients
with SC disease and any of the sickle thalassemia
compound disorders (including Sb0 and SS-a thalasse-
mia) may have considerably more target cells than
patients with uncomplicated SS. Patients with SC
disease may also demonstrate C crystals in some RBCs
[10]. C crystals and targets by themselves, without
sickle cells, of course may suggest homozygosity for
hemoglobin C.
• Spherocytes have two common causes: immune-mediated
hemolysis and hereditary spherocytosis (HS). Some patients
with HS will demonstrate occasional ‘mushroom cell’
or ‘pincer cell’ variants: these cells resemble sphero-
cytes with mirror-image indentations, resulting in an
appearance similar to a button mushroom. RBC mor-
phology is not usually very helpful in differentiating
immune hemolysis from HS: further testing (such as
direct antiglobulin testing and flow cytometry [11])
may be required. It should be noted that spherocytosis
may also be seen in neonates with gram-negative sepsis
and in patients with thermal burns, as well as in other
hemolytic anemias including G6PD deficiency.
• Elliptocytosis is most commonly due to iron deficiency
or hereditary elliptocytosis (HE). Although there are
several other causes of elliptocytosis, as a practical
matter if iron deficiency is excluded then elliptocytosis
is most likely due to HE. Parents with typical HE may
have newborns with a much more abnormal pheno-
type, featuring severe microschistocytosis as well as
elliptocytosis. These infants may have either heredi-
tary elliptocytosis with infantile poikilocytosis (HEIP)
or hereditary pyropoikilocytosis (HPP) [12]. In South
East Asian ovalocytosis (SEAO), the elliptocytes show
a transverse (as opposed to longitudinal) zone of cen-
tral pallor, or two zones of pallor separated by a trans-
verse bar of cytoplasm, or even a zone of central
pallor divided into two or three spokes like the open
spaces on a sleigh bell. SEAO is considered hemato-
logically benign, although there is a suggestion that
it may be responsible for transient anemia in the
newborn period [13].
• Schistocytes generally reflect intravascular hemolysis.
When seen with thrombocytopenia, schistocytes sug-
gest microangiopathic hemolytic anemia (MAHA), a
group of conditions consisting primarily of thrombotic
thrombocytopenic purpura (TTP), hemolytic uremic
syndrome (HUS), and disseminated intravascular
coagulopathy (DIC). Morphology is not useful in dif-
ferentiating among these three conditions, nor among
their subtypes (such as congenital vs. acquired TTP or
typical vs. atypical HUS). Morphology is also unreli-
able in predicting the severity of a case of MAHA: a
patient with more schistocytes is not necessarily ‘more
sick’ than a patient with fewer schistocytes. There are
other important causes of schistocytosis, including
vasculitis, intracardiac hemolysis (e.g., due to a septal
defect or prosthetic cardiac valve), thermal burn,
march hemoglobinuria, the HELLP syndrome in preg-
nancy, and the Kasabach–Merritt phenomenon in
infants. All of these lesions share the common patho-
genetic step of extrinsic mechanical injury to the red
blood cell.
Many hemolytic anemias show multiple poikilo-
cytes: G6PD deficiency, for example, often shows not
only bite and blister cells but also schistocytes and
spherocytes. The RBC morphology may not so much
suggest a single diagnosis as several relevant avenues
for clinical and laboratory follow-up. A patient with
bite cells and spherocytes may benefit from G6PD
screening and a direct antiglobulin test, for example.
This problem is particularly notable in neonates, in
whom the usual hemolytic morphologies may not be
clearly evident. Neonatal hemolysis may lead to a
very broad range of poikilocytosis, without the same
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 J. FORD | RED BLOOD CELL MORPHOLOGY 357

‘classic’ patterns as are relied upon in adults: oxidative
hemolysis, for example, may lead to more schistocyto-
sis than bite/blister cells. The morphologic differential
diagnosis for hemolysis in a neonate must therefore
be broader than in an adult.
Morphology in the assessment of macrocytic anemia
The usual approach to macrocytosis is to differentiate
between megaloblastic and nonmegaloblastic causes:
megaloblastosis is seen with B12 and folate deficiency,
MDS and CDA, HIV infection, and rare inborn errors
of metabolism, while nonmegaloblastic causes include
liver and thyroid disease, alcohol, Down syndrome,
aplastic anemia, and reticulocytosis. Medications can
be responsible for both megaloblastic and nonmega-
loblastic anemia, while RBC agglutination may lead to
spurious macrocytosis.
Red blood cell morphology usually plays a small
but important role in this differentiation of megalob-
lastic from nonmegaloblastic causes. Important preli-
minary findings include agglutination, polychromasia
(reticulocytosis), target cells (liver disease or alcohol),
and a dual population (MDS or post transfusion).
Oval macrocytosis and severe macrocytosis (e.g.,
>115 fL) are both classically found in megaloblastic
anemia, while round macrocytosis is seen in non-
megaloblastic anemia. Circulating nRBCs may show
dysplastic features suggesting megaloblastic change:
that is, large immature nuclei within mature red
cytoplasm.
In many patients with macrocytic anemia, the RBC
morphology is quite bland: for example, marrow fail-
ure (e.g., Diamond–Blackfan anemia, idiopathic aplas-
tic anemia, etc.) may produce morphologically
unremarkable RBCs.
CONCLUSION
The review of red blood cell morphology is a critical
step in the evaluation of a patient with anemia. It can
be very useful in evaluating microcytic, normocytic,
and macrocytic anemias and is especially helpful in
the work-up of patients with hemolysis. Assessment
of RBC morphology can be the best tool for laboratory
hematology professionals to recommend clinical and
laboratory follow-up in a patient with anemia and to
select the right tests for definitive diagnosis.

REFERENCES
1. Cornbleet J. Spurious results from auto-
mated hematology cell analyzers. Lab Med
1983;14:509–14.
2. Zandecki M, Genevieve F, Gerard J, Godon
A. Spurious counts and spurious results on
haematology analysers: a review. Part II:
white blood cells, red blood cells, haemo-
globin, red cell indices and reticulocytes.
Int J Lab Hematol 2007;29:21–41.
3. Ford J. Approach to disorders of red blood
cells. In: Non-neoplastic hematopathology
and infections, 1st edn. Cualing HD, Bharg-
ava P, Sandin RL (eds). Hoboken: Wiley-
Blackwell, 2012: 45–64.
4. Lockitch G, Berry B, Roland E, Wadsworth
L, Kaikov Y, Mirhady F. Seizures in a
10-week-old infant: lead poisoning from an
unexpected source. Can Med Assoc
J 1991;145:1465–8.
5. Demir A, Yarali N, Fisgin T, Duru F, Kara
A. Most reliable indices in differentiation
between thalassemia trait and iron defi-
ciency anemia. Pediatr Int 2002;44:612–16.
6. Beyan C, Kaptan K, Ifran A. Predictive value
of discrimination indices in differential diag-
nosis of iron deficiency anemia and beta-thal-
assemia trait. Eur J Haematol 2007;78:524–6.
7. Vallance H, Ford J. Carrier testing for auto-
somal-recessive disorders. Crit Rev Clin Lab
Sci 2003;40:473–97.
8. Skogerboe KJ, West SF, Smith C, Terashita
ST, LeCrone CN, Detter JC, Tait JF. Screen-
ing for alpha-thalassemia. Correlation of
hemoglobin H inclusion bodies with DNA-
determined genotype. Arch Pathol Lab Med
1992;116:1012–18.
9. Fessas P. Inclusions of hemoglobin in ery-
throblasts and erythrocytes of thalassemia.
Blood 1963;21:21–32.
10. Diggs LW, Bell A. Intraerythrocytic hemo-
globin crystals in sickle cell – hemoglobin C
disease. Blood 1965;25:218–23.
11. King MJ, Behrens J, Rogers C, Flynn C,
Greenwood D, Chambers K. Rapid flow
cytometric test for the diagnosis of
membrane cytoskeleton-associated haemo-
lytic anaemia. Br J Haematol 2000;111:
924–33.
12. Gallagher PG. Hereditary elliptocytosis:
spectrin and protein 4.1R. Semin Hematol
2004;41:142–64.
13. Laosombat V, Viprakasit V, Dissaneevate S,
Leetanaporn R, Chotsampancharoen T,
Wongchanchailert M, Kodchawan S, Thong-
noppakun W, Duangchu S. Natural history
of Southeast Asian Ovalocytosis during the
first 3 years of life. Blood Cells Mol Dis
2010;45:29–32.

© 2013 Blackwell Publishing Ltd, Int. Jnl. Lab. Hem. 2013, 35, 351–357