Original Article

DOI: 10.21276/APALM.1303

HbA2 and Fetal haemoglobin in The Diagnosis of

Thalassemia and Hemoglobinopathies
Sandhya Venkatachala1* and Manjula Rajendran2
Dept. of Pathology, Apollo Hospitals Bangalore, India
1

2
Dept. of Pathology, Madurai Medical college, Madurai, India

ABSTRACT
Background: Hemoglobin (Hb) disorders which include hemoglobinopathies and Thalassemia affect 7% of the world population. Capillary
electrophoresis is useful for screening and follow up of Hb disorders .
Aim: To evaluate HbA2 and HbF (fetalhemoglobin) in the diagnosis of Thalassemia and hemoglobinopathies.
Material and Methods: 100 consecutive Capillary Hemoglobin electrophoresis done as a part of screening programme for Hb disorders
from Jan2016 to june 2016 was included in the study. Children <1 yr of age and individuals with recent blood transfusion were excluded .
Hb, RBC count and MCV were recorded.
Results: Of the 100 Hb electrophoresis performed, 57 normal and 43 abnormal patterns were seen. Among the abnormal Hb patterns, β
thalassemia trait (βTT) was the most common constituting 58.2% followed by Sickle cell (HbS) trait(11.7%), HbE trait(9.3%) and HbE/ β
Thalassemia (7.0%). The HbA2 levels in normal, βTT, Sickle cell trait , HbE trait and HbE/ β thalassemia were 2.12%(SD 0.5), 4.9%(SD
0.62), 3.28%(SD 0.43), 3.98%(SD 0.67) respectively . The difference in HbA2 were significant (p value <0.0001).The difference in HbA2
levels between HbE trait and HbE disease was also significant (p value 0.036).Based on the HbF levels Sickle cell hemoglobinopathy was
further classified.
Conclusion: The difference in HbA2 levels in normal subjects, Thalassemia and hemoglobinopathies are statistically significant. The
percentage of HbF in sickle cell gives information about coexisting hemoglobin disorder. In HbEhemoglobinopathy, HbA2 along with HbF
identifies a specific group HbE/ β Thalassemia which often needs clinical intervention.

Keywords: Hemoglobin A2, Fetal Haemoglobin, Hemoglobinopathy, Thalassemia, Capillary Electrophoresis

Introduction to evaluate HbA2 andHbF in the diagnosis of Thalassemia

Hemoglobin (Hb) disorders are a frequent genetic disease and hemoglobinopathies .
affecting 7% of world population.[1] Hemoglobinopathies
Material and Methods
result from a structural defect in the globin chain where
100 consecutive cases of Hb electrophoresis done as a part
as Thalassemias are due to a quantitative defect in the
of screening programme for hemoglobin disorders from
globin chain production.They are detected in populations
Jan 2016 to June 2016 were included in the study. Children
during programmes run for prevention of Hbdisorders or
less than one year of age and individuals with a history of
in patients with clinical suspicion or familial history of
blood transfusion in the past three months were excluded in
Hb disorder. Capillary electrophoresis has been used for
the study. Hemoglobin electrophoresis was done by Sebia
precise and accurate first line screening and follow up Hb
Minicap Flex piercing capillary electrophoresis method.[2]
disorders.[2] DNA or protein analysis are recommended K- EDTA anticoagulated blood was used. Hb, RBC count
for a definitive diagnosis in difficult cases. HbA2 and and MCV were recorded in each case. Reference range by
HbF along with the specific abnormal band, point to the Sebia CE-HbA 96.8% to 97.8% and HbA2- 2.2% to 3.2% .
diagnosis of Hb disorder. Few studies have separately
evaluated HbA2andHbF in Hb disorders.[3,4] Capillary Results
electrophoresis(CE) and high performance liquid Of the 100 Hb electrophoresis performed 57 showed
chromatography (HPLC) were used respectively for normal pattern (Fig 1) with HbA ranging between 97.1%
hemoglobin separation respectively in these studies. But and 99%( Mean 97.85,SD 0.52) and HbA2 between 1%
both HbA2 and HbF have not been evaluated together in and 3.6% (mean 2.12,SD 0.5). HbF of 0.5% was seen
Hb disorders by CE. So the present study was undertaken in one of the cases. Hb, RBC count and MCV ranged

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Venkatachala et al. A-447

between 5gm% to 15.8gm% ,4.15to5.4x1012 /L and 70-118 fl (SD 1.1). One case each of Sickle cell disease(SCD)
femtolitres respectively. The lowest HbA2 observed was (Fig3B) , heterozygous HbS/ β thalassemia( Fig 4A)
1% which corresponded to Hb of5 gm% and MCV of 70 and heterozygous HbS/ Heriditary persistence of fetal
fl. Marginally elevated HbA2 of 3.6% was seen in the case hemoglobin (HPFH) (Fig 4B) were seen . HbF of 20.6%,
with MCV of 118 and Hb of 10gm%. 9.0% and 32.8% were seen in these cases respectively. In
addition heterozygous HbS/HPFH showed elevated HbA2
The 43 abnormal electrophoresis pattern included levels of 8.4%.
26 cases of Thalassemia ,8 cases each of sickle cell
hemoglobinopathy and HbE hemoglobinopathy, one case HbE hemoglobinopathy included eight cases (table 4).
of HbD hemoglobinopathy. Furthur classification and HbE trait was the most common .Charateristic HbE band
distribution of cases are shown in table 1. was seen (Fig5A) in addition to HbA and HbA2. HbA,
HbE and HbA2 were 79.95% (SD 19.6) , 22.9(SD 2.8)
Thalassemia out numbered hemoglobinopathies. The most and 3.98 (SD 0.67). HbF of 0.6% was seen in one of the
common abnormal Hb pattern was β thalassemia trait (βTT) cases . The mean RBC count and MCV were 4.99x1012(SD
(Fig2A ). An elevated HbA2 level between 3.8% and 6.2% 0.65) and 76.1fl (SD 1.33).A single case of HbE disease
(4.9, SD 0.62) was observed. HbF was seen in 13 of the was present (Fig5B ).Three cases showed higher HbF of
25 cases and varied between 0.3%to 6%.The mean RBC 11%(SD 1.05) and HbA2 of 4.33(SD 0.15) along with HbE
count and MCV were 5.59 x10 12(SD 0.84) and 64.2 (SD levels of 84.66 (SD 0.97). HbA was nil. They constituted
4.08) (Table 2). A single case of α Thalassemia was seen the double heterozygous HbE/β° thalassemia (Fig 5C)
with HbH band(28.3%) (Fig2B) .HbA of 69.6% , HbA2 of
2.1% were recorded. The Hb, RBC and MCV were 13gm/ HbD hemoglobinopathy was comprised of a single case
dl, 4.8x1012 and 83 fl respectively. of HbD trait as shown in Fig6 with HbD of30.8%, HbA
of 66.1% and HbA2 of 3.1% . The Hb, RBC and MCV
The details of eight cases of Sickle cell hemoglobinopathy were 10gm/dl, 4.99x1012 and 66.7fl respectively. MCV
are shown in table 3. The five cases of SCT showed HbS in the ascending order in HbS/ β thalassemia, HbE/ β
band (Fig3A ) in addition to HbA. Average HbS was thalassemia, HbE disease, βTT, HbD, SCD, HbE trait, SCT
30.46 (SD7.2) and HbA2 was 3.28 (SD 0.43). HbF was and α Thalassemia were 52.3fl,62.5fl (SD 1.5),63.4 fl, 64.2
seen in two cases amounting to 0.6% and 1.8%. The mean fl (SD 4.08), 66.7fl , 70fl , 76.1fl (SD 1.33), 81.8 fl (SD 1.1)
RBC count and MCV were 4.7x1012 (SD 0.51) and 81.88 and 83fl respectively.
Table 1: Shows the distribution of Abnormal hemoglobins
Abnormal hemoglobin electrophoresis patterns No. of cases (n=43) Percentage
Thalassemia :
α Thalassemia (HbH) 1 2.3
β Thalassemia trait 25 58.2
Sickle cell hemoglobinopathy :
Sickle cell disease 1 2.3
Sickle cell trait 5 11.7
Double heterozygous Sickle cell/ β thalassemia 1 2.3
Compound heterozygous HbS/HPFH 1 2.3
HbE hemoglobinopathy 1 2.3
HbE disease 4 9.3
HbE trait 3 7.0
HbE/ β Thalassemia
HbD hemoglobinopathy 1 2.3
Table 2: Shows electrophoresis pattern, Hemoglobin, RBC count and MCV in Beta Thalassemia Trait.
HbA% HbA2% HbF% Hb(gm/dl) RBC(x1012/L) MCV(fl)
94.3 5.7 --- 10.4 5.2 64.3
94.6 5.4 ---- 11.9 6.16 62.5
88.7 4.8 6.5 8.6 3.68 75.5
95.1 4.9 ---- 12.2 6.68 59.3
3.4 4.7 1.9 10.1 5.22 62.7

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A-448 HbA2 and HbF in Hemoglobinopathies

HbA% HbA2% HbF% Hb(gm/dl) RBC(x1012/L) MCV(fl)

96.4 3.8 ---- 8.4 5.3 64.3
95.5 4.5 ---- 8.7 4.5 60.5
95.1 4.5 0.9 11 6.4 59.5
94.7 5.3 ---- 9.8 4.83 60.6
94.6 5.1 0.3 12.5 6.5 62.9
96.2 3.8 ---- 8.9 4.1 69.7
93.1 6.2 0.7 10.3 5.89 58
94.7 4.8 0.5 9.6 5.28 60.3
95.8 3.8 0.5 11.6 4.85 77
92.9 4.5 2.6 13.1 6.18 68.8
95.1 4.9 ----- 12.4 6.6 59.2
94.2 5.5 0.3 12.9 6.61 63.6
94.5 5.1 0.4 11.5 5.4 69.6
95 5 ---- 8.9 4.64 64
94.6 5.4 ---- 10.4 5.21 66
93.5 5.7 0.8 11 6.3 63
94.8 5.2 ---- 12.5 6.6 64
94.3 5.2 0.5 9 6 68
94.7 5 ----- 10.5 5.8 63
95.5 4 0.5 10.8 5.9 62.2
Table 3 : Shows electrophoresis pattern, Hemoglobin, RBC count and MCV inSickle cell Hemoglobinopathy :
Sickle cell hemoglobinopathy
HbA% HbA2% HbS% HbF% Hb(gm/dl) RBC(x1012/L) MCV(fl)
(8 cases )
Sickle cell disease(1) ---- 2.8 76.6 20.6 8.3 3.81 70
60.6 3.7 35.7 --- 11.1 4.3 80.4
57.7 2.7 39.6 ---- 10 4.8 82.6
Sickle cell trait (5) 74.9 3.2 21.3 0.6 11.5 5.5 82
69.1 3.1 27.8 ---- 11 4.7 81.2
66.6 3.7 27.9 1.8 10.5 4.2 83.2
Double heterozygous Sickle cell/
5.7 8.4 76.9 9.0 5.2 3.19 52.3
βThalassemia (1)
Compound heterozygous HbS/
--- 1.3 65.9 32.8 10.2 3.27 91.2
HPFH ( 1)
Table 4: Shows electrophoresis pattern, Hemoglobin, RBC count and MCV in HbE hemoglobinopathy :
HbE hemoglobinopathy (8) HbA HbA2 HbE HbF HB RBC MCV
HbE disease (1) --- 5.2 94.8 --- 8.5 4.2 63.4
71.1 4 24.9 --- 11.7 4.8 75.4
72.3 3.6 24.1 --- 14.3 5.9 75
HbE trait (4)
72.7 3.4 23.9 --- 12.1 4.36 78
75.7 4.9 18.8 0.6 11.9 4.9 76
--- 4.5 84.9 10.6 9 4.7 61
HbE/ β Thalassemia (3 ) --- 4.2 83.6 12.2 9.2 4.8 64
--- 4.3 85.5 10.2 9.7 5.2 62.5

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Venkatachala et al. A-449

Fig. 1: Shows normal pattern of hemoglobin electrophoresis.

Fig. 2: A Shows elevated HbA2 in beta thalassemia trait. B Shows HbH band in alpha thalassemia. 

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A-450 HbA2 and HbF in Hemoglobinopathies

Fig. 3: A Shows HbS in addition to HbA in sickle cell trait. B Shows HbS with HbF in the absence of HbA in Sickle cell disease.

Fig. 4: A Shows elevated HbA2, HbF and HbS in heterozygous HbS- beta thalassemia. B Shows elevated HbF in the presence
of HbS in heterozygous HbS-HPFH.

Fig. 5: A Shows HbE in addition to HbA in HbE trait. HbA2 is increased . B Shows HbEonly withelevated HbA2 in HbE disease
.C Shows elevated HbF and HbA2 in addition to HbE in HetrozygousHbE-beta thalassemia.

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Venkatachala et al. A-451

Fig. 6: Shows HbD in addition to HbA and HbA2 in HbD trait.

Discussion 0.5% HbF seen in one of our cases are in accordance with
No screening programme is 100% specific and sensitive normal adult HbF levels of <1%.[4]
for the diagnosis of Hb disorders. A combination of βTT was the most common abnormal Hb followed by HbS
haematological, biochemical and molecular analysis trait, HbE trait and HbE/ β thalassemia. This is comparable
including Hb separation on CE, globin chain separation with other studies.[8,9,10,11]HbS trait was the second most
on reverse phase chromatography, sequencing of globin common Hb disorder in the present study while HbE trait
genes, detection of globin gene deletions by PCR and occupied the second position in other studies across the
measurement of δ:β globin chain ratios using spectrometry Indian population.[9,10] However Balgir and others have found
would provide a complete work up for a Hb disorder.[5] Sickle cell anemia more common in Orissa, Eastern India.
However Assessment of HbA2 and HbF along with specific
bands play a vital role in the diagnosis of Hb disorders. CE HbA2 levels in βTT was 4.9% (SD 0.62) (range 3.8%to
separates the Hb bands with sufficient clarity compared to 6.2%) . A range of 3.5% to5.5% and 5.23%(SD 0.63) have
the other methods of electrophoresis.[2,6] been seen in otherstudies using capillary electrophoresis.
[3,5]
HbA2 levels upto 6.9% have been observed.[12] High
Mean HbA2 levels of 2.12% (SD 0.5) seen in the 57 HbA2 levels over 6.5% characterise a subgroup of β
normal Hb electrophoresisis below the mean HbA2 thalassemia caused by deletions that remove the regulatory
seen in βTT (4.9%) , HbE hemoglobinopathy( HbE
elements in the promoter region of β gene. These are often
trait -3.98%,HbE/β thal-4.33%) and SCT(3.28%). This
accompanied by increase in HbF[5]An increase in HbF>1%
difference was statistically significant ( p<0.0001). A low
in a healthy adult points to a genetic or acquired pathology.
HbA2 of 1% was seen in a case of Iron deficiency anemia [4]
HbF of 2% and 6.5% were seen in the present study in
in the present study . Mosca and others have reported
two cases of βTT . Polymorphisms of BCL11A gene has
similar findings and have attributed the decreased HbA2
been associated with high levels of HbF in normal persons
levels in Iron deficiency to the inhibition of δ globin
, β thalassemia and in sickle cell anemia.[4,13] Pernicious
synthesis by low iron levels and to the preferential
anemia, aplastic anemia, chronic renal failure and Diabetes
binding of β to α chain rather than δ chains. One of the
mellitus are some of the acquired causes of elevated HbF.[4]
cases with MCV of 118fl showed HbA2 level of 3.6%
and was a case of VitB12 deficiency. Megaloblastic HbA2 levels in sickle cell trait was( 3.28 % ,SD 0.43)
anemia and hyperthyroidism elevate HbA2 levels .[7] A significantly more than normal (2.12, SD 0.5) (p<0.0001)

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A-452 HbA2 and HbF in Hemoglobinopathies

Mean HbA2 levels 0.2%to 1% higher than normal were was no HbA these cases probably represented HbE/β°
noted in sickle cell trait by Craver R and others.[12]The thalassemia. Praising and others have similarly concluded
modest increase in HbA2 in SCT is due to the increased that a combination of HbA2 levels > 6% and HbF varying
avidity of normal δ chains for α chains compared to HbS β from 5%to 15% would differentiate HbE/β thalassemia
chain.[14]No significant difference in HbA2 between normal from HbE disease.[18] Identifying HbE/β Thalassemia
subjects and SCT was recorded by Ajjack and others in their is important since it is clinically associated with a more
study of sickle cell hemoglobinopathy by CE who found severe disease compared to HbE trait and HbE disease.[17]
a HbS of 39.3% (SD 13.8)in SCT.[15]This is comparable
α Thalassemia and HbD were the less common Hb
to HbS of 30.46% (SD 14.4) seen in the present study .
disorder in the present study similar to the other studies
Studies show mean HbF levels of 1.4% and 2.14% in SCT.
by Vani and others who reported 1.6% and 0.7% of these
[13,15]
In the present study, fetal hemoglobin was identified
cases respectively.[8] The predominant feature in HbH
in two of the five cases(mean 1.2%)
disease is the presence of HbH ranging between 0.8%
Fetal Hb is the major modulator of hematological and to 40% with normal or slightly reduced HbA2.[19]In the
clinical features in sickle cell disease . HbF levels declines present study, HbH of 28.3% and HbA2 of 2.1% were
at a lower rate in sickle cell disease compared to normal observed. HbD common in Punjab also known as HbD-
individuals stabilising at 5 yrs of age at 5%to 8%.[13] Los Angels can be inherited in heterozygous state with
However some patients with sickle cell hemoglobinopathy HbA as in the present study and in the rarest form of
have high levels of HbF. This includes 3 groups of sickle homozygous state- HbDD. Association with HbS and
cell patients – sickle cell disease with Senegal/Saudi-Indian Thalassemia also occur.[20].MCV was lower in HbE/ β
haplotype or BCL11A polymorphisms and compound Thalassemia compared to β Thalassemia, HbE trait and
heterozygous for HbS/HPFH. HbF in the former group SCT in the ascending order . A similar pattern has been
varied between 11% to 20%, while HbF levels of 30% described by Vani and others.[8] The other Hb disorders
(SD 2) was associated with the latter group (HbS/HPFH). were single cases inadequate for comparison.
[16]
Furthur in HbS/HPFH a pancellular distribution of HbF
is a characteristic feature. In the present study two cases Conclusion
showed high HbF levels of 20.65 and 32.8% along with Thus the quantification of HbF differentiates the three
HbS in the absence of HbA and were designated as Sickle groups of sickle cell hemoglobinopathy patients, those of
cell disease and compound heterozygous HbS/HPFH Senegal/Saudi Indian haplotype, BCL11A polymorphisms
respectively. Elevated HbF along with elevated HbA2, Vs heterozygous HbS/HPFH . Furthur the presence of
HbS and HbA is double heterozygous HbS/β Thalassemia , elevated HbA2 and HbF in HbE hemoglobinopathy
a single case in the present study. identifies HbE/β Thalassemia , an entity needing clinical
intervention. Assesment of HbA 2 and HbF in conjunction
HbE is the second common hemoglobinopathy after with specific abnormal Hb band and HbA thus plays a
sickle cell hemoglobinopathy in South-east Asia which pivotal role in the diagnosis of hemoglobinopathy and
includesNorth eastern India, Thailand, Malaysia, Nepal, Thalassemia. Quantification of HbA2 and HbF thus
Bangladesh and Vietnam. [17] In the present study, HbE throws light on the pattern of inheritance – homozygous/
hemoglobinopathy accounted for 18.6% abnormal Hb heterozygous / double heterozygous which is confirmed by
similar to Sickle cell hemoglobinopathy. HbE trait was molecular analysis.
more frequent followed by HbE/β Thalassemia and HbE
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*Corresponding author:
Dr. Sandhya.V, D3 -508, L&T Southcity apartment, JP Nagar 7th phase, Arekere MICO layout, Bangalore-560076,India
Phone: +91 9591627364, 080-26554334
Email: [email protected]
Date of Submission : 01.02.2017
Date of Acceptance : 29.05.2017
Financial or other Competing Interests: None. Date of Publication : 31.08.2017

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