S H O RT C O M M U N I C AT I O N
JIACM 2005; 6(1): 42-4
Detecting Patients with
Glucose-6-Phosphate Dehydrogenase Deficiency
GA Oni*, RAE Johnson*, OO Oguntibeju**
Abstract
Glucose-6-phosphate dehydrogenase (G-6-PD) deficiency was screened in male (n = 150) and female (n = 100) patients at Obafemi
Awolowo University Teaching Hospital Complex (OAUTHC) lle-lfe, Nigeria, using a simple, reliable and cost-effective qualitative
method. Forty (26.7%) of the male patients and 35 (35%) of the female patients were G-6-PD deficient. The prevalence rate of G-6PD deficiency was significant (p < 0.05) between genders. Overall, the prevalence rate of G-6-PD deficiency in this population was
high, and this is of great concern. The results suggest quantitative and genetic analysis with a larger sample size.
Keywords : Glucose-6-phospate dehydrogenase, Deficiency, Methaemoglobin reduction test, Out-patients.
Introduction
Research reports1-3 have shown that glucose-6-phosphate
dehydrogenase (G-6-PD) deficiency is a frequent and a Xchromosome-linked enzyme abnormality. As G-6-PD plays
an important role in maintaining erythrocytes, G-6-PD
deficiency could possibly result in acute haemolysis after
exposure to various oxidative conditions, including viral
and bacterial infections, medications and fava beans
(favism)3. An association has been observed between
prevalence of G-6-PD deficiency and malaria, especially
in tropical countries such as Nigeria4.
The glucose-6-phosphate dehydrogenase enzyme
catalyses the oxidation of glucose-6-phosphate to 6phosphogluconate, while simultaneously reducing the
oxidised form of nicotinamide adenine dinucleotide
phosphate (NADP+) to nicotinamide adenine dinucleotide
phosphatase (NADPH). It is interesting to note that NADPH
maintains glutathione in its reduced form. It is also known
that red blood cells depend upon glucose-6-phosphate
dehydrogenase activity since it is the only source of
NADPH that protects the cells against oxidative stress2,5.
Glucose-6-phosphate dehydrogenase deficiency is
believed to affect about 400 million people globally5. The
rate of prevalence is high among Africans and Asians3.
Reports showed that severity resulting from G-6-PD
deficiency varies significantly between races with more
severe deficiency variant occurring in the Mediterranean
population, and the milder form in the African population6.
Available evidence demonstrates that majority of patients
are asymptomatic while few present with neonatal
jaundice, history of infection, or drug-induced haemolysis.
In some cases, gallstone formation may be a prominent
feature, and splenomegaly may be present in others3.
Haemolytic anaemia due to G-6-PD deficiency could
be severe and even life-threatening7. The screening of
patients for G-6-PD deficiency is not a common
practice in the health-care delivery services of most
African countries. However, there is a need for regular
screening of patients to be able to establish patients
with G-6-PD deficiency, since patients may harbour
illnesses or receive drugs that could precipitate
haemolytic crisis. Information on the prevalence of
persons with G-6-PD deficiency is very scanty. Due to
paucity of information on G-6-PD deficiency, it is
important to detect and inform G-6-PD-deficient
persons in and from areas in which malaria and
bacterial infections are pandemic before exposing
them to oxidative stress in order to avoid acute
haemolytic attack. It is against this background that
we examined G-6-PD deficiency among male and
female patients attending the out-patient department
of the Obafemi Awolowo University (OAU) Teaching
Hospital Complex, Ile-Ife, Nigeria, using a comparatively
simple and cost-effective method, with shorter
incubation time.
* School of Medical Laboratory Sciences,
Obafemi Awolowo University Teaching Hospital (OAUTH) Complex, Ile-Ife,Nigeria.
** School of Health Technology, Central University of Technology, Free State, Bloemfontein 9300, South Africa.
Subjects and Methods
PD deficiency than their male counterparts.
A total of 250 (male, n = 150; female, n = 100) patients
(aged 18 - 45 years) attending the outpatient department
of the OAUTH Complex, Ile-Ife, Osun State, Nigeria were
recruited into the study. The protocol of the study was
explained to the patients and verbal informed consent
was obtained from each patient before inclusion into the
study. Patients with acute viral and bacterial infection, or
chronic illnesses such as diabetes, or patients who had
blood transfusion four weeks before the time of
recruitment or those with sickle-cell disease were not
included in this study. Five ml of blood was collected from
each patient via vene-puncture into sterile ACD sample
tubes and tests were performed within one hour of
collection.
The current study revealed the prevalence rate of persons
with G-6-PD deficiency following qualitative screening.
The outcome of this study provided useful clinical and
survey information for the patients who participated in
the study, as well as the health institutions and
professionals, especially in an environment where malaria
is endemic, viral and bacterial infections are common, and
self-medication is practised. The study revealed that 26.7%
of the male patients were deficient in contrast to 35% of
females. This figure is higher than the percentage reported
by Luzzatto and Testa7 among same ethnic group. Both
authors reported 22% G-6-PD deficiency in the studied
population without gender differentiation. The prevalence
of G-6-PD deficiency was significantly (p < 0.05) higher in
the female group. These differences in percentage
prevalence of G-6-PD deficiency observed in this study
and that of Luzzatto and Testa7 may be related to the level
of anaemia, inter-assay variation, methodology and the
problem of self-medication. The difference according to
gender is similar to that reported by Owa and
Osanyintuyi6.
The methaemoglobin reduction test was used and the
principle states that sodium nitrite converts haemoglobin
to methaemoglobin. When no methylene blue was added,
methaemoglobin persisted, but incubation of the blood
sample with methylene blue allowed stimulation of the
pentose phosphate pathway in persons with normal G-6PD levels. The methaemoglobin was reduced during the
incubation period. However, in G-6-PD deficient persons,
the blockage in the pentose phosphate pathway
prevented this reduction. With this test, the blood sample
from a normal person gave a clear red colour similar to
that in the normal reference tube, whereas blood sample
from a deficient person indicated a brown colour. The
detailed technique of methaemoglobin reduction test
applied in the current study is described in a paper by
Owa and Osanyintuyi6.
Although, the relationship between the prevalence rate
of G-6-PD deficiency and malaria endemicity was not
examined in this study. However, a previous study
reported by Iwat et al (2003) suggested that such a
relationship exists. This study is limited by its qualitative
and cross-sectional nature. Nonetheless, it is simple, costeffective, and less time-consuming, and since the method
does not require electricity, it could be effectively adopted
in communities with inconsistent electricity.
Results and discussion
References
The result of this study was reported as normal or deficient
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male, representing 60% of the studied population, while
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showed that 40 of the 150 male patients were G-6-PD
deficient (26.7%), while 110 of the same group were
normal (73.3%). In the female group, 35 of the 100 patients
were G-6-PD deficient (35%), while 65 of the same gender
were normal (65%). The result indicated that the female
patients showed higher prevalence rate (p < 0.05) of G-6-
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Journal, Indian Academy of Clinical Medicine
Vol. 6, No. 1
January-March, 2005