Case report

Case report
A Patient with G6PD Deficiency and Falciparum Malaria
* M Nateghpour 1, A Miahipour 1, M Yousefi1, A Mohammadiha 1, Y Fagani 2
1Dept. of Medical Parasitology and Mycology, School of Public Health & Institute of Public Health
Research, Tehran University of Medical Sciences, Iran
2Infections Diseases Ward, Bou-Ali Hospital, Tehran, Iran
(Received 3 Nov 2006; accepted 3Mar 2007)
Abstract
A 20 year old male patient from Afghanistan with a history of G6PD deficiency and clinical manifestations of
malaria referred to Bou-Ali Hospital in Tehran, capital of Iran. Giemsa stained thick blood films revealed an
infection of Plasmodium falciparum with 33700 parasite/μL of blood. The patient was successfully treated
according to malaria treatment guideline.
Key words: G6PD deficiency, Falciparum, Malaria, Iran
Introduction
lucose-6-phosphate-dehydrogenase
(G6PD) is a cytoplasmic enzyme
that is essential for a cells capacity to
withstand oxidant stress. The geographic
correlation of G6PD deficiency distribution
with the endemicity of malaria suggests
that such enzymopathy has risen in
frequency through natural selection by
falciparum malaria.
Motulsky and Allison (1, 2) suggested
that individuals with G6PD deficiency
trait might be more than normally resistant
to falciparum malaria. These authors
and later some others found a notable
correlation between the prevalence of
such enzymopathy of human and the endemicity
of Plasmodium falciparum malaria
in some areas of the world. The suggestion
of such inherent relative resistance
to falciparum malaria in the enzyme
deficient subjects has been supported by
low parasitaemia and low mortality in
G6PD deficient patients (3-5). Nevertheless,
this hypothesis does not seem to
constitute the whole story. Some evidences
have been put forward by the
some researchers (6-8).
Case report
In this report, we introduce a twenty year
old Afghani worker resident in Tehran,
capital of Iran with a history of traveling
to some villages located on the southeast
borderland of Iran, three weeks before to
feel clinical signs. The patient with typical
malaria symptoms (chilliness, fever,
and sweating), headache, and hemoglobinuria
referred to Bou-Ali Hospital in
Tehran. The laboratory analysis of blood
revealed as: G6PD partial deficiency (using
colorimetry and fluorescence activity
methods), WBC 3100/ micro/L, eosinophils
3%, RBC 3.47 million/μl, SGOT 173 IU/L,
G
*Correspondent author: Tel: +98 21 88989130,
E-mail: nateghpourm@sina.tums.ac.ir
M Nateghpour et al: A Patient with G6PD…
44
SGPT 147 IU/L, hemoglobin 10.2 g/dl
and hematocrit 29.6%. Giemsa stained
thick and thin blood films indicated P.
falciparum malaria infection with high
parasitaemia of 33700/ μl. The patient
was successfully treated according to malaria
treatment guideline.
Discussion
Malaria-protection hypothesis of G6PD deficiency
seems to be a conflicting negotiation
between relevant investigators.
While Powell and Brewer (9) showed no
significant difference between corresponding
mean levels of parasitaemia in G6PD
deficient people compared to G6PD normal
individuals, Gilles and co-workers
found that the incidence of G6PD deficiency
in children with sever malaria is
significantly lower than that of control
children (5). In another investigation, 700
children of both sexes from a rural area of
holoendemic malaria (P. falciparum) were
studied (10). The investigators found that
there was no evidence that enzyme-deficient
subjects had any greater resistance
against malaria. In three cross-sectional
studies using IFA and the blue dye, decolorization
G6PD tests by Edrissian et
al. in Hormozgan Province, a malarious
area in southern Iran; different results were
found out. In the first study, the G6PD
deficient individuals had significantly lower
seropositive rate and considerably lower
total geometric mean of reciprocal titers
with P. falciparum antigen as compared
to the G6PD normal subjects, but not in
P. vivax antigen. However, in the second
and third studies no such distinct serological
differences between G6PD deficient
patients with falciparum malaria and
G6PD normal subjects were observed
(11). Our reported case, parasitologically,
was alike to those were found out by Edrissian
et al. in the second and third studies.
Acknowledgements
Authors would like to thank Mrs A Motavali
Haghi and staffs of medical lab of
Bou-Ali Hospital for their technical assistance.
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