European Review for Medical and Pharmacological Sciences
2013; 17: 994-995
Protective role of G6PD deficiency in
poisoning by aluminum phosphide;
are there possible new treatments?
Corresponding Author: Nasim Zamani MD; e-mail: email@example.com
Aluminum phosphide (AlP) is an insecticide and rodenticide available in Asian markets and is a major
cause of death in many countries including Iran. No definite treatment has yet been established for it. We
suggest a possible treatment method for AlP poisoning based on two cases available in the literature.
A 24-year-old known case of G6PD deficiency was referred to us two days after ingestion of one AlP
tablet. His poisoning had been conservatively managed. After two days, he referred again with icter with-
out ingestion of any oxidant. He was conscious, febrile, icteric and had sinus tachycardia. Lab tests
showed normal ABG, electrolytes, PT and PTT, negative Coombs’ test results, and normal hepatobiliary
ultrasonography. Normal WBC, platelet count and hemoglobin of 9.3 mg/dL dropping to 3.9 mg/L were
documented. Hemoglobinuria was detected. By the next day, he improved and was discharged complete-
Another case of G6PD deficiency exposed to ALP2was a 22-year-old presenting with nausea, epigastric
distress, vomiting and cola-coloured urine after ingestion of one ALP tablet. He denied taking any other intox-
icant. On admission, he was conscious, icteric, and normotensive with mild tachycardia. Urine sample was
deep brown. ABG and renal tests were normal. Liver function tests showed unconjugated hyperbilirubi-
naemia. A G6PD assay obtained showed deficient activity. He was conservatively amanged, improved, and
The interesting point is that with a total mortality rate of almost 71% for rice tablet3, there are two cases
of ALP poisoning presenting with definite signs and symptoms of this fatal toxicity and survive. Is it possible
that these patients’ common feature – G6PD deficiency – has a role in their outcome?
G6PD deficiency is the most common enzymatic disorder of RBCs in humans4. It causes sudden de-
struction of erythrocytes in contact with fava beans, several medications, toxins and poisons, and meta-
bolic abnormalities5. G6PD deficiency, as known, has a protective effect against falciparum malaria attrib-
uted to the vulnerability of the parasites to the oxidative stress induced by G6PD deficiency6. It was sug-
gested that the parasite oxidized the NADPH in RBC of the host to maintain its own glutathione (GSH) in
reduced form. It was then hypothesized that G6PD-deficient erythrocytes would protect against fulminant
malaria infection because utilization of NADPH by both the host erythrocyte and malaria parasite would
overwhelm the limited ability of the G6PD deficient red cells to regenerate NADPH and the resultant
decrement in GSH would lead to oxidant-induced hemolysis. In fact, it seems that the oxidative stress
caused by a toxin in a G6PD-deficient patient lyses the RBCs and inhibits further dissemination of the
parasites. Oxidation of the host RBCs does not let the parasite to keep its own glutathione in reduced
form and this damages the parasite6.
On the other hand, the theory of oxidative stress and extra-mitochondrial release of free oxygen radi-
cals has been suggested as a potential cause of ALP poisoning and death7. It seems that if we can pre-
vent the oxidative stress caused by the phosphine gas, we can save the patient. The interesting point is
that in two patients with G6PD deficiency and extensive hemolysis, the patients survived. This may mind
that in these patients, the extensive RBC lysis has prevented the disseminated oxidative stress distribut-
ing by the phosphine-damaged RBCs. The other interesting idea is that can we possibly prevent further
oxidative stress in ALP-poisoned patients by routes of extracorporeal elimination of the damaged RBCs?
Can, for instance, blood exchange prevent the disseminated oxidative stress that is induced and distrib-
uted in the body by damaged RBCs? This may need further studies evaluating such idea in ALP-poi-
Conflict of Interest
References Download full-text
1) FARNAGHI F, OWLIAEY H, HASSANIAN-MOGHADDAM H, SHADNIA S, MONTAZMANESH N, MEHRPOUR O, ZAMANI N.
Intravascular haemolysis due to Glucose‐6‐Phosphate dehydrogenase deficiency in a patient with aluminum phos-
phide poisoning. Accepted for publication in Indian J Forensic Sci Toxicol 2013.
2) SRINIVAS R, AGARWAL R, JAIRAM A, SAKHUJA V. Intravascular haemolysis due to glucose-6-phosphate dehydrogenase
deficiency in a patient with aluminium phosphide poisoning. Emerg Med J 2007; 24: 67-68.
3) MEHRPOUR O. Hyperglycemia in acute aluminum phosphide poisoning as potential prognostic factor. Hum Exp
Toxicol 2006; 27: 591-595.
4) GALDER BE. Glucose 6 Phosphate Dehydrogenase deficiency and related disorders of hexose monophosphate shunt
and glutathione metabolism. In: Lee GR, Foerster J, Lukens J, et al, eds. Wintrobe’s Clinical Hematology, 10th edn.
William & Wilkins, 1999.
5) TRIPATHY V, REDDY BM. Present status of understanding on the G6PD deficiency and natural selection. J Postdrag
Med 2007; 53: 193-202.
6) GREENE LS. G6PD deficiency as protection against falciparum malaria: an epidemiologic critique of population and ex-
perimental studies. Yearbook of Physical Anthropology, 1993.
7) MEHRPOUR O, JAFARZADEH M, ABDOLLAHI M. A systematic review of aluminium phosphide poisoning. Arh Hig Rada
Toksikol 2012; 63: 61-73.
N. Zamani, O. Mehrpour1
Department of Clinical Toxicology, Loghman Hakim Hospital,
Shahid Beheshti University of Medical Sciences, Tehran, Iran
1Medical Toxicology and Drug Abuse Research Center (MTDRC),
Birjand University of Medical Sciences, Birjand, Iran
Letter to the Editor