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Glucose-6-phosphate Dehydrogenase (G6PD) Deficiency and its Relation to Covid-19

Article Information

Ayse Sahin Tutak1*, Hakan Sezgin Sayiner2

1Department of Internal Medicine, Adiyaman University School of Medicine, Adiyaman, Turkey

2Department of Infectious Disease, Adiyaman University School of Medicine, Adiyaman, Turkey

*Corresponding author: Ayse Sahin Tutak, Department of Internal Medicine, Adiyaman University School of Medicine, Adiyaman, Turkey

Received: 22 November 2021; Accepted: 14 December 2021; Published: 20 December 2021

Citation: Ayse Sahin Tutak, Hakan Sezgin Sayiner. Glucose-6-phosphate Dehydrogenase (G6PD) Deficiency and its Relation to Covid-19. Archives of Clinical and Biomedical Research 5 (2021): 1000-1003.

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Keywords

Covid-19; Glucose-6-phosphate Dehydrogenase

Covid-19 articles

Article Details

Short Communication

Glucose-6-phosphate dehydrogenase (G6PD) def-iciency is the most common enzymopathy world-wide. It is prevalent in approximately 400 million people in East and Southeast Asia and central Africa [1, 2].  G6PD is an enzyme with X-linked recessive inheritance. Its level of activity varies among individuals and due to various drugs and foods. The level of enzyme activity decreases with aging. Clinically, men develop conditions, while women are carriers. G6PD deficiency is classified by the level of enzyme activity, and patients may suffer from mild/moderate G6PD deficiency.  In the most severe type, the level of enzyme activity is below 10% [3]. It catalyzes the first and rate-limiting reaction step in the hexose monophosphate (HMP) pathway G6PD and provides the conversion of NADP to NADPH (nicotinamide adenine dinucleotide phosphate). G6PD deficiency results in a lack of NADPH production. NADPH plays an important role in maintaining the integrity of the cell membrane in erythrocytes [4] and protects the erythrocytes against oxidative stress. Its deficiency may result in hemolysis of different severity and endothelial dysfunction in different tissues due to exposure to various factors. G6PD is also known to be essential in preventing opacification of the eye and for the development of cells of the lens. Studies on different age groups have found a strong correlation between G6PD deficiency in erythrocyte cells and cataract formation [5, 6]. One of the factors in the etiology of neonatal jaundice is G6PD deficiency [7]. G6PD deficiency has been found to vary from 1.5% to 35% in infants with jaundice [8].

G6PD activity changes depending on nutrition, hormones, and especially NADPH concentration [9]. The level of enzyme activity may also change due to various viral and bacterial causes. G6PD deficiency have been detected in patients with HIV, hepatitis viruses (A, B and E), and cytomegalovirus [10, 11]. It has been observed that some drugs activate and some inhibit the enzyme in some individuals with G6PD deficiency [12, 13].

Due to the Covid-19 pandemic, mortality rates have been increasing worldwide day by day. According to a meta-analysis, high levels of patient monitoring at ICU and mortality in men due to Covid-19 indicate the common enzyme deficiency with X-linked recessive inheritance [16].  Previous studies have suggested that oxidative stress contributes to the pathogenesis of severe SARS-CoV-2 infection [14], and researchers have found that cells with G6PD deficiency are more susceptible to infection [15].  Therefore, G6PD deficiency can cause vulnerability to SARS-CoV-2, while the treatment with HCQ, steroids, antibiotics, and antiemetics may also affect the level of G6PD enzyme activity positively or negatively. Drugs with negative effect will cause a decrease in NADPH levels, increasing the severity of oxidative stress, resulting in increased mortality and morbidity.

COVID-19 includes clinical presentations of various severities ranging from death due to severe acute respiratory failure to simple myalgia. There is no solid evidence on the cause of this broad range of clinical conditions. Based on the observations during the monitoring of patients in ICU that

  1. A high number of individuals of the same family had a severe condition and/or resulted in death;
  2. Individuals or their first-degree relatives who had an indication for ICU hospitalization or resulted in mortality had a history of cataract;
  3. Men have more severe clinical presentations and a higher mortality rate;
  4. Individuals or their children admitted to ICU had a history of neonatal jaundice;
  5. There is a partial coherence between the world map showing the regions of G6PD deficiency and the map showing mortality rates due to Covid-19 (Since the non-coherent countries are at low socioeconomic levels, reliability of their data should be considered);
  6. Monitoring of the patients in ICU showed a moderate methemoglobinemia and hyperbilirubinemia in arterial blood gas; more studies analyzing the genetic basis of individual response to coronavirus infections are also warranted [17]. We believe that the patients with severe and complicated clinical presentations may have G6PD deficiency, and the patients with G6PD deficiency will have a more severe course of disease.

We are of the opinion that it will have a worldwide impact on mortality and morbidity to screen the patients with the above-mentioned clinical pre-sentations for the history of G6PD deficiency and to determine their treatment and diet accordingly, as well as to carry out studies on it using multi-centered patient data.

References

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  2. Nkhoma ET, Poole C, Vannappagari V, Hall SA, Beutler E. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood Cells Mol Dis 42 (2009): 267-78.
  3. Fairbanks VF, Klee GG. Biochemical aspects of hematology. In:Burtis CA, Ashwood ER, eds. Tietz text book of clinical chemistry USA: WB Saunders Co (1994): 1974-9.
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  5. Orzalesi N, Sorcinelli R and Guiso G. “Increased incidence of cataracts in male subjects deficient in 62 glucose 6-phosphate dehydrogenase”, Arch Ophthalmol 99 (1981): 69-70.
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  8. Madan N, Sundaram KR, Bhargava SK, Sood SK. Glucose-6- phosphate dehydrogenase deficiency and neonatal hyperbilirubinemia. Indian J Med Res 90 (1989): 306-313.
  9. Ayala A, Fabregat I, Machado A. “The role of NADPH in the regulation of glucose-6-phosphate and 6-phospho gluconate dehydrogenase in rat adipose tissue” Mol Cell Biochem 105 (1991): 1-5.
  10. Au WY, Ngai CW, Chan WM, Leung RY, Chan SC. Hemolysis and methemoglobinemia due to hepatitis E virus infection in patient with G6PD deficiency. Ann Hematol 90 (2011): 1237–8.
  11. A raujo T, Katiyar V, Gonzales Zamora JA. Acute retroviral syndrome presenting with hemolytic anemia induced by G6PD deficiency. Trop Med Infect Dis 4 (2018): 6.
  12. Özmen I, Çiftçi M, Küfrevioglu ÖI, Çürük MA. “Investigation of Glucose 6-Phosphate Dehydrogenase (G6PD) Kinetics for Normal and G6PD Deficient Persons and the Effects of some Drugs” Journal of Enzyme Inhibition and Medicinal Chemistry 19 (2004): 45-50.
  13. Dar SA, Wahid M, Haque S, Almalki SS, Akhter N. Hydroxychloroquine (HCQ) use in G6PD deficient COVID-19 patients and the risk of Acute Hemeolytic Anaemia (AHA). Eur Rev Med Pharmacol Sci 24 (2020): 7923-7924.
  14. Delgado-Roche L, Mesta F. Oxidative stress as key player in severe acute respiratory syndrome coronavirus (SARS-CoV) infection. Arch Med Res (2020).
  15. Wu YH, Tseng CP, Cheng ML, Ho HY, Shih SR, et al. Glucose-6-phosphate dehydrogenase deficiency enhances human coronavirus 229 E infection. J Infect Dis 197 (2008): 812-816.
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  17. Marta Galanti, Jeffrey Shaman. Direct Observation of Repeated Infections with Endemic Coronaviruses, the Journal of Infectious Diseases 223 (2021): 409–415.

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