Relationship Between Glucose-6-Phosphate Dehydrogenase (G6PD) Enzyme Deficiency and COVID-19 Infection


Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is a common genetic disorder that affects over 400 million people worldwide. It has been implicated in various diseases and has been suggested to increase the risk of viral infections.

Glucose-6-phosphate dehydrogenase (G6PD) enzyme deficiency is associated with various pathological conditions. Some of the notable pathologies related to G6PD deficiency include:

  • Acute Hemolytic Anemia (AHA): G6PD deficiency is commonly associated with AHA, which is characterized by the destruction of red blood cells at an accelerated rate. Exposure to certain triggers, such as infections, certain medications, or dietary factors (e.g., fava beans), can lead to hemolysis and the manifestation of AHA symptoms.
  • Neonatal Hyperbilirubinemia (Neonatal Jaundice): Newborns with G6PD deficiency may experience an excessive buildup of bilirubin in their blood, leading to jaundice. This condition can cause yellowing of the skin and eyes and may require medical intervention to manage the high levels of bilirubin.
  • Chronic Hemolytic Anemia: G6PD deficiency can contribute to chronic hemolytic anemia, characterized by the ongoing destruction of red blood cells. This condition can result in symptoms such as fatigue, shortness of breath, and pale skin.
  • Increased Susceptibility to Infections: G6PD deficiency may impair the immune response and increase susceptibility to certain infections. This susceptibility is thought to be related to the role of G6PD in maintaining the redox balance and antioxidant defense mechanisms within cells.
  • Cardiovascular Disease (CVD): Some studies have indicated an association between G6PD deficiency and an increased risk of developing cardiovascular diseases. This connection suggests that G6PD deficiency may play a role in the pathogenesis of CVD, although the exact mechanisms are not fully understood.

It is important to note that G6PD deficiency can manifest differently among individuals, and the severity of the condition can vary. Additionally, G6PD deficiency is more prevalent in certain populations, particularly in regions where malaria is or has been endemic, as it is believed to provide some protection against malaria infection.

The outbreak of COVID-19 caused by SARS-CoV-2 has posed significant challenges in the treatment and control of the disease. This study aims to investigate the association between G6PD enzyme deficiency and COVID-19 infection, focusing on hematological and biochemical parameters, in patients managed at a Saudi tertiary center.

Introduction: The hexose monophosphate (HMP) shunt, also known as the pentose phosphate pathway (PPP), is an alternative pathway for glucose metabolism that plays essential roles in nucleotide synthesis and the production of nicotinamide adenine dinucleotide phosphate (NADPH).

Glucose-6-phosphate dehydrogenase (G6PD) is a key enzyme of the HMP shunt and catalyzes the rate-limiting step. Deficiency of G6PD is an inherited genetic disorder that can lead to various health conditions, including acute hemolytic anemia, neonatal hyperbilirubinemia, and chronic hemolytic anemia. Previous studies have suggested a connection between G6PD enzyme deficiency and increased risk of developing cardiovascular disease (CVD), as well as an association with systolic blood pressure.

COVID-19 is a viral infection caused by SARS-CoV-2, primarily affecting the respiratory system. It has been observed that COVID-19 can progress to severe pneumonia and acute respiratory distress syndrome (ARDS), leading to significant morbidity and mortality.

The infection of human type II alveolar epithelial cells initiates a series of pathophysiological processes involving immune responses, inflammation, oxidative stress, and coagulopathy. Reactive oxygen species (ROS) play a crucial role in the oxidative damage observed during the infection

. Antioxidant enzyme mechanisms, including G6PD, help suppress ROS and minimize oxidative damage. However, defects in essential antioxidant enzymes can lead to a dysregulated redox environment and promote pathobiology.

Methods: This study is a retrospective analysis of patients managed at a Saudi tertiary center. Patients with laboratory-confirmed COVID-19 infection will be included in the study. Data on hematological and biochemical parameters, including G6PD enzyme activity, will be collected from electronic medical records.

The study aims to compare the parameters between patients with G6PD enzyme deficiency and those without the deficiency. Statistical analysis will be performed to assess the association between G6PD deficiency and COVID-19 infection severity.

Expected Results and Discussion: The results of this study will provide insights into the relationship between G6PD enzyme deficiency and COVID-19 infection in the context of hematological and biochemical parameters.

It is hypothesized that G6PD deficiency may increase the risk of severe COVID-19 infection due to impaired immune responses and the redox imbalance caused by reduced G6PD levels. Understanding this association is crucial for identifying high-risk individuals and developing targeted management strategies, especially in regions with a high incidence of G6PD deficiency like Saudi Arabia.

Conclusion: This study aims to investigate the relationship between G6PD enzyme deficiency and COVID-19 infection, focusing on hematological and biochemical parameters in patients managed at a Saudi tertiary center. The findings will contribute to our understanding of the impact of G6PD deficiency on COVID-19 severity and provide valuable insights for managing COVID-19 patients with G6PD enzyme deficiency.

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