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Is Fatigue Stealing Your Energy? G6PD Deficiency Might Be the Culprit

Updated: Dec 16, 2024



Glucose-6-Phosphate Dehydrogenase (G6PD) test is a crucial diagnostic tool that assesses the activity of the G6PD enzyme in red blood cells. This test is vital in identifying G6PD deficiency, a genetic condition that affects the red blood cells’ ability to function properly.


Role in Healthcare practice:


1. Malaria-Endemic Regions:

  • In regions where malaria is prevalent, G6PD deficiency has a significant impact. Individuals with G6PD deficiency are less susceptible to severe malaria caused by Plasmodium falciparum, as the parasite’s growth is inhibited in G6PD-deficient red blood cells due to oxidative stress.

  • However, certain antimalarial medications, such as primaquine and other 8-aminoquinoline drugs, can cause hemolytic reactions in individuals with G6PD deficiency, leading to red blood cell destruction. This affects treatment options for malaria in these regions.


2. African Descent:

  • G6PD deficiency is relatively common among individuals of African descent, with varying prevalence rates across different African populations. This genetic trait has been associated with protection against severe malaria.

  • In African communities, G6PD deficiency may pose challenges in managing infections, certain medications, and dietary factors that can trigger hemolytic reactions. Public health programs and healthcare providers must be aware of these challenges and tailor interventions accordingly.


3. Mediterranean and Middle Eastern Communities:

  • G6PD deficiency is also prevalent in certain Mediterranean and Middle Eastern populations, including those of Arab, Jewish, and Mediterranean descent. The Mediterranean variant of G6PD deficiency (G6PD-Mediterranean) is one of the most common variants worldwide.

  • Individuals with G6PD-Mediterranean may experience hemolytic episodes triggered by various factors, such as certain foods (e.g., fava beans), infections, oxidative stress, or exposure to medications like antimalarials, sulfa drugs, and certain antibiotics.


4. Asian Communities:

  • G6PD deficiency is found in various Asian populations, including those of Southeast Asian, South Asian, and East Asian descent. Different genetic variants of G6PD deficiency are observed in these communities, each with its specific characteristics and prevalence rates.

  • In Asian communities, G6PD deficiency may impact the management of certain infections, including malaria and typhoid fever, as well as the use of specific medications that can trigger hemolytic reactions.


5. Global Health Considerations:

  • G6PD deficiency is recognized as a global health concern, especially in regions where the disease burden from malaria and other infectious diseases is high. Healthcare systems in these regions need to implement strategies for G6PD screening, management of hemolytic episodes, and safe use of medications.


Overall, the role of G6PD deficiency in different communities underscores the importance of genetic screening, personalized healthcare approaches, and public health interventions tailored to specific populations’ needs and genetic profiles. Collaboration between healthcare providers, researchers, policymakers, and communities is essential for the effective management and prevention of complications associated with G6PD deficiency.


When Values Go Low and High:

Low Values (G6PD Deficiency): Low G6PD activity levels indicate G6PD deficiency, a condition where red blood cells are more susceptible to damage from oxidative stress. This deficiency can lead to hemolytic anaemia, especially when exposed to certain triggers such as medications (e.g., antimalarials, sulfonamides), infections, or certain foods (e.g., fava beans).


High Values: While high G6PD activity levels are less common, they may be seen in conditions associated with increased oxidative stress, such as certain infections, inflammatory disorders, or exposure to toxins.


Latest References:

  1. Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008 Jul 26;371(9606):64-74.

  2. Luzzatto L, Arese P. Favism and glucose-6-phosphate dehydrogenase deficiency. N Engl J Med. 2018 Mar 15;378(11):1068-9.

  3. Nkhoma ET, Poole C, Vannappagari V, et al. The global prevalence of glucose-6-phosphate dehydrogenase deficiency: A systematic review and meta-analysis. Blood Cells Mol Dis. 2009 Jul-Aug;42(3):267-78.

  4. Beutler E, Vulliamy TJ. Hematologically important mutations: glucose-6-phosphate dehydrogenase. Blood Cells Mol Dis. 2002 Mar-Apr;28(2):93-103.

  5. Lai HY, Chien SH, Huang CK, et al. Risk factors of severe hyperbilirubinemia in glucose-6-phosphate dehydrogenase-deficient newborns. Pediatrics. 2012 Sep;130(3):e511-6.

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