Reagent | G6PDH
A Biomarker of G6PDH Deficiency
Benefits of the Randox G6PDH Assay
A correlation coefficient of r=0.9903 was displayed when the Randox G6PDH assay was compared to commercially available methods.
The Randox G6PDH assay displayed a precision of <4.65% CV.
The Randox G6PDH assay has a reconstituted stability of 4 weeks when stored at +2oC to +8oC.
Dedicated G6PDH controls available
Dedicated G6PDH controls available offering a complete testing package.
Applications available detailing instrument-specific settings for the convenient use of the Randox G6PDH assay on a variety of clinical chemistry analysers.
|PD410||R1 1 x 100ml (L)|
R2 1 x 2ml
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|PD2616||750T (Screen Test)|
R1a 3 x 25ml (L)
R1b 1 x 80ml
R3 1 x 2ml
R4 1 x 20ml
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|(L) Indicates liquid option|
Instrument Specific Applications (ISA’s) are available for a wide range of biochemistry analysers. Contact us to enquire about your specific analyser.
The G6PD gene provides the instructions for marking the glucose-6-phosphate dehydrogenase (G6PDH) enzyme 1. G6PDH is a cytosolic enzyme located on the long arm of the X-chromosome of bodily cells and so is an inherited x-linked disorder. G6PDH is involved in the normal processing of carbohydrate and the prevention of cellular damage from reactive oxygen species (ROS). In doing so, G6PDH provides substrates to prevent oxidative damage. G6PDH plays a critical role in red blood cells, protecting them from damage and premature destruction. The two main products of G6PDH are: ribose-5-phosphatase which is important for DNA, the chemical cousin of RNA; and NADPH which protects the body from ROS 1, 2.
Glucose-6-phosphate dehydrogenase (G6PDH/G6PD) deficiency is the most common enzyme deficiency in the pentose phosphate pathway, affecting more than 400 million people globally. G6PDH deficiency is an X-linked recessive disorder mainly affecting RBC’s 2.
A defect in the G6PDH enzyme results in premature haemolysis (break down of RBC’s). If the bone marrow cannot compensate for the reduction of RBC’s, haemolytic anaemia can occur. Many individuals that are glucose-6-phosphate dehydrogenase deficient are asymptomatic most of the time, however when they are exposed to certain triggering factors, they can develop acute haemolytic anaemia (AHA), which can be life-threatening, especially in children. Symptoms associated with G6PDH deficiency can include paleness, jaundice, dark urine, fatigue, shortness of breath, a sudden rise in body temperature, lower back pain, splenomegaly (enlarged spleen) and a rapid heart rate. Other symptoms can include nausea, diarrhoea or abdominal discomfort. It has been noted that glucose-6-phosphate dehydrogenase deficiency is a significant cause of mild to severe jaundice in new-borns. Early and accurate diagnosis of G6PDH deficiency is essential in ensuring the successful management of haemolytic anaemia 1, 2.
Of all malaria cases reported in Latin America and the Caribbean, 42% are attributed to Brazil. However, in recent years, progress has been made towards the elimination of the malaria burden, reaching the lowest levels in the past 35 years (143, 910 cases and 41 confirmed malaria-related deaths). Whilst the transmission area of malaria has significantly reduced, 99.5% of Brazil’s malaria burden is attributed to the Amazon Basin 3. The predominant contributor to the malaria outbreak in Brazil is attributed to the plasmodium vivax parasites which can cause severe and fatal complications in glucose-6-phosphate dehydrogenase (G6PDH) deficient individuals. Individuals infected with malaria are treated with primaquine, however, in G6PDH deficient individuals, this treatment can induce haemolytic anaemia, and so, G6PDH screening is vital 4.
A Brazilian study, published in the Malaria Journal prospectively evaluated 516 male volunteers within the Alto do Juruá, an area characterized by a high prevalence of plasmodium vivax, to determine the prevalence of G6PDH. The study found that 4.5% of the study group were G6PDH deficient and were at a high risk of haemolytic anaemia if treated with primaquine. As such, the routine screening of G6PDH deficiency in Brazil to personalize the treatment of patients with vivax malaria, is crucial for malaria elimination 4.
Chloroquine, an anti-malaria drug, has been selected to aid in treating those with COVID-19 following preliminary research and a limited study in Australia which highlighted that chloroquine showed promise in eradicating the virus. Moreover, Chinese research highlighted the efficacy and safety of chloroquine in treating pneumonia in COVID-19 patients 5.
It is believed that COVID-19 is expected to spread to areas where G6PDH deficiency is more common, however, serious consideration must be given to treatment decisions using chloroquine as chloroquine-induced haemolysis is the result to decreased G6PDH activity 6.
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Reagents Resource Hub
 Genetics Home Reference. G6PD gene. https://ghr.nlm.nih.gov/gene/G6PD (accessed 13 March 2020).
 Richardson SR, O’Malley GF. Glucose 6 Phosphate Dehydrogenase (G6PD) Deficiency. Treasure Island (FL): StatPearls Publishing; 2019.
 Ferreira MU, Castro MC. Challenges for malaria elimination in Brazil. Malaria Journal 2016; 15(284): 1-18.
 Dombrowski JG, Souza RM, Curry J, Hinton L, Silva NR, et al. G6PD deficiency alleles in a malaria-endemic region in the Western Brazilian Amazon. Malaria Journal 2017; 16(253): 1-9.
 Vick DJ. Chloroquine Is Not a Harmless Panacea for COVID-19 — There’s a real safety concern with malaria drug. https://www.medpagetoday.com/infectiousdisease/covid19/85552 (accessed 12 June 2020).
 Kassi EN, Papavassiliou KA, Papavassiliou AG. G6PD and chloroquine: Selecting the treatment against SARS-CoV-2?. Journal of Cellular and Molecular Medicine 2020; 24(): 4913-4914.
Featured Reagent – G6PDH
Featured Reagent | G6PDH
Glucose-6-phosphate dehydorgenase (G6PDH/G6PD) deficiency is an x-linked and sex-linked metabolic disorder, commonly affecting men more so than women1. The G6PDH enzyme is critical for the proper functioning of red blood cells (RBC’s). Depleated levels of G6PDH can cause the premature destruction of RBC’s (haemolysis). If the bone marrow cannot compensate for the reduction in RBC’s, heamolyic anaemia can develop. It is important to note that a deficiency in the G6PDH enzyme is not enough to promote the onset of haemolysis, but rather additional factors are required to promote the onset of symptoms2.
Some of the common side effects of G6PDH deficiency include: paleness, dark urine, yellowing of the skin and whites of the eyes, a rapid heart rate and shortness of breath. Common triggers for the development of haemolytic anaemia in those who are G6PDH deficient include: bacterial and viral infections, certain drugs (medications and antibiotics to treat malaria), and favism (inhaling the pollen from fava plants and ingesting fava beans)3
G6PDH deficiency has been recognised as a significant cause of mild to severe jaundice in newborns. It has been noted that those with this disorder commonly will not experience any signs or symptoms making them unaware that they have the condition3.
Haemolytic anaemia is an umbrella term used to describe the premature destruction of red blood cells (RBC’s). This disorder encompasses numerous conditions including: autoantibodies, medications, underlying malignancy, bone marrow failure, infection and heredity conditions including sickle cell disease or haemoglobinopathies4 5.
The severity of haemolytic anaemia depends on whether the onset of haemolysis is gradual or rapid and on the extent of RBC destruction. Patients with mild haemolysis can be asymptomatic whereas the anaemia in severe haemolysis can be life-threatening and can cause angina and cardiopulmonary decompensation. Haemolytic anaemia is an intravascular phenomenon meaning that this type of haemolysis occurs within the blood vessels and is caused by the following conditions: prosthetic cardiac valves, glucose-6-phosphate dehydrogenase (G6PDH) deficiency, thrombotic thrombocytopenic purpura, disseminated intravascular coagulation, transfusion of ABO incompatible blood and paroxysmal nocturnal haemoglobinuria (PNH)6.
Heredity disorders can also cause haemolysis due to the erythrocyte membrane and haemoglobin abnormalities, and enzymatic defects. Some hereditary disorders include: G6PDH deficiency, hereditary spherocytosis and sickle cell anaemia6.
Glucose-6-phosphate dehydrogenase (G6PDH) is a cytosolic enzyme located on the X-chromosome found in bodily cells. G6PDH is involved in the normal processing of carbohydrates and plays a critical role in RBC, protecting them from damage and premature destruction. The two main products of G6PDH are ribose-5-phosphate which is important for DNA, the chemical cousin of RNA. The chemical reaction produces NADPH which protects bodily cells from reactive oxygen species1.
Benefits of the G6PDH Assay
A niche assay from Randox meaning that Randox are one of the only manufacturers to offer a G6PDH assay in an automated biochemistry format.
Superior stability of 4 weeks upon reconstitution and stored at +2°C to +8°C. Many other commercially available assays offer only 5 days stability, leading to product wastage.
Minimal interference as the sample pre-wash step included in the Randox G6PDH testing method serves to purify the sample, leading to no known interferences being observed.
Excellent correlation coefficient of r=0.99 when compared against other commercially available methods.
Lyophilised reagent for enhanced stability.
G6PDH controls offering a complete testing package.
Applications available detailing instrument-specific settings for the convenient use of the Randox G6PDH assay on a wide range of clinical chemistry analsyers.
 Croom, Edward. Progress in Molecular Biology and Translational Science. 2012. ISBN 9780124158139 / ISSN 1877-1173.
 National Organization for Rare Disorders. Glucose-6-Phosphate Dehydrogenase Deficiency. [Online] no date. [Cited: January 31, 2019.] https://rarediseases.org/rare-diseases/glucose-6-phosphate-dehydrogenase-deficiency.
 U.S. National Library of Medicine. Glucose-6-phosphate dehydrogenase deficiency. [Online] May 2017. [Cited: January 30, 2019.] https://ghr.nlm.nih.gov/condition/glucose-6-phosphate-dehydrogenase-deficiency.
 National Heart, Lung, and Blood Institute. Hemolytic Anemia. [Online] no date. [Cited: January 28, 2019.] https://www.nhlbi.nih.gov/health-topics/hemolytic-anemia.
 BMJ Publishing Group. Hemolytic anemia. BMJ Best Practice. [Online] March 2018. [Cited: January 28, 2019.] https://bestpractice.bmj.com/topics/en-us/98.
 Schick, Paul. Hemolytic Anemia. Medscape. [Online] December 29, 2018. [Cited: Janaury 28, 2018.] https://emedicine.medscape.com/article/201066-overview.
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G6PDH Quality Control
The Randox Acusera G6PDH control is designed specifically to monitor the accuracy and precision of G6PDH assays. Two levels of control are available covering both normal and deficient concentration ranges.
Features & Benefits
- Lyophilised for enhanced stability
- Stabilised red-cell haemolysate
- Assayed target values provided
- Stable to expiry date at 2°C – 8°C
- Reconstituted stability of 5 days at 2°C – 8°C
|G6PDH Control Deficient||6 x 0.5 ml||1||PD2617|
|G6PDH Control Normal||6 x 0.5 ml||1||PD2618|