Gene:
G6PD
glucose-6-phosphate dehydrogenase

PharmGKB contains no dosing guidelines for this . To report known genotype-based dosing guidelines, or if you are interested in developing guidelines, click here.

PharmGKB gathers information regarding PGx on FDA drug labels from the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels", and from FDA-approved FDA and EMA-approved (European Medicines Agency) EMA labels brought to our attention. Excerpts from the label and downloadable highlighted label PDFs are manually curated by PharmGKB.

Please note that some drugs may have been removed from or added to the FDA's "Table of Pharmacogenomic Biomarkers in Drug Labels" without our knowledge. We periodically check the table for additions to this table and update PharmGKB accordingly.

There is currently no such list for European drug labels - we are working with the EMA to establish a list of European Public Assessment Reports (EPAR)s that contain PGx information. We are constructing this list by initially searching for drugs for which we have PGx-containing FDA drug labels - of these 44 EMA EPARs were identified and are being curated for pgx information.

We welcome any information regarding drug labels containing PGx information approved by the FDA, EMA or other Medicine Agencies around the world - please contact feedback.


last updated 10/25/2013

FDA Label for chloroquine and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for chloroquine (Aralan) states caution should be taken when administering treatment to G6PD deficient individuals due to the possibility of hematological effects. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests, however the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 12/13/2013

FDA Label for chlorpropamide and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for chlorpropamide (DIABINESE) states that caution should be used in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency due to the risk for hemolytic anemia, and that a non-sulfonylurea alternative should be considered in this subset of patients. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests, however the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 12/13/2013

FDA Label for dabrafenib and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The drug label for dabrafenib (TAFINLAR) states that it is indicated for use in patients with unresectable or metastatic melanoma with a BRAF V600E mutation, as detected by an FDA-approved test. The label also notes that patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency have a risk for developing hemolytic anemia, and that these patients should be closely observed when taking dabrafenib.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for dapsone and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved label for dapsone gel provides a precautionary warning that G6PD deficient individuals may be at an increased risk of hemolytic adverse reactions, as oral dapsone treatment is associated with dose-related hemolysis and hemolytic anemia in these individuals. This enzyme deficiency is due to underlying genetic variants in the G6PD gene and can be tested for by enzyme activity or genetic tests.

There's more of this label. Read more.


last updated 12/17/2013

FDA Label for glibenclamide and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Although the glibenclamide (glyburide; GLYNASE PresTab) drug label does not specifically mention genetic testing, the FDA highlight precaution labeling prior to initiating treatment with glibenclamide for G6PD deficient individuals due to risk of hemolytic anemia. Treatment of patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency with sulfonylurea agents can lead to hemolytic anemia; caution should be used in patients with G6PD deficiency and a non-sulfonylurea alternative should be considered.

There's more of this label. Read more.


last updated 12/17/2013

FDA Label for glimepiride and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for glimepiride (AMARYL) states that caution should be used in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency due to the risk for hemolytic anemia, and that a non-sulfonylurea alternative should be considered in this subset of patients. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests, however the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 12/17/2013

FDA Label for glipizide and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for glipizide (GLUCOTROL) states that caution should be used in patients with glucose 6-phosphate dehydrogenase (G6PD) deficiency due to the risk for hemolytic anemia, and that a non-sulfonylurea alternative should be considered in this subset of patients. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests, however the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 12/17/2013

FDA Label for mafenide and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for mafenide (SULFAMYLON) mentions that fatal hemolytic anemia with disseminated intravascular coagulation has been reported following treatment with SULFAMYLON cream, possibly due to a glucose-6-phosphate dehydrogenase (G6PD) deficiency. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests. However, the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 12/17/2013

FDA Label for methylene blue and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Although the methylene blue drug label does not specifically mention genetic testing, precaution prior to initiating treatment with methylene blue is highlighted for G6PD deficient individuals, a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests.

There's more of this label. Read more.


last updated 12/18/2013

FDA Label for nalidixic acid and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Nalidixic acid is used to treat urinary tract infections due to gram-negative bacteria. Although the nalidixic acid (NegGram) drug label does not specifically mention genetic testing, the FDA highlight precaution labeling prior to initiating treatment with nalidixic acid for G6PD deficient individuals due to an association with hemolytic anemia.

There's more of this label. Read more.


last updated 12/18/2013

FDA Label for nitrofurantoin and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Nitrofurantion is used to treat urinary tract infections caused by certain strains of bacteria. A link between nitrofurantoin-induced hemolytic anemia and G6PD deficiency is highlighted in the Warnings section. Hemolysis appears to be linked to a glucose-6-phosphate dehydrogenase deficiency in the red blood cells of the affected patients.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for norfloxacin and G6PD

Actionable PGx

Summary

Norfloxacin is used to treat urinary tract infections, sexually transmitted diseases and prostatitis caused by certain microorganisms. The label reports hemolytic reactions have been seen in G6PD deficient individuals in association with this drug.

There's more of this label. Read more.


last updated 12/18/2013

FDA Label for pegloticase and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Pegloticase is used to treat chronic gout. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are treated with pegloticase are at risk of hemolysis and methemoglobinemia. Pegloticase is contraindicated for such patients.

There's more of this label. Read more.


last updated 12/20/2013

FDA Label for primaquine and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Primaquine is used to prevent vivax malaria relapse. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are treated with primaquine are at risk of moderate to severe hemolytic reactions. Patients with cytochrome b5 reductase deficiency (CYB5R3, also known as NADH methemoglobin reductase) who are treated with primaquine are at risk of methemoglobinemia.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for probenecid and G6PD

Actionable PGx

Summary

Probenecid is used to treat chronic gouty arthritis. An association between probenecid-induced hemolytic anemia and G6PD deficiency is highlighted in the Adverse Reactions section of the probenecid label.

There's more of this label. Read more.


last updated 12/20/2013

FDA Label for quinine and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

The FDA-approved drug label for quinine (QUALAQUIN) states that it is contraindicated in patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to the risk for hemolysis. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests, however the drug label does not specifically mention testing.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for rasburicase and G6PD

This label is on the FDA Biomarker List
Genetic testing required

Summary

The drug label recommends screening patients at higher risk for G6PD deficiency (e.g., patients of African or Mediterranean ancestry) prior to starting Elitek(rasburicase) therapy. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are treated with rasburicase are at risk of severe hemolysis. Rasburicase is contraindicated for such patients.

There's more of this label. Read more.


last updated 01/14/2014

FDA Label for sodium nitrite and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

Sodium nitrite is intended for sequential use with sodium thiosulfate, in order to treat acute and life-threatening cyanide poisoning. Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency who are treated with sodium nitrite are at risk for a hemolytic crisis. Alternative treatments should be considered in these individuals, or they should be monitored for an acute drop in hematocrit. G6PD deficiency is a condition caused by variants in the G6PD gene which can be determined by enzymatic or genetic tests. However, the drug label does not specifically mention testing

There's more of this label. Read more.


last updated 01/15/2014

FDA Label for succimer and G6PD

This label is on the FDA Biomarker List
Informative PGx

Summary

Succimer (CHEMET) is used for treating lead poisoning in pediatric patients with blood lead levels greater than 45 mcg/dL. The drug label notes that succimer has been used to treat five patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency without any adverse reactions.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for sulfadiazine and G6PD

Actionable PGx

Summary

Sulfadiazine is an antimicrobial topical drug used to prevent and treat wound sepsis in second and third degree burns. A link between sulfadiazine-induced hemolytic anemia and G6PD deficiency is highlighted in the Warnings section of the label.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for sulfasalazine and G6PD

Actionable PGx

Summary

Sulfasalazine is used to treat and prolong remission for ulcerative colitis. The label warns that people with G6PD are susceptible to hemolytic anemia on this drug.

There's more of this label. Read more.


last updated 10/25/2013

FDA Label for sulfisoxazole and G6PD

Actionable PGx

Summary

Erythromycin ethylsuccinate and sulfisoxazole acetyl is used to treat acute otitis media in children caused by certain strains of Haemophilus influenzae. The label warns that hemolysis may occur in G6PD deficient patients on this drug.

There's more of this label. Read more.


last updated 12/18/2013

FDA Label for vitamin c and G6PD

This label is on the FDA Biomarker List
Actionable PGx

Summary

MoviPrep, a solution containing Vitamin C, is a laxative used for colon cleansing in preparation for a colonoscopy. Because it contains Vitamin C (ascorbic acid), the label warns that hemolytic reactions are possible in those with G6PD deficiency.

There's more of this label. Read more.



European Medicines Agency (EMA) Label for methylene blue and BLVRB, CYB5R3, G6PD

Actionable PGx

Summary

The EMA European Public Assessment Report (EPAR) for methylthioninium chloride Proveblue (also known as methylene blue) contains information regarding contraindication of the drug in patients with G6PD deficiency due to risk of hemolytic anemia, and in patients with a deficiency in NADPH reductase (encoded by the BLVRB gene). The label also states that failure to respond to the drug may indicate a deficiency in cytochrome b5 reductase (CYB5R3) or G6PD.

There's more of this label. Read more.


European Medicines Agency (EMA) Label for rasburicase and G6PD

Actionable PGx

Summary

The EMA European Public Assessment Report (EPAR) contraindicates the use of rasburicase (Fasturtec) in patients with G6PD deficiency due to a risk of hemolytic anemia or methemoglobinemia. Testing or screening for G6PD deficiency is not mentioned.

There's more of this label. Read more.


Clinical Variants that meet the highest level of criteria, manually curated by PharmGKB, are shown below. Please follow the link in the "Position" column for more information about a particular variant. Each link in the "Position" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

To see more Clinical Variants with lower levels of criteria, click the button at the bottom of the table.

Disclaimer: The PharmGKB's clinical annotations reflect expert consensus based on clinical evidence and peer-reviewed literature available at the time they are written and are intended only to assist clinicians in decision-making and to identify questions for further research. New evidence may have emerged since the time an annotation was submitted to the PharmGKB. The annotations are limited in scope and are not applicable to interventions or diseases that are not specifically identified.

The annotations do not account for individual variations among patients, and cannot be considered inclusive of all proper methods of care or exclusive of other treatments. It remains the responsibility of the health-care provider to determine the best course of treatment for a patient. Adherence to any guideline is voluntary, with the ultimate determination regarding its application to be made solely by the clinician and the patient. PharmGKB assumes no responsibility for any injury or damage to persons or property arising out of or related to any use of the PharmGKB clinical annotations, or for any errors or omissions.

? = Mouse-over for quick help

This is a non-comprehensive list of genetic tests with pharmacogenetics relevance, typically submitted by the manufacturer and manually curated by PharmGKB. The information listed is provided for educational purposes only and does not constitute an endorsement of any listed test or manufacturer.

A more complete listing of genetic tests is found at the Genetic Testing Registry (GTR).

PGx Test Variants Assayed Related Drugs?
Labor für Humangenetik Synlab MVZ Humane Genetik München. Test for Glucose-6-Phosphate Dehydrogenase Deficiency Variant in G6PD
Emory Molecular Genetics Laboratory Emory University School of Medicine. Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region, deletion/duplication analysis
The Rare Disease Company, Centogene GmbH. Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region
Medical Genetics Laboratory Diagenom GmbH. Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region
Hehr Laboratory, Center for Human Genetics Regensburg University of Regensburg. Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region
MVZ Dortmund, Dr. Eberhard and Partner, Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of exons: 2-13
Molecular Genetics Center for Human Genetics and Laboratory Medicine Martinsried, Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region
Molecular Biology Center, GENETAQ, Test for Glucose-6-Phosphate Dehydrogenase Deficiency Sequence analysis of the entire coding region
Molecular Genetics Laboratory ARUP Laboratories, Glucose-6-Phosphate Dehydrogenase (G6PD) 2 Mutations G6PDA-202A_376G , rs1050829 , rs1050828
Molecular Diagnostics Division, Genome Research Group Centre for Cellular and Molecular Biology. Test for Glucose-6-Phosphate Dehydrogenase Deficiency rs137852339 , rs5030868 , rs78478128
PerkinElmer Genetics, Inc. Test for Glucose-6-Phosphate Dehydrogenase Deficiency G6PDA-202A_376G , rs72554665 , rs5030868 , rs1050829 , rs1050828 , Sequence analysis of the entire coding region
Bioscientia GmbH Center for Human Genetics. Glucose-6-Phosphate Dehydrogenase Deficiency G6PDA-202A_376G , rs72554665 , rs5030869 , rs5030868 , rs1050829 , rs1050828
bio.logis Center for Human Genetics. Test for Glucose-6-Phosphate Dehydrogenase Deficiency G6PDA-202A_376G , rs72554665 , rs5030869 , rs5030868 , rs1050829 , rs1050828

The table below contains information about pharmacogenomic variants on PharmGKB. Please follow the link in the "Variant" column for more information about a particular variant. Each link in the "Variant" column leads to the corresponding PharmGKB Variant Page. The Variant Page contains summary data, including PharmGKB manually curated information about variant-drug pairs based on individual PubMed publications. The PMIDs for these PubMed publications can be found on the Variant Page.

The tags in the first column of the table indicate what type of information can be found on the corresponding Variant Page on the appropriate tab.

Links in the "Drugs" column lead to PharmGKB Drug Pages.

Variant?
(138)
Alternate Names / Tag SNPs ? Drugs ? Alleles ?
(+ chr strand)
Function ? Amino Acid?
Translation
VIP No VIP available No VIP available A- 680T_376G N/A N/A N/A
VIP CA VA A-202A_376G N/A N/A N/A
VIP No VIP available No VIP available A-968C_376G N/A N/A N/A
No VIP available CA VA B (wildtype) N/A N/A N/A
VIP CA VA Mediterranean Haplotype N/A N/A N/A
rs1050828 153764217C>T, 16571G>A, 202G>A, 292G>A, 4682155C>T, Asahi, G6PD:202G>A, Val68Met, Val98Met
C > T
Not Available
Val68Met
rs1050829 153763492T>C, 17296A>G, 376A>G, 466A>G, 4681430T>C, A, Asn126Asp, Asn156Asp, G6PD:376A>G, G6PD:A
A > C
A > T
Missense
Asn156Asp
rs5030868 153762634G>A, 18154C>T, 4680572G>A, 563C>T, 653C>T, Mediterranean, Ser188Phe, Ser218Phe
G > A
Not Available
Ser218Phe
rs72554665 1376G>C, 1376G>T, 1466G>C, 1466G>T, 153760484C>A, 153760484C>G, 20304G>C, 20304G>T, 4678422C>A, 4678422C>G, Canton, c.1376G>T, c.1466G>T
C > G
C > A
Not Available
Arg459Leu
Arg459Pro
Alleles, Functions, and Amino Acid Translations are all sourced from dbSNP 138

Overview

Alternate Names:  None
Alternate Symbols:  G6PD1
PharmGKB Accession Id: PA28469

Details

Cytogenetic Location: chrX : q28 - q28
GP mRNA Boundary: chrX : 153759606 - 153775787
GP Gene Boundary: chrX : 153756606 - 153785787
Strand: minus
The mRNA boundaries are calculated using the gene's default feature set from NCBI, mapped onto the UCSC Golden Path. PharmGKB sets gene boundaries by expanding the mRNA boundaries by no less than 10,000 bases upstream (5') and 3,000 bases downstream (3') to allow for potential regulatory regions.

Background

Molecular Structure and function

The G6PD enzyme is conserved throughout evolution, with human G6PD sharing around 93% amino acid identity with rat and 37% with E. coli [Articles:2606104, 8119488]. G6PD is encoded by a gene on the X chromosome (Xq28) [Articles:6930669, 2194676, 2364435], contrary to an early report describing the G6PD enzyme as a fusion protein encoded by genes on chromosomes 6 and X [Article:2758468]. The G6PD gene is around 18kb in length and consists of 13 exons and 12 introns, and was originally cloned in 1986 [Articles:3515319, 3012556, 2428611]. The G6PD gene is found on the minus chromosomal strand - please note that for standardization, the PharmGKB presents all allele base pairs on the positive chromosomal strand, therefore the alleles within our variant annotations will differ (in a complementary manner) from those in this VIP summary that are given on the minus strand as reported in the literature.

The promoter region of the G6PD gene shares some sequence homology with other housekeeping genes, and contains elements for tissue-specific expression which regulate transcription in response to oxidative stress, hormones, nutrients and growth factors [Articles:2428611, 8119488]. Alternative transcriptional start sites and mRNA splice variants have been described [Articles:2910917, 2836867, 3515319, 2428611, 8466644]. The G6PD mature peptide of 514 amino acids in length (59KDa) is active as a dimer or tetramer, and 1 molecule of NADP+ is bound per protein subunit [Articles:10745013, 8466644, 5781270, 7857286, 921782]. The binding of NADP+ is thought to be integral to the enzyme's stability and thus its function, as point mutations close to the NADP+ and dimer interface result in severe G6PD deficiency, revealed by the crystal structure of the Canton variant [Article:10745013] and site directed mutagenesis studies [Article:9492308].

G6PD is a cytoplasmic protein and has two main roles within the cell: the production of NADPH and Ribose-5-phosphate (reviewed in [Articles:17611006, 20122995]. Both are synthesized by steps within the Pentose Phosphate Pathway (PPP), also known as the Hexose Monophosphate Shunt (HMPS), e.g. [Article:539595] (reviewed in [Articles:18177777, 17611006]. NADPH is essential to maintain the redox state of the cell and relieves oxidative stress through the reduction of glutathione, which in turn reduces hydrogen peroxide and oxidative free radicals (reviewed in [Articles:2633878, 8119488, 18177777, 20122995, 17611006]. Ribose-5-phosphate is required for glycolysis and for DNA and RNA biosynthesis (reviewed in [Articles:18177777, 17611006, 2633878, 8119488, 20122995]). Alternative pathways can be utilized for the biosynthesis of nucleic acids, but G6PD is essential for a cell's ability to cope with oxidative stress [Article:7489710]. Tumor suppressor protein p53 has been shown to regulate the PPP by binding to G6PD, preventing dimer formation and thus NADP+ binding, inhibiting NADPH production [Article:21336310]. Several p53 mutants associated with tumors were shown to lack this inhibitory property, and therefore disregulation of G6PD in cancer cells may result in increased cell growth through unregulated glucose biosynthesis and the production of NADPH [Articles:21336310, 20122995].

G6PD is expressed in all cells, but its role is particularly important in red blood cells (rbcs), which do not have mitochondria and are therefore dependent upon G6PD as the only source of NADPH to relieve oxidative stress and protect the hemoglobin beta chain from oxidation (See the PharmGKB Oxidative Stress Regulatory Pathway (reviewed in [Articles:17611006, 18177777, 2633878]). In addition, enzyme levels fall during the rbc lifespan [Article:2633878]. When the required levels of NADPH cannot be maintained, the amount of reduced glutathione falls, resulting in oxidative damage which can ultimately lead to lysis of rbcs (reviewed in [Articles:17611006, 19233695, 18177777]). Under normal conditions, G6PD activity in rbcs is only around 2% of its capacity, inhibited through a negative feedback loop with NADPH (reviewed in [Articles:2633878, 9581796]). However under oxidative pressure, oxidation of NADPH releases the inhibitory effect and G6PD enzyme activity increases, enabling enhanced reducing activity to deal with the additional stress (reviewed in [Articles:2633878, 9581796]). In G6PD deficient rbcs where enzyme activity can be below 10% of the normal value, homeostasis can be maintained and most G6PD deficient individuals remain asymptomatic (reviewed in [Article:2633878]). However, the deficiency becomes apparent under oxidative stress conditions when an increased demand in NADP/NADPH turnover cannot be met (reviewed in [Article:2633878]).

G6PD as an important pharmacogene

We have known for more than 2000 years that the ingestion of fava beans can have dire consequences in some individuals, and could indeed be why Pythagoras imposed abstinence from beans amongst his followers (Brumbaugh and Schwartz, 1980) [Article:11678777]. However, it wasn't until the 20th century that a deficiency in the G6PD enzyme was discovered to be the underlying cause of 'Favism', and the connection that agents other than fava beans can cause similar adverse events in G6PD deficient individuals (discussed in [Articles:18177777, 13618370]). In the 1950s, it was observed that a subset of African-American soldiers were more likely to develop an adverse reaction to the anti-malarial drug primaquine, compared to their Caucasian counterparts [Articles:14945981, 14945980]. This susceptibility to primaquine-induced intravascular hemolysis led to the discovery of a deficiency in G6PD enzyme activity in rbcs [Article:13360274].

More than 400 variations of the G6PD enzyme have now been described, based on clinical manifestations and biochemical properties, and G6PD deficiency is the most prevalent enzyme deficiency in the world (reviewed in [Articles:18177777, 17611006, 7949118, 12064901, 8364584]), affecting an estimated 4.9% of the world's population (more than 300 million people) [Article:19233695]. Polymorphic variants in G6PD are those of significant frequencies (1-70%) in specific human populations - these fall into World Health Organization (WHO) class II and III (see Table I) [Articles:2633878, 5316621, 17611006, 7949118]. Different polymorphic variants have arisen in different geographical areas, for example the Canton variant is predominantly found in Chinese and South East Asian populations [Articles:1953767, 12064901, 17018380, 11499668], reviewed in [Article:17611006]. It is hypothesized that higher population densities of humans due to the development of agriculture facilitated malaria endemisms, and introduced a selective pressure for the spread of G6PD variants (reviewed in [Article:17611006]). Nevertheless, G6PD deficient variants can also occur sporadically due to de novo mutations (reviewed in [Article:17611006]). Most of the genetic variants tend to be single point mutations, and the lack of large or out-of-frame deletions may indicate that total absence of enzyme activity is fatal [Articles:17611006, 2633878, 8364584, 7949118, 3393536]. In-frame deletions are usually associated with the most severe clinical manifestations (class I) (reviewed in [Articles:17611006, 8364584, 7949118]), such as the novel G6PD Tondela variant, a 6 amino acid deletion identified in a heterozygous woman with chronic hemolytic anemia (see Table 1) [Article:21397531].

The mechanism underlying the G6PD deficient phenotype may vary depending on the location of the mutation in the enzyme's 3D structure, and include alterations to protein assembly, dimer formation and stability, interaction with substrates, and protein turnover (reviewed in Bautista, J.M. and Luzzatto, L., Glucose 6-phosphate dehydrogenase. In: Swallow D.M. & Edwards. Y.H., Editors. Protein Dysfunction in Human Genetic Disease. Oxford: BIOS Scientific Publishers; 1997, p. 33-56). Studies suggest that most G6PD variants result in G6PD enzyme instability (reviewed in [Articles:17611006, 5316621]), and variants which cause the most severe deficiency (resulting in CNSHA) are found predominantly at or near the dimer interface of the G6PD protein in exon 10 [Article:8639919], though not exclusively. Different gene variants can confer similar effects on enzyme function and clinical manifestations, and conversely, the same genetic variation can result in different molecular and clinical phenotypes [Articles:8364584, 12064901, 7906668]. Therefore G6PD variants based on enzyme biochemistry may have been characterized differently yet have the same underlying genetic mutation [Articles:2572288, 2912069, 2602358]. The term 'haplotype' is used in this review to define a set of linked alleles in G6PD that are inherited together. The B haplotype is considered the 'wild type' precursor sequence, as alignment of Human and Chimpanzee DNA sequences have shown [Article:2572288]. Variants which differ from the B wild type are often named with the region where the population in which the variant was found [Articles:12064901, 6075369]. Even though attempts have been made to standardize nomenclature since 1967 [Article:6075369], there are still instances where haplotype names have been used to refer to more than one set of variations (see text on haplotype A-). It should be noted that many studies do not screen the whole G6PD gene, and therefore some genetic variants may be unreported and may be a factor underlying differences in biochemical properties.

Exogenous agents can trigger hemolytic anemia in G6PD deficient individuals by inducing oxidative stress in rbcs (reviewed in [Articles:17018377, 18177777, 17611006]). These include certain food items, therapeutic drugs, infections, and exposure to chemicals (for example hair dye containing naphthol) [Articles:17018377, 18177777, 17611006, 20085579]. G6PD variants have been classified into 5 WHO categories according to the severity of clinical manifestation resulting from the genotype (see Table 1), with class II and III the most common type of polymorphic G6PD deficient variant [Articles:8364584, 2633878]. Due to lower rbc G6PD activity, patients carrying class I sporadic variants (associated with CNSHA) are highly susceptible to hemolytic anemia caused by the same drugs that can induce adverse reactions in carriers of polymorphic G6PD variants (reviewed in PMID: 17611006].

Table 1: Classification of G6PD variants

WHO Class Enzyme Activity Associated Phenotype Variant Example Genotyping Reference
I severe deficiency Congenital Non-Spherocytic Hemolytic Anemia (CNSHA) Tondela, Palermo [Articles:21397531, 20085579]
II <10% severely deficient Risk of acute hemolytic anemia Mediterranean, Canton [Articles:3393536, 2263506, 1953767]
III 10-60% moderate deficiency Risk of acute hemolytic anemia A- Haplotype, Asahi [Articles:2572288, 2836867, 11852882]
IV 60-150% normal activity No clinical manifestations B (wildtype), A [Article:3446582]
V 150% enhanced activity Hektoen [Articles:4974311, 5492291]

Table based on [Articles:18177777, 2633878, 8364584, 7949118, 5316621].

Testing for G6PD deficiency

G6PD variants that result in enzyme deficiency confer a G6PD deficient phenotype in hemizygous males (with one copy of the G6PD gene) and homozygous females (for example; [Articles:20520804, 10747271]). To diagnose a phenotype of G6PD deficiency in heterozygous females is more difficult, as the extent of enzyme deficiency activity can vary greatly within heterozygous individuals, due to X-linked mosaicism [Articles:7949118, 13868717, 10747271]. This pattern of gene inactivation is random therefore female heterozygotes will have G6PD deficient rbcs combined with those expressing normal G6PD activity, and the population sizes of these cells can vary from 50:50, to minimal levels or a majority of G6PD deficient cells [Articles:2633878, 13868717, 7949118]. Genotyping is therefore essential to establish heterozygosity in females; however this can make prediction of drug response difficult without phenotypic information of G6PD enzyme activity levels. For example, 75% of females genetically heterozygous for the Mediterranean variant had normal G6PD activity, whereas 25% were enzyme deficient, as assessed by a colorimetric test [Article:20520804]. Testing for both genotype and enzyme function is the ideal method, however due to various factors, including the impracticalities and costs of genotyping in the field, many studies and clinics have solely tested G6PD enzyme activity, making the association of causative variants difficult. In a meta-analysis of 280 studies, less than 8% used DNA analysis to assess G6PD deficiency [Article:19233695].

G6PD and therapeutic drug response

The WHO recommends testing of drugs to predict for risk of hemolysis in G6PD deficient individuals if the drugs are to be prescribed in areas of high prevalence of G6PD deficiency [Article:2633878]. As a consequence of adverse reactions in individuals with G6PD deficiency, the FDA has introduced warnings or precautions on the drug labeling of primaquine, chloroquine, dapsone, rasburicase, avandaryl tablets (glimepiride + rosiglitazone maleate) and glucovance tablets (metformin + glibenclamide) (FDA website). These highlight the possible risk of hemolytic anemia in G6PD deficient individuals upon drug intake. It should be noted that numerous factors can contribute to drug-induced hemolytic anemia in G6PD deficient individuals, including high dosage, other drugs taken in combination, concurrent infections and other genetic variants, as discussed in [Articles:1984194, 20701405, 18177777]. Therefore it may be that many drugs which have been reported to cause hemolysis in individual case studies can be taken safely by G6PD deficient individuals, for example aspirin, vitamin C and chloroquine (discussed further below). These drugs however should be administered with caution especially in combination with other drugs or at high doses, with possible monitoring of rbc or hemoglobin levels [Articles:1984194, 20701405]. Readdressing the safety of drugs in these individuals could make effective therapeutics available (as discussed in [Article:20701405]). More information and comprehensive advice on unsafe drugs in G6PD deficient individuals can be found at http://www.favism.org. Outlined below are several drug subsets and the possible consequences of drug intake for G6PD deficient individuals:

G6PD deficiency and anti-malarial drugs

It is hypothesized that variants associated with G6PD deficiency have remained prevalent in the human population due to positive selective pressures, in particular resistance to uncomplicated and severe malaria (reviewed in [Articles:17611006, 18177777]). At the same time G6PD deficiency confers susceptibility to hemolytic anemia triggered by some anti-malarial drug treatments [Article:19233695]. The prevalence of G6PD deficiency in malaria endemic regions where anti-malarial drugs are required is an important public health issue [Articles:21311583, 19233695]. It should be noted that hemolysis is also a phenotype induced by malaria infection; therefore distinguishing whether this is truly a drug-induced effect may be difficult (as discussed in [Articles:15183620, 20194698]). Another important consideration in areas where malaria is endemic is the financial and practical costs of G6PD screening [Articles:20520804, 18177777]. However, the wide-scale drug-based eradication of malaria is likely to require G6PD deficiency testing [Article:21311583], and thus the application of pharmacogenomics in the treatment of G6PD deficient individuals.

Race-specific differences in sensitivity to hemolytic anemia after treatment with aminoquinolines have been reported since the 1920s (reviewed in [Article:13618370]). In 1956 a deficiency in the G6PD enzyme was determined as the underlying cause of 'primaquine-sensitivity' [Articles:14945981, 14945980, 13360274]. Metabolism of primaquine mediated by CYP proteins is thought to be one of the mechanisms behind the drug sensitivity, as the resulting metabolites induce formation of methemoglobin and reactive oxygen intermediates [Article:19616568]. Alternatives to primaquine have been sought for use in areas where G6PD deficiency is prevalent. However, unfortunately numerous anti-malarial drugs can also induce hemolysis in G6PD deficient individuals, including dapsone which has FDA drug labeling precautions [Articles:20194698, 19690618, 19112496] (reviewed in: [Article:20701405]. The WHO released guidelines after a Technical Consultation in 2004 for the use of Lapdap™ (a combination of chloroproguanil and dapsone) due to safety concerns in G6PD deficient individuals, recommending use only if malaria infection is confirmed, testing for G6PD deficiency and avoiding drug treatment in these individuals, as discussed in [Article:20599264].

FDA labeling of chloroquine advises that caution should be taken when administering this drug to G6PD deficient individuals, though it is not contraindicated. Treatment of normal rbcs with chloroquine in vitro does not boost the PPP, and does not reduce the survival of G6PD deficient rbcs transferred into wild type recipients [Article:1247492] (Chan, T.K., Todd, D., Tso, S.C., Red cell survival studies in glucose 6 phosphate dehydrogenase deficiency. Bulletin of the Hong Kong Medical Association, 1974. 26(1): p. 41-48). However, a high dose of chloroquine (600mg) for the prophylaxis of malaria was reported to induce severe hemolytic anemia in 50 soldiers, all G6PD deficient [Article:79931]. G6PD deficiency may also increase the risk of side affects such as pruritus induced by chloroquine [Article:15027776]. Chloroquine treatment combined with primaquine for P. vivax infection has been associated with significantly decreased hemocrit levels [Article:16969059], though the development of hemolysis in G6PD deficient individuals has been affiliated with primaquine administration rather than chloroquine [Article:20963329]. Severe hemolysis has been reported in several children treated with combinations of chloroquine, chloramphenicol, aspirin and primaquine [Article:1708959]. On the other hand, chloroquine treatment combined with methylene blue or elubaquine does not induce severe adverse effects in individuals with G6PD deficiency [Articles:15655011, 16179085, 16969059]. To conclude, the safety of chloroquine in G6PD deficient individuals is indefinite, and seems to depend on numerous factors including dosage, concurrent drugs and infections, as discussed in [Articles:1984194, 20701405].

When comparing G6PD deficient and G6PD 'normal' children with uncomplicated malaria infection in a trial of artesunate+amodiaquine or artemether-lumefantrine (also known as Artemisinin-based Combination Therapy (ACT)), no significant differences in adverse events were observed, indicating these drug combinations are a promising alternative (see PharmGKB Artemisinin and Derivatives, Pharmacokinetics Pathway) and Amodiaquine Pathway, Pharmacokinetics [Article:18575626].

G6PD deficiency and cancer therapeutics

Several agents involved in the treatment of cancer patients have the potential to result in severe adverse side effects in G6PD deficient individuals, due to induction of oxidative stress in rbcs. Carmustine (BCNU) treatment results in a deficiency in glutathione reductase in erythrocytes, platelets and leukocytes [Articles:539595, 870569]. This lowers levels of reduced glutathione and leads to insufficient removal of hydrogen peroxide and susceptibility to oxidative hemolysis, particularly in rbcs that are G6PD deficient [Articles:539595, 870569]. Doxorubicin (Adriamycin) stimulates the PPP but to a lower extent in G6PD deficient rbcs, and results in oxidative stress through the accumulation of hydrogen peroxide due to an inability to increase G6PD activity (see PharmGKB Doxorubicin Pathway (Cancer Cell), Pharmacodynamics [Articles:539595, 21048526]. This response can also be mirrored in "normal" rbcs when cells are pretreated with carmustine before doxorubicin treatment, resulting in diminished glutathione stability and enhanced susceptibility to oxidative stress [Article:539595]. A number of cases of methemoglobinemia and acute hemolysis after treatment with rasburicase in G6PD deficient individuals have been described [Articles:20196170, 16204390, 19654083]. The FDA labeling has contraindicated rasburicase for G6PD deficient individuals.

The anti-leukemia drug daunorubicin is metabolized into the less-potent form daunorubinol, a process dependent on NADPH via G6PD [Article:8648264]. This biotransformation was greatly reduced in rbcs from A- or Mediterranean G6PD deficient individuals, and thus may have implications in the clinic, raising the issue of whether or not the drug is more effective in these individuals due to prolonged exposure to the more active form and possible toxicity concerns [Article:8648264]. NADPH inhibitors, including primaquine aldehyde, were also shown to reduce daunorubicin metabolism and daunorubinol appearance [Article:8648264].

Aspirin

A child carrying the Mediterranean variant who was diagnosed with systemic arthritis and prescribed a daily dose of 100mg/kg aspirin subsequently developed severe hemolytic anemia, with no sign of viral or bacterial infection [Article:2502894]. Hemolysis was reported in a male administered 1.5g aspirin for a fever (likely a viral infection), who later was found to be G6PD deficient and had a family history of Jaundice [Article:13836342]. However, in 22 healthy G6PD deficient individuals, normal therapeutic doses of aspirin for 4 days (50mg/kg daily) had no effect on rbc count or hemoglobin levels [Article:993904]. Therefore the effect of aspirin on G6PD deficient individuals may be dependent on the variant type and pre-existing clinical conditions (such as an infection or inflammatory disease) [Article:714540]. Dosage is also likely to contribute, as exemplified in the above studies and demonstrated by in vitro studies in which higher levels of aspirin were required to see a drop in GSH levels in the blood from sensitive patients [Article:13836342].

G6PD deficiency and diabetes mellitus treatment

Glibenclamide (glyburide) has been shown to induce acute hemolysis in diabetic patients carrying the A- haplotype or the Mediterranean variant [Articles:8562390, 15126005], though it should be noted that these seem to be sporadic case studies, as discussed in [Article:20701405]. FDA labeling of glucovance tablets, which contain glyburide and metformin HCl, cautions use in G6PD deficient individuals as sulfonylurea agents can result in hemolytic anemia, and advise using a non-sulfonylurea alternative (FDA MedWatch).

G6PD Variants and Haplotypes

A selection of the most studied G6PD variants and known haplotypes are discussed in the separate VIP variant sections (see Variant Summaries), and their association with drug response is summarized in Table 2.

Table 2: Polymorphic G6PD Variants and Haplotypes associated with drug response

Variants Genotyped Drug or Treatment Associated Response Reference*
A- Haplotype
202A/ 376G (rs1050828 and rs1050829) Glibenclamide Acute hemolysis [Article:15126005] (case study)
202A (rs1050828) Sulfadoxine-pyrimethamine and artemisinin plus primaquine Increased risk of developing moderate anemia [Article:20194698] (n=562 total population genotyped, 8.4% heterozygous, 3.9% homo/hemizygous). #
202A (rs1050828) Chlorproguanil-dapsone Increased risk of a drop in hemoglobin levels, compared to sulfadoxine-pyrimethamine treatment. [Article:15183620] (n=1480 total study group treated with CD, n=370 treated with SP. n=237 treated with CD had a >20g/L fall in hemoglobin and of these 35% were carriers of this variant, defined as G6PD deficient), compared to 24% treated with SP.
202A (rs1050828) Chlorproguanil-dapsone-artesunate Severe decreases in hemoglobin levels and increased risk of blood transfusion [Article:19112496] 13% were carriers of this variant and defined as A- G6PD deficient, in n=343 total genotyped.
202A (rs1050828) Sulphadoxine-pyrimethamine coadministered with amodiaquine Increased risk of requiring a blood transfusion [Article:19112496] 11% were carriers of this variant and defined as A- G6PD deficient in n=359 total genotyped.
202A (rs1050828), 376G (rs1050829), 680T (rs137852328), 968C (rs76723693), 542G (rs5030872) Chlorproguanil-dapsone-artesunate Severe reduction in hemoglobin levels and an increased risk of requiring a blood transfusion [Article:19690618] n=800 genotyped. G6PD deficient individuals were defined as A- hemizygous males (17% of n=388), and homozygous A-/A- females (4% of n=412).
Not specified Rasburicase Hemolytic anemia [Article:20196170] (case study)
Not specified Daunorubicin Reduced drug metabolism [Article:8648264]
Not specified Methylene Blue Hemolysis in an individual with methemoglobinemia [Article:5091568] (case study)
Not specified Vitamin C (high dose of 80g intravenously, 2 days) Hemolysis [Article:1138591] (case study)
Mediterranean Variant
563T (rs5030868) Glibenclamide Acute hemolysis [Article:8562390] (case study)
Not specified Aspirin (high dose of 100mg/kg daily) Severe hemolytic anemia in a child with systemic arthritis [Article:2502894] (case study)
Not specified Daunorubicin Reduced drug metabolism [Article:8648264] (in vitro)
Not specified Rasburicase Severe G6PD deficiency was revealed during treatment. [Article:19654083] (case study)

Table key:
*: For each reference, details of whether the study was a single case study, or total study numbers and percentage of individuals carrying the indicated G6PD allele, are given in the reference column.
#: Please note in this study heterozygous 202A individuals were considered G6PD A, and hemizygous/ homozygous 202A individuals were classified as G6PD A-.

The G6PD gene is found on the minus chromosomal strand. Please note that for standardization, the PharmGKB presents all allele base pairs on the positive chromosomal strand, therefore the alleles within our variant annotations and haplotypes will differ (in a complementary manner) from those in this VIP summary that are given on the minus strand as reported in the literature.

Citation PharmGKB summary: very important pharmacogene information for G6PD. Pharmacogenetics and genomics. 2012. McDonagh Ellen M, Thorn Caroline F, Bautista José M, Youngster Ilan, Altman Russ B, Klein Teri E. PubMed
History

Submitted by Ellen M. McDonagh, Caroline F. Thorn, Jose M. Bautista, Ilan Youngster, Teri E. Klein and Russ B. Altman (October 2011)

Variant Summaries rs1050828, rs1050829, rs5030868, rs72554665
Haplotype Summaries G6PD Mediterranean Haplotype, G6PD A- 680T_376G, G6PD A-202A_376G, G6PD A-968C_376G
Drugs
Diseases
Pathways
Phenotypes resistance to malaria infection

Appendix

A database with G6PD mutational and structural data is available at http://www.bioinf.org.uk/g6pd/ established by Dr Andrew C.R. Martin's Group at UCL. A list of pharmacogenomic biomarkers in Drug labels, including G6PD-deficiency, can be found at: http://www.fda.gov/Drugs/ScienceResearch/ResearchAreas/Pharmacogenetics/ucm083378.htm and information on drug safety at MedWatch; http://www.fda.gov/Safety/MedWatch/default.htm. Information related to genetic tests are available for G6PD deficiency; http://www.ncbi.nlm.nih.gov/sites/GeneTests/lab/clinical_disease_id/2339.

Haplotype Overview

The A- G6PD alleles are composed of two genetic variants - rs1050829 allele C + a second variant, either rs1050828 allele T (position 202), rs137852328 allele A (position 680) or rs76723693 (position 968) [Articles:12064901, 2572288, 2836867, 3393536].

The Mediterranean variant (rs5030868 allele A at position 563) has been found with a second variant (rs2230037 allele A at position 437) in Mediterranean and Middle Eastern populations [Articles:2912069, 2321910, 2393028, 1978554].

Source: PharmGKB

All alleles in the download file are on the positive chromosomal strand. PharmGKB considers the first haplotype listed in each table as the reference haplotype for that set.

PharmGKB Curated Pathways

Pathways created internally by PharmGKB based primarily on literature evidence.

  1. Methylene Blue Pathway, Pharmacodynamics
    A stylized diagram showing the mechanisms that can cause methemoglobin production in erythrocytes and the control mechanisms to prevent methemoglobinemia, including methylene blue treatment which requires NADPH from the Pentose Phosphate Pathway.
  1. Oxidative Stress Regulatory Pathway (Erythrocyte)
    A simplified diagram to show several of the regulatory mechanisms that prevent oxidative stress in red blood cells, many of which require NADPH from the Pentose Phosphate Pathway.
  1. Pentose Phosphate Pathway (Erythrocyte)
    A simplified diagram to show the role of G6PD in generating NADPH in red blood cells - this can then be utilized in the Oxidative Stress Regulatory and Methylene Blue Pathways.
  1. Uric Acid-Lowering Drugs Pathway, Pharmacodynamics
    A stylized diagram showing the drugs that act to prevent uric acid formation or enhance its excretion, and adverse reactions associated with these drugs.

External Pathways

Links to non-PharmGKB pathways.

  1. Pentose phosphate pathway (hexose monophosphate shunt) - (Reactome via Pathway Interaction Database)
No related genes are available

Curated Information ?

Evidence Drug Class
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
artemisinin and derivatives

Curated Information ?

Publications related to G6PD: 155

No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
G6PD testing in support of treatment and elimination of malaria: recommendations for evaluation of G6PD tests. Malaria journal. 2013. Domingo Gonzalo J, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Humanized mouse model of glucose 6-phosphate dehydrogenase deficiency for in vivo assessment of hemolytic toxicity. Proceedings of the National Academy of Sciences of the United States of America. 2013. Rochford Rosemary, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
PharmGKB summary: methylene blue pathway. Pharmacogenetics and genomics. 2013. McDonagh Ellen M, et al. PubMed
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Rasburicase Causing Severe Oxidative Hemolysis and Methemoglobinemia in a Patient with Previously Unrecognized Glucose-6-Phosphate Dehydrogenase Deficiency. Acta haematologica. 2013. Cheah Chan Y, et al. PubMed
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An in vivo drug screening model using glucose-6-phosphate dehydrogenase deficient mice to predict the hemolytic toxicity of 8-aminoquinolines. The American journal of tropical medicine and hygiene. 2013. Zhang Peng, et al. PubMed
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Genetic Variants That Confer Resistance to Malaria are Associated with Red Blood Cell Traits in African Americans: An Electronic Medical Record-Based Genome Wide Association Study. G3 (Bethesda, Md.). 2013. Ding Keyue, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Malaria pharmacogenomics: return to the future. Pharmacogenomics. 2013. Gil Jp. PubMed
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Lethal effect of a single dose of rasburicase in a preterm newborn infant. Pediatrics. 2013. Zaramella Patrizia, et al. PubMed
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Clinical spectrum and severity of hemolytic anemia in glucose 6-phosphate dehydrogenase-deficient children receiving dapsone. Blood. 2012. Pamba Allan, et al. PubMed
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Haemolysis risk in methylene blue treatment of G6PD-sufficient and G6PD-deficient West-African children with uncomplicated falciparum malaria: a synopsis of four RCTs. Pharmacoepidemiology and drug safety. 2012. Müller Olaf, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Artemisinin-resistant Plasmodium falciparum in Pursat province, western Cambodia: a parasite clearance rate study. The Lancet infectious diseases. 2012. Amaratunga Chanaki, et al. PubMed
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Methemoglobinemia and hemolysis in a patient with G6PD deficiency treated with rasburicase. American journal of hematology. 2012. Sonbol Mohamad Bassam, et al. PubMed
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Glucose-6-phosphate dehydrogenase deficiency and safety of methylene blue. Drug safety : an international journal of medical toxicology and drug experience. 2012. Müller Olaf, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
PharmGKB summary: very important pharmacogene information for G6PD. Pharmacogenetics and genomics. 2012. McDonagh Ellen M, et al. PubMed
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Methemoglobinemia induced by rasburicase in a pediatric patient: A case report and literature review. Journal of oncology pharmacy practice : official publication of the International Society of Oncology Pharmacy Practitioners. 2011. Ng John S, et al. PubMed
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A randomized trial of a single-dose rasburicase versus five-daily doses in patients at risk for tumor lysis syndrome. Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 2011. Vadhan-Raj S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Blue cures blue but be cautious. Journal of pharmacy & bioallied sciences. 2011. Sikka Pranav, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Prospective-retrospective biomarker analysis for regulatory consideration: white paper from the industry pharmacogenomics working group. Pharmacogenomics. 2011. Patterson Scott D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Chronic hemolytic anemia is associated with a new glucose-6-phosphate dehydrogenase in-frame deletion in an older woman. Blood cells, molecules & diseases. 2011. Manco Licínio, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Stress response and cytoskeletal proteins involved in erythrocyte membrane remodeling upon Plasmodium falciparum invasion are differentially carbonylated in G6PD A(-) deficiency. Free radical biology & medicine. 2011. Méndez Darío, et al. PubMed
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Diabetes mellitus and glucose-6-phosphate dehydrogenase deficiency: from one crisis to another. Diabetes & metabolism. 2011. Carette C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
A research agenda for malaria eradication: diagnoses and diagnostics. PLoS medicine. 2011. malERA Consultative Group on Diagnoses and Diagnostics, et al. PubMed
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Systematic review of pharmacoeconomic studies of pharmacogenomic tests. Pharmacogenomics. 2010. Beaulieu Mathieu, et al. PubMed
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Ciprofloxacin-induced acute haemolytic anaemia in a patient with glucose-6-phosphate dehydrogenase Mediterranean deficiency: a case report. Annals of hematology. 2010. Sansone Stefano, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review. Drug safety : an international journal of medical toxicology and drug experience. 2010. Youngster Ilan, et al. PubMed
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The rise and fall of the antimalarial Lapdap: a lesson in pharmacogenetics. Lancet. 2010. Luzzatto Lucio. PubMed
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In Tanzania, hemolysis after a single dose of primaquine coadministered with an artemisinin is not restricted to glucose-6-phosphate dehydrogenase-deficient (G6PD A-) individuals. Antimicrobial agents and chemotherapy. 2010. Shekalaghe Seif A, et al. PubMed
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The impact of phenotypic and genotypic G6PD deficiency on risk of plasmodium vivax infection: a case-control study amongst Afghan refugees in Pakistan. PLoS medicine. 2010. Leslie Toby, et al. PubMed
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A ghostly presence-G6PD deficiency. American journal of hematology. 2010. Bain Barbara J. PubMed
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Metabolic genes in cancer: their roles in tumor progression and clinical implications. Biochimica et biophysica acta. 2010. Furuta Eiji, et al. PubMed
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Glucose 6-phosphate dehydrogenase Palermo R257M: a novel variant associated with chronic non-spherocytic haemolytic anaemia. British journal of haematology. 2010. Rigano Paolo, et al. PubMed
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Clinical aspects of hemolysis in patients with P. vivax malaria treated with primaquine, in the Brazilian Amazon. The Brazilian journal of infectious diseases : an official publication of the Brazilian Society of Infectious Diseases. 2010. Ramos Júnior Wilson M, et al. PubMed
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Glucose-6-phosphate dehydrogenase deficiency and malaria: cytochemical detection of heterozygous G6PD deficiency in women. The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society. 2009. Peters Anna L, et al. PubMed
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Cytochrome P(450)-dependent toxic effects of primaquine on human erythrocytes. Toxicology and applied pharmacology. 2009. Ganesan Shobana, et al. PubMed
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Allelic heterogeneity of G6PD deficiency in West Africa and severe malaria susceptibility. European journal of human genetics : EJHG. 2009. Clark Taane G, et al. PubMed
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[A severe G6PD deficiency revealed during a chemotherapy protocol including rasburicase]. Annales de biologie clinique. 2009. Joly P, et al. PubMed
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The global prevalence of glucose-6-phosphate dehydrogenase deficiency: a systematic review and meta-analysis. Blood cells, molecules & diseases. 2009. Nkhoma Ella T, et al. PubMed
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Chlorproguanil-dapsone-artesunate versus artemether-lumefantrine: a randomized, double-blind phase III trial in African children and adolescents with uncomplicated Plasmodium falciparum malaria. PloS one. 2009. Premji Zul, et al. PubMed
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Exchange transfusion as treatment for rasburicase induced methemoglobinemia in a glucose-6-phosphate dehydrogenase deficient patient. Pediatric blood & cancer. 2008. Bhat Priya, et al. PubMed
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Glucose-6-phosphate dehydrogenase deficiency. Lancet. 2008. Cappellini M D, et al. PubMed
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Methemoglobinemia and hemolytic anemia caused by rasburicase administration in a newly diagnosed child with Burkitt lymphoma/leukemia. Pediatric blood & cancer. 2008. Borinstein Scott C, et al. PubMed
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An open label, randomised trial of artesunate+amodiaquine, artesunate+chlorproguanil-dapsone and artemether-lumefantrine for the treatment of uncomplicated malaria. PloS one. 2008. Owusu-Agyei Seth, et al. PubMed
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High risk of severe anaemia after chlorproguanil-dapsone+artesunate antimalarial treatment in patients with G6PD (A-) deficiency. PloS one. 2008. Fanello Caterina I, et al. PubMed
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G6PD deficiency: the genotype-phenotype association. Blood reviews. 2007. Mason Philip J, et al. PubMed
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Catalase deficiency may complicate urate oxidase (rasburicase) therapy. Free radical research. 2007. Góth László, et al. PubMed
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Aniline-induced methaemoglobinaemia in a glucose-6-phosphate dehydrogenase enzyme deficient patient. Anaesthesia and intensive care. 2007. Mullick P, et al. PubMed
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X-linked G6PD deficiency protects hemizygous males but not heterozygous females against severe malaria. PLoS medicine. 2007. Guindo Aldiouma, et al. PubMed
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G6PD (AC)n and (CTT)n microsatellites in Mexican Mestizos with common G6PD African variants. Blood cells, molecules & diseases. 2007. Vaca Gerardo. PubMed
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Glucose 6-phosphate dehydrogenase deficiency: from genotype to phenotype. Haematologica. 2006. Luzzatto Lucio. PubMed
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Incidence and complete molecular characterization of glucose-6-phosphate dehydrogenase deficiency in the Guangxi Zhuang autonomous region of southern China: description of four novel mutations. Haematologica. 2006. Yan Tizhen, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Primaquine: report from CDC expert meeting on malaria chemoprophylaxis I. The American journal of tropical medicine and hygiene. 2006. Hill David R, et al. PubMed
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Safety and tolerability of elubaquine (bulaquine, CDRI 80/53) for treatment of Plasmidium vivax malaria in Thailand. The Korean journal of parasitology. 2006. Krudsood Srivicha, et al. PubMed
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Recognition and management of methemoglobinemia and hemolysis in a G6PD-deficient patient on experimental anticancer drug Triapine. American journal of hematology. 2006. Foltz Lynda M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Glucose-6-phosphate dehydrogenase variants associated with favism in Thai children. International journal of hematology. 2006. Laosombat Vichai, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Coexistence of five G6PD variants indicates ethnic complexity of Phuket islanders, Southern Thailand. Journal of human genetics. 2006. Ninokata Aya, et al. PubMed
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Methylene blue for malaria in Africa: results from a dose-finding study in combination with chloroquine. Malaria journal. 2006. Meissner Peter E, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Hemolysis and methemoglobinemia secondary to rasburicase administration. The Annals of pharmacotherapy. 2005. Browning Linda A, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Drug-induced haemolysis and methaemoglobinaemia in glucose 6-phosphate dehydrogenase deficiency. British journal of haematology. 2005. Dalal Bukal I, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Postoperative methemoglobinemia with associated G-6-P-D deficiency in infant cardiac surgery--enigmas in diagnosis and management. Paediatric anaesthesia. 2005. Maddali Madan Mohan, et al. PubMed
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Safety of the combination of chloroquine and methylene blue in healthy adult men with G6PD deficiency from rural Burkina Faso. Tropical medicine & international health : TM & IH. 2005. Mandi Germain, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Rapid screening for glucose-6-phosphate dehydrogenase deficiency and haemoglobin polymorphisms in Africa by a simple high-throughput SSOP-ELISA method. Malaria journal. 2005. Enevold Anders, et al. PubMed
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Safety of the methylene blue plus chloroquine combination in the treatment of uncomplicated falciparum malaria in young children of Burkina Faso [ISRCTN27290841]. Malaria journal. 2005. Meissner Peter E, et al. PubMed
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Prolonged hemolysis and methemoglobinemia following organic copper fungicide ingestion. Veterinary and human toxicology. 2004. Yang Chen-Chang, et al. PubMed
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Glibenclamide-induced acute haemolytic anaemia revealing a G6PD-deficiency. Diabetes research and clinical practice. 2004. Vinzio Stéphane, et al. PubMed
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Comparison of chlorproguanil-dapsone with sulfadoxine-pyrimethamine for the treatment of uncomplicated falciparum malaria in young African children: double-blind randomised controlled trial. Lancet. 2004. Alloueche A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Estrogen receptor-mediated regulation of oxidative stress and DNA damage in breast cancer. Carcinogenesis. 2004. Mobley James A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Molecular basis of G6PD deficiency in India. Blood cells, molecules & diseases. 2004. Sukumar Sridevi, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Rasburicase (recombinant urate oxidase) for the management of hyperuricemia in patients with cancer: report of an international compassionate use study. Cancer. 2003. Bosly André, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Treatment-specific changes in gene expression discriminate in vivo drug response in human leukemia cells. Nature genetics. 2003. Cheok Meyling H, et al. PubMed
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Urate-oxidase in the prevention and treatment of metabolic complications in patients with B-cell lymphoma and leukemia, treated in the Société Française d'Oncologie Pédiatrique LMB89 protocol. Annals of oncology : official journal of the European Society for Medical Oncology / ESMO. 2002. Patte C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
A single mutation 202G>A in the human glucose-6-phosphate dehydrogenase gene (G6PD) can cause acute hemolysis by itself. Blood. 2002. Hirono Akira, et al. PubMed
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Hemolytic anemia after methylene blue therapy for aniline-induced methemoglobinemia. Veterinary and human toxicology. 2002. Liao Yao-Pan, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Hematologically important mutations: glucose-6-phosphate dehydrogenase. Blood cells, molecules & diseases. 2002. Beutler Ernest, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Pulmonary toxicity with mefloquine. The European respiratory journal. 2001. Udry E, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Metoclopramide-induced methemoglobinemia in a patient with co-existing deficiency of glucose-6-phosphate dehydrogenase and NADH-cytochrome b5 reductase: failure of methylene blue treatment. Haematologica. 2001. Karadsheh N S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Distribution of glucose-6-phosphate dehydrogenase mutations in Southeast Asia. Human genetics. 2001. Iwai K, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
The lower susceptibility to Plasmodium falciparum malaria of Fulani of Burkina Faso (west Africa) is associated with low frequencies of classic malaria-resistance genes. Transactions of the Royal Society of Tropical Medicine and Hygiene. 2001. Modiano D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Glucose-6-phosphate dehydrogenase mutations and haplotypes in Mexican Mestizos. Blood cells, molecules & diseases. 2000. Arámbula E, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Human glucose-6-phosphate dehydrogenase: the crystal structure reveals a structural NADP(+) molecule and provides insights into enzyme deficiency. Structure (London, England : 1993). 2000. Au S W, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Red cell glucose-6-phosphate dehydrogenase status and pyruvate kinase activity in a Nigerian population. Tropical medicine & international health : TM & IH. 2000. May J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Hemolytic crisis after excessive ingestion of fava beans in a male infant with G6PD Canton. International journal of hematology. 1999. Shibuya A, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Methylene blue-induced hyperbilirubinemia in neonatal glucose-6-phosphate dehydrogenase (G6PD) deficiency. The Journal of maternal-fetal medicine. 2000. Gauthier T W. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Methemoglobinemia: etiology, pharmacology, and clinical management. Annals of emergency medicine. 1999. Wright R O, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Haemolytic potential of three chemotherapeutic agents and aspirin in glucose-6-phosphate dehydrogenase deficiency. Eastern Mediterranean health journal = La revue de santé de la Méditerranée orientale = al-Majallah al-ṣiḥḥīyah li-sharq al-mutawassiṭ. 1999. Ali N A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Management of a case of chloroquine-resistant falciparum malaria in a pregnant woman with glucose-6-phosphate dehydrogenase (G6PD) deficiency. American journal of perinatology. 1999. Cultrera R, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Drug-induced pneumonia associated with hemizygote glucose-6-phosphate-dehydrogenase deficiency. European journal of haematology. 1998. Drent M. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Methemoglobinemia induced by methylene blue pertubation during laparoscopy. Acta anaesthesiologica Scandinavica. 1998. Bilgin H, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Treatment of high-risk, refractory acquired methemoglobinemia with automated red blood cell exchange. Journal of clinical apheresis. 1998. Golden P J, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Urate oxidase in prevention and treatment of hyperuricemia associated with lymphoid malignancies. Leukemia : official journal of the Leukemia Society of America, Leukemia Research Fund, U.K. 1997. Pui C H, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Glucose-6-phosphate dehydrogenase deficiency severely restricts the biotransformation of daunorubicin in human erythrocytes. The Journal of laboratory and clinical medicine. 1996. Amitai Y, et al. PubMed
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Glyburide-induced acute haemolysis in a G6PD-deficient patient with NIDDM. British journal of haematology. 1996. Meloni G, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Natural selection of hemi- and heterozygotes for G6PD deficiency in Africa by resistance to severe malaria. Nature. 1995. Ruwende C, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
G6PD deficiency. Blood. 1994. Beutler E. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
G6PD Ferrara I has the same two mutations as G6PD A(-) but a distinct biochemical phenotype. Human genetics. 1994. Cappellini M D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Glucose-6-phosphate dehydrogenase: a "housekeeping" enzyme subject to tissue-specific regulation by hormones, nutrients, and oxidant stress. The FASEB journal : official publication of the Federation of American Societies for Experimental Biology. 1994. Kletzien R F, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Concise review: methemoglobinemia. American journal of hematology. 1993. Mansouri A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available VIP No VIP available
Variants of glucose-6-phosphate dehydrogenase are due to missense mutations spread throughout the coding region of the gene. Human mutation. 1993. Vulliamy T, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Two commonly occurring nucleotide base substitutions in Chinese G6PD variants. Biochemical and biophysical research communications. 1991. Chiu D T, et al. PubMed
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Hemolytic anemia due to G6PD deficiency and urate oxidase in a kidney-transplant patient. Clinical nephrology. 1991. Ducros J, et al. PubMed
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Glucose-6-phosphate dehydrogenase deficiency. The New England journal of medicine. 1991. Beutler E. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
The NT 1311 polymorphism of G6PD: G6PD Mediterranean mutation may have originated independently in Europe and Asia. American journal of human genetics. 1990. Beutler E, et al. PubMed
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Hemolytic reactions to nitrofurantoin in patients with glucose-6-phosphate dehydrogenase deficiency: theory and practice. DICP : the annals of pharmacotherapy. 1990. Gait J E. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
G6PD Canton a common deficient variant in South East Asia caused by a 459 Arg----Leu mutation. Nucleic acids research. 1990. Stevens D J, et al. PubMed
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[Recurrent acute renal failure during the course of hemolytic crisis in a patient with glucose-6-phosphate dehydrogenase deficiency]. Polski tygodnik lekarski (Warsaw, Poland : 1960). 1991. Syzdół P, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Ascorbic-acid-induced haemolysis in G-6-PD deficiency. Lancet. 1990. Mehta J B, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Human red cell glucose-6-phosphate dehydrogenase is encoded only on the X chromosome. Cell. 1990. Mason P J, et al. PubMed
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Human red cell glucose-6-phosphate dehydrogenase: all active enzyme has sequence predicted by the X chromosome-encoded cDNA. Cell. 1990. Beutler E, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Common glucose-6-phosphate dehydrogenase (G6PD) variants from the Italian population: biochemical and molecular characterization. Annals of human genetics. 1990. Viglietto G, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Drug-induced haemolysis and renal failure in children with glucose-6-phosphate dehydrogenase deficiency in Afghanistan. Annals of tropical paediatrics. 1990. Choudhry V P, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Glucose-6-phosphate dehydrogenase. Characteristics revealed by the rat liver enzyme structure. European journal of biochemistry / FEBS. 1989. Jeffery J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Molecular heterogeneity of glucose-6-phosphate dehydrogenase A-. Blood. 1989. Beutler E, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Two structural genes on different chromosomes are required for encoding the major subunit of human red cell glucose-6-phosphate dehydrogenase. Cell. 1989. Kanno H, et al. PubMed
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Two point mutations are responsible for G6PD polymorphism in Sardinia. American journal of human genetics. 1989. De Vita G, et al. PubMed
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Aspirin-induced acute haemolytic anaemia in glucose-6-phosphate dehydrogenase-deficient children with systemic arthritis. Acta haematologica. 1989. Meloni T, et al. PubMed
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Glucose-6-phosphate dehydrogenase deficiency. WHO Working Group. Bulletin of the World Health Organization. 1989. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Diverse point mutations in the human glucose-6-phosphate dehydrogenase gene cause enzyme deficiency and mild or severe hemolytic anemia. Proceedings of the National Academy of Sciences of the United States of America. 1988. Vulliamy T J, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Molecular cloning and nucleotide sequence of cDNA for human glucose-6-phosphate dehydrogenase variant A(-). Proceedings of the National Academy of Sciences of the United States of America. 1988. Hirono A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
A single nucleotide base transition is the basis of the common human glucose-6-phosphate dehydrogenase variant A (+). Genomics. 1987. Takizawa T, et al. PubMed
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A phase-III clinical trial of mefloquine in children with chloroquine-resistant falciparum malaria in Thailand. Bulletin of the World Health Organization. 1987. Chongsuphajaisiddhi T, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
Trials of mefloquine in vivax and of mefloquine plus 'fansidar' in falciparum malaria. Lancet. 1985. Harinasuta T, et al. PubMed
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Phenazopyridine-induced hemolytic anemia in a patient with G6PD deficiency. Acta haematologica. 1983. Tishler M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available VA No VIP available No VIP available
A phase II clinical trial of mefloquine in patients with chloroquine-resistant falciparum malaria in Thailand. Bulletin of the World Health Organization. 1983. Harinasuta T, et al. PubMed
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Acute hemolytic anaemia due to phenazopyridine hydrochloride in G-6-PD deficient subject. Lancet. 1982. Mercieca J E, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Influence of double genetic polymorphism on response to sulfamethazine. Clinical pharmacology and therapeutics. 1982. Woolhouse N M, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Localization of loci for hypoxanthine phosphoribosyltransferase and glucose-6-phosphate dehydrogenase and biochemical evidence of nonrandom X chromosome expression from studies of a human X-autosome translocation. Proceedings of the National Academy of Sciences of the United States of America. 1980. Pai G S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
The effect of BCNU and adriamycin on normal and G6PD deficient erythrocytes. American journal of hematology. 1979. Sagone A L, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Haemoglobinopathies and G.-6-P.D. deficiency in Laos. Lancet. 1978. Sicard D, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Aspirin-induced hemolysis: the role of concomitant oxidant (H2O2) challenge. Pediatric research. 1978. Stockman J A, et al. PubMed
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Hemolysis during BAL chelation therapy for high blood lead levels in two G6PD deficient children. Clinical pediatrics. 1978. Janakiraman N, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Severe generalized glutathione reductase deficiency after antitumor chemotherapy with BCNU" [1,3-bis(chloroethyl)-1-nitrosourea]. The Journal of laboratory and clinical medicine. 1977. Frischer H, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Evaluation of the hemolytic role of aspirin in glucose-6-phosphate dehydrogenase deficiency. The Journal of pediatrics. 1976. Glader B E. PubMed
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Haemolytic effect of two sulphonamides evaluated by a new method. British journal of haematology. 1976. Gaetani G D, et al. PubMed
No Dosing Guideline available No Drug Label available CA VA No VIP available No VIP available
Hyperlactatemia and hemolysis in G6PD deficiency after nitrofurantoin ingestion. The American journal of the medical sciences. 1976. Lavelle K J, et al. PubMed
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Letter: Ascorbic acid-induced hemolysis in G-6-PD deficiency. Annals of internal medicine. 1975. Campbell G D, et al. PubMed
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Acute haemolytic anaemia in typhoid fever. Indian journal of pediatrics. 1972. Bakshi S, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Characteristics and distribution of glucose-6-phosphate dehydrogenase-deficient variants in South China. American journal of human genetics. 1972. Chan T K, et al. PubMed
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Failure of methylene blue treatment in toxic methemoglobinemia. Association with glucose-6-phosphate dehydrogenase deficiency. Annals of internal medicine. 1971. Rosen P J, et al. PubMed
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Chloramphenicol-induced hemolysis in Caucasian glucose-6-phosphate dehydrogenase deficiency. Annals of internal medicine. 1971. McCaffrey R P, et al. PubMed
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Human glucose-6-phosphate dehydrogenase variants. Bulletin of the World Health Organization. 1971. Yoshida A, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
Amino acid substitution (histidine to tyrosine) in a glucose-6-phosphate dehydrogenase variant (G6PD Hektoen) associated with over-production. Journal of molecular biology. 1970. Yoshida A. PubMed
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Typhoid fever in Hong Kong junk family. British medical journal. 1969. Forrest C R, et al. PubMed
No Dosing Guideline available No Drug Label available No Clinical Annotation available No Variant Annotation available No VIP available No VIP available
A new structural variant of glucose-6-phosphate dehydrogenase with a high production rate (G6PD Hektoen). The Journal of laboratory and clinical medicine. 1969. Dern R J, et al. PubMed
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Nomenclature of glucose-6-phosphate dehydrogenase in man. American journal of human genetics. 1967. PubMed
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Hemolysis in typhoid fever. British medical journal. 1967. La Grutta A, et al. PubMed
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A single amino Acid substitution (asparagine to aspartic Acid) between normal (b+) and the common negro variant (a+) of human glucose-6-phosphate dehydrogenase. Proceedings of the National Academy of Sciences of the United States of America. 1967. Yoshida A. PubMed
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Haemolysis in typhoid fever in children with G-6-PD deficiency. British medical journal. 1967. Hersko C, et al. PubMed
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A Chinese variant of glucose-6-phosphate dehydrogenase. The Journal of laboratory and clinical medicine. 1966. McCurdy P R, et al. PubMed
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Severe anemia with hemolysis and megaloblastic erythropoiesis. A reaction to nitrofurantoin administered during pregnancy. JAMA : the journal of the American Medical Association. 1965. Pritchard J A, et al. PubMed
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METHEMOGLOBIN REDUCTION. STUDIES OF THE INTERACTION BETWEEN CELL POPULATIONS AND OF THE ROLE OF METHYLENE BLUE. Blood. 1963. BEUTLER E, et al. PubMed
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The normal human female as a mosaic of X-chromosome activity: studies using the gene for C-6-PD-deficiency as a marker. Proceedings of the National Academy of Sciences of the United States of America. 1962. BEUTLER E, et al. PubMed
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Haemolytic jaundice following aspirin administration to a patient with a deficiency of glucose-6-phosphate dehydrogenase in erythrocytes. Acta haematologica. 1960. SZEINBERG A, et al. PubMed
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Haemolytic jaundice following aspirin administration to a patient with a deficiency of glucose-6-phosphate dehydrogenase in erythrocytes. Acta haematologica. 1960. SZEINBERG A, et al. PubMed
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Methaemoglobin reduction test: a new, simple, in vitro test for identifying primaquine-sensitivity. Bulletin of the World Health Organization. 1960. BREWER G J, et al. PubMed
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The hemolytic effect of primaquine and related compounds: a review. Blood. 1959. BEUTLER E. PubMed
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Enzymatic deficiency in primaquine-sensitive erythrocytes. Science (New York, N.Y.). 1956. ALVING A S, et al. PubMed

LinkOuts

Entrez Gene:
2539
OMIM:
305900
UCSC Genome Browser:
NM_000402
RefSeq RNA:
NM_000402
NM_001042351
RefSeq Protein:
NP_000393
NP_001035810
MutDB:
G6PD
ALFRED:
LO000338O
HuGE:
G6PD
Comparative Toxicogenomics Database:
2539
HumanCyc Gene:
HS08467
HGNC:
4057

Common Searches