Lab result explainedBlood count (CBC)Last updated November 11, 2026

G6PD test: normal range, what a deficient result means and what to avoid

G6PD test (G6PD) · Stand-alone enzyme assay; part of the hemolysis work-up and of newborn screening in some states and countries · reported in U/g Hb (units of enzyme activity per gram of hemoglobin); also reported as a percentage of the normal median or as U per 10 to the 12th red cells

Glucose-6-phosphate dehydrogenase (G6PD) is an enzyme inside red blood cells that protects them from oxidative damage, and the G6PD test measures how much of it is working. Red cells have no nucleus and cannot make new proteins, so they rely on G6PD to produce NADPH, the molecule that keeps their antioxidant defenses charged. When activity is low, exposure to certain drugs, infections or fava beans overwhelms the cell and it breaks apart, causing a sudden episode of hemolytic anemia. Normal activity on the quantitative test is roughly 7 to 20 units per gram of hemoglobin (U/g Hb), with each lab setting its own range; deficiency is usually defined as less than 30 percent of the normal median, and values between 30 and 80 percent are called intermediate.

G6PD deficiency is the most common enzyme disorder in the world, affecting around 400 million people. The gene sits on the X chromosome, so it mainly affects males: about 10 to 14 percent of African American men carry the A- variant, which leaves 10 to 15 percent of normal activity and causes self-limited episodes, while the Mediterranean variant found in people of Italian, Greek, Middle Eastern, Sephardic Jewish and South Asian ancestry leaves under 10 percent and causes more severe hemolysis. Women who carry one copy have a mixture of normal and deficient red cells and test anywhere from deficient to normal, which is why a quantitative result matters more for them than a simple screen.

The test is ordered in three situations: to explain an episode of hemolysis or unexplained jaundice in a newborn, before prescribing a drug that is dangerous in deficiency (primaquine and tafenoquine for malaria, rasburicase, dapsone, methylene blue), and as newborn screening in regions where deficiency is common. The most important pitfall is timing. Right after a hemolytic episode the oldest, most deficient cells have been destroyed and the young replacement cells have the most enzyme, so a test taken during or just after a crisis can read falsely normal; if the suspicion is strong, it is repeated about three months later.

G6PD at a glance

What it is: a measure of the activity of glucose-6-phosphate dehydrogenase, the enzyme that protects red cells from oxidative damage; either a qualitative screen (normal or deficient) or a quantitative assay in U/g Hb or as a percentage of normal.
Normal (adults): roughly 7–20 U/g Hb depending on the lab and method; many labs report 60–150 percent of the adjusted normal median as normal. Labs differ; use the printed range.
Deficient: below 30 percent of normal (often under 4 U/g Hb) in the classification used for drug safety; the 2022 WHO classes are A (under 20 percent, chronic hemolysis), B (under 45 percent, hemolysis with triggers) and C (60–150 percent, normal). Intermediate (30–80 percent) is seen mostly in female carriers.
Low G6PD means risk of hemolysis after triggers: fava beans, oxidant drugs (primaquine, tafenoquine, dapsone, rasburicase, methylene blue, nitrofurantoin, sulfonamides), naphthalene mothballs, henna and infections. Between episodes most people are well.
False-normal: a test done during or within 2 to 3 months of a hemolytic episode, or after a transfusion, can read normal because young red cells have the most enzyme. Repeat when the reticulocyte count is normal.
Newborns: screened in some US states and widely abroad; a deficient result means watching closely for jaundice in the first week and avoiding triggers for life.

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What G6PD measures

G6PD is the first enzyme of the pentose phosphate pathway, and in red cells it is the only source of NADPH. NADPH recycles glutathione, which neutralizes the hydrogen peroxide and free radicals generated continuously by oxygen-carrying hemoglobin and in bursts during infection or after exposure to oxidant drugs. In a deficient cell the glutathione reserve collapses under oxidative load, hemoglobin precipitates into clumps called Heinz bodies, the membrane is damaged, and the cell either bursts in the circulation (intravascular hemolysis, with dark urine) or is pulled apart in the spleen, leaving the bite and blister cells seen on a blood smear. Because old red cells have the least enzyme, episodes in the milder A- variant stop on their own after the old cells are gone.

Two kinds of test are in use. The fluorescent spot test and similar screens mix blood with substrate and report whether NADPH is produced: normal or deficient. They are cheap and fast but miss intermediate activity, which includes most female carriers, and the newer point-of-care devices used before antimalarial treatment have the same limitation. The quantitative spectrophotometric assay measures the rate of NADPH formation and reports activity in units per gram of hemoglobin (or per 10 to the 12th red cells), which the lab converts to a percentage of the normal male median. Genetic testing for specific variants is available and is useful in families and in women with intermediate results, but it does not replace the activity measurement, since more than 200 variants exist.

Activity is highest in reticulocytes and falls as cells age, so anything that raises the proportion of young cells inflates the result: an acute hemolytic episode, recent blood loss, treated iron or B12 deficiency, and a transfusion within the past 3 months (donor cells carry donor enzyme). A white cell count above about 20,000 can also raise the measured activity because white cells contain much more G6PD than red cells. No fasting is needed, and the sample is drawn into an EDTA tube; results in babies are interpreted against newborn ranges, which are higher than adult ranges because newborn red cells are young.

Normal range for G6PD

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

Group	Typical range (U/g Hb (units of enzyme activity per gram of hemoglobin); also reported as a percentage of the normal median or as U per 10 to the 12th red cells)	Notes
Adults, normal (quantitative)	Roughly 7–20 U/g Hb (varies with method and temperature; 4.6–13.5 and 8.8–13.4 are both published)	Labs differ widely because assays run at different temperatures. Always compare against the printed range or the percentage of normal.
Normal, WHO class C / older class IV	60–150 percent of the normal male median	Unrestricted use of all drugs, including primaquine and tafenoquine (tafenoquine requires activity above 70 percent).
Intermediate	30–80 percent of normal (some labs 30–60)	Mostly women with one deficient X chromosome; a mixed population of normal and deficient cells. Qualitative screens usually call these normal, yet primaquine can still cause significant hemolysis. Quantitative testing is needed.
Deficient, moderate (older WHO class III, e.g. the A- variant)	10–30 percent of normal	Common in people of African ancestry (about 10 to 14 percent of African American men). Hemolysis with triggers is self-limited because young cells retain enough enzyme.
Deficient, severe (older WHO class II, e.g. Mediterranean, Canton, Kaiping)	Below 10 percent of normal	Hemolysis with triggers can be severe and prolonged; favism is largely confined to this group. Includes most people of Mediterranean, Middle Eastern and South Asian ancestry with deficiency.
WHO 2022 class A	Below 20 percent with chronic hemolysis even without triggers	Rare variants causing chronic nonspherocytic hemolytic anemia from birth; previously class I.
WHO 2022 class B	Below 45 percent, acute hemolysis only with triggers	Merges the older class II and III variants; the 2022 revision uses activity and clinical phenotype rather than ancestry.
Newborns	Higher than adult values (young red cells); deficiency is still defined against age-specific cut-offs	A deficient newborn is at increased risk of significant jaundice; the AAP recommends G6PD testing in jaundiced infants with relevant ancestry, a family history or a poor response to phototherapy.

High or normal G6PD after a hemolytic episode (false-normal result)

There is no disease caused by too much G6PD, and a result above the reference range is not a concern in itself. A high reading usually reflects a high proportion of young red cells, which carry the most enzyme: reticulocytosis after bleeding or hemolysis, recovery from iron, B12 or folate deficiency, a recent transfusion, or a very high white cell count contaminating the assay. In those settings a high value is a laboratory artifact rather than a finding about your health.

The clinically important version of a high or normal result is the false-normal. During and for weeks after a hemolytic crisis, the oldest and most enzyme-poor cells have already been destroyed and the marrow has flooded the blood with reticulocytes, so a person with genuine deficiency, particularly the A- variant, can test squarely in the normal range. If you were tested because of jaundice, dark urine or a sudden drop in hemoglobin and the result came back normal, the test should be repeated about 3 months later, once the reticulocyte count is back to baseline, or a genetic test ordered.

A normal result in a woman also needs care. Because of X-inactivation, a carrier has two red cell populations and her average activity can fall anywhere between deficient and normal. A qualitative screen reporting normal does not exclude a significant deficient population, and trials of primaquine in heterozygous women with intermediate activity have documented falls in hemoglobin of 2 to 3 g/dL. For drug-safety decisions, women are assessed with a quantitative result, and the threshold for using tafenoquine is activity above 70 percent.

Common causes

Testing during or within 3 months of a hemolytic episode
The deficient old cells are gone and young cells with high activity dominate; the A- variant in particular reads normal in this window. Repeat when the reticulocyte count has normalized.
Recent blood transfusion
Donor red cells carry donor enzyme for up to 3 months and raise the measured activity toward normal.
Reticulocytosis from any cause
Recovery from bleeding, treated iron or B12 deficiency, and chronic hemolysis of other causes all raise the proportion of young cells and the average enzyme activity.
Female carrier (heterozygote) with mostly normal cells
Depending on X-inactivation, a carrier can have 80 percent normal cells and test normal while still having a vulnerable deficient population.
Very high white cell count
White cells contain far more G6PD than red cells; counts above about 20,000 per µL can inflate a whole-blood assay unless the lab removes them.
Laboratory variation
Assays run at 30 °C or 37 °C and different reagent systems give different absolute numbers, so a value above one lab's range may be mid-range at another; the percentage of normal is more comparable.

Symptoms that can go with it

None; a high or normal G6PD causes no symptoms
If the result is normal but you recently had dark urine, jaundice, back pain or a sudden drop in hemoglobin, the symptoms still need explaining, and a repeat test in 3 months is reasonable
A woman with a normal screen who has had hemolysis after a drug, infection or fava beans should ask for a quantitative test

Low G6PD (G6PD deficiency)

A low result means your red cells have less protection against oxidative stress than normal and can be destroyed in large numbers when exposed to a trigger. Most of the time, and for most people with the deficiency, nothing happens: red cells cope with everyday oxidative load, blood counts are normal, and the condition is silent. The problem is episodic. Within 24 to 72 hours of a trigger, hemoglobin falls, often by 2 to 4 g/dL, bilirubin and LDH rise, haptoglobin disappears, urine turns dark from hemoglobin, and the person feels weak, breathless and sometimes has back or abdominal pain. In the A- variant the episode stops on its own within a week as the old cells are cleared; in the Mediterranean variant it can be deeper and longer and sometimes needs a transfusion.

How low matters. Below 10 percent of normal (the Mediterranean, Canton and similar variants, WHO class B with severe phenotype) carries a risk of serious hemolysis from fava beans and from a long list of drugs. Between 10 and 30 percent (the A- variant) the triggers are mostly drugs and infections, and favism is unusual. Between 30 and 80 percent, intermediate, the person is almost always a female carrier whose deficient cells can still hemolyze with primaquine or tafenoquine. The rare class A variants with under 20 percent activity cause chronic hemolysis even without triggers, with an enlarged spleen, gallstones and a persistently raised reticulocyte count from childhood.

In a newborn, a deficient result is mainly about jaundice. Deficient babies clear bilirubin less well and may also hemolyze with triggers such as naphthalene-treated clothing, henna or maternal fava bean intake while breastfeeding, so bilirubin peaks higher and later than in other babies and the risk of kernicterus, bilirubin damage to the brain, is higher. The American Academy of Pediatrics lists G6PD deficiency as a neurotoxicity risk factor that lowers the bilirubin threshold for phototherapy and exchange transfusion. After the newborn period, the practical consequence of a low result is a lifelong list of things to avoid and a note in the medical record so that no one prescribes a dangerous drug.

Common causes

Inherited G6PD variants (X-linked)
More than 200 variants are known. The A- variant (about 10 to 15 percent residual activity) is common in people of sub-Saharan African ancestry; the Mediterranean variant (under 10 percent) across the Mediterranean, Middle East and South Asia; Canton, Kaiping, Mahidol and Viangchan variants across East and Southeast Asia. Males with the gene are deficient; females with one copy are intermediate to deficient.
Fava beans (favism)
Vicine and convicine in fresh or dried fava (broad) beans generate oxidants that trigger severe hemolysis, usually within 24 hours, in people with the Mediterranean and similar severe variants; children aged 1 to 5 are most affected. Other beans and legumes do not cause it.
Antimalarial drugs: primaquine and tafenoquine
The best-studied triggers. Primaquine causes dose-dependent hemolysis in deficient people, and tafenoquine's long half-life makes hemolysis prolonged, so testing is required before either is prescribed; tafenoquine needs activity above 70 percent.
Other high-risk drugs
Dapsone, rasburicase, methylene blue, toluidine blue, nitrofurantoin, phenazopyridine, sulfonamide antibiotics (sulfamethoxazole, sulfadiazine), sulfasalazine, nalidixic acid and some quinolones (ciprofloxacin and others carry warnings). Aspirin and acetaminophen at normal doses are considered safe by most reviews; high-dose aspirin is used with caution.
Infections
The commonest trigger of hemolysis in daily life. Bacterial pneumonia, hepatitis A and B, typhoid, cytomegalovirus, influenza and COVID-19 have all caused episodes; neutrophils release oxidants as they fight the infection.
Chemicals and household exposures
Naphthalene (mothballs and some toilet deodorizer blocks, including clothing stored with them), henna applied to the skin of infants, aniline dyes, and some industrial solvents.
Diabetic ketoacidosis and other metabolic stress
Acidosis and dehydration during DKA have precipitated hemolysis in deficient people, and the acute illness itself adds oxidative load.
High-dose vitamin C and other supplements
Intravenous vitamin C in gram doses has caused severe hemolysis in case reports; menadione (vitamin K3, not the K1 used in newborns), and in some reports high-dose vitamin K analogs and isobutyl nitrite have done the same.
Newborn exposures
In deficient newborns, triggers include naphthalene-treated bedding, henna, fava beans eaten by a breastfeeding mother, and infection; all increase the risk of dangerous jaundice in the first week.

Symptoms that can go with it

None between episodes in the great majority of people
Sudden fatigue, weakness, breathlessness and a fast heartbeat starting 1 to 3 days after a trigger
Dark, tea- or cola-colored urine from hemoglobin
Yellowing of the eyes and skin (jaundice)
Back, abdominal or flank pain during the episode
Pale skin, dizziness or fainting when the hemoglobin drop is large
In newborns: jaundice that is deeper or lasts longer than usual, poor feeding or sleepiness in the first week
In the rare chronic forms: an enlarged spleen, gallstones and lifelong mild anemia

Read it alongside

Reticulocyte count — tells you whether the test was taken in the false-normal window; a high reticulocyte count means the result should be repeated in 3 months.
Hemoglobin and hematocrit — show how much blood has been lost during an episode and whether a transfusion is being considered.
Haptoglobin, LDH and indirect bilirubin — confirm that hemolysis is occurring; in a G6PD crisis haptoglobin is usually undetectable and LDH very high.
Peripheral blood smear — bite cells, blister cells and (with a special stain) Heinz bodies are characteristic of oxidative hemolysis and separate it from other causes.
Direct Coombs test — negative in G6PD hemolysis; a positive result points to an immune cause instead.
Urine dipstick for blood — positive for heme with no red cells on microscopy during intravascular hemolysis (hemoglobinuria).
Newborn bilirubin, total and direct — the result that drives treatment decisions in a deficient baby.
Hemoglobin electrophoresis — sickle cell trait and thalassemia trait are common in the same populations and can coexist; both change how an episode behaves.

What usually happens next

If the result is deficient, expect it to be recorded prominently in your chart and to be asked to carry the information (a wallet card or medical alert) so that primaquine, dapsone, rasburicase, methylene blue, nitrofurantoin and sulfonamides are not prescribed; ask your clinician or pharmacist for the current list.
If you were tested during or soon after an episode of jaundice or dark urine and the result is normal or intermediate, ask for a repeat quantitative test about 3 months later, once the reticulocyte count is normal, or for genetic testing if the suspicion is strong.
Women who test normal on a screening test but have had hemolysis, or who need primaquine or tafenoquine, should ask for a quantitative assay reported as a percentage of normal; the screen cannot detect intermediate activity.
For a deficient newborn, expect bilirubin checks over the first week, advice on avoiding naphthalene, henna and fava beans (including in the breastfeeding mother's diet), and a note to re-test later in infancy if the first result was borderline.
Family members may want testing, since brothers of a deficient male have a 50 percent chance of being affected if the mother is a carrier, and all daughters of a deficient male are carriers.

Diet, lifestyle and natural levers with evidence

What can move G6PD once the cause is known. Nothing here replaces finding the cause.

Avoid fava beans completely

Strong evidence

Fava (broad) beans contain vicine and convicine, which are converted in the gut to compounds that generate hydrogen peroxide inside red cells. In people with severe variants, eating them causes hemolysis within 24 hours, with hemoglobin falls of 3 to 5 g/dL in children, and favism remains the leading cause of hospital admission for acute hemolysis in Mediterranean and Middle Eastern countries. Fresh beans are more dangerous than dried or cooked, but none is safe. Other beans, lentils, peas, peanuts and soy do not contain these compounds and do not need to be avoided; many lists circulating online include foods with no evidence behind them.

Breastfeeding mothers of deficient infants should also avoid fava beans; neonatal favism through breast milk has been reported.

Know the drug and chemical list and tell every prescriber

Strong evidence

Evidence-based reviews narrow the list of drugs that definitely cause hemolysis in G6PD deficiency to a manageable set: primaquine, tafenoquine, dapsone, rasburicase, methylene blue, toluidine blue, nitrofurantoin, phenazopyridine, sulfonamides, sulfasalazine and nalidixic acid, with quinolones and high-dose aspirin as use-with-caution. Avoiding these and naphthalene (mothballs) prevents most episodes outright. Acetaminophen, most antibiotics other than those listed, and normal-dose aspirin are considered safe; carrying the list prevents both dangerous prescriptions and unnecessary avoidance of safe medicines.

Be cautious with high-dose vitamin C and oxidant supplements

Preliminary evidence

Severe hemolysis, kidney injury and death have been reported after intravenous vitamin C in doses of 30 to 100 g in people with unrecognized G6PD deficiency, and oral doses in the several-gram range have been implicated in a few cases. Ordinary dietary vitamin C and standard supplement doses (up to around 500 mg) have not caused episodes. Menadione (vitamin K3), isobutyl nitrite and some herbal products with oxidant properties are also listed as triggers. Clinics that give intravenous vitamin C should test G6PD first.

Tell any practitioner offering high-dose intravenous vitamin C or glutathione infusions that you have G6PD deficiency before treatment.

Folic acid in the chronic forms

Moderate evidence

People with the rare class A variants that cause ongoing hemolysis, and anyone recovering from a major episode, have a red cell turnover several times normal and can run short of folate; 1 mg of folic acid a day is routine supportive care in hematology guidelines for chronic hemolytic anemia. It does not raise G6PD activity or prevent episodes; it keeps the marrow able to replace lost cells. Most people with the common variants, who are well between episodes, do not need it.

Vitamin E in the Mediterranean variant

Preliminary evidence

A small 1980 study gave 800 IU of vitamin E a day for a year to people with Mediterranean-type deficiency and chronic low-grade hemolysis and found a rise in hemoglobin of about 1 g/dL, a longer red cell survival and a fall in reticulocytes; a later trial failed to confirm the benefit, and no study has shown that vitamin E prevents a triggered episode. It is not a substitute for avoiding triggers.

High-dose vitamin E increases bleeding risk with anticoagulants and antiplatelet drugs.

When to see a clinician promptly

Dark or cola-colored urine, yellow eyes, breathlessness, a racing heart, dizziness or fainting within 1 to 3 days of a new medicine, an infection or eating fava beans: an acute hemolytic episode, needs same-day assessment and sometimes a transfusion.
A newborn known or suspected to be deficient who looks yellow in the first 24 hours, is unusually sleepy, feeds poorly or is jaundiced beyond the first week: urgent bilirubin check.
Very little urine, or urine that stays dark for more than a day, during an episode: free hemoglobin can injure the kidneys.
Before starting primaquine, tafenoquine, dapsone, rasburicase, methylene blue, nitrofurantoin or a sulfonamide if you have not been tested or do not know your result.
Recurrent episodes of jaundice or anemia with an enlarged spleen or gallstones, which suggest one of the chronic variants and need hematology review.
A normal result in a woman or in anyone tested right after an episode when the history strongly suggests deficiency, to arrange a repeat quantitative or genetic test.

Frequently asked questions

What is the normal range for a G6PD test?

On the quantitative assay most labs report normal adult activity somewhere between about 7 and 20 units per gram of hemoglobin, but the absolute numbers depend on the method and the temperature the assay is run at, so ranges such as 4.6 to 13.5 and 8.8 to 13.4 U/g Hb are both in use. Many labs now also report the result as a percentage of the normal male median: 60 to 150 percent is normal, 30 to 80 percent intermediate, and below 30 percent deficient. Newborns have higher values because their red cells are young. Always compare against the range printed on your report.

What does a low G6PD result mean?

It means your red cells have reduced protection against oxidative stress and can be destroyed rapidly after exposure to certain triggers, causing an episode of hemolytic anemia with fatigue, jaundice and dark urine. Between episodes most people are completely well. The result is inherited and lifelong. The practical steps are to avoid fava beans, naphthalene mothballs and a specific list of drugs, to make sure the deficiency is recorded in your medical record, and, for a newborn, to watch closely for jaundice in the first week.

What foods should I avoid with G6PD deficiency?

Fava beans (broad beans) are the only food proven to cause hemolysis, and they should be avoided completely, fresh, dried or cooked, especially by people with the Mediterranean variant and by children. Breastfeeding mothers of deficient infants should avoid them too. Many online lists add soy, other legumes, blueberries, tonic water, artificial food colorings and menthol; there is no good evidence that these cause hemolysis at normal intake, and avoiding them is not necessary. Very high doses of vitamin C, particularly intravenous, are the one supplement with documented risk.

Which drugs are unsafe with G6PD deficiency?

The drugs with clear evidence of causing hemolysis are primaquine, tafenoquine, dapsone, rasburicase, methylene blue, toluidine blue, nitrofurantoin, phenazopyridine, sulfonamide antibiotics such as sulfamethoxazole (in Bactrim or Septra) and sulfadiazine, sulfasalazine and nalidixic acid. Ciprofloxacin and other quinolones, chloroquine, high-dose aspirin and glibenclamide are listed as use with caution. Acetaminophen, ibuprofen at normal doses, penicillins, cephalosporins, macrolides and most other common drugs are considered safe. Tell every prescriber and pharmacist, and ask them to check before any new medicine.

Why was my G6PD test normal if I had hemolysis?

Because the test was probably done at the wrong time. During and for weeks after a hemolytic episode the oldest red cells, which have the least enzyme, have been destroyed, and the marrow has released young cells that carry the most. In the common A- variant the average activity can read entirely normal in this window. A recent transfusion has the same effect because donor cells carry donor enzyme. The test should be repeated about 3 months later, when the reticulocyte count is normal, or a genetic test ordered. Women can also test normal on a screen while carrying a significant deficient cell population.

Is G6PD deficiency part of newborn screening?

Not everywhere. It is included in the routine newborn screening panel in a few US states and jurisdictions (Pennsylvania and the District of Columbia among them) and is universal in many countries where the deficiency is common, including much of the Mediterranean, the Middle East and East and Southeast Asia. Elsewhere, the American Academy of Pediatrics recommends testing a jaundiced newborn when the family's ancestry or history makes deficiency likely, or when jaundice is severe or responds poorly to phototherapy. Parents who know they carry the trait can ask for the test at birth.

Can women have G6PD deficiency?

Yes. The gene is on the X chromosome, so men with one deficient copy are fully affected and women need two copies to be fully deficient, which happens in populations where the variant is common. Women with one copy are carriers, and because of random X-inactivation their red cells are a mix of normal and deficient; their measured activity can be anywhere from deficient to normal. They can still hemolyze with strong triggers such as primaquine, fava beans or a serious infection, and a qualitative screen often misses them, so a quantitative test is recommended before antimalarial treatment.

Does G6PD deficiency affect life expectancy?

For the common variants, no. Most people have no symptoms at all and normal blood counts throughout life, provided triggers are avoided, and the trait is thought to have persisted because it gives partial protection against severe malaria. The risks are concentrated in the newborn period (severe jaundice) and in acute episodes after a trigger, which are treatable. The rare chronic variants cause lifelong mild anemia, gallstones and an enlarged spleen and are followed by a hematologist.

References

Glucose-6-phosphate dehydrogenase (G6PD) test. MedlinePlus, US National Library of Medicine (2022)
Luzzatto L, Ally M, Notaro R. Glucose-6-phosphate dehydrogenase deficiency. Blood (2020)
Cappellini MD, Fiorelli G. Glucose-6-phosphate dehydrogenase deficiency. Lancet (2008)
Luzzatto L, Bancone G, Dugué PA, et al.. New WHO classification of genetic variants causing G6PD deficiency. Bulletin of the World Health Organization (2024)
Youngster I, Arcavi L, Schechmaster R, et al.. Medications and glucose-6-phosphate dehydrogenase deficiency: an evidence-based review. Drug Safety (2010)
Kemper AR, Newman TB, Slaughter JL, et al.. Clinical practice guideline revision: management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics (2022)
Chu CS, Bancone G, Nosten F, White NJ, Luzzatto L. Primaquine-induced haemolysis in females heterozygous for G6PD deficiency. Malaria Journal (2018)
Corash L, Spielberg S, Bartsocas C, et al.. Reduced chronic hemolysis during high-dose vitamin E administration in Mediterranean-type glucose-6-phosphate dehydrogenase deficiency. New England Journal of Medicine (1980)
Kaplan M, Hammerman C. Glucose-6-phosphate dehydrogenase deficiency and severe neonatal hyperbilirubinemia: a complexity of interactions between genes and environment. Seminars in Fetal and Neonatal Medicine (2010)
Luzzatto L, Seneca E. G6PD deficiency: a classic example of pharmacogenetics with on-going clinical implications. British Journal of Haematology (2014)
Glucose-6-phosphate dehydrogenase (G6PD) deficiency. Merck Manual Professional Version (2024)
Testing for G6PD deficiency for safe use of primaquine in malaria treatment. Centers for Disease Control and Prevention, Malaria (2023)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.