Hemolytic Anemia Due to G6PD Deficiency

Hemolytic anemia due to G6PD deficiency happens when red blood cells (RBCs) break down faster than the body can replace them because they lack enough of an enzyme called glucose-6-phosphate dehydrogenase (G6PD). G6PD helps RBCs make NADPH, which keeps glutathione in a reduced, protective form. Without enough G6PD, RBCs cannot handle oxidative stress from infections, certain foods, or some medicines. Their hemoglobin becomes damaged (forming Heinz bodies), parts of the cell membrane are removed in the spleen (forming “bite cells”), and RBCs are destroyed in the circulation or spleen, causing sudden anemia, jaundice, and dark urine. G6PD deficiency is X-linked, so it affects males more often, and it is the most common enzyme defect worldwide. NCBI+1

Hemolytic anemia due to G6PD deficiency happens when red blood cells (RBCs) break faster than the body can replace them because they lack enough of the enzyme glucose-6-phosphate dehydrogenase (G6PD). G6PD normally makes NADPH, which keeps glutathione reduced so RBCs can neutralize oxidants. Without enough G6PD, exposures such as infections, certain medicines, and fava beans create oxidative stress that damages RBCs and causes jaundice, dark urine, weakness, and sometimes newborn jaundice. Most people are well between episodes; hemolysis usually starts 1–3 days after a trigger and settles as new, enzyme-rich RBCs appear. G6PD deficiency is one of the world’s most common enzyme disorders. ASH Publications+3MedlinePlus+3NCBI+3

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Other names

This condition is also called: G6PD deficiency with acute hemolytic anemia, favism-related hemolytic anemia (when triggered by fava beans), X-linked non-spherocytic hemolytic anemia due to G6PD deficiency, and oxidant-induced hemolysis in G6PD deficiency. These names all describe the same core problem: RBC breakdown after oxidative stress in a person who has low G6PD activity. Medscape

G6PD runs the first step of the pentose phosphate pathway in RBCs. This step makes NADPH. NADPH lets RBCs recycle glutathione, the main “shield” against oxidants like hydrogen peroxide. When G6PD is low, oxidants damage hemoglobin and the RBC membrane. Damaged hemoglobin clumps (Heinz bodies) and the spleen “bites” them out, producing bite cells. The result is hemolysis (RBC destruction), which raises bilirubin and causes jaundice, anemia, and dark urine. In severe, fast hemolysis, hemoglobin spills into urine (hemoglobinuria) and the blood test shows low haptoglobin, high LDH, and high indirect bilirubin. NCBI+1

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Types

1. Acute hemolytic episodes: Sudden anemia after a trigger such as infection, certain drugs, or fava beans; usually self-limited once the trigger stops. Medscape

2. Favism: Hemolysis after eating fava beans or inhaling their pollen; more common with Mediterranean variants. Medscape

3. Drug- or chemical-induced hemolysis: After exposure to specific medicines (for example, primaquine, tafenoquine, dapsone, nitrofurantoin, methylene blue, rasburicase) or chemicals (for example, naphthalene in mothballs). CDC+3World Health Organization+3FDA Access Data+3

4. Infection-triggered hemolysis: Viral or bacterial infections increase oxidant stress and can precipitate hemolysis even without drugs. NCBI

5. Neonatal jaundice due to G6PD deficiency: Newborns can develop early, significant jaundice and, if untreated, risk kernicterus; many programs now emphasize screening or targeted testing. AAFP+1

6. Chronic non-spherocytic hemolytic anemia (CNSHA): Rare, severe G6PD variants cause ongoing hemolysis even without triggers. Medscape

7. Variants by enzyme activity (updated WHO classes): The WHO updated its system in 2022–2024; the big change is merging prior class II and III variants into a broader “Class B” based on median residual activity. This better matches clinical risk. World Health Organization+1

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Causes and common triggers

1. Fava beans (favism) – contain oxidant compounds (vicine/convicine) that overwhelm low-G6PD RBCs, causing rapid hemolysis. Medscape

2. Primaquine (antimalarial) – classic high-risk oxidant; WHO and guidelines require G6PD testing before use. World Health Organization

3. Tafenoquine (antimalarial) – long-acting 8-aminoquinoline; contraindicated without adequate G6PD activity. World Health Organization

4. Dapsone (antibacterial/anti-inflammatory) – strong oxidant; well-documented cause of hemolysis in G6PD deficiency. EBM Consult

5. Rasburicase (urate oxidase) – FDA-boxed warning and contraindicated in G6PD deficiency because it generates peroxide. FDA Access Data+1

6. Methylene blue (for methemoglobinemia) – contraindicated in G6PD deficiency; it can worsen hemolysis and may not work. FDA Access Data+1

7. Nitrofurantoin (urinary antibiotic) – recognized trigger in G6PD deficiency, especially at higher doses or prolonged use. NCBI

8. Phenazopyridine (urinary analgesic) – oxidant stressor; avoid or use extreme caution. NCBI

9. Sulfonamides / TMP-SMX – classic oxidant antibiotics (e.g., sulfamethoxazole); can trigger hemolysis. NCBI

10. Chloroquine/other older antimalarials – listed among agents that may trigger hemolysis in susceptible persons. NCBI

11. Naphthalene (mothballs) – environmental chemical; well-described cause of acute oxidative hemolysis in G6PD deficiency. CDC+1

12. Henna (lawsone dye) – can cause hemolysis in infants and older patients with G6PD deficiency after skin, hair, or nail use. Pediatrics Publications+1

13. Severe bacterial or viral infections – infections raise oxidant stress and can be the sole trigger for an episode. NCBI

14. Diabetic ketoacidosis or acute metabolic stress – metabolic derangements can precipitate hemolysis in susceptible people. PMC

15. Certain analgesics / high-dose aspirin – some lists include acetylsalicylic acid and acetaminophen as potential triggers; use caution and clinical judgment. NCBI

16. Quinolones (selected) – some members have been implicated; caution is prudent in confirmed G6PD deficiency. NCBI

17. Chloramphenicol – older antibiotic associated with oxidative hemolysis risk in G6PD-deficient patients. NCBI

18. Isoniazid (anti-TB) – appears on caution/avoid lists in several summaries; risk varies; weigh benefits vs risks. NCBI

19. Vitamin K analogues like menadione (K3) – linked to hemolysis; avoid these forms in G6PD deficiency. Baebies

20. Aniline dyes / miscellaneous oxidants – various industrial or household oxidants may trigger episodes; detailed history helps. ATSDR

Note: Different lists exist, and evidence strength varies by drug. Two agents are consistently contraindicated (methylene blue, rasburicase). Antimalarials primaquine and tafenoquine require prior G6PD testing. For other drugs, use risk–benefit judgment and local guidance. FDA Access Data+2FDA Access Data+2

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Common symptoms and signs

1. Sudden tiredness and weakness – fewer RBCs carry less oxygen, so you feel exhausted quickly. Medscape

2. Pale skin or inside eyelids – classic sign of anemia. Medscape

3. Yellow eyes and skin (jaundice) – bilirubin from broken RBCs builds up. NCBI

4. Dark brown or cola-colored urine – hemoglobin or its breakdown products spill into urine during brisk hemolysis. Medscape

5. Fast heartbeat (palpitations) – heart beats quicker to move the reduced oxygen around. Medscape

6. Shortness of breath – low oxygen capacity makes you winded. MedlinePlus

7. Dizziness or light-headedness – brain gets less oxygen. MedlinePlus

8. Headache – another common effect of anemia and hemolysis. MedlinePlus

9. Back or abdominal pain – kidneys and spleen react to the hemolysis; spasms may occur. Medscape

10. Fever or signs of infection – when an infection is the trigger. NCBI

11. Nausea or poor appetite – common during acute illness. MedlinePlus

12. Enlarged spleen (splenomegaly) – spleen filters damaged RBCs and may enlarge. NCBI

13. Irritability or lethargy in infants – an early sign of significant jaundice/hemolysis. AAFP

14. Poor feeding in newborns – often accompanies significant neonatal jaundice. AAFP

15. Confusion (severe cases) – very low oxygen or complications; urgent care is needed. NCBI

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Diagnostic tests

A) Physical examination (at the bedside)

1. General appearance and vital signs – look for pallor, jaundice, fever, fast heart and breathing rates; these point to acute hemolysis and stress. Medscape

2. Scleral inspection and skin check – yellowing of eyes/skin shows rising bilirubin. NCBI

3. Abdominal palpation for spleen size – the spleen may enlarge while filtering damaged RBCs. NCBI

4. Hydration and mucous membranes – severe hemolysis can dehydrate; assess capillary refill. (Supportive bedside assessment aligning with anemia care.) Medscape

5. Neonatal jaundice assessment – visual check plus a bilirubin measurement pathway when jaundice is suspected; very important to prevent kernicterus. AAFP

B) “Manual” or microscopy-based tests

6. Peripheral blood smear – looks for Heinz bodies (with supravital stain) and “bite cells.” These are classic in oxidant hemolysis. Medscape

7. Reticulocyte count (manual or automated) – rises as the marrow tries to replace lost RBCs. Medscape

8. Manual bilirubin checks in newborns (TcB → TSB) – transcutaneous bilirubin screening followed by serum confirmation when indicated. AAFP

9. Urine dipstick and microscopy – detects hemoglobinuria and bilirubin in brisk hemolysis. Medscape

10. Heinz body preparation (crystal violet / brilliant cresyl blue) – specific supravital stains make denatured hemoglobin visible. Medscape

C) Laboratory and pathology (the core tests)

11. Complete blood count (CBC) – shows anemia; MCV is usually normal; white cells/platelets help rule out other causes. Medscape

12. Indirect and direct bilirubin – indirect (unconjugated) bilirubin generally rises with hemolysis. Medscape

13. Lactate dehydrogenase (LDH) – increases with RBC destruction. Medscape

14. Serum haptoglobin – falls because it binds free hemoglobin released during hemolysis. Medscape

15. Direct antiglobulin (Coombs) test – usually negative in G6PD hemolysis; helps exclude autoimmune hemolytic anemia. Medscape

16. Quantitative G6PD enzyme assay (spectrophotometric) – gold-standard to confirm deficiency; measure when the patient is stable (reticulocytosis can temporarily “normalize” results). Medscape

17. Fluorescent spot test – a rapid screen showing whether NADPH is produced; useful but less accurate in females and during acute hemolysis. NCBI

18. Point-of-care quantitative tests/biosensors – newer tests can quantify activity at the bedside and support safe antimalarial use. Medscape

19. Newborn G6PD testing pathway – major guidelines advise testing for G6PD in infants with severe, unexpected, or persistent jaundice or when phototherapy needs escalate. AAFP

20. Genetic testing (variant analysis) – identifies the specific G6PD variant; useful for counseling, for females with mosaicism, and for borderline enzyme results. WHO has also updated variant classification to better match activity and risk. pediatric.testcatalog.org+1

D) Electro-diagnostic / monitoring (supportive)

1. Pulse oximetry and basic ECG are not specific for G6PD deficiency, but they monitor severity (tachycardia from anemia; oxygenation in very ill patients). These are supportive tools while definitive lab tests confirm the diagnosis. Medscape

E) Imaging (when complications are suspected)

1. Abdominal ultrasound may be used to evaluate splenomegaly or pigment gallstones if there is recurrent or chronic hemolysis. Neuroimaging is sometimes considered in infants with severe hyperbilirubinemia to assess for kernicterus, but bilirubin management follows clinical pathways first. Imaging is adjunctive, not diagnostic of G6PD deficiency itself. AAFP

Non-pharmacological treatments (therapies & others)

(Each item: description ~purpose, ~mechanism)

1. Immediate trigger stop & “reverse the last dose.” As soon as hemolysis is suspected, stop the likely oxidant (drug/food/chemical) and treat infection. This removes the ongoing source of oxidative stress so remaining RBCs aren’t further damaged, allowing the bone marrow to catch up. Medscape

2. Hydration with close urine monitoring. Encourage oral fluids (or IV if needed) and watch urine output/color. Hydration dilutes free hemoglobin and supports kidney perfusion, lowering acute kidney injury risk during brisk hemolysis. Medscape

3. Infection control (early medical care). Infections are the most common hemolysis trigger; get prompt evaluation and appropriate therapy (antibiotics chosen to be G6PD-safe). Treating the infection decreases inflammatory oxidants and stops the hemolytic cascade. PMC

4. Patient education & a personal “avoid list.” Teach patients to avoid fava beans, mothballs, and high-risk medicines; give a written list and links to up-to-date drug databases (e.g., G6PD.org). Education prevents future crises by reducing exposure. NCBI+2PMC+2

5. Medical alert identification. Wearing a bracelet/card stating “G6PD deficiency—avoid oxidant drugs (e.g., primaquine, tafenoquine, methylene blue, rasburicase)” speeds safe decisions in emergencies. Mechanism: prompts clinicians to choose non-oxidant options. CDC+1

6. Neonatal screening & early jaundice pathway. Where available, screen newborns for G6PD and monitor bilirubin closely; start phototherapy early if jaundice rises. Screening and standardized pathways lower exchange transfusions and bilirubin-related brain injury. Nature+1

7. Phototherapy (newborns). Blue light converts bilirubin into water-soluble forms for excretion, reducing neurotoxicity risk in G6PD-related jaundice. Use current AAP 2022 thresholds and escalate if near exchange levels. Wiley Online Library+1

8. Planned malaria prevention without oxidants. For travelers in malaria areas, emphasize mosquito avoidance (nets, repellents, clothing) and consult on G6PD-safe chemoprophylaxis if indicated. This prevents infection-triggered hemolysis and avoids contraindicated drugs. CDC

9. Work/home toxin avoidance. Remove or avoid naphthalene mothballs and similar oxidants at home/work. This eliminates a well-documented cause of severe hemolysis and methemoglobinemia in G6PD-deficient children and adults. PMC+1

10. Routine follow-up after a crisis. Recheck hemoglobin, reticulocytes, bilirubin, LDH, and renal function about 1–2 weeks after an episode to ensure recovery and catch complications. This tracks marrow response and organ safety. Medscape

11. Dietary counseling (what to avoid & safe patterns). Avoid fava beans and educate about hidden fava (e.g., some flours); otherwise follow a balanced diet. Mechanism: minimizing oxidant exposure while meeting nutrition needs for recovery. The Blood Project

12. Family counseling & cascade testing. Because G6PD deficiency is X-linked, offer information to family members (especially males). Early knowledge prevents avoidable exposures. MedlinePlus

13. Printed/phone list of safe/unsafe drugs. Use a reputable database (e.g., G6PD.org; national hospital lists) and keep it handy. This operationalizes avoidance in day-to-day care. g6pd.org+1

14. Travel letter & records. For people in/going to malaria regions, carry proof of G6PD status and a physician letter; this helps clinicians select safe regimens quickly. CDC

15. Fever care plan (non-drug measures first). Cool fluids, light clothing, and tepid sponging while arranging safe antipyretics. Lowering fever reduces metabolic stress and perceived dyspnea. PMC

16. Avoid “self-treating” with unknown herbal products. Some supplements can be oxidants; avoid unless known to be safe. Mechanism: lowers unrecognized oxidative exposures. BPS Publications

17. Peri-operative flagging. Ensure anesthetists know the diagnosis; they will avoid oxidant agents and plan monitoring. Mechanism: reduces intra-operative oxidative stress. ClinPGx

18. Newborn feeding guidance when mother eats fava. Maternal fava ingestion has been linked to hemolysis/jaundice in G6PD-deficient infants; counsel to avoid during breastfeeding if infant is G6PD-deficient. NCBI

19. Community/registry programs. Local education programs and registries (when available) improve awareness and rapid, appropriate care for at-risk groups. King’s College Hospital

20. Written action plan for red/dark urine or jaundice. Clear steps: stop trigger, hydrate, seek urgent care, bring drug list. Mechanism: faster care reduces complications. Medscape

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Drug treatments

Important note: There is no enzyme-replacement or curative drug for G6PD deficiency today; treatment is supportive and trigger-avoidance. Some drugs below are for complications (e.g., infection, malaria) and were selected because major guidelines consider them acceptable or preferred when G6PD deficiency is present. Always check local protocols and patient specifics. PMC

1. Folic acid — 1 mg orally once daily long-term in chronic hemolysis; short courses after severe episodes. Purpose: support RBC production; Mechanism: supplies folate for DNA synthesis during reticulocytosis; Side effects are uncommon at this dose. Medscape+1

2. Isotonic IV fluids (e.g., 0.9% saline) — rate per hemodynamics. Purpose: maintain renal perfusion and dilute free hemoglobin; Mechanism: supports kidney clearance during hemolysis; Adverse effects: fluid overload if over-given. Medscape

3. Packed RBC transfusion — dose by weight/hemoglobin; often considered when Hb ~<7 g/dL or symptomatic (context-dependent). Purpose: rapidly restore oxygen-carrying capacity; Risks: transfusion reactions, iron overload with repeated use. Emergency Med

4. Acetaminophen (paracetamol) — 325–1,000 mg PO q6–8h PRN (max per label). Purpose: treat fever/pain without oxidative stress; Generally considered safe at therapeutic doses. Winnipeg Regional Health Authority

5. Ibuprofen — 200–400 mg PO q6–8h with food. Purpose: analgesia/antipyresis; At standard doses it is commonly used and not a typical oxidant trigger. Verywell Health

6. Amoxicillin — 500 mg PO q8h (typical adult dose) for susceptible infections. Purpose: treat bacterial triggers; Mechanism: beta-lactam; generally safe in G6PD deficiency. PMC

7. Cephalexin / Ceftriaxone — 500 mg PO q6h; or 1–2 g IV daily. Purpose: treat bacterial infections; Cephalosporins are generally acceptable choices. PMC

8. Azithromycin — 500 mg day 1 then 250 mg daily ×4. Purpose: respiratory infections; Not an oxidant drug; well tolerated. PMC

9. Artemether-lumefantrine (ACT) — per malaria protocols. Purpose: treat falciparum malaria without using oxidant 8-aminoquinolines; Mechanism: artemisinin derivative; Considered safe with respect to G6PD. CDC

10. Atovaquone-proguanil — per label for malaria treatment/prophylaxis. Purpose: non-oxidant option for malaria; Mechanism: mitochondrial and folate pathway inhibition; generally acceptable in G6PD deficiency. CDC

11. Doxycycline — 100 mg PO bid (as part of malaria therapy or for bacterial infections). Purpose: adjunct/alternative therapy; Mechanism: protein synthesis inhibition; not a known G6PD oxidant at therapeutic doses. CDC

12. Chloroquine (where sensitive species) — per local malaria guidance. Purpose: relapse prevention in G6PD-deficient patients who cannot take primaquine/tafenoquine (long prophylaxis strategy). CDC

13. Vitamin C (ascorbic acid) for methemoglobinemia when G6PD-deficient — adult regimens vary in reports (e.g., 1–5 g IV q6h; follow local guidance). Purpose: reduce methemoglobin when methylene blue is contraindicated; Side effects: high doses can cause GI upset, oxalate issues in renal impairment. Medscape+1

14. Safe antiemetics (e.g., ondansetron) — 4–8 mg PO/IV PRN. Purpose: prevent vomiting/dehydration during crises; not an oxidant trigger at standard doses. Medscape

15. Proton-pump inhibitor if GI bleeding risk — e.g., pantoprazole 40 mg daily. Purpose: protect stomach if hemolysis crisis coincides with stress gastritis; choose agents without known oxidative risk. Medscape

16. Antibiotic selection for neonatal sepsis evaluation — choose regimens compatible with G6PD deficiency while following neonatal sepsis protocols; aim is to treat infection early to remove a major hemolysis trigger. Medscape

17. Avoid methylene blue for methemoglobinemia in known/suspected G6PD deficiency (list here as a “do-not-use”). If methemoglobinemia is life-threatening and options are limited, specialist care is essential. PMC+1

18. Avoid rasburicase (tumor lysis) — it generates hydrogen peroxide during uric acid breakdown and can cause catastrophic hemolysis/methemoglobinemia in G6PD deficiency. Screen before use. FDA Access Data+1

19. Avoid primaquine/tafenoquine unless quantitative G6PD activity is normal; in partial deficiency, only specialist-supervised regimens are considered. CDC+1

20. Iron — only if lab-confirmed iron deficiency (not routine in acute hemolysis). Purpose: correct coexisting deficiency; otherwise free iron from hemolysis and normal stores make supplementation unnecessary. AAFP

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Dietary molecular supplements

1. Folate (diet + tablet) — Folate-rich foods (leafy greens, beans—not fava—citrus) plus 1 mg/day folic acid in chronic hemolysis helps marrow make new RBCs; it does not prevent triggers but supports recovery. Medscape

2. Vitamin E — Antioxidant that may reduce oxidative damage in RBC membranes; small/older studies suggest benefit, but evidence is mixed and not definitive; avoid high doses that raise bleeding risk. Discuss case-by-case. UTMB Health Research Expert Profiles+2New England Journal of Medicine+2

3. Vitamin C — Regular dietary intake is fine; high-dose IV/PO is reserved for methemoglobinemia when methylene blue cannot be used. Do not self-dose high amounts chronically. Medscape

4. Selenium — Despite antioxidant rationale, there’s no proven benefit for G6PD hemolysis; avoid high-dose supplementation outside deficiency. AAFP

5. General multivitamin (standard dose) — May help meet daily needs during recovery; avoid formulations with unproven high-dose antioxidants. Evidence for preventing hemolysis is lacking. PMC

6. Protein-adequate diet — Adequate protein supports erythropoiesis (RBC building). There’s no G6PD-specific protein therapy; keep it balanced and avoid fava products. NCBI

7. Iron-rich foods — Only emphasize if labs show deficiency; otherwise iron loading isn’t helpful in acute hemolysis. AAFP

8. Hydration — Water is not a “supplement,” but maintaining fluid intake is a core nutritional behavior that supports kidney clearance during hemolysis. Medscape

9. B12-rich foods — Helpful if deficiency exists, but B12 is not a specific therapy for G6PD hemolysis; check levels first. NCBI

10. Herbal products — Avoid products with uncertain oxidant effects; adverse supplement reactions have been reported in hemolytic conditions; use only with clinician guidance. BPS Publications

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Immunity-booster / regenerative / stem-cell drugs

There are currently no approved “immunity boosters,” regenerative drugs, or stem-cell drugs that treat G6PD deficiency. Research explores antioxidants, enzyme stabilizers, gene addition/editing, and hematopoietic stem-cell (HSC) approaches, but none are standard of care. Below are research directions for context only.

1. Antioxidant strategies (research) — Many antioxidants have been tested; overall clinical benefit is limited or inconsistent. Focus remains on avoidance plus supportive care. PMC

2. Small-molecule enzyme stabilizers (preclinical) — Compounds aiming to stabilize mutant G6PD to restore activity are under study but not approved. PMC

3. Gene addition (viral vectors) to HSCs (preclinical) — Concept: add a functional G6PD copy to stem cells to produce normal RBCs; still experimental. PMC

4. CRISPR/base editing (preclinical) — Correcting the G6PD mutation ex vivo in HSCs is theoretically curative; studies are at lab/animal stages. PMC

5. Allogeneic HSCT (exceptional cases) — Not standard for isolated G6PD deficiency given risk/benefit; may be considered only in unusual, severe, transfusion-dependent scenarios within research/exception pathways. Haematologica

6. “Immune boosters” — No evidence that OTC “immune boosters” prevent G6PD hemolysis; some herbal products may even be oxidants—avoid unsupervised use. BPS Publications

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Surgeries/procedures

1. Phototherapy (newborns) — Noninvasive “light treatment” converts bilirubin to excretable forms; start per AAP 2022 curves and escalate if levels approach exchange thresholds. AAFP+1

2. Exchange transfusion (newborns) — If bilirubin is at/near exchange threshold or refractory to intensive phototherapy, exchange transfusion rapidly lowers bilirubin; do not use G6PD-deficient donor blood. Pediatrics Publications+1

3. Packed RBC transfusion (children/adults) — For severe symptomatic anemia; follow restrictive thresholds with clinical judgment. Emergency Med

4. Cholecystectomy (pigment gallstones) — Chronic/recurrent hemolysis raises bilirubin and pigment stone risk; symptomatic stones are managed surgically as usual. PubMed+1

5. Renal support (dialysis) in AKI — Rarely, severe hemolysis causes kidney injury; standard renal replacement therapy may be needed until recovery. Medscape

Splenectomy is generally not recommended in typical G6PD deficiency, but may be considered in rare transfusion-dependent chronic non-spherocytic cases with symptomatic splenomegaly—specialist decision only. AAFP+1

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Preventions

1. Avoid fava beans (and foods made with them). The Blood Project

2. Avoid mothballs/naphthalene at home. PMC

3. Never take primaquine/tafenoquine without quantitative G6PD testing documented as normal. CDC

4. Do not use rasburicase if G6PD-deficient. FDA Access Data

5. Avoid/flag methylene blue for methemoglobinemia—ask for alternatives. PMC

6. Treat infections early (they’re major triggers). PMC

7. Carry a medical alert card listing “G6PD deficiency—avoid oxidants.” g6pd.org

8. Use reputable drug lists/databases and ask clinicians before new meds. g6pd.org

9. Neonatal screening/early bilirubin follow-up in newborns. Nature

10. Malaria prevention with nets/repellent and G6PD-safe regimens when needed. CDC

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When to see a doctor

Seek urgent care for sudden yellow skin/eyes, dark or red urine, severe fatigue, shortness of breath, fast heartbeat, fever, or after any exposure to a known trigger (drug, fava beans, mothballs). Newborns with jaundice or poor feeding need prompt evaluation, especially if there’s family history or known G6PD deficiency. King’s College Hospital+1

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What to eat & what to avoid

1. Avoid: Fava (broad) beans in any form (whole, flour, hidden in mixes). The Blood Project

2. Avoid: Mothballs/naphthalene exposure around stored foods/closets. PMC

3. Okay: Standard balanced diet with fruits/vegetables/whole grains; no need for special “G6PD diet.” NCBI

4. Folate-rich foods: leafy greens, citrus, lentils (but not fava). Medscape

5. Hydrate well, especially during illness. Medscape

6. During breastfeeding if infant is G6PD-deficient: caregivers should avoid fava intake. NCBI

7. Be careful with herbal products (unknown oxidant risk). BPS Publications

8. Iron-rich foods only if iron deficiency is proven. AAFP

9. Vitamin E/C: use food sources; don’t megadose without clinician advice. PMC

10. Ask before new supplements; bring your G6PD card to clinic visits. g6pd.org

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FAQs

1) Is G6PD deficiency curable with medicine?
No. There is currently no approved medicine that restores G6PD in RBCs; care focuses on avoidance and supportive treatment. PMC

2) What are the most important things to avoid?
Fava beans, mothballs (naphthalene), and oxidant drugs such as primaquine/tafenoquine, methylene blue, and rasburicase. FDA Access Data+4The Blood Project+4PMC+4

3) Can I take acetaminophen or ibuprofen for fever?
Yes—at standard doses, these are common choices; always follow labels and your doctor’s advice. Verywell Health

4) Why are infections so risky?
They increase oxidants inside RBCs and are the leading cause of hemolysis episodes—treat them early. PMC

5) What about vitamin E or other antioxidants?
Evidence is mixed/limited; do not self-prescribe high doses. Discuss with your clinician. PMC+1

6) How are newborns managed?
Screen where available, monitor bilirubin, start phototherapy per AAP 2022 curves, and do exchange transfusion if indicated. AAFP

7) Is methylene blue safe for me?
No—methylene blue is contraindicated in G6PD deficiency; vitamin C and other measures are used instead for methemoglobinemia. Medscape

8) Do I need folic acid tablets?
Often yes if there’s chronic hemolysis (or during recovery) to support RBC production—commonly 1 mg/day. Medscape

9) Can I ever take primaquine or tafenoquine?
Only if quantitative G6PD activity is normal; otherwise they can cause dangerous hemolysis. CDC

10) Why do some people get gallstones?
Chronic/recurrent hemolysis increases bilirubin and pigment stone formation; symptomatic stones are treated normally (e.g., cholecystectomy). PubMed

11) Is splenectomy helpful?
Generally not recommended; reserved for rare, transfusion-dependent chronic non-spherocytic cases with specialist oversight. AAFP

12) What if I get methemoglobinemia?
Because methylene blue is unsafe, clinicians may use ascorbic acid or transfusion/hyperbaric oxygen depending on the situation. NCBI

13) Do I need a special diet?
No special diet beyond avoiding fava beans and maintaining balanced nutrition/hydration. The Blood Project

14) Should my family be tested?
G6PD deficiency is X-linked; offer information/testing to relatives—especially males—in at-risk families. MedlinePlus

15) Where can I check if a medication is safe?
Use reputable lists (e.g., G6PD.org) and ask your clinician/pharmacist before starting anything new. g6pd.org

Disclaimer: Each person’s journey is unique, treatment plan, life style, food habit, hormonal condition, immune system, chronic disease condition, geological location, weather and previous medical  history is also unique. So always seek the best advice from a qualified medical professional or health care provider before trying any treatments to ensure to find out the best plan for you. This guide is for general information and educational purposes only. Regular check-ups and awareness can help to manage and prevent complications associated with these diseases conditions. If you or someone are suffering from this disease condition bookmark this website or share with someone who might find it useful! Boost your knowledge and stay ahead in your health journey. We always try to ensure that the content is regularly updated to reflect the latest medical research and treatment options. Thank you for giving your valuable time to read the article.

The article is written by Team RxHarun and reviewed by the Rx Editorial Board Members

Last Updated: September 17, 2025.

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