Glucose-6-Phosphate Dehydrogenase (G6PD), in Visit Clinic

If you have G6PD deficiency, red blood cells are vulnerable to oxidative stress. Triggers — certain drugs, infections, fava beans or chemicals — can cause acute hemolytic anemia, leading to jaundice, dark urine, fatigue, shortness of breath and rapid heart rate. Some people have chronic mild anemia; newborns may develop severe jaundice. Management focuses on avoiding triggers and treating complications.

Glucose‑6‑phosphate dehydrogenase (G6PD) catalyzes the first, rate‑limiting step of the pentose phosphate pathway, converting glucose‑6‑phosphate to 6‑phosphogluconolactone while producing NADPH. NADPH keeps glutathione reduced, protecting red blood cells from oxidative damage and enabling detoxification of reactive oxygen species. The pathway also supplies ribose‑5‑phosphate for nucleotide synthesis and supports lipid biosynthesis.

Glucose‑6‑phosphatase and G6PD are distinct enzymes. Glucose‑6‑phosphatase (ER lumen of hepatocytes and renal cells) hydrolyzes glucose‑6‑phosphate to free glucose in gluconeogenesis and glycogenolysis; deficiency causes glycogen storage disease type I with severe fasting hypoglycaemia and lactic acidosis. G6PD (cytosolic) catalyses the first step of the pentose‑phosphate pathway, producing NADPH and ribose‑5‑phosphate; its deficiency causes oxidative hemolytic anaemia triggered by drugs, infections, or fava beans.

Fava (broad) beans are the classic food trigger that can cause acute hemolysis in people with G6PD deficiency. Other dietary oxidants—such as quinine in tonic water and some food additives—might contribute in susceptible individuals. Most hemolytic episodes are caused by specific drugs, infections, or chemicals, so avoid known triggers and consult a clinician for personalized guidance.

Yes — most people with G6PD deficiency can live a normal, long life. With awareness and avoidance of triggers (certain drugs, fava beans, severe infections), prompt treatment of hemolytic episodes, and routine medical follow‑up, complications are uncommon. Severe chronic anemia is rare; education, newborn screening, and genetic counseling help manage risks and maintain healthy outcomes.

People with G6PD deficiency can often donate blood if they are well, not experiencing or recently recovered from haemolysis, and meet standard donor criteria. You should disclose your G6PD status to the blood service because some centres may defer donation or restrict use of your blood for certain recipients (for example neonates). Check local blood‑service guidance and speak with your clinician before donating.