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G6PD deficiency is a common inherited enzyme disorder that affects the ability of red blood cells to protect themselves from oxidative damage. It occurs due to mutations in the G6PD gene, resulting in reduced levels of the glucose-6-phosphate dehydrogenase enzyme. The condition is inherited in an X-linked pattern, making it more common in males, although females can also be affected.

Many individuals with G6PD deficiency remain symptom-free until exposed to certain triggers. These may include specific medications, severe infections, fava beans, or chemicals such as naphthalene found in mothballs. Exposure to these triggers can cause rapid destruction of red blood cells, known as haemolysis, leading to symptoms such as sudden fatigue, pale skin, jaundice, dark urine, rapid heartbeat, and shortness of breath. In newborns, G6PD deficiency may also cause significant neonatal jaundice.

Diagnosis is confirmed through enzyme activity testing and, when required, genetic analysis. Management focuses on avoiding known triggers, treating infections promptly, and educating patients about medications and foods that may provoke haemolytic episodes. Severe cases may require blood transfusions or supportive hospital care during acute haemolysis. With early diagnosis, trigger avoidance, and appropriate medical guidance, most individuals with G6PD deficiency can maintain good health and lead normal, active lives.