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Introduction Clinical definition glucose-6-phosphate dehydrogenase (G6PD) deficiency is an X-linked genetic disorder that causes an intrinsic hemolytic anemia Epidemiology prevalence 7.1% worldwide most common enzyme disorder of erythrocytes demographics more severe in males than females common in areas where malaria is endemic Pathophysiology G6PD affects the pentose phosphate (hexose monophosphate) pathway this pathway generates nicotinamide dinucleotide phosphate (NADPH), which protects red blood cells against oxidative stress in red blood cells (without mitochondria), this pathway is the only source of NADPH acute hemolytic anemia following exposure to oxidative stressors oxidative stressors cause G6PD deficiency is thought to decrease risk of severe malaria Genetics inheritance pattern X-linked mutations G6PD gene encoding the G6PD enzyme Prognosis natural history of disease typically asymptomatic until exposed to oxidative stressors Presentation Symptoms primary symptoms neonatal hyperbilirubinemia on day 2-4 acute hemolytic anemia following exposure to precipitants, typically within 24-72 hours after ingestion Physical exam jaundice Studies Labs complete blood count and reticulocyte count bite cells ↑ indirect bilirubin ↓ haptoglobin ↑ lactate dehydrogenase urine hemoglobinuria G6PD activity assays indication screening fluorescent spot test most sensitive methemoglobin reduction test Quantitative assays indications confirmation of diagnosis spectrophotometry analysis Differential jaundice at birth (rather than delayed onset of jaundice) normal G6PD enzyme activity spherocytosis seen on peripheral blood smear Treatment Conservative avoid oxidative stressors Medical blood transfusion indication Complications Recurrence of acute hemolysis Create a free account or log in to see the cards.

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The only double-blind trial (n=16) found weak objective improvements but no change in subjective sleep quality