<unk>  deficiency was first discovered more than 50 years ago. Prisoner volunteers were given primaquine and some of them developed hemolytic anemia.<unk>  deficiency may be classified to into 5 subtypes. It is understood that<unk>  deficiency is the result of reduced<unk> -6-phosphate<unk>  enzyme levels.<unk>  deficiency is an X-linked disorder.<unk> -6-phosphate<unk>  enzyme oxidizes<unk> -6-phosphate to<unk> -phosphogluconolactone in pentose phosphate pathway ( HMP shunt). The most common cause of<unk>  deficiency is due to genetic disorder. Less common cause of<unk>  deficiency include neutrophil dysfunction.<unk>  deficiency is affecting 400 million people worldwide. patients of all age groups may develop favism, but more often and severe in children. African, Middle Eastern and South Asian people are affected the most. Men are more commonly affected by<unk>  deficiency. Common risk factors in the development of<unk>  deficiency include some foods such as fava beans, some medications and infections. The symptoms of<unk>  deficiency typically develop after exposure to some foods and medications. Common complications of<unk>  deficiency include acute hemolytic anemia and neonatal jaundice.Diagnostic study of choice for<unk>  deficiency include quantitative laboratory assay, Beutler fluorescent spot test and DNA testing for mutated genes. The mainstay of treatment for<unk>  deficiency is avoidance of the foods such as fava beans and drugs that cause hemolysis. Pharmacologic medical therapy is recommended among patients with chronic hemolysis. Blood transfusion can be considered in acute phase of hemolysis.
Glucose-6-phosphate dehydrogenase deficiency
Pyridoxamine 5-prime-phosphate oxidase deficiency
Aldolase A deficiency
Alpha-ketoglutarate dehydrogenase deficiency
ALA dehydratase deficiency
Ornithine transcarbamylase deficiency
Pyruvate dehydrogenase deficiency
Pyruvate kinase deficiency