<unk>  deficiency is the second most common human enzyme defect after ALDH2 deficiency, being present in more than 400 million people worldwide.<unk>  deficiency resulted in 4,100 deaths in 2013 and 3,400 deaths in 1990. African, Middle Eastern and South Asian people are affected the most, including those who have these ancestries. A side effect of this disease is that it confers protection against malaria, in particular the form of malaria caused by Plasmodium falciparum, the most deadly form of malaria. A similar relationship exists between malaria and sickle-cell disease. One theory to explain this is that cells infected with the Plasmodium parasite are cleared more rapidly by the spleen. This phenomenon might give<unk>  deficiency carriers an evolutionary advantage by increasing their fitness in malarial endemic environments. In vitro studies have shown that the Plasmodium falciparum is very sensitive to oxidative damage. This is the basis for another theory, that is that the genetic defect confers resistance due to the fact that the<unk> -deficient host has a higher level of oxidative agents that, while generally tolerable by the host, are deadly to the parasite.
Glucose-6-phosphate dehydrogenase deficiency
Pyruvate kinase deficiency
Ribose-5-phosphate isomerase deficiency
Hereditary spherocytosis
Glutaminase deficiency
Sickle cell disease
6-phosphogluconate dehydrogenase deficiency
Aldolase A deficiency