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| ==Epidemiology and Demographics== | | ==Epidemiology and Demographics== |
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| '''Epidemiology'''
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| In the United States congenital methemoglobinemia is rare. Deficiency of cytochrome b5 reductase endemic only in some Native American tribes like Navajo and Athabaskan Alaskans.
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| The acquired methemoglobinemia is the most common form, and most cases are related to topical anesthetic use during medical procedures.
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| '''Demographics'''
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| Infants, particularly those younger than 6 months are most susceptible to methemoglobinemia. This is due to the fact that the NADH methemoglobin reducase activity and concentration, the main protective enzyme, against oxidative stress is not fully mature in infants.
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| There is no difference between females and males regarding the frequency of acquired methemoglobinemia. From the congenital type of MetHB Both cytochrome b5 reductase deficiency and pyruvate kinase deficiency are autosomal recessive diseases and the Hb M has autosomal dominant pattern of inheritance. On the other hand G6PD deficiency is X-linked, therefore the risk of acquired methemoglobinemiais greater in males.,
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| The congenital cytochrome b5 reductase deficiency type of methemoglobinemia is endemic in some Native American tribes (Navajo and Athabaskan Alaskans) and the Yakutsk people in Siberia.
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| The highest prevalence of G6PD deficiency is observed in the malaria-endemic regions: Sub-Saharan Afria, West Asia and Arabian Peninsula, as well as in people of Mediterranean descent. As a result these populations are at higher risk for acquired methemoglobinemia.
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| ==References== | | ==References== |