Methemoglobinemia epidemiology and demographics: Difference between revisions
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'''Epidemiology''' | '''Epidemiology''' | ||
In the United States congenital methemoglobinemia is rare. Deficiency of cytochrome b5 reductase endemic only in some Native American tribes like Navajo <ref>{{J Pediatr. 1964 Dec;65:928-31. | In the United States congenital [[methemoglobinemia]] is rare. Deficiency of [[cytochrome b5 reductase]] [[endemic]] only in some Native American tribes like Navajo <ref>{{J Pediatr. 1964 Dec;65:928-31. | ||
HEREDITARY METHEMOGLOBINEMIA DUE TO DIAPHORASE DEFICIENCY IN NAVAJO INDIANS. | HEREDITARY METHEMOGLOBINEMIA DUE TO DIAPHORASE DEFICIENCY IN NAVAJO INDIANS. | ||
BALSAMO P, HARDY WR, SCOTT EM. pmid=14244100}}</ref> and Athabaskan Alaskans, and the Yakutsk people in Siberia. <ref>{{J Pediatr Hematol Oncol. 2017 Jan;39(1):42-45. | BALSAMO P, HARDY WR, SCOTT EM. pmid=14244100}}</ref> and Athabaskan Alaskans, and the Yakutsk people in Siberia. <ref>{{J Pediatr Hematol Oncol. 2017 Jan;39(1):42-45. | ||
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Burtseva TE1, Ammosova TN, Protopopova NN, Yakovleva SY, Slobodchikova MP. pmid=27879543 }}</ref> | Burtseva TE1, Ammosova TN, Protopopova NN, Yakovleva SY, Slobodchikova MP. pmid=27879543 }}</ref> | ||
The acquired methemoglobinemia is the most common form, and most cases are related to topical or local | The [[acquired]] [[methemoglobinemia]] is the most common form, and most cases are related to topical or local [[anesthetics]] use during medical procedures. | ||
'''Demographics''' | '''Demographics''' | ||
Infants, particularly those younger than 4 months are most susceptible to methemoglobinemia. This is due to the fact that the NADH methemoglobin reductase activity and concentration (the main protective enzyme against oxidative stress) is not fully mature in infants. | Infants, particularly those younger than 4 months are most susceptible to [[methemoglobinemia]]. This is due to the fact that the [[NADH methemoglobin reductase]] activity and concentration (the main protective [[enzyme]] against [[oxidative stress]]) is not fully mature in infants. | ||
Both cytochrome b5 reductase deficiency and pyruvate kinase deficiency are autosomal recessive diseases and the Hb M has autosomal dominant pattern of inheritance. | 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 methemoglobinemia is greater in males. 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. <ref>{{Malar J. 2013 Nov 15;12:418. doi: 10.1186/1475-2875-12-418. | On the other hand ([G6PD]] deficiency is [[X-linked]], therefore the risk of acquired methemoglobinemia is greater in males. 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. <ref>{{Malar J. 2013 Nov 15;12:418. doi: 10.1186/1475-2875-12-418. | ||
Spatial distribution of G6PD deficiency variants across malaria-endemic regions. | Spatial distribution of G6PD deficiency variants across malaria-endemic regions. | ||
Howes RE1, Dewi M, Piel FB, Monteiro WM, Battle KE, Messina JP, Sakuntabhai A, Satyagraha AW, Williams TN, Baird JK, Hay SI. pmid=24228846 }}</ref> <ref>{{ Adv Parasitol. 2013;81:133-201. doi: 10.1016/B978-0-12-407826-0.00004-7. | Howes RE1, Dewi M, Piel FB, Monteiro WM, Battle KE, Messina JP, Sakuntabhai A, Satyagraha AW, Williams TN, Baird JK, Hay SI. pmid=24228846 }}</ref> <ref>{{ Adv Parasitol. 2013;81:133-201. doi: 10.1016/B978-0-12-407826-0.00004-7. | ||
Revision as of 16:00, 14 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Template:Aksiniya K. Stevasarova, M.D.
Overview
Congenital (Hereditary) Methemoglobinemia
There are three main congenital conditions that lead to methemoglobinemia:
1. Cytochrome b5 reductase deficiency and pyruvate kinase deficiency
3. Presence of abnormal hemoglobin (Hb M)
Acquired or Acute Methemoglobinemia
Most common cause include different oxidant drugs, toxins or chemicals
Epidemiology and Demographics
Epidemiology
In the United States congenital methemoglobinemia is rare. Deficiency of cytochrome b5 reductase endemic only in some Native American tribes like Navajo [1] and Athabaskan Alaskans, and the Yakutsk people in Siberia. [2]
The acquired methemoglobinemia is the most common form, and most cases are related to topical or local anesthetics use during medical procedures.
Demographics
Infants, particularly those younger than 4 months are most susceptible to methemoglobinemia. This is due to the fact that the NADH methemoglobin reductase activity and concentration (the main protective enzyme against oxidative stress) is not fully mature in infants. 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 methemoglobinemia is greater in males. 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. [3] [4] [5]
- ↑ {{J Pediatr. 1964 Dec;65:928-31. HEREDITARY METHEMOGLOBINEMIA DUE TO DIAPHORASE DEFICIENCY IN NAVAJO INDIANS. BALSAMO P, HARDY WR, SCOTT EM. pmid=14244100}}
- ↑ {{J Pediatr Hematol Oncol. 2017 Jan;39(1):42-45. Enzymopenic Congenital Methemoglobinemia in Children of the Republic of Sakha (Yakutia). Burtseva TE1, Ammosova TN, Protopopova NN, Yakovleva SY, Slobodchikova MP. pmid=27879543 }}
- ↑ {{Malar J. 2013 Nov 15;12:418. doi: 10.1186/1475-2875-12-418. Spatial distribution of G6PD deficiency variants across malaria-endemic regions. Howes RE1, Dewi M, Piel FB, Monteiro WM, Battle KE, Messina JP, Sakuntabhai A, Satyagraha AW, Williams TN, Baird JK, Hay SI. pmid=24228846 }}
- ↑ {{ Adv Parasitol. 2013;81:133-201. doi: 10.1016/B978-0-12-407826-0.00004-7. G6PD deficiency: global distribution, genetic variants and primaquine therapy. Howes RE1, Battle KE, Satyagraha AW, Baird JK, Hay SI.pmid=23384623}}
- ↑ Template:Pmid=1917622