Methemoglobinemia risk factors
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aksiniya Stevasarova, M.D.
Overview
- The risk factors for the formation of methemoglobinemia can be divided into two groups: congenital risk factors and acquired risk factors.
Congenital Risk Factors for 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 Risk Factors for Methemoglobinemia
- Some of the most common risk factors include different oxidant drugs, toxins and chemicals.
Risk Factors
Congenital Risk Factors for Methemoglobinemia
- There are three main congenital risk factors that lead to methemoglobinemia:
1. Cytochrome b5 reductase deficiency and pyruvate kinase deficiency
3. Presence of abnormal hemoglobin (Hb M)
- Both cytochrome b5 reductase deficiency and pyruvate kinase deficiency can lead to NADH deficiency which in turn will lead to decreased ability to remove MetHb from the blood. Cytochrome b5 reductase deficiency is an autosomal recessive disorder with at least 2 forms that we know of.
The most common form, is the Ib5R deficiency, where cyt b5 reductase is absent only in RBCs, and the levels of MetHb are around 10% to 35%. [1]
- The second type, which is much less common, is the IIb5R deficiency, where MetHb levels vary between 10% and 15% and the [[cyt
b5 reductase]] is absent in all cells. This form is associated with mental retardation, microcephaly, and other neurologic problems. The lifespan of the affected individuals is greatly affected and patients usually die very young. [2]
- Congenital deficiency in G6PD can lead to decreased levels of NADPH and thus compromising the function of the diaphorase II enzyme system. [3]
- Abnormal hemoglobins like Hb M, including Hb Ms, Hb MIwate, Hb MBoston, Hb MHyde Park, and Hb MSaskatoon, an autosomal dominant condition, can also lead to methemoglobinemia. In case of amino acid substitution in the alpha-chain of hemoglobin, we observe cyanosis at birth, and infants with beta chain amino acid substitution will present with cyanosis later around 4-6 months of age. [4]
Acquired Risk Factors for Methemoglobinemia
- Some of the most common risk factors that can cause excessive formation of methemoglobin include different oxidant drugs, toxins and chemicals.[5] [1]
1. Drug Induced
• Anesthetics[6] like benzocaine[7], lidocaine[8], prilocaine[9]
• Antimalarial drugs like Primaquine phosphate (in nicotinamide adenine dinucleotide (NADH) methemoglobin reductase deficient individuals)
• Dapsone
2. Contaminated well water (in premature infants and infants younger than 4 months) [12]ref> [www.epa.gov/dwstandardsregulations]</ref>
3. Solid foods (not well cooked vegetables high in nitrates in premature infants and infants younger than 4 months) [13] [14]
References
- ↑ 1.0 1.1 do Nascimento TS, Pereira RO, de Mello HL, Costa J (2008). "Methemoglobinemia: from diagnosis to treatment". Rev Bras Anestesiol. 58 (6): 651–64. PMID 19082413.
- ↑ Percy MJ, Barnes C, Crighton G, Leventer RJ, Wynn R, Lappin TR (2012). "Methemoglobin reductase deficiency: novel mutation is associated with a disease phenotype of intermediate severity". J Pediatr Hematol Oncol. 34 (6): 457–60. doi:10.1097/MPH.0b013e318257a492. PMID 22627575.
- ↑ Rehman A, Shehadeh M, Khirfan D, Jones A (2018). "Severe acute haemolytic anaemia associated with severe methaemoglobinaemia in a G6PD-deficient man". BMJ Case Rep. 2018. doi:10.1136/bcr-2017-223369. PMID 29592989.
- ↑ Alonso-Ojembarrena A, Lubián-López SP (2016). "Hemoglobin M Disease as a Cause of Cyanosis in a Newborn". J Pediatr Hematol Oncol. 38 (3): 173–5. doi:10.1097/MPH.0000000000000489. PMID 26694193.
- ↑ Hall AH, Kulig KW, Rumack BH (1986). "Drug- and chemical-induced methaemoglobinaemia. Clinical features and management". Med Toxicol. 1 (4): 253–60. PMID 3537620.
- ↑ Faust AC, Guy E, Baby N, Ortegon A (2018). "Local Anesthetic-Induced Methemoglobinemia During Pregnancy: A Case Report and Evaluation of Treatment Options". J Emerg Med. 54 (5): 681–684. doi:10.1016/j.jemermed.2018.01.039. PMID 29519718.
- ↑ Rodriguez LF, Smolik LM, Zbehlik AJ (1994). "Benzocaine-induced methemoglobinemia: report of a severe reaction and review of the literature". Ann Pharmacother. 28 (5): 643–9. doi:10.1177/106002809402800515. PMID 8069004.
- ↑ Gay HC, Amaral AP (2018). "Acquired Methemoglobinemia Associated with Topical Lidocaine Administration: A Case Report". Drug Saf Case Rep. 5 (1): 15. doi:10.1007/s40800-018-0081-4. PMC 5889764. PMID 29627919.
- ↑ Shamriz O, Cohen-Glickman I, Reif S, Shteyer E (2014). "Methemoglobinemia induced by lidocaine-prilocaine cream". Isr Med Assoc J. 16 (4): 250–4. PMID 24834764.
- ↑ Khan M, Paul S, Farooq S, Oo TH, Ramshesh P, Jain N (2017). "Rasburicase-Induced Methemoglobinemia in a Patient with Glucose-6- Phosphate Dehydrogenase Deficiency". Curr Drug Saf. 12 (1): 13–18. doi:10.2174/1574886312666170111151246. PMID 28078984.
- ↑ Messmer AS, Nickel CH, Bareiss D (2015). "P-chloroaniline poisoning causing methemoglobinemia: a case report and review of the literature". Case Rep Emerg Med. 2015: 208732. doi:10.1155/2015/208732. PMC 4377359. PMID 25861488.
- ↑ Brunato F, Garziera MG, Briguglio E (2003). "A severe methaemoglobinemia induced by nitrates: a case report". Eur J Emerg Med. 10 (4): 326–30. doi:10.1097/01.mej.0000103472.32882.db. PMID 14676514.
- ↑ [www.fda.gov/Drugs/DrugSafety/ucm250024.htm]
- ↑ [www.fda.gov/forconsumers/consumerupdates/ucm306062.htm]