Methoglobinemia is a condition in which ferrous iron within hemoglobin is oxidized to ferric iron resulting in impaired oxygen and carbon dioxide transport leading to cyanosis. It occurs as an acquired or congenital variant. Acquired methemoglobinemia occurs from exposure to oxidizing agents such as nitrates, nitrites, aniline dyes and medications such as lidocaine, prilocaine antimalarials. We report 1 14 months old girl with acquired methemoglobinemia who developed cyanosis after ingestion of potato wafers consisting of monosodium glutamate.

Methemoglobinemia is a condition in which ferrous iron within hemoglobin is oxidized to ferric iron resulting in impaired oxygen and carbon dioxide transport leading to cyanosis. This ferric state leads to the formation of methemoglobin that causes brownish discoloration of the blood. In healthy normal children, the ferric iron is reduced to ferrous state by the aid of cytochrome b5 oxidase (methemoglobin reductase) along with other systems such as NADH reductase, glutathione reductase and Glucose-6-phosphate dehydrogenase (G-6-PD). Normal concentration of methemoglobin is maintained below 1% in healthy individuals by these enzyme systems (1). Methemoglobinemia occurs as an acquired or congenital variant. Acquired methemoglobinemia is more common and occurs from exposure to oxidizing agents such as nitrates, nitrites, aniline dyes and medications such as lidocaine, prilocaine antimalarials. Pyridium etc (2). It is seen more commonly in premature infants and infants younger than 4 months of age due to presence of fetal hemoglobin and decreased levels of NADH reductase at that age group. Congenital methemoglobinemia is due to either presence of altered hemoglobin (Hemoglobin M) or NADH reductase deficiency. Patients with congenital methemoglobinemia are generally asymptomatic other than cyanosis from birth. Acquired methemoglobinemia is usually mild but can be severe depending upon the cause and can present with cyanosis, dyspnea, lethargy-headache, dizziness and deterioration of mental functioning. A history of exposure to a known toxin or drug may be elicited. (1) We report a child with acquired methemoglobinemia who developed cyanosis after ingestion of potato wafers consisting of monosodium glutamate.

	1.	Conkling PR. Brown blood: understanding methemoglobinemia. N C Med J. Mar 1986; 47: 109-111.
	2.	Ash-Bernal R, Wise R, Wright SM. Acquired methemoglobinemia: a retrospective series of 138 cases at 2 teaching hospitals. Medicine (Baltimore). 2004; 83: 265-273
	3..	Henretig FM, Gribetz B, Kearney T, Lacouture P, Lovejoy FH. Interpretation of color change in blood with varying degree of methemoglobinemia. J Toxicol Clin Toxicol. 1988; 26: 293-301.
	4.	Herman MI, Chyka PA, Butler AY, Rieger SE. Methylene blue by intraosseous infusion for methemoglobinemia. Ann Emerg Med. 1999; 33: 111-113

Last Updated on 01-09-2005 Vol 2 Issue 9 Art # 42

Shah I. Methemoglobinemia.Pediatric Oncall [serial online] 2005 [cited 2005 September 1];2. Art # 42. Available from: