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The presence of methemoglobin in the blood.



the appearance of methemoglobin in the blood as a result of the toxic effect of various chemical substances (nitrates and nitrites, aniline, pyridine) that are capable of converting hemoglobin to methemoglobin (MtHb) upon entering the body through the skin, digestive tract, or lungs. With considerable methemoglobinemia, oxygen starvation, or hypoxia, may result. Methemoglobin may be excreted with the urine (methemoglobinuria); this is sometimes damaging to the kidneys. Methemoglobinemia is treated with antidotes (methylene blue, ascorbic acid) and oxygen therapy.

References in periodicals archive ?
As a result of the prolonged absorption time and enterohepatic recirculation of DDS, methaemoglobinaemia may persist for several days following DDS ingestion.
This may explain the undetectability of cases of methaemoglobinaemia in routine hospital work, which depend on the use of pulse oxymetry.
Methaemoglobinaemia also increases the risk of haemolysis due to oxidant damage to erythrocytes, either directly or through the formation of free radicals.
The next day repeat arterial blood co-oximetry revealed methaemoglobinaemia of 23%.
Other adverse effects in humans include the formation of methaemoglobinaemia, which can cause cyanosis in sufficient quantities.
The 4% methaemoglobinaemia for Case 1 was therefore considered a false result, although this was not confirmed.
Asymptomatic methaemoglobinaemia and its implications.
I read with interest the article by Mullick et al describing management of case of aniline-induced methaemoglobinaemia in a G6PD deficient patient (1).
Methaemoglobinaemia after inhalation of nitric oxide in infant with pulmonary hypertension.
Neither patient developed methaemoglobinaemia or raised nitrogen dioxide concentrations.
Drug-induced oxidant damage to red cells presents in a variety of disorders of which methaemoglobinaemia and/or intravascular haemolysis are the main components.