Methemoglobinemia is acquired when the normal mechanisms responsible for the elimination of methemoglobin are overwhelmed by an exogenous oxidant stress, such as a drug or chemical agent (Table 183-1). Drugs rarely produce clinically significant methemoglobinemia in conventional doses, although subclinical methemoglobinemia may go unrecognized. Currently, most cases of methemoglobinemia are due to phenazopyridine (a commonly used agent for the symptomatic treatment of urinary tract infections), benzocaine (a topical anesthetic), and dapsone (an antibiotic often used in HIV-related therapy) ( Table 183-1). Many of these compounds require metabolism to the "active" oxidant, and a substantial time delay until toxicity may occur. Methemoglobinemia can affect any age group and, due to undeveloped methemoglobin reduction mechanisms, the perinatal and infant age groups are more susceptible than older age groups. This explains the relatively common development of methemoglobinemia in infants given certain nitrogenous vegetables (e.g., spinach) or well-water that contains high nitrate levels. Bacteria within the gastrointestinal flora are capable of converting nitrates to the nitrite form, accounting for the toxicity of nitrates in well water and vegetables. Another common cause of acquired infantile methemoglobinemia is gastroenteritis, although the exact cause remains undefined.3
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