Infantile methemoglobinemia associated with acute diarrheal illness

Lebby, Tom; Roco, Joseph J.; Arcinue, Edgardo L.

doi:10.1016/0735-6757(93)90086-q

Cited by 24 publications

(20 citation statements)

References 6 publications

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“…It is becoming increasingly clear, however, that the early authors were correct to be cautious, and now it appears that there is an association between gastrointestinal illness and symptoms of methemoglobinemia in the absence of exogenous nitrate exposure (Bricker et al 1983; Dagan et al 1988; Danish 1983; Gebara and Goetting 1994; Kay et al 1990; Lebby et al 1993; Smith et al 1988; Yano et al 1982). Yano et al (1982) suggested that diarrhea produces an oxidant stress that increases MetHb production and that acidosis impairs the MetHb reductase systems.…”

Section: Discussionmentioning

confidence: 99%

Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion

Fewtrell¹

2004

Environ Health Perspect

498

204

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On behalf of the World Health Organization (WHO), I have undertaken a series of literature-based investigations examining the global burden of disease related to a number of environmental risk factors associated with drinking water. In this article I outline the investigation of drinking-water nitrate concentration and methemoglobinemia. The exposure assessment was based on levels of nitrate in drinking water greater than the WHO guideline value of 50 mg/L. No exposure–response relationship, however, could be identified that related drinking-water nitrate level to methemoglobinemia. Indeed, although it has previously been accepted that consumption of drinking water high in nitrates causes methemoglobinemia in infants, it appears now that nitrate may be one of a number of co-factors that play a sometimes complex role in causing the disease. I conclude that, given the apparently low incidence of possible water-related methemoglobinemia, the complex nature of the role of nitrates, and that of individual behavior, it is currently inappropriate to attempt to link illness rates with drinking-water nitrate levels.

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Section: Discussionmentioning

confidence: 99%

Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion

Fewtrell¹

2004

Environ Health Perspect

498

204

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“…Moreover, unexpected contamination of running water would have been followed by outbreaks of toxic methemoglobinemia 13 -a fact that was not observed. In contrast, the relation between methemoglobinemia and diarrhea is well known 10,20 with or without some degree of metabolic acidosis in infants, particularly in those with weight at or below the 10th percentile for age. 8,9 However, none of these circumstances occurred in our patients.…”

Section: Discussionmentioning

confidence: 99%

Methemoglobinemia and Consumption of Vegetables in Infants

Benito²,

2001

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ABSTRACT. Objective. To assess clinical and epidemiologic data of 7 infants diagnosed with acquired methemoglobinemia at the pediatric emergency department between 1993 and 1998. All cases were attributed to the consumption of mixed vegetables.Methods. Medical records were reviewed to collect anamnestic data; history of food ingestion; and results of physical examination, pulse oximetry, gasometry, cooximetry, urinalysis, and outcome. Local health authorities provided information on nitrate concentration in running water and in vegetables of common consumption in the area.Results. The mean age of the patients was 8.14 months (range: 7-13). None of the infants was undernourished, had diarrhea, or was given any drug. Drinking water showed a nitrate concentration of 3 to 6 ppm. All were fed homemade purée of mixed vegetables, prepared in advance and kept in the refrigerator for 12 to 27 hours. Silver beets were a common ingredient. No case showed metabolic acidosis. Methemoglobin level ranged between 10% and 58%. Three cases had nitrituria. Silver beets in our area were the vegetables with the highest nitrate concentration (mean: 3200 mg/kg).Conclusions. Consumption of silver beets and incorrect storage of homemade purées of mixed vegetables were potential causes of methemoglobinemia in this series. The disease may occur in children older than 6 months of age. Nitrituria in a cyanotic infant may suggest the diagnosis of methemoglobinemia. Pediatrics 2001; 107:1024 -1028; methemoglobinemia, nitrates, nitrites, food analysis, infant food, food preservation.ABBREVIATIONS. Sao 2 , oxygen saturation; Hb, hemoglobin. M ethemoglobinemia is a rare cause of cyanosis in pediatric patients. Methemoglobin, a derivative of hemoglobin in which the iron component has been oxidized from the Fe 2ϩ to the Fe 3ϩ state, imparts a characteristic brownish color to blood and is unable to transport oxygen. 1,2 Under physiologic conditions, methemoglobin reduction is accomplished primarily by red cell reduced nicotinamide adenine dinucleotide reductase so efficiently that there is Ͻ1% of methemoglobin in the circulating blood. Hereditary methemoglobinemia is attributable either to deficiency of erythrocyte methemoglobin reductase or to the presence of one of the M hemoglobins. Acquired methemoglobinemia is induced by oxidizing agents, particularly chlorates and inorganic and organic nitrites, or by exposure to certain drugs or their metabolites.The most common sources of nitrate exposure are well water, which is mixed with infant formula, consumption of some vegetables with high nitrate concentration, administration of oxidant drugs, and the presence of diarrheal episodes. After ingestion, nitrates are converted to nitrites by fecal organisms, rapidly absorbed from the intestine by passive diffusion reaching the systemic circulation without undergoing first-pass metabolism in the liver (extrahepatic metabolism). Nitrites are potent oxidant agents of ferrohemoglobin. Infants younger than 6 months old are particularly susceptible to nitrate-...

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“…The cyanosis resolved after treatment with methylene blue and discontinuation of metoclopramide. Although diarrheal illness with acidosis has been associated with methemoglobinemia in infants, 9,10 the neonate in the current report did not experience significant diarrhea or acidosis.…”

Section: Case Reportmentioning

confidence: 70%

“…11 Transient methemoglobinemia associated with acute diarrheal illness and acidosis has also been reported, although the mechanism for this association is not clear. 9 Metoclopramide, a derivative of orthoprocainamide, is primarily metabolized (at the first pass through the gut wall or liver) to metoclopramide N-4-sulfate, but as much as 25-40% of the parent compound may undergo renal clearance. 17 In addition, CYP2D6 may also be involved in the metabolism of metoclopramide.…”

Section: Case Reportmentioning

confidence: 99%

Methemoglobinemia Associated with Metoclopramide Therapy in a Neonate

Palmer

James

2004

The Journal of Pediatric Pharmacology and Therapeutics

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With the removal of cisapride from the U.S. market, practitioners have increasingly used other medications, such as metoclopramide, to treat gastroesophageal reflux in pediatric patients. We describe the case of a neonate who developed methemoglobinemia after receiving metoclopramide at doses slightly above the recommended age-appropriate dosage. Health care providers should be aware of this potentially serious side effect in young infants who receive this medication.

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Infantile methemoglobinemia associated with acute diarrheal illness

Cited by 24 publications

References 6 publications

Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion

Drinking-Water Nitrate, Methemoglobinemia, and Global Burden of Disease: A Discussion

Methemoglobinemia and Consumption of Vegetables in Infants

Methemoglobinemia Associated with Metoclopramide Therapy in a Neonate

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