Methemoglobinemia and Heinz Body Hemolytic Anemia Due to Phenazopyridine Hydrochloride

Greenberg, Mortimer S.; Wong, Helena

doi:10.1056/nejm196408272710902

Cited by 47 publications

(7 citation statements)

References 9 publications

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“…Methaemoglobinaemia is the major recognized complication of acute overdosage with this drug (Wander and Pascoe, 1965). Hepatotoxicity and transient elevation of the blood urea have also been reported (Wander and Pascoe, 1965); Heinzbody haemolytic anaemia has been associated with methaemoglobinaemia in adult patients treated with Pyridium (Greenberg and Wong, 1964). The present patient had no evidence of hepatic damage, but there was a significant elevation of blood urea for several days indicating transient renal toxicity.…”

Section: Discussionsupporting

confidence: 59%

Acute Pyridium Poisoning

Soutter

Harley

Walker-Smith

1969

J Paediatrics Child Health

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A 2 year old female infant was admitted with a short history of vomiting yellow-brown material and passing yellow urine. Acute poisoning with Pyridium was suspected on clinical grounds and later demonstrated chemically. She developed methaemoglobinaemia which responded well to methylenc blue intravenously and saline enemata. She also had evidence of haemolysis and transient renal toxicity, but she made a complete recovery. Sand, R. E. and Edelmann, C. M. Jr. (1961). Pyridium-induced rnethemoglobinemia. 1. Pediar., 58, 845. Wander. H. J. and Pascoe, D. J. (1965). Phenylazopyridine hydrochloride poisoning. Report of case and review of literature. Anier. J . Dis. Child., 110, 105.

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Section: Discussionsupporting

confidence: 59%

Acute Pyridium Poisoning

Soutter

Harley

Walker-Smith

1969

J Paediatrics Child Health

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“…Single megadoses produced central nervous system depression, methemoglobinemia, hemolytic anemia, and up to 50% mortality [19]. Methemoglobinemia is one of the earliest recognized side effects of Pyridium® overdose [13,14]. The pathology of methemoglobin is the oxidation to the trivalent (ferric) iron rather than the normal bivalent (ferrous) iron, thereby increasing the affinity to the bound oxygen and decreasing its availability to tissues [20].…”

Section: Discussionmentioning

confidence: 99%

“…Acute renal failure (ARF) is a rare but reported side effect [3][4][5][6][7][8][9][10]. Methemoglobinemia, hemolytic anemia, and skin pigmentation accompanies the transient renal failure in some of the reported cases [11][12][13][14][15]. We report a case of acute renal failure due to suicidal Pyridium® overdose in a young female with no prior documented kidney disease despite being infected with human immunodeficiency virus (HIV).…”

Section: Introductionmentioning

confidence: 99%

Acute renal failure due to phenazopyridine (Pyridium®) overdose: case report and review of the literature

et al. 2006

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Phenazopyridine (Pyridium) is a commonly used urinary tract analgesic. It has been associated with yellow skin discoloration, hemolytic anemia, methemoglobinemia, and acute renal failure, especially in patients with preexisting kidney disease. We report a 17-year-old female with vertically transmitted human immunodeficiency virus (HIV) infection, presenting with acute renal failure and methemoglobinemia following a suicidal attempt with a single 1,200 mg ingestion of Pyridium. She had no prior evidence of HIV nephropathy. The patient had a progressive nonoliguric renal failure on the 3rd day following the ingestion. She was treated with N-acetylcysteine, intravenous carnitine, and alkalinization of the urine. Her kidney biopsy revealed acute tubular necrosis with no glomerular changes. After 7 days of conservative management, she was discharged home with normal kidney function. To our knowledge, this is the second smallest amount of Pyridium overdose resulting in acute renal failure with no previous history of kidney disease.

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“…to a sulfonamide preparation containing PAP [20] , led to a study of the in vitro effects of PAP on red cells containing Hb Zurich. Greenberg and Wong [2] demonstrated that PAP added to normal blood in drug/ hemoglobin molar ratios of 10 to 100 led to a marked increase in the rate of methemoglobin formation. However, at a molar ratio of 44: 1, GSH levels remained stable after the addition of glucose.…”

Section: Discussionmentioning

confidence: 99%

“…Phenazopyridine (PAP), a commonly used urinary tract analgesic, causes methemoglobinemia and Heinz body hemolytic anemia in normal individuals when taken in overdose or administered to subjects with renal insufficiency [ 11. Although it has been recommended that the drug not be used in subjects deficient in glucose-6phosphate dehydrogenase (G6PD) [2,3], there are no reports of untoward reactions in such a setting. Also unreported are the in vivo or in vitro effects of the drug on red cells containing an unstable hemoglobin.…”

Section: Introductionmentioning

confidence: 99%

Unique sensitivity of Hb Zürich to oxidative injury by phenazopyridine: Reversal of the effects by elevating carboxyhemoglobin levels in vivo and in vitro

et al. 1983

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Phenazopyridine (PAP) causes a hemolytic anemia in normal individuals who receive an overdose or in patients with decreased renal function given therapeutic doses. There are no reports of PAP-induced hemolysis in individuals with unstable hemoglobins. Therapeutic doses of PAP administered to a subject with Hb Zürich (His E7 (63) beta leads to Arg) caused a severe hemolytic anemia with many large Heinz bodies appearing in the red cells. Incubation of whole blood from three asymptomatic Hb Zürich subjects with PAP at a molar ratio of PAP/Hb of 1.3/1 produced a moderate to marked increase in methemoglobin (MHb) and Heinz body formation accompanied by a slight to moderate decrease in levels of reduced glutathione. The rates of MHb formation were proportional to the concentration of PAP. In two of the subjects the rates of formation of Heinz bodies and MHb were substantially higher than in the third subject. Red cells from five normal adults were not affected. In Hb Zürich red cells the affinity of the abnormal beta chain for carbon monoxide is much greater than that of the normal alpha and beta chains. The two subjects with higher rates of MHb and Heinz body formation were nonsmokers with in vivo carboxyhemoglobin (HbCO) levels of 4-6%. The third subject with low rates of MHb and Heinz body formation was a smoker with in vivo HbCO levels of 15-18%. Increasing levels of HbCO from 8.2% to 14.3% by the in vitro addition of CO caused a marked reduction in the rate of Heinz body formation and a moderate decrease in MHb formation. Rates of MHb formation similar to those observed in normal red cells occurred at HbCO percentages of 89.2 and 99.2. Red cells containing Hb Zürich are extremely sensitive to oxidative injury by PAP, either in vivo or in vitro. The degree of oxidative injury diminishes as the level of HbCO increases, a phenomenon that is enhanced by preferential binding of CO to the abnormal beta subunit of Hb Zürich.

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Methemoglobinemia and Heinz Body Hemolytic Anemia Due to Phenazopyridine Hydrochloride

Cited by 47 publications

References 9 publications

Acute Pyridium Poisoning

Acute Pyridium Poisoning

Acute renal failure due to phenazopyridine (Pyridium®) overdose: case report and review of the literature

Unique sensitivity of Hb Zürich to oxidative injury by phenazopyridine: Reversal of the effects by elevating carboxyhemoglobin levels in vivo and in vitro

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