- General Drug Summary
- Description
- An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29)
- Also Known As
- Acetasol; Analgesine; Anodynin; Anodynine; Antipirin; Antipyrin; Antipyrinum; Azophen; Azophenum; Fenazon [czech]; Fenazona [inn-spanish]; Fenazone; Phenazone; Phenozone
- Structure
- Summary In Neonatal Jaundice
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1 record(s) for Antipyrine NA in Neonatal Jaundice.
- PMID
- Drug Name
- Efficacy
- Evidence
- Summary
- prolongation of the plasma half-life of antipyrine maybe lead to Neonatal jaundice
- Serum gamma-glutamyl transpeptidase, D-glucaric acid excretion and plasma half-life of antipyrine in newborns with severe jaundice of unknown etiology and due to glucose-6-phosphate dehydrogenase deficiency in Greece. Helvetica paediatrica acta, 1981 [Go to PubMed]
- Serum gamma-glutamyl transpeptidase (gamma-GT) activity, urinary D-glucaric acid (D-GA) excretion and plasma half-life of antipyrine were measured in 22 healthy children as well as in 45 full-term newborns on the 10th day of life. Of these 45 newborns, 20 had jaundice of unknown etiology, 14 had jaundice due to G-6 PD deficiency, and 11 were normal and served as controls. Serum gamma-GT activity was found to be within the normal range in the 22 healthy children, whereas it was in the upper range of the norm in all newborns during the neonatal period. Urinary D-GA excretion was normal in the healthy children and in control known etiology and in 57% of babies with jaundice due to G-6-PD deficiency. Plasma half-life of antipyrine was normal (less than 30 h) in the 22 healthy children, whereas it was prolonged (greater than 30 h) in 9% of the normal newborns, in 60% of the newborns with jaundice of unknown etiology and in 7% of the newborns with jaundice due to G-6-PD deficiency. These findings suggest that in svere neonatal jaundice of unknown etiology there is a greatly reduced excretion of endogenously formed D-GA as well as prolongation of the plasma half-life of antipyrine. This is probably due to decreased activity of the liver enzymes involved in the metabolism of glucuronic acid and the oxidation of antipyrine. These defects probably contributed to the unconjugated hyperbilirubinemia observed in these newborns.