NEOMYCIN

Fetal Risk Summary

Neomycin is an aminoglycoside antibiotic. Small amounts of neomycin (about 3%) are absorbed from the normal gastrointestinal tract (GI) after oral and rectal administration (1). Larger systemic amounts may be obtained if GI motility is impaired. A single 4-g oral dose has produced peak plasma concentrations of 2.5–6.1 µg/mL 1–4 hours after the dose (1).

No reports describing the passage of neomycin across the placenta to the fetus have been located, but this should be expected (see other aminoglycosides Amikacin, Gentamicin, Kanamycin, Streptomycin, and Tobramycin).

Ototoxicity, which is known to occur after oral, topical, and parenteral neomycin therapy, has not been reported as an effect of in utero exposure. However, eighth cranial nerve toxicity in the fetus is well known following exposure to kanamycin and streptomycin and may potentially occur with neomycin.

Oral neomycin therapy, 2 g daily, depresses urinary estrogen excretion, apparently by inhibiting steroid conjugate hydrolysis in the gut (2). The fall in estrogen excretion resembles the effect produced by ampicillin but occurs about 2 days later. Urinary estriol was formerly used to assess the condition of the fetoplacental unit, depressed levels being associated with fetal distress. This assessment is now made by measuring plasma conjugated estriol, which is not usually affected by neomycin.

The Collaborative Perinatal Project monitored 50,282 mother-child pairs, 30 of which had 1st trimester exposure to neomycin (3). No evidence was found to suggest a relationship to large categories of major or minor malformations or to individual defects.

The population-based dataset of the Hungarian Case-Control Surveillance of Congenital Abnormalities, covering the period of 1980–1996, was used to evaluate the teratogenicity of aminoglycoside antibiotics (parenteral gentamicin, streptomycin, tobramycin, and oral neomycin) in a study published in 2000 (4). A case group of 22,865 women who had fetuses or newborns with congenital malformations were compared to 38,151 women who had no newborns with structural defects. A total of 38 cases and 42 controls were treated with aminoglycosides. There were 12 cases (0.05%) and 14 controls (0.04%) treated with oral neomycin (odds ratio 1.4, 95% confidence interval 0.7–3.1). A case-control pair analysis for the 2nd and 3rd months of gestation also failed to show a risk for teratogenicity. The investigators concluded that there was no detectable teratogenic risk for structural defects for any of the aminoglycoside antibiotics (4). They also concluded, although it was not investigated in this study, that the risk of deafness after in utero aminoglycoside exposure was small.

Breast Feeding Summary

No reports describing the use of neomycin during human lactation have been located. Small amounts of other aminoglycosides (e.g., see Gentamicin) are excreted into breast milk and absorbed by the nursing infant. Neomycin was excreted into the milk of lactating cows and ewes after a single 10-mg/kg IM dose that produced peak concentrations of approximately 35 µg/mL at 1–2 hours (5). The very limited systemic bioavailability of oral neomycin in humans (about 3% for a normal GI tract), however, suggests that clinically insignificant amounts of neomycin would appear in breast milk.

References

1. American Hospital Formulary Service. Drug Information 2000. Bethesda, MD: American Society of Health-System Pharmacists, 2000:73–4.
2. Pulkkinen M, Willman K. Reduction of maternal estrogen excretion by neomycin. Am J Obstet Gynecol 1973;115:1153.
3. Heinonen OP, Slone D, Shapiro S. Birth Defects and Drugs in Pregnancy. Littleton, MA: Publishing Sciences Group, 1977:297–301.
4. Czeizel AE, Rockenbauer M, Olsen J, Sorensen HT. A teratological study of aminoglycoside antibiotic treatment during pregnancy. Scand J Infect Dis 2000;32:309–13.
5. Ziv G, Sulman FG. Distribution of aminoglycoside antibiotics in blood and milk. Res Vet Sci 1974;17:68–74.