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Ototoxicity in preterm infants: effects of genetics, aminoglycosides, and loud environmental noise

E Zimmerman1, A Lahav

  • 1Department of Newborn Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Journal of Perinatology : Official Journal of the California Perinatal Association
|August 11, 2012
PubMed

Insights

Aminoglycoside treatment and NICU noise may cause hearing loss in preterm infants. Mitochondrial DNA mutations can worsen this risk, necessitating protective strategies.

Area of Science:

  • Neonatal Medicine
  • Otolaryngology
  • Genetics

Background:

  • Hearing loss is common in extremely preterm infants with unknown causes.
  • Aminoglycosides and Neonatal Intensive Care Unit (NICU) noise are suspected contributors to ototoxicity.
  • Mitochondrial DNA mutations are linked to aminoglycoside-induced hearing loss.

Purpose of the Study:

  • To systematically review research on ototoxicity in extremely preterm neonates.
  • To elucidate mechanisms of aminoglycoside, noise, and mitochondrial DNA mutation interactions.
  • To recommend strategies for minimizing ototoxicity risk in NICU infants.

Main Methods:

  • Systematic literature review.
  • Analysis of multifactorial mechanisms of ototoxicity.
  • Discussion of clinical care improvements.

Main Results:

  • Aminoglycosides and NICU noise can damage auditory hair cells.
  • Mitochondrial DNA mutations exacerbate aminoglycoside-induced ototoxicity.
  • Combined factors potentiate hearing impairment risk.

Conclusions:

  • Ototoxicity in preterm infants is multifactorial, involving genetics and environment.
  • Strategies to reduce noise and judicious aminoglycoside use are crucial.
  • Further research and clinical vigilance are needed to protect infant hearing.

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