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Aminoglycoside-induced deafness during treatment of acute leukaemia
  1. M Bitner-Glindzicz1,2,
  2. V Osei-Lah3,4,
  3. I Colvin5,
  4. T Sirimanna3,
  5. D Lucas5,
  6. B Mac Ardle5,
  7. D Webb6,
  8. A Shankar7,
  9. J Kingston6,7,
  10. L Jenkins8,
  11. S Rahman1,9
  1. 1Clinical and Molecular Genetics Unit, UCL Institute of Child Health and Great Ormond Street Hospital NHS Trust, London, UK
  2. 2UCL Ear Institute, London, UK
  3. 3Department of Audiological Medicine, Great Ormond Street Hospital NHS Trust, London, UK
  4. 4Department of Audiological Medicine, Queen Alexandra Hospital, Portsmouth, UK
  5. 5Nuffield Hearing and Speech Centre, Royal National Throat Nose and Ear Hospital, London, UK
  6. 6Department of Haematology and Oncology, Great Ormond Street Hospital NHS Trust, London, UK
  7. 7Department of Paediatric Haematology and Oncology, The Royal London Hospital, Whitechapel, London, UK
  8. 8North Thames (East) Regional Clinical Molecular Genetics Laboratory, Great Ormond Street Hospital NHS Trust, London, UK
  9. 9MRC Centre for Neuromuscular Diseases, National Hospital for Neurology and Neurosurgery, Queen Square, London, UK
  1. Correspondence to Maria Bitner-Glindzicz, Clinical and Molecular Genetics Unit, UCL Institute of Child Health and Great Ormond Street Hospital NHS Trust, 30 Guilford St, London WC1N 1EH, UK; mbitnerg{at}ich.ucl.ac.uk

Abstract

Three unrelated children from ethnically diverse backgrounds who were treated for acute leukaemia became profoundly and irreversibly deaf during treatment. Aminoglycoside levels were within the therapeutic range. Genetic testing showed all three to have a maternally inherited mutation of mitochondrial DNA, m.1555A>G, known to cause sensitivity to the ototoxic effects of aminoglycosides. One child has received a cochlear implant, and another will be implanted shortly. Children diagnosed with acute leukaemia should be tested for this mutation at diagnosis, and alternative antibiotics chosen for the treatment of sepsis. Consideration should be given to elective testing of other groups of patients likely to receive aminoglycosides.

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Footnotes

  • Funding MB-G and SR have received funding from SPARKS.

  • Competing interests MB-G and SR have been awarded funding from SPARKS to determine the prevalence of m.1555A>G in the UK.

  • Patient consent Parental consent obtained.

  • Provenance and peer review Not commissioned; externally peer reviewed.

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