Handbook of clinical drug data.pdf - Me and My Life

DRUG-INDUCED OTOTOXICITY 85978. Karbassi M, Nikou S. Acute uveitis in patients with acquired immunodeficiency syndrome receiving prophylacticrifabutin. Arch Ophthalmol 1995;113:699–701.79. Cayley FE, Majumdar SK. Ocular toxicity due to rifampicin. Br Med J 1976;1:199–200.80. Lyons RW. Orange contact lenses from rifampin. N Engl J Med 1979;300:372–3. Letter.81. Harris J, Jenkins P. Discoloration of soft contact lenses by rifampicin. Lancet 1985;2:1133. Letter.82. Nayfield SG, Gorin MB. Tamoxifen-associated eye disease: a review. J Clin Oncol 1996;14:1018–26.83. Wild JM et al. Characteristics of a unique visual field defect attributed to vigabatrin. Epilepsia1999;40:1784–94.84. Kälviäinen R et al. Vigabatrin, a gabaergic antiepileptic drug, causes concentric visual field defects. Neurology1999;53:922–6.85. Albert DM et al. Ocular complications of vincristine therapy. Arch Ophthalmol 1967;78:709–13.Drug-Induced OtotoxicityDrug-induced ototoxicity can affect hearing (auditory or cochlear function), balance(vestibular function), or both, depending on the drug. Drugs of almost everyclass have been reported to produce tinnitus, as have placebos. The agents in thistable are associated with measurable changes in hearing or vestibular defect whenadministered systemically.AminoglycosidesAminoglycoside antibiotics can cause cochlear and vestibular toxicities. Cochlear toxicity presentsas progressive hearing loss, starting with the highest tones and advancing to lower tones. Thus,considerable damage can occur before the patient is cognizant of it. Vestibular damage presentsas dizziness, vertigo, or ataxia. Both forms of ototoxicity are usually bilateral and potentially reversible,but permanent damage is common and can progress after aminoglycoside discontinuation.Estimates of the prevalence of aminoglycoside-induced ototoxicity vary widely depending onthe criteria applied. Clinically detectable ototoxicity probably occurs in as many as 5% of patients,with a much higher percentage demonstrating audiometrically detectable damage. Mostaminoglycoside-induced ototoxicity is associated with parenteral therapy, but it has followedtopical, oral, and irrigation use of these drugs, especially neomycin. A patient should receivedosages by these routes that are no greater than the dosages given by injection. Possible predisposingfactors for ototoxicity are decreased renal function, long duration of therapy, large totaldosage, plasma levels exceeding the therapeutic range, previous aminoglycoside use, concurrentuse of other ototoxic drugs, dehydration, and old age. There is some evidence of an inherited susceptibilityto aminoglycoside-induced ototoxicity. Hearing impairment is less common in neonatesand children. Two meta-analyses found no difference in the effects on hearing of single daily dosingand multiple daily dosing of aminoglycosides. The comparative effects on vestibular functionhave not been adequately investigated. Serial audiometry might be useful in early detection ofototoxicity. Each aminoglycoside has a slightly different spectrum of ototoxicity; the table belowserves as a general guide to their relative ototoxic potentials. 1–10RELATIVE OTOTOXIC POTENTIALDRUG COCHLEAR VESTIBULARAmikacin +++ ++Gentamicin ++ +++