Animoglycosides are bactericidal agents that bind to the 30 S bacterial ribosome and inhibit protein synthesis. Agents include gentamicin, tobramycin, amikacin, kanamycin, streptomycin, spectinomycin, and netilmicin. Aminoglycosides have a low therapeutic to toxic ratio, with ototoxicity and nephrotoxicity being common adverse effects. All aminoglycosides have the potential to damage vestibular and cochlear sensory cells, but neomycin is by far the most ototoxic. The incidence of hearing loss related to aminoglycoside has been reported to be between 2 and 25 percent. Hearing loss correlates closely with high-dose or prolonged therapy. Nephrotoxicity results from damage to the proximal renal tubules and correlates with drug dose, therapy duration, volume status, and extremes of age. Mild renal insufficiency may result in 10 to 25 percent of patients using aminoglycosides, as reflected in elevations in serum creatine. Renal damage is largely reversible with cessation of therapy, but renal function should be monitored closely during therapy.
An interesting adverse effect of aminoglycoside use is possible neuromuscular blockade. The aminoglycosides are believed to inhibit the release of acetylcholine presynaptically and block binding postsynaptically. Myasthenia gravis patients appear to be at greatest risk for weakness related to aminoglycoside usage due to a potential curare-like effect, but apnea has been reported in neurologically normal individuals after they have received intraperitoneal neomycin. Aminoglycosides may also prolong the effects of the non-depolarizing paralytic agents.
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