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Toxicity aminoglycosides

Resistance to drug toxic effects has also been observed in children. The incidence of aminoglycoside toxicity has been reported to be much lower in infants and children than in adults [39,48]. Diminished tissue sensitivity has been suggested as an explanation. [Pg.669]

Fischel-Ghodsian N. Genetic factors in aminoglycoside toxicity. Ann NY Acad Sci 1999 884 99-109. [Pg.142]

A major clinical distinction between the effects on the inner ear and the kidney is the fact that the renal effects are reversible while the effects on the inner ear are irreversible, leading to permanent loss of balance or auditory function. Furthermore, renal insults can more easily be monitored and thereby largely prevented, while monitoring of impending auditory or vestibular damage is not always possible. Ototoxic side effects frequently develop after cessation of aminoglycoside treatment, sometimes delayed by weeks. This review will therefore focus on the ototoxic side effects as a major unresolved issue in aminoglycoside toxicity. [Pg.256]

Figure 9.2. Mechanisms of aminoglycoside toxicity. This schematic representation summarizes the principles of aminoglycoside toxicity discussed in the text. Treatment with the drugs leads to the formation of reactive oxygen species through a redox-active complex with iron and unsaturated fatty acid or by triggering superoxide production by way of NADPH oxidase. An excess of reactive oxygen species, not balanced by intracellular antioxidant systems, will cause an oxidative imbalance potentially severe enough to initiate cell death pathways. Augmenting cellular defenses by antioxidant therapy can reverse the imbalance and restore homeostasis to protect the cell. Figure 9.2. Mechanisms of aminoglycoside toxicity. This schematic representation summarizes the principles of aminoglycoside toxicity discussed in the text. Treatment with the drugs leads to the formation of reactive oxygen species through a redox-active complex with iron and unsaturated fatty acid or by triggering superoxide production by way of NADPH oxidase. An excess of reactive oxygen species, not balanced by intracellular antioxidant systems, will cause an oxidative imbalance potentially severe enough to initiate cell death pathways. Augmenting cellular defenses by antioxidant therapy can reverse the imbalance and restore homeostasis to protect the cell.
Nephrotoxicity/Ototoxicity Because of reported cases of deafness and potential nephrotoxic effects, closely observe patients. Refer to the Warning Box in the Aminoglycosides, Parenteral monograph concerning aminoglycoside toxicity. Pregnancy. [Pg.1652]

Peloquin CA, Berning SE, Nitta AT, Simone PM, Goble M, Huitt GA, Iseman MD, Cook JL, Curran-Everett D. Aminoglycoside toxicity Daily versus thrice-weekly dosing for treatment of mycobacterial diseases. Clin Infect Dis 2004 38 1538M 4. [Pg.221]

Adverse effects. Aminoglycoside toxicity is a risk when the dose administered is high or of long duration, and the risk is higher if renal clearance is inefficient (because of disease or age), other potentially nephrotoxic drugs are co-administered (e.g. [Pg.224]

Strategies for minimizing aminoglycoside toxicity include early bedside detection of cochlear and vestibular dysfunction, which should lead to prompt withdrawal, use of short periods of treatment, dosing intervals of at least 12 hours, monitoring of serum concentrations, and awareness of relative contraindications, such as renal or hepatic dysfunction, old age, hearing impairment, and previous recent aminoglycoside exposure (3). [Pg.118]

Slaughter RL, CappeUetty DM. Economic impact of aminoglycoside toxicity and its prevention through therapeutic drug monitoring. Pharmacoeconomics 1998 14(4) 385-94. [Pg.136]

It is still controversial whether vancomycin can cause ototoxicity when given alone. However, vancomycin can augment the ototoxicity of aminoglycosides (30). Tinnitus and dizziness have been noted, resolving on withdrawal (31). Hearing loss can be transient or permanent. If vancomycin is combined with aminoglycosides, toxicity may be additive (32). [Pg.3595]

Hostetler KY, Hall LB, Inhibition of kidney lysosomal phospholipases A and C by aminoglycoside antibiotics possible mechanism of aminoglycoside toxicity, Proc Nat Acad Sci, 1982,79 1663-67. [Pg.288]

Some drugs may be less toxic in pediatric patients than in adults. Aminoglycosides appear to be less toxic in infants than in adults. In adults, aminoglycoside toxicity is related to both peripheral compartment accumulation and the individual patient s inherent sensitivity to these tissue concentrationsAlthough neonatal peripheral tissue compartments for gentamicin have been reported to closely resemble those of adults with similar renal function, gentamicin is rarely nephrotoxic in infants. This dissimilarity in the incidence of nephrotoxicity implies that newborn infants may have less inherent tissue sensitivity for toxicity than adults. [Pg.94]

Campochiaro PA, Lim JL. Aminoglycoside toxicity in the treatment of endophthalmitis. Arch Ophthalmol 1994 112 48-53. [Pg.23]

Campochiaro PA, Conway BP. Aminoglycoside toxicity a survey of retinal specialists. Arch Ophthalmol 1991 109 946-950. [Pg.95]

LLC-PK] cells appear to be an acceptable model for the study of aminoglycoside toxicity due to the following observations (1) A recent study confirmed in vivo observations that gentamicin was more toxic to LLC-PKi monolayers when exposed at the apical side, which... [Pg.133]

The principal aminoglycoside toxicities are neuromuscular paralysis, ototoxicity, and nephrotoxicity. Neuromuscular paralysis is a relatively rare comphcation resulting from high aminoglycoside concentrations at the neuromuscular junctions following, for example, rapid bolus iatravenous injection or peritoneal instillation, rather than the normal intravenous infusion. The mechanism apparently involves an inhibition of both the presynaptic release of acetjicholine and the acetylcholine postsynaptic receptors (51). [Pg.482]

E. M. Priuska, K. Clark-Baldwin, V. L. Pecoraro, and J. Schacht, NMR studies of iron-gentamicin complexes and the implications for aminoglycoside toxicity, Inorg. Chim. Acta, 273... [Pg.294]

D. Bodmer, D. Brors, K. Pak, B. Gloddek, and A. F. Ryan, Rescue of auditory hair cells from aminoglycoside toxicity by Clostridium difficile toxin B, an inhibitor of the small GTPases Rho/ Rac/Cdc42, Hear. Res., 172 (2002) 81-86. [Pg.295]


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