Gentamicin Sulfate

Gentamicin Sulfate Chemical formula
Synonyms: Gentamicin sulfát; Gentamicin Sulphate sulfate de; Gentamicini sulfas; Gentamicino sulfatas; Gentamicinsulfat; Gentamicin-szulfát; Gentamisiinisulfaatti; Gentamisin Sülfat; Gentamycyny siarczan; NSC-82261; Sch-9724; Sulfato de gentamicina.
Cyrillic synonym: Гентамицина Сульфат.

💊 Chemical information

CAS — 1403-66-3 (gentamicin); 1405-41-0 (gentamicin sulfate).
ATC — D06AX07; J01GB03; S01AA11; S02AA14; S03AA06.
ATC Vet — QD06AX07; QJ01GB03; QS01AA11; QS02AA14; QS03AA06.


In Chin., Eur., Int., Jpn, US, and Viet.

Ph. Eur. 6.2

(Gentamicin Sulphate). A mixture of the sulfates of antimicrobial substances produced by Micromonospora purpurea, the main components being gentamicins C1, C1a, C2, C2a, and C2b. It contains 20 to 40% of gentamicin C1, 10 to 30% of gentamicin C1a; the sum of gentamicins C2, C2a, and C2b is 40 to 60%. The potency is not less than 590 units/mg, calculated with reference to the anhydrous substance. A white or almost white hygroscopic powder. Freely soluble in water; practically insoluble in alcohol. A 4% solution in water has a pH of 3.5 to 5.5. Store in airtight containers.

USP 31

(Gentamicin Sulfate). The sulfate salt, or a mixture of such salts, of antibiotic substances produced by the growth of Micromonospora purpurea. The content of gentamicin C1 is between 25 and 50%, the content of gentamicin C1a is between 10 and 35%, and the sum of the contents of gentamicin C2a and gentamicin C2 is between 25 and 55%. It has a potency equivalent to not less than 590 micrograms of gentamicin per mg, calculated on the dried basis. A white to buff powder. Freely soluble in water; insoluble in alcohol, in acetone, in chloroform, in ether, and in benzene. pH of a 4% solution in water is between 3.5 and 5.5. Store in airtight containers.


The aminoglycosides are inactivated in vitro by various penicillins and cephalosporins via an interaction with the beta-lactam ring, the extent of inactivation depending on temperature, concentration, and duration of contact. The different aminoglycosides vary in their stability, with amikacin apparently the most resistant and tobramycin the most susceptible to inactivation; gentamicin and netilmicin are of intermediate stability. The beta lactams also vary in their ability to produce inactivation, with ampicillin, benzylpenicillin, and antipseudomonal penicillins such as carbenicillin and ticarcillin producing marked inactivation. Inactivation has also been reported with clavulanic acid. Gentamicin is also incompatible with furosemide, heparin, sodium bicarbonate (the acid pH of gentamicin solutions may liberate carbon dioxide), and some solutions for parenteral nutrition. Interactions with preparations having an alkaline pH (such as sulfadiazine sodium), or drugs unstable at acid pH (for example erythromycin salts), might reasonably be expected. Given their potential for incompatibility, gentamicin and other aminoglycosides should not generally be mixed with other drugs in syringes or infusion solutions nor given through the same intravenous line. When aminoglycosides are given with a beta lactam, they should generally be given at separate sites. General references. 1. Henderson JL, et al. In vitro inactivation of gentamicin, tobramycin, and netilmicin by carbenicillin, azlocillin, or mezlocillin. Am J Hosp Pharm 1981; 38: 1167–70. 2. Tindula RJ, et al. Aminoglycoside inactivation by penicillins and cephalosporins and its impact on drug-level monitoring. Drug Intell Clin Pharm 1983; 17: 906–8. 3. Navarro AS, et al. In-vitro interaction between dibekacin and penicillins. J Antimicrob Chemother 1986; 17: 83–9. 4. Courcol RJ, Martin GR. Comparative aminoglycoside inactivation by potassium clavulanate. J Antimicrob Chemother 1986; 17: 682–4.


There was an average 16% potency loss of gentamicin sulfate from solutions containing 10 and 40 mg/mL when stored at 4° or 25° in plastic disposable syringes for 30 days, and a brown precipitate formed in several. Storage in glass disposable syringes for 30 days produced an average 7% potency loss, which was considered acceptable, but storage for longer resulted in precipitate formation in some cases and was not recommended. 1 1. Weiner B, et al. Stability of gentamicin sulfate injection following unit dose repackaging. Am J Hosp Pharm 1976; 33: 1254–9.

💊 Adverse Effects

The aminoglycosides can produce irreversible, cumulative ototoxicity. This affects both the cochlea (manifest as hearing loss, initially of higher tones, and which, because speech recognition relies greatly on lower frequencies, may not be at first apparent) and the vestibular system (manifest as dizziness or vertigo). The incidence and relative toxicity with different aminoglycosides is a matter of some dispute, but netilmicin is probably less cochleotoxic than gentamicin or tobramycin, and amikacin more so. Netilmicin also exhibits less vestibular toxicity than gentamicin, tobramycin, or amikacin, while streptomycin produces a high incidence of vestibular damage. Vestibular damage is more common than hearing loss in patients receiving gentamicin. Reversible nephrotoxicity may occur and acute renal failure has been reported, often in association with the use of other nephrotoxic drugs. Renal impairment is usually mild, although acute tubular necrosis and interstitial nephritis have occurred. Decreased glomerular filtration rate is usually seen only after several days, and may even occur after therapy has stopped. Electrolyte disturbances (notably hypomagnesaemia, but also hypocalcaemia and hypokalaemia) have occurred. The nephrotoxicity of gentamicin is reported to be largely due to the gentamicin C 2 component. Although particularly associated with high plasma concentrations, many risk factors have been suggested for ototoxicity and nephrotoxicity in patients receiving aminoglycosides—see Precautions below. Aminoglycosides possess a neuromuscular-blocking action and respiratory depression and muscular paralysis have been reported, notably after absorption from serous surfaces. Neomycin has the most potent action and several deaths have been associated with its use. Hypersensitivity reactions have occurred, especially after local use, and cross-sensitivity between aminoglycosides may occur. Very rarely, anaphylactic reactions to gentamicin have occurred. Some hypersensitivity reactions have been attributed to the presence of sulfites in parenteral formulations, and endotoxic shock has also been reported. Infrequent effects reported for gentamicin include blood dyscrasias, purpura, nausea and vomiting, stomatitis, and signs of liver dysfunction such as increased serum-aminotransferase values and increased serum-bilirubin concentrations. Neurotoxicity has occurred, with both peripheral neuropathies and central symptoms being reported including encephalopathy, confusion, lethargy, hallucinations, convulsions, and mental depression. Atrophy or fat necrosis has been reported at injection sites. There have been isolated reports of meningeal irritation, arachnoiditis, polyradiculitis, and ventriculitis after intrathecal, intracisternal, or intraventricular use of aminoglycosides. Subconjunctival injection of gentamicin may lead to pain, hyperaemia, and conjunctival oedema, while severe retinal ischaemia has followed intra-ocular injection.

Effects on the ears.

Reviews and references to aminoglycoside-induced ototoxicity.
1. Cone LA. A survey of prospective, controlled clinical trials of gentamicin, tobramycin, amikacin, and netilmicin. Clin Ther 1982; 5: 155–62
2. Kahlmeter G, Dahlager JI. Aminoglycoside toxicity—a review of clinical studies published between 1975 and 1982. J Antimicrob Chemother 1984; 13 (suppl A): 9–22
3. Brummett RE, Fox KE. Aminoglycoside-induced hearing loss in humans. Antimicrob Agents Chemother 1989; 33: 797–800
4. Mattie H, et al. Determinants of efficacy and toxicity of aminoglycosides. J Antimicrob Chemother 1989; 24: 281–93
5. Schacht J. Aminoglycoside ototoxicity: prevention in sight? Otolaryngol Head Neck Surg 1998; 118: 674–7
6. Nakashima T, et al. Vestibular and cochlear toxicity of aminoglycosides—a review. Acta Otolaryngol 2000; 120: 904–11
7. Darlington CL, Smith PF. Vestibulotoxicity following aminoglycoside antibiotics and its prevention. Curr Opin Investig Drugs 2003; 4: 841–6
8. Rizzi MD, Hirose K. Aminoglycoside ototoxicity. Curr Opin Otolaryngol Head Neck Surg 2007; 15: 352–7.

Effects on the kidneys.

Reviews and references to aminoglycoside-induced nephrotoxicity.
1. Cone LA. A survey of prospective, controlled clinical trials of gentamicin, tobramycin, amikacin, and netilmicin. Clin Ther 1982; 5: 155–62
2. Lietman PS, Smith CR. Aminoglycoside nephrotoxicity in humans. Rev Infect Dis 1983; 5 (suppl 2): S284–93
3. Kahlmeter G, Dahlager JI. Aminoglycoside toxicity—a review of clinical studies published between 1975 and 1982. J Antimicrob Chemother 1984; 13 (suppl A): 9–22
4. Kohlhepp SJ, et al. Nephrotoxicity of the constituents of the gentamicin complex. J Infect Dis 1984; 149: 605–14
5. Mattie H, et al. Determinants of efficacy and toxicity of aminoglycosides. J Antimicrob Chemother 1989; 24: 281–93
6. Appel GB. Aminoglycoside nephrotoxicity. Am J Med 1990; 88 (suppl 3C): 16S–20S
7. Bertino JS, et al. Incidence of and significant risk factors for aminoglycoside-associated nephrotoxicity in patients dosed by using individualized pharmacokinetic monitoring. J Infect Dis 1993; 167: 173–9
8. Swan SK. Aminoglycoside nephrotoxicity. Semin Nephrol 1997; 17: 27–33
9. Baciewicz AM, et al. Aminoglycoside-associated nephrotoxicity in the elderly. Ann Pharmacother 2003; 37: 182–6
10. Rougier F, et al. Aminoglycoside nephrotoxicity. Curr Drug Targets Infect Disord 2004; 4: 153–62
11. Martínez-Salgado C, et al. Glomerular nephrotoxicity of aminoglycosides. Toxicol Appl Pharmacol 2007; 223: 86–98.

Endotoxin reactions.

Reports of endotoxin reactions associated with intravenous gentamicin have been received by the CDC and the FDA in the USA.1 Although endotoxin concentrations in the injections used were within USP limits, giving a single daily dose rather than divided doses was thought to have resulted in toxic serum concentrations of endotoxins.1,2
1. CDC. Endotoxin-like reactions associated with intravenous gentamicin—California, 1998. MMWR 1998; 47: 877–80
2. Krieger JA, Duncan L. Gentamicin contaminated with endotoxin. N Engl J Med 1999; 340: 1122.

💊 Treatment of Adverse Effects

Aminoglycosides may be removed by haemodialysis or to a much lesser extent by peritoneal dialysis. Calcium salts given intravenously have been used to counter neuromuscular blockade; the effectiveness of neostigmine has been variable.

💊 Precautions

Gentamicin is contra-indicated in patients with a known history of hypersensitivity to it, and probably in those hypersensitive to other aminoglycosides. It should be avoided in patients with myasthenia gravis, and great care is required in patients with parkinsonism and other conditions characterised by muscular weakness. The risk of ototoxicity and nephrotoxicity from aminoglycosides is increased at high plasma concentrations and it is therefore generally desirable to determine dosage requirements by individual monitoring. In patients receiving standard multiple-dose regimens of gentamicin, dosage should be adjusted to avoid peak plasma concentrations above 10 micrograms/mL, or trough concentrations (immediately before next dose) exceeding 2 micrograms/mL. Local guidelines on serum concentration should be consulted where oncedaily dosage regimens are used. Monitoring is particularly important in patients receiving high doses or prolonged courses, in infants and the elderly, and in patients with renal impairment, who generally require reduced doses. The BNF also considers monitoring to be important in patients with cystic fibrosis or significant obesity; again, altered doses may be required. See Pharmacokinetics below for other patient groups in whom pharmacokinetics may be altered. Impaired hepatic function or auditory function, bacteraemia, fever, and perhaps exposure to loud noises have also been reported to increase the risk of ototoxicity, while volume depletion or hypotension, liver disease, or female sex have been reported as additional risk factors for nephrotoxicity. Regular assessment of auditory and renal function is particularly necessary in patients with additional risk factors. Topical application of gentamicin into the ear is contraindicated in patients with known or suspected perforation of the ear drum. Use of aminoglycosides during pregnancy may damage the eighth cranial nerve of the fetus.

Breast feeding.

A study1 involving 10 mothers given gentamicin and their breast-fed infants found measurable gentamicin concentrations in the serum of 5 of the 10 neonates, indicating that appreciable gastrointestinal absorption had occurred. It was, however, considered that these low concentrations would not cause clinical effects and the American Academy of Pediatrics2 also considers that the use of gentamicin is usually compatible with breast feeding.
1. Celiloglu M, et al. Gentamicin excretion and uptake from breast milk by nursing infants. Obstet Gynecol 1994; 84: 263–5
2. American Academy of Pediatrics. The transfer of drugs and other chemicals into human milk. Pediatrics 2001; 108: 776–89. Correction. ibid.; 1029. Also available at: pediatrics%3b108/3/776 (accessed 27/05/04)

Interference with assay procedures.

The implications of drug interference with assays for aminoglycosides have been reviewed.1 Other antimicrobials and antineoplastics may alter the results of microbiological assays but this can be overcome by selection of an appropriate assay organism. Microbiological assays for aminoglycosides in samples also containing imipenem could be accomplished by using cysteine hydrochloride to inactivate imipenem, since it is stable to most beta-lactamases and resistant strains are extremely rare.2 Because aminoglycosides may be inactivated by penicillins and cephalosporins, it has been recommended that aminoglycoside sampling times should be chosen to coincide with a trough plasma concentration for the beta lactam. Samples should be frozen if there is to be a delay before they are assayed3 or a penicillinase added. However, one group of workers have reported loss of gentamicin activity after storage at −60° before assay.4 Furthermore, there have been reports that concentrations of aminoglycosides in patients also receiving beta lactams have been overestimated using a homogeneous enzyme immunoassay, probably because of an inability to differentiate between active drug and inactivated products.5,6 The radionuclide gallium-67 interferes with radio-enzymatic assays, and it has been suggested that an agar diffusion method should be used in patients who have received a gallium scan.7,8 Heparin has been shown to produce underestimation of aminoglycoside concentrations when using microbiological, enzymatic, or immunoassays.9-11 It has been recommended that either serum should be used or that blood samples should not be collected in heparinised tubes or from indwelling catheter lines. Some consider that concentrations of heparin reached in the blood of patients receiving heparin are too low to affect gentamicin.12 Falsely low concentrations have also been reported in microbiological assays in the presence of zinc salts.13 Heat treatment of whole blood to inactivate human immunodeficiency virus leads to an increase in the concentration of gentamicin subsequently found on assay.14
1. Yosselson-Superstine S. Drug interferences with plasma assays in therapeutic drug monitoring. Clin Pharmacokinet 1984; 9: 67–87
2. McLeod KM, et al. Gentamicin assay in the presence of imipenem. J Antimicrob Chemother 1986; 17: 828–9
3. Tindula RJ, et al. Aminoglycoside inactivation by penicillins and cephalosporins and its impact on drug-level monitoring. Drug Intell Clin Pharm 1983; 17: 906–8
4. Carlson LG, et al. Potential liabilities of gentamicin homogeneous enzyme immunoassay. Antimicrob Agents Chemother 1982; 21: 192–4
5. Ebert SC, Clementi WA. In vitro inactivation of gentamicin by carbenicillin, compared by Emit and microbiological assays. Drug Intell Clin Pharm 1983; 17: 451
6. Dalmady-Israel C, et al. Ticarcillin and assay of tobramycin. Ann Intern Med 1984; 100: 460
7. Bhattacharya I, et al. Effects of radiopharmaceuticals on radioenzymatic assays of aminoglycoside antibiotics: interference by gallium-67 and its elimination. Antimicrob Agents Chemother 1978; 14: 448–53
8. Shannon K, et al. Interference with gentamicin assays by gallium-67. J Antimicrob Chemother 1980; 6: 285–300
9. Nilsson L. Factors affecting gentamicin assay. Antimicrob Agents Chemother 1980; 17: 918–21. Correction. ibid.; 18: 839
10. Nilsson L, et al. Inhibition of aminoglycoside activity by heparin. Antimicrob Agents Chemother 1981: 20: 155–8
11. O’Connell MB, et al. Heparin interference with tobramycin, netilmicin, and gentamicin concentrations determined by Emit. Drug Intell Clin Pharm 1984; 18: 503–4
12. Regamey C, et al. Inhibitory effect of heparin on gentamicin concentrations in blood. Antimicrob Agents Chemother 1972; 1: 329–32
13. George RH, Healing DE. The effect of zinc on aminoglycoside assay. J Antimicrob Chemother 1978; 4: 186
14. Eley A, et al. Effect of heat on gentamicin assays. Lancet 1987; ii: 335–6.

💊 Interactions

Use of other nephrotoxic drugs (including other aminoglycosides, vancomycin, some cephalosporins, ciclosporin, cisplatin, and fludarabine), or of potentially ototoxic drugs such as etacrynic acid and perhaps furosemide, may increase the risk of aminoglycoside toxicity. It has been suggested that use of an antiemetic such as dimenhydrinate may mask the early symptoms of vestibular ototoxicity. Care is also required if other drugs with a neuromuscular-blocking action are used. The neuromuscular-blocking properties of aminoglycosides may be sufficient to provoke severe respiratory depression in patients given general anaesthetics or opioids. There is a theoretical possibility that the antibacterial effects of aminoglycosides could be reduced by bacteriostatic antibacterials, but such combinations have been used successfully in practice. Since aminoglycosides have been shown to be incompatible with some beta lactams in vitro (see Incompatibility, above), these antibacterials should be given separately if both are required; antagonism in vivo has been reported only in a few patients with severe renal impairment, in whom aminoglycoside activity was diminished. Aminoglycosides exhibit synergistic activity with a number of beta lactams in vivo (see Antimicrobial Action, below). Renal excretion of zalcitabine may be reduced by aminoglycosides. For a report of severe hypocalcaemia in a patient treated with aminoglycosides and bisphosphonates. Gentamicin may inhibit α-galactosidase activity and should not be used with agalsidase alfa or beta.

💊 Antimicrobial Action

Gentamicin is an aminoglycoside antibiotic and has a bactericidal action against many Gram-negative aerobes and against some strains of staphylococci. Mechanism of action. Aminoglycosides are taken up into sensitive bacterial cells by an active transport process which is inhibited in anaerobic, acidic, or hyperosmolar environments. Within the cell they bind to the 30S, and to some extent to the 50S, subunits of the bacterial ribosome, inhibiting protein synthesis and generating errors in the transcription of the genetic code. The manner in which cell death is brought about is imperfectly understood, and other mechanisms may contribute, including effects on membrane permeability. Spectrum of activity. The following pathogenic organisms are usually sensitive to gentamicin (but see also Resistance, below). Many strains of Gram-negative bacteria including species of Brucella, Calymmatobacterium, Campylobacter, Citrobacter, Escherichia, Enterobacter, Francisella, Klebsiella, Proteus, Providencia, Pseudomonas, Serratia, Vibrio, and Ye rsini a. Some activity has been reported against isolates of Neisseria, although aminoglycosides are rarely used clinically in neisserial infections. Among the Gram-positive organisms many strains of Staphylococcus aureus are highly sensitive to gentamicin. Listeria monocytogenes and some strains of Staph. epidermidis may also be sensitive to gentamicin, but enterococci and streptococci are usually insensitive to gentamicin. Some actinomycetes and mycoplasmas have been reported to be sensitive to gentamicin, but mycobacteria are insensitive at clinically achievable concentrations; anaerobic organisms, yeasts, and fungi are resistant. Activity with other antimicrobials. Gentamicin exhibits synergy with beta lactams, probably because the effects of the latter on bacterial cell walls enhance aminoglycoside penetration. Enhanced activity has been demonstrated with a penicillin (such as ampicillin or benzylpenicillin) and gentamicin against the enterococci, and gentamicin has been combined with an antipseudomonal penicillin such as ticarcillin for enhanced activity against Pseudomonas spp., and with vancomycin for enhanced activity against staphylococci and streptococci. Resistance to the aminoglycosides may be acquired by three main mechanisms. The first is by mutation of ribosomal target sites leading to reduced affinity for binding; this type of resistance is generally only relevant for streptomycin and, even then, it appears to be rare in Gram-negative bacteria. Secondly, penetration of aminoglycosides into bacterial cells is by an oxygen-dependent active transport process and resistance may occur because of elimination or reduction of this uptake; when it occurs this generally results in crossresistance to all aminoglycosides. Thirdly, and by far the most important cause of resistance to the aminoglycosides, is inactivation by enzymatic modification. Three main classes of enzyme conferring resistance have been found, operating by phosphorylation, acetylation, or addition of a nucleotide group, usually adenyl. Enzyme production is usually plasmid-determined and resistance can therefore be transferred between bacteria, even of different species. Resistance to other antibacterials may be transferred at the same time. In Staph. aureus, transfer of resistance is more likely when these drugs are used topically. Each type of enzyme produces characteristic patterns of resistance, but their overlapping and variable affinities for their substrates result in a wide range of permutations of cross-resistance to the different aminoglycosides. The different enzymes vary in their distribution and prevalence in different locations, and at different times, presumably with variations in antibacterial usage, but relationships to the use of specific aminoglycosides are difficult to establish. These variations in drug sensitiv ity require local testing to determine resistance and establish susceptibility of bacteria to the aminoglycoside being used, but such local variations mean that estimates of the incidence of resistance are of limited value. In general, the occurrence of resistant pathogens seems to have been greater in southern than in northern Europe, and perhaps greater in the USA than in Europe. There has been particular concern over the increasing incidence of high-level gentamicin resistance among enterococci (in up to 50% of isolates from some centres), since they already possess inherent or acquired resistance to many drugs, including vancomycin in some cases. A similar problem exists with gentamicin resistance in meticillin-resistant strains of Staph. aureus. Such multiply-resistant strains pose a major therapeutic problem in those centres where they occur, since the usual synergistic combinations with other antibacterials are ineffective. However, results from some centres indicate that rational use of a wider range of aminoglycosides (including amikacin which is not affected by most of the aminoglycoside-degrading enzymes) has resulted in a modest decline in overall aminoglycoside resistance.
1. Mingeot-Leclercq M-P, et al. Aminoglycosides: activity and resistance. Antimicrob Agents Chemother 1999; 43: 727–37
2. Kotra LP, et al. Aminoglycosides: perspectives on mechanisms of action and resistance and strategies to counter resistance. Antimicrob Agents Chemother 2000; 44: 3249–56
3. Barclay ML, Begg EJ. Aminoglycoside adaptive resistance: importance for effective dosage regimens. Drugs 2001; 61: 713–21
4. Magnet S, Blanchard JS. Molecular insights into aminoglycoside action and resistance. Chem Rev 2005; 105: 477–98.

💊 Pharmacokinetics

Gentamicin and other aminoglycosides are poorly absorbed from the gastrointestinal tract but are rapidly absorbed after intramuscular injection. Average peak plasma concentrations of about 4 micrograms/mL have been attained in patients with normal renal function 30 to 60 minutes after an intramuscular dose equivalent to gentamicin 1 mg/kg, which is similar to concentrations achieved after intravenous infusion. There may be considerable individual variation. Several doses are required before plasma equilibrium concentrations occur and this may represent the saturation of binding sites in body tissues such as the kidney. Binding of gentamicin to plasma proteins is usually low. On parenteral use, gentamicin and other aminoglycosides diffuse mainly into extracellular fluids. However, there is little diffusion into the CSF and even when the meninges are inflamed effective concentrations may not be achieved; diffusion into the eye is also poor. Aminoglycosides diffuse readily into the perilymph of the inner ear. They cross the placenta but only small amounts have been reported in breast milk. Systemic absorption of gentamicin and other aminoglycosides has been reported after topical use on denuded skin and burns and on instillation into, and irrigation of, wounds, body-cavities (except the urinary bladder), and joints. The plasma elimination half-life for gentamicin has been reported to be 2 to 3 hours though it may be considerably longer in neonates and patients with renal impairment. Gentamicin and other aminoglycosides do not appear to be metabolised and are excreted virtually unchanged in the urine by glomerular filtration. At steady state at least 70% of a dose may be recovered in the urine in 24 hours and urine concentrations in excess of 100 micrograms/mL may be achieved. However, gentamicin and the other aminoglycosides appear to accumulate in body tissues to some extent, mainly in the kidney, although the relative degree to which this occurs may vary with different aminoglycosides. Release from these sites is slow and small amounts of aminoglycosides may be detected in the urine for up to 20 days or more after treatment stops. Small amounts of gentamicin appear in the bile. The pharmacokinetics of the aminoglycosides are affected by many factors, which may become significant because of the relatively small difference between therapeutic and toxic concentrations, reinforcing the need for monitoring.
Absorption from intramuscular sites may be reduced in critically ill patients, especially in conditions that reduce perfusion such as shock, resulting in reduced plasma concentrations. Plasma concentrations may also be reduced in patients with conditions which expand extracellular fluid volume or increase renal clearance including ascites, cirrhosis, heart failure, malnutrition, spinal cord injury, burns, cystic fibrosis, and possibly leukaemia. Clearance is also reportedly increased in intravenous drug abusers, and in patients who are febrile.
In contrast, renal impairment or reduced renal clearance for any reason (for example in neonates with immature renal function, or in the elderly in whom glomerular function tends to decline with age) can result in markedly increased plasma concentrations and/or prolonged half-lives. However, in neonates initial plasma concentrations may actually be reduced, due to a larger volume of distribution. Plasma concentrations may also be higher than expected for a given dose in obese patients (in whom extracellular volume is low relative to weight), and in patients with anaemia.
Renal clearance, and hence plasma concentrations, of aminoglycosides may vary according to a circadian cycle, and it has been suggested that this should be taken into account when determining and comparing plasma aminoglycoside concentrations.

💊 Uses and Administration

Gentamicin is an aminoglycoside antibiotic used, often with other antibacterials, to treat severe systemic infections due to sensitive Gram-negative and other organisms (see Antimicrobial Action, above). Such infections include biliary-tract infections (acute cholecystitis or cholangitis), brucellosis, cat scratch disease, cystic fibrosis, endocarditis (in the treatment and prophylaxis of endocarditis due to streptococci, enterococci, or staphylococci), endometritis, gastroenteritis, granuloma inguinale, listeriosis, meningitis, otitis externa, otitis media, pelvic inflammatory disease, peritonitis, plague, pneumonia, septicaemia, skin infections such as in burns or ulcers (given systemically for pseudomonal and other Gram-negative infections), tularaemia, and urinary-tract infections (acute pyelonephritis), as well as in the prophylaxis of surgical infection and the treatment of immunocompromised patients and those in intensive care. It may be used as part of a multi-drug regimen for the treatment of inhalation and gastrointestinal anthrax. Gentamicin is also applied topically for localised infections. For details of these infections and their treatment, see under Choice of Antibacterial. Gentamicin is often used with other antibacterials to extend its spectrum of activity or increase its efficacy, e.g. with a penicillin for enterococcal and streptococcal infections, or an antipseudomonal beta lactam for pseudomonal infections, or with metronidazole or clindamycin for mixed aerobic-anaerobic infections.

Administration and dosage.

Gentamicin is used as the sulfate but doses are expressed in terms of gentamicin base. For many of the infections above it is given intramuscularly every 8 hours to provide a total daily dose of 3 to 5 mg/kg. In the prophylaxis and treatment of streptococcal and enterococcal endocarditis, a dose of 1 mg/kg every 8 hours with a penicillin or vancomycin has been suggested for treatment in the UK; a suggested dose for prophylaxis in high-risk patients is 120 mg before induction of anaesthesia, with a penicillin or vancomycin or teicoplanin. For urinary-tract infections, if renal function is not impaired, 160 mg once daily may be used. Gentamicin sulfate may also be given intravenously in similar doses to those used intramuscularly, but there is some disagreement as to the appropriate method, since intravenous infusion has been associated with both subtherapeutic and excessive trough concentrations of gentamicin, while bolus intravenous injection may increase the risk of neuromuscular blockade. In the USA, intravenous infusion over 30 minutes to 2 hours is favoured, but sources in the UK differ, with some licensed product information recommending infusion over no more than 20 minutes, in a limited fluid volume, while other products should not be given by slow infusion, recommending bolus injection over at least 2 to 3 minutes, and yet others allow use in a similar way to the USA. The course of treatment should generally be limited to 7 to 10 days. As gentamicin is poorly distributed into fatty tissue it has been suggested that dosage calculations should be based on an estimate of lean bodyweight. Doses in infants and children are usually somewhat higher than those in adults but exact dosage recommendations vary. One regimen is gentamicin 3 mg/kg every 12 hours in premature infants and those up to 2 weeks of age, with older neonates and children receiving 2 mg/kg every 8 hours. Alternatively, 2.5 mg/kg every 12 hours in the first week of life, 2.5 mg/kg every 8 hours or 3 mg/kg every 12 hours in infants and neonates, and 1.5 to 2 mg/kg every 8 hours in children has been given. Dose adjustment and monitoring. Dosage should be adjusted in all patients according to plasma-gentamicin concentrations, and this is discussed in more detail under Administration and Dosage, below. Once-daily dosage. In many centres, the total daily requirement is increasingly given as a single dose (see Once-daily Dosage, below). In suitable patients this appears to be as safe and effective as conventional regimens, and is more convenient. However, it is not suitable for all patients, especially those with endocarditis, extensive burns, or renal impairment (creatinine clearance less than 20 mL/minute). With once-daily dosage, traditional methods of monitoring peak and trough plasma concentrations may not be applicable and local guidelines on dosage and plasma concentrations should be consulted. Other routes. Gentamicin has sometimes been given orally for enteric infections and to suppress intestinal flora and has occasionally been given by inhalation in cystic fibrosis. In meningitis it has been given intrathecally or intraventricularly usually in doses of 1 to 5 mg daily with intramuscular therapy. Gentamicin has also been given by subconjunctival injection. A bone cement impregnated with gentamicin is used in orthopaedic surgery. Acrylic beads containing gentamicin and threaded on to surgical wire are implanted in the management of bone infections. Gentamicin has also been applied topically for skin infections in concentrations of 0.1%, but such use may lead to the emergence of resistance and is considered inadvisable. Concentrations of 0.3% are used in preparations for topical application to the eyes and ears. A liposomal formulation of gentamicin is under investigation.
1. Edson RS, Terrell CL. The aminoglycosides. Mayo Clin Proc 1999; 74: 519–28.

Administration and dosage.

CONCENTRATION MONITORING. Measurements of aminoglycoside plasma concentrations are routinely performed to individualise dosage regimens, both in terms of dose given and dosing interval, in order to attain the desired therapeutic range as quickly as possible.1This entails measurement of both peak concentrations to monitor efficacy and trough concentrations to avoid accumulation and thereby prevent toxicity. Dosage should be adjusted in all patients according to these concentrations, but this is of particular importance where factors such as age, renal impairment, or high dosage may predispose to toxicity. Although there has been some dispute about the relationship between plasma concentrations and toxicity it is generally recommended that, for multiple daily dosing with gentamicin, trough plasma concentrations (measured just before the next dose) should be less than 2 micrograms/mL, and peak concentrations should reach at least 4 micrograms/mL but not exceed 10 micrograms/mL. In the UK, peak concentrations are generally measured 1 hour after intramuscular and intravenous doses, but practice has varied between centres and countries and this may lead to difficulties when comparing figures. Methods exist for calculating aminoglycoside dosage requirements, though none has been universally accepted. Simple pharmacokinetic methods involve linear dosage adjustment based on peak or trough concentrations or area under the concentrationtime curve, or the use of predictive nomograms.1 For most patients receiving once-daily dosage (see below), the nomogram is the method of choice, primarily because of its simplicity. However, it has not been validated for children and does not work in patients with either a very high clearance of aminoglycosides or a high volume of distribution, such as those with ascites, burns, or cystic fibrosis, or in other conditions such as pregnancy where the fixed dose assumed in the construction of the nomogram is irrelevant. When a nomogram cannot be applied, a more sophisticated pharmacokinetic method is required, using either Bayesian statistics or non-Bayesian methods such as that of Sawchuk and Zaske.2,3 Bayesian methods are favoured when the patient population’s pharmacokinetic parameters are well known because of their good predictive performance. Otherwise, the Sawchuk and Zaske method is the method of choice because of its robustness and the lack of requirement for prior information about the distribution of parameters within the population.1
1. Tod MM, et al. Individualising aminoglycoside dosage regimens after therapeutic drug monitoring: simple or complex pharmacokinetic methods? Clin Pharmacokinet 2001; 40: 803–14
2. Sawchuk RJ, Zaske DE. Pharmacokinetics of dosing regimens which utilize multiple intravenous infusions: gentamicin in burn patients. J Pharmacokinet Biopharm 1976; 4: 183–95
3. Sawchuk RJ, et al. Kinetic model for gentamicin dosing with the use of individual patient parameters. Clin Pharmacol Ther 1977; 21: 362–9.
1. Isemann BT, et al. Optimal gentamicin therapy in preterm neonates includes loading doses and early monitoring. Ther Drug Monit 1996; 18: 549–55
2. Logsdon BA, Phelps SJ. Routine monitoring of gentamicin serum concentrations in pediatric patients with normal renal function is unnecessary. Ann Pharmacother 1997; 31: 1514–18
3. Murphy JE, et al. Evaluation of gentamicin pharmacokinetics and dosing protocols in 195 neonates. Am J Health-Syst Pharm 1998; 55: 2280–9
4. Yeung MY, Smyth JP. Targeting gentamicin concentrations in babies: the younger the baby, the larger the loading dose and the longer the dose interval. Aust J Hosp Pharm 2000; 30: 98–101
5. Stickland MD, et al. An extended interval dosing method for gentamicin in neonates. J Antimicrob Chemother 2001; 48: 887–93
6. Rastogi A, et al. Comparison of two gentamicin dosing schedules in very low birth weight infants. Pediatr Infect Dis J 2002; 21: 234–40
7. Chattopadhyay B. Newborns and gentamicin—how much and how often? J Antimicrob Chemother 2002; 49: 13–16
8. Murphy JE. Prediction of gentamicin peak and trough concentrations from six extended-interval dosing protocols for neonates. Am J Health-Syst Pharm 2005; 62: 823–7
9. Hale LS, Durham CR. A simple, weight-based, extended-interval gentamicin dosage protocol for neonates. Am J Health-Syst Pharm 2005; 62: 1613–16
10. Khan AM, et al. Extended-interval gentamicin administration in malnourished children. J Trop Pediatr 2006; 52: 179–84.
1. Traynor AM, et al. Aminoglycoside dosing weight correction factors for patients of various body sizes. Antimicrob Agents Chemother 1995; 39: 545–8.
IN RENAL IMPAIRMENT. Although a number of nomograms, schedules, and rules have been devised for the calculation of aminoglycoside dosage in renal impairment, where possible dosage modification should be based on the monitoring of individual pharmacokinetic parameters. Standard dosage calculation methods should not be used for patients undergoing dialysis as they may require supplementary post-dialysis doses. Individualised regimens based on an initial dose (for moderate to severe infections) of 2 to 2.5 mg/kg, modified in the obese or those with excessive fluid retention, and with subsequent doses after haemodialysis ranging from 1 to 1.8 mg/kg, have been reported to be effective.1 Serum-aminoglycoside concentrations were not routinely requested unless treatment for more than 4 days was thought likely, and the target concentration was adjusted both for the agressiveness of therapy required and the individual haemodialysis regimen. Typically, about 50% of a dose was eliminated in a haemodialysis session.
1. Dager WE, King JH. Aminoglycosides in intermittent hemodialysis: pharmacokinetics with individual dosing. Ann Pharmacother 2006; 40: 9–14.
ONCE-DAILY DOSAGE. The concept of giving aminoglycosides once daily rather than in divided doses is attractive on the grounds of convenience and economy. The rationale cited by proponents of single daily doses for preferring high intermittent plasma concentrations includes the prolonged postantibiotic effect of aminoglycosides (persistent antibacterial activity after plasma concentrations have fallen below the MIC), potentially higher antibacterial concentrations at the site of infection, and theoretical reductions in the incidence of adaptive resistance, with no apparent increase in nephrotoxicity. Clinical studies have generally included small numbers of patients with uncomplicated infections and have excluded patients with altered pharmacokinetic profiles, but several metaanalyses have been published which have concluded that once-daily administration appears to be at least as effective as, and no more toxic than, multiple daily dosing in such patient populations.1-7 Similar results have been seen in children.8,9 Many centres now use such regimens in suitable patients. Several methods for calculating doses and monitoring treatment have been proposed.10-12 There is insufficient information for pregnant or breast-feeding women, or patients with burns or impaired renal or hepatic function.12-14 However, preliminary reports suggest that once-daily use may be practical in trauma patients,15 and children with neutropenia,16 or cystic fibrosis.17,18Once daily dosage may, though, be inappropriate for elderly patients19 (due to an increased incidence of nephrotoxicity), patients in whom the volume of drug distribution or clearance is difficult to predict or markedly abnormal,20 and in the treatment of enterococcal endocarditis.12 In the UK, the BNF states that a once-daily high dose regimen should be avoided in patients with endocarditis, extensive burns, or creatinine clearance less than 20 mL/minute. For mention of an increase in endotoxin reactions associated with the use of single daily doses see under Adverse Effects, above.
1. Barza M, et al. Single or multiple daily doses of aminoglycosides: a meta-analysis. BMJ 1996; 312: 338–45
2. Hatala R, et al. Once-daily aminoglycoside dosing in immunocompetent adults: a meta-analysis. Ann Intern Med 1996; 124: 717–25
3. Ferriols-Lisart R, Alos-Almiñana M. Effectiveness and safety of once-daily aminoglycosides: a meta-analysis. Am J HealthSyst Pharm 1996; 53: 1141–50
4. Munckhof WJ, et al. A meta-analysis of studies on the safety and efficacy of aminoglycosides given either once daily or as divided doses. J Antimicrob Chemother 1996; 37: 645–63
5. Bailey TC, et al. A meta-analysis of extended-interval dosing versus multiple daily dosing of aminoglycosides. Clin Infect Dis 1997; 24: 786–95
6. Ali MZ, Goetz MB. A meta-analysis of the relative efficacy and toxicity of single daily dosing versus multiple daily dosing of aminoglycosides. Clin Infect Dis 1997; 24: 796–809
7. Hatala R, et al. Single daily dosing of aminoglycosides in immunocompromised adults: a systematic review. Clin Infect Dis 1997; 24: 810–15
8. Nestaas E, et al. Aminoglycoside extended interval dosing in neonates is safe and effective: a meta-analysis. Arch Dis Child Fetal Neonatal Ed 2005; 90: F294–F300
9. Contopoulos-Ioannidis DG, et al. Extended-interval aminoglycoside administration for children: a meta-analysis. Pediatrics 2004; 114: e111–8
10. Begg EJ, et al. A suggested approach to once-daily aminoglycoside dosing. Br J Clin Pharmacol 1995; 39: 605–9
11. Prins JM, et al. Validation and nephrotoxicity of a simplified once-daily aminoglycoside dosing schedule and guidelines for monitoring therapy. Antimicrob Agents Chemother 1996; 40: 2494–9
12. Freeman CD, et al. Once-daily dosing of aminoglycosides: review and recommendations for clinical practice. J Antimicrob Chemother 1997; 39: 677–86
13. Rodvold KA, et al. Single daily doses of aminoglycosides. Lancet 1997; 350: 1412
14. Anonymous. Aminoglycosides once daily? Drug Ther Bull 1997; 35: 36–7
15. Finnell DL, et al. Validation of the Hartford nomogram in trauma surgery patients. Ann Pharmacother 1998; 32: 417–21
16. Tomlinson RJ, et al. Once daily ceftriaxone and gentamicin for the treatment of febrile neutropenia. Arch Dis Child 1999; 80: 125–31
17. Bragonier R, Brown NM. The pharmacokinetics and toxicity of once-daily tobramycin therapy in children with cystic fibrosis. J Antimicrob Chemother 1998; 42: 103–6
18. Vic P, et al. Efficacy, tolerance, and pharmacokinetics of once daily tobramycin for pseudomonas exacerbations in cystic fibrosis. Arch Dis Child 1998; 78: 536–9
19. Koo J, et al. Comparison of once-daily versus pharmacokinetic dosing of aminoglycosides in elderly patients. Am J Med 1996; 101: 177–83
20. Gerberding JL. Aminoglycoside dosing: timing is of the essence. Am J Med 1998; 105: 256–8.

Ménière’s disease.

Gentamicin and streptomycin have been used for medical ablation in advanced Ménière’s disease. Although gentamicin given systemically is considered to be more ototoxic than streptomycin, evidence from animal studies suggests that intratympanic use may be less ototoxic. This, and a higher incidence of adverse effects with streptomycin, has meant that intratympanic gentamicin is now preferred. Intratympanic gentamicin has been reported to control vertigo symptoms in the majority of patients, although some experience a worsening of their hearing loss immediately after treatment.1-8 However, the ideal regimen for intratympanic gentamicin has yet to be defined.
1. Nedzelski JM, et al. Chemical labyrinthectomy: local application of gentamicin for the treatment of unilateral Meniere’s disease. Am J Otol 1992; 13: 18–22
2. Pyykkö I, et al. Intratympanic gentamicin in bilateral Meniere’s disease. Otolaryngol Head Neck Surg 1994; 110: 162–7
3. Quaranta A, et al. Intratympanic therapy for Ménière’s disease: high-concentration gentamicin with round-window protection. Ann N Y Acad Sci 1999; 884: 410–24
4. Longridge NS, Mallinson AI. Low-dose intratympanic gentamicin treatment for dizziness in Meniere’s disease. J Otolaryngol 2000; 29: 35–9
5. Quaranta A, et al. Intratympanic therapy for Ménière’s disease: effect of administration of low concentration of gentamicin. Acta Otolaryngol 2001; 121: 387–92
6. Marzo SJ, Leonetti JP. Intratympanic gentamicin therapy for persistent vertigo after endolymphatic sac surgery. Otolaryngol Head Neck Surg 2002; 126: 31–3
7. Cohen-Kerem R, et al. Intratympanic gentamicin for Menière’s disease: a meta-analysis. Laryngoscope 2004; 114: 2085–91
8. Postema RJ, et al. Intratympanic gentamicin therapy for control of vertigo in unilateral Menière’s disease: a prospective, doubleblind, randomized, placebo-controlled trial. Acta Otolaryngol 2008; 128: 876–80.

💊 Preparations

BP 2008: Gentamicin and Hydrocortisone Acetate Ear Drops; Gentamicin Cream; Gentamicin Ear Drops; Gentamicin Eye Drops; Gentamicin Injection; Gentamicin Ointment; USP 31: Gentamicin and Prednisolone Acetate Ophthalmic Ointment; Gentamicin Injection; Gentamicin Sulfate Cream; Gentamicin Sulfate Ointment; Gentamicin Sulfate Ophthalmic Ointment; Gentamicin Sulfate Ophthalmic Solution.

Proprietary Preparations

Arg.: Gentaderm; Gentamina; Gentapharma; Gentaren; Gentatenk†; Genticol†; Gentoler; Glevomicina; Plurisemina; Provisual; Rupegen†; Sintepul; Ultradermis†; Austral.: Genoptic; Austria: Garamycin†; Gentax; Refobacin; Sulmycin; Belg.: Geomycine; Braz.: Emisgenta; Garacin; Garamicina; Garamin; Gentac†; Gentagran; Gentamicil; Gentamil; Gentaron; Gentax†; Vitromicin†; Canad.: Alcomicin; Diogent†; Garamycin; Garatec†; Chile: Gentalyn; Oftagen; Cz.: Garamycin; Megental†; Ophtagram†; Denm.: Garamycin; Gentacoll; Hexamycin; Fin.: Gensumycin; Gentacoll; Fr.: Gentalline; Ger.: Gencin; Gent-Ophtal; Genta; Gentamytrex; Ophtagram†; Refobacin; Sulmycin; Terramycin N; Gr.: Dabroson; Garamycin; Hong Kong: Garamycin; Genoptic; Miramycin; Optigen†; Hung.: Garamycin; India: Andregen; Biogaracin; G-80†; Garamycin; Gensyn†; Gentacip; Gentasporin; Genticyn; Genticyn Eye/Ear†; Indon.: Bioderm; Dermabiotik; Dermagen; Ethigent; Garabiotic; Garamycin; Garapon; Garexin; Gentacyl; Gentamerck; Gentamisin; Ikagen; Isotic Timact; Konigen; Licogenta; Nichogencin; Ottogenta; Sagestam; Salgen; Salticin; Timact; Ximex Konigen; Irl.: Cidomycin; Genticin; Israel: Cidomycin†; Gentatrim; Lacromycin; Opti-Genta; Ital.: Ciclozinil; Dergesol; Eutopic; Gentacream; Gentalyn; Gentamen; Gentibioptal†; Genticol; Gentomil; Nemalin; Ribomicin; Tacigen; Malaysia: Beagenta; Garamycin; Gentamed†; Gentamytrex†; Miramycin; Mex.: Barmicil†; Beramicina; Fustermicina; G-I; Garacoll; Garakacin; Garalen; Garamicina; Geclicin; Genemicin; Genkova; Genrex; Genser; Genta; Genta-Micron; Gentacin†; Gentamil; Gentanacin†; Gentapat; Gentarim†; Gentazaf Z; Gentazol; Gentialoquin; Geracin; Ikatin; Lifegram; Lisibac†; Progen; Quilagen; Servigenta; Tamigen; Tondex; Tremax; Yectamicina; Neth.: Garacol; Garamycin; Gentamytrex; Norw.: Garamycin; Gensumycin; NZ: Genoptic; Philipp.: Garamycin; Gentamytrex; Migentax; Minoglen; Obogen; Opthagen; Orimed; Rocygen; Servigenta; Tangyn; Topigen; Pol.: Garamycin; Gentamytrex†; Port.: Cronocol; Garalone; Genta Gobens; Gentalin; Gentocil; Ophtagram; Septopal; S.Afr.: Cidomycin; Garacoll†; Garamycin; Genoptic†; Sabax Gentamix; Sterisol Fermentmycin; Singapore: Garamycin†; Genoptic; Gentamytrex; Miramycin; Spain: Coliriocilina Gentam†; Genta Gobens; Gentamedical†; Gentamival; Genticina†; Gevramycin; Gevramycin Topica; Rexgenta; Swed.: Garamycin; Gensumycin; Switz.: Garamycin; Ophtagram; Thai.: Garamycin†; Genta; Genta-Oph; Gentac†; Gentacin; Gental; Grammicin; Grammixin; Miramycin; Skinfect; Versigen; Turk.: Genmisin; Genta; Gentagut; Gentamed; Genthaver; Gentreks; Getamisin; Getasin; UAE: Gental; UK: Cidomycin; Garamycin†; Genticin; USA: Garamycin; Genoptic; Gentacidin; Gentak; Gentasol; Ocu-Mycin; Venez.: Catogen†; Gentalyn; Gentamicil†; Gentamilan; Gentisul; Kincinat†; Refobacin†; Solgenta; Yectamicina†. Multi-ingredient: Arg.: Adenil; Aeromicrosona C†; Anginotrat; Bacticort; Bacticort Complex; Bactisona; Becortin; Betacort Plus; Blamy; Calmurid; Cevaderm; Cicatrizol; Ciprocort; Cuta Crema; Denvercrem; Dercotex; Dermizol G; Dermizol Trio; Dermoperative; Dermosona; Dermovit†; Dexamytrex; Diprogenta; Factor Dermico; Filoderma; Filoderma Plus; Gentacler; Gentasol; Gentocelina†; Griseocrem; Hifamonil Crema; Lazar-Cort Complex; Linfol Dermico; Lisoderma; Macril; Micozol Compuesto†; Microsona C; Miklogen; Monizol Cort Crema; Novo Bacticort Complex†; Novo Bacticort†; Otalex G; Otonorthia; Pancutan; Provisual Compuesto; Prurisedan Biotic†; Quadriderm; Quiacort G; Quiacort G Plus; Septopal†; Sirotamicin BG; Start NP†; Tribiocort; Tricur; Tridermal; Triefect†; Triliver; Triplex; Vitacortil; Austral.: Celestone VG†; Palacos E with Garamycin; Palacos R with Garamycin; Septopal; Austria: Decoderm Compositum; Decoderm trivalent; Dexagenta; Diprogenta; Septopal; Voltamicin; Belg.: Decoderm Compositum; Dexagenta-POS; Duracoll; Garasone†; Infectoflam; Palacos LV avec Gentamicine†; Palacos R avec Gentamicine†; Septopal; Braz.: Cauterex; Cremederme; Dexamytrex†; Diprogenta; Emecort†; Garasone; Gentacort; Gino-Cauterex; Microbiogen†; PanEmecort†; Permut; Poliderms; Quadriderm; Quadrikin; Quadrilon; Quadriplus; Qualiderm; Septopal; Tetraderm; Canad.: Diprogen†; Garasone; Pentasone; Valisone-G; Chile: Diprospan G; Gentasone; Labosona G; Mixgen; Oftagen Compuesto; Palacos E con Gentamicina; Palacos R con Gentamicina; Perlas De PMMA con Gentamicina; Pred G†; Vilterm†; Cz.: Belogent; Clenigen†; Dexa-Gentamicin; Garasone; Infectoflam†; Septopal†; Voltamicin†; Denm.: Septopal; Fin.: Celestoderm cum Garamycin; Palacos R cum Gentamicin†; Septopal; Fr.: Collatamp G†; Indobiotic; Palacos LV avec Gentamicine; Palacos R avec Gentamicine; Ger.: Betagentam; Cibaflam; CMW mit Gentamicin; Copal; Decoderm Comp; Dexa-Gentamicin; Dexamytrex; Diprogenta; Inflanegent; Palamed G; Refobacin-Palacos R; Septocoll; Septopal; SmartSet GHV; Sulmycin mit Celestan-V; Terracortril N; Gr.: Celestoderm-V/GA; Dexamytrex; Efemoline; Garamat; Gentadex; Luzin; Palacos R with Gentamycin†; Propiogenta; Septopal†; Hong Kong: Becogem; Celestoderm-V with Garamycin; Clobeta-G; Conazole; Dermafacte; Diprogenta; Garasone; Lycobeta-G; Quadriderm; Septopal; Triderm; Triditol-G; Hung.: Garasone; Gentason; Septopal; Vipsogal†; Voltamicin†; India: Betamil-GM; Betnederm GM; Betnovate-GM; Candiderma†; ClobenG; Cloderm GM; Clomycin; Cutinorm†; Diclogenta; Ecodax†; EumosoneG; Fourderm; Fourderm AF; Gentacip D; Genticyn B Eye/Ear†; Genticyn HC†; Lobate-G; Lobate-GM; Quiss; Septopal; Sigmaderm; Tenovate G; Translipo-Triple; Indon.: Benoson G; Betagentam; Betasin; Biocort; Celestoderm-V with Garamycin; Cinogenta; Digenta; Diprogenta; Diprosta; Garasone; Genolon; Gentacortin; Gentasolon; Isotic Betaracin; Mastroson; Salgen Plus; Sinobiotik; Skilone; Skinal; Sonigen; Irl.: Gentisone HC; Israel: Aflumycin; Betacorten-G; Cicloderm-C; Diprogenta; Triderm; Ital.: Batasalgin; Betacream; Citrizan Antibiotico; Dermabiolene; Egerian; Fidagenbeta; Formomicin; Genalfa; Genatrop; Gentacort; Gentalyn Beta; Kamelyn; Sterozinil; Vasosterone Oto; Voltamicin†; Malaysia: B-Mycin; Beprogent; Betagen; Betamethasone G; Celestoderm-V with Garamycin†; Dexa-Gentamicin†; Dexamytrex†; Diprogenta; Garasone; Gentadexa; Infectoflam†; Joysun; Septopal†; Mex.: Barmicil Compuesto; Beclogen; Betrigen; Clotricina; Diprosone G; Garamicina-V; Garasone; Miclobet; Prubagen; Quadriderm NF; Triderm; Neth.: Dexagenta-POS; Dexamytrex; Septopal; Norw.: Septopal; NZ: CMW Gentamicin; Palacos with Garamycin; VacuMix Plus with CMW gentamicin; Philipp.: Dexamytrex; Diprogenta; Garasone; Infectoflam; Ophtasone; Quadriderm; Quadrotopic; Septopal; Triderm; Pol.: Bedicort G; Dexamytrex; Diprogenta; Triderm; Port.: Dexamytrex; Diprogenta; Epione; Gentadexa; Indobiotic; Quadriderme; Rus.: Akriderm Genta (Акридерм Гента); Akriderm GK (Акридерм ГК); Belogent (Белогент); Betagenot (Бетагенот); Celestoderm-V with Garamycin (Целестодерм-В с Гарамицином); Dexa-Gentamicin (ДексаГентамицин); Triderm (Тридерм); S.Afr.: Celestoderm-V with Garamycin†; Diprogenta; Garasone†; Palacos R with Garamycin; Quadriderm; Septopal; Singapore: B-Tasone-G; Beprogent; Celestoderm-V with Garamycin†; Combiderm; Conazole; Dexamytrex; Diprogenta; Garasone; Gentriderm; Gentrisone; Infectoflam; Modaderm; Neoderm; Quadriderm†; Refobacin Bone Cement R; Refobacin-Palacos R†; Septopal†; TriMicon; Triderm; Voltamicin†; Spain: Celestoderm Gentamicina; Cuatroderm; Diprogenta; Epitelizante; Flugen; Flutenal Gentamicina; Gentadexa; Interderm; Novoter Gentamicina; Swed.: Celeston valerat med gentamicin; Septopal†; Switz.: Diprogenta; Indobiotic†; Infectoflam; Ophtasone; Quadriderm; Septopal; Triderm; Voltamicin; Thai.: Beprogent; Beprogenta; Dexamytrex; Diprogenta†; Genquin; Gental-F; Infectoflam; Pred Oph; Refobacin-Palacos R; Septopal; Turk.: Indobiotic; UK: Collatamp EG; Gentisone HC; Palacos LV with Gentamicin; Palacos R with Gentamicin; Septopal; Vipsogal; USA: Pred G; Venez.: Betaderm con Gentamicina; Celestoderm con Gentalyn; Diprogenta; Garabet; Garasone; Gentidexa; Gentisor†; Propiogenta†; Quadriderm; Triderm; Tridetarmon.
Published March 18, 2019.