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Amikacin
side effects, nutrient depletions, herbal interactions and health notes:

Data provided by Applied Health

reports: Animal studies and case reports indicate that renal tubular damage due to aminoglycosides, such as gentamicin, can lead to hypokalemia combined with hypocalcemia, hypomagnesemia and alkalosis. adverse effects: The toxicities of aminoglycosides include toxicity to the kidneys and ears (vestibular and auditory) and, rarely, neuromuscular blockade and hypersensitivity reactions. These adverse reactions are more common when aminoglycosides are given in combination with vancomycin. Nephrotoxicity results from renal cortical accumulation resulting in tubular cell degeneration and sloughing. Ototoxicity is usually irreversible. The prescribing physician should closely monitor (draw aminoglycoside and vancomycin serum levels) patients for these potential side effects.1

research: Akbar et al have noted that this phenomenon may be especially common among children with cystic fibrosis who have a history of repeated use of aminoglycosides2

nutritional support: Individuals using aminoglycosides, especially on a repeated or chronic basis, should consult with their prescribing physician and/or a nutritionally oriented healthcare professional about nutritional support to restore normal levels of these important minerals. Patients undergoing extended treatment with aminoglycosides may need to have their doctor regularly monitor their kidney function along with magnesium and potassium status. Serum creatinine, BUN and creatinine clearance should be measured prior to initiating therapy and should be monitored throughout treatment. In this regard, many nutritionally-oriented practitioners find that testing magnesium levels in red blood cells is far more reliable than testing serum magnesium. Only after such assessment should supplementation with magnesium or potassium be undertaken and then only under close supervision by the prescribing physician. Calcium supplementation in the range of 800-1000 mg per day may beneficial for individuals being treated with aminoglycosides. Slow-K and Micro-K are typical examples of the potassium supplementation suggested by most physicians. Potassium levels can be further enhanced by eating several pieces of fruit each day. However, increasing potassium intake by any means is usually contraindicated and often dangerous in patients with reduced kidney function, especially those on dialysis. Supplementation of magnesium in the dosage range of 300-500 mg per day is usually appropriate but should be done in consultation with the prescribing doctor or a nutritionally-oriented physician. Magnesium supplementation can be risky in patients with kidney damage and is usually contraindicated in such cases. It is also important to note that magnesium is needed to maintain intracellular potassium.3

: Free radical generation due to aminoglycosides plays an important role in drug-induced damage to the liver, kidneys and inner ear. Alpha-lipoic acid is a powerful antioxidant and free radical scavenge4

Sandhya et al found that lipoic acid administration brought about a decrease in the degree of lipid peroxidation due to gentamicin in rats. Conlon et al conducted studies using guinea pigs to the investigate the ability of the alpha-lipoic acid (100 mg/kg/day) to attenuate the cochlear damage induced by 450 mg/kg/day, i.m. of the aminoglycoside amikacin. Their results showed that animals receiving alpha-lipoic acid in combination with amikacin demonstrated a significantly less severe changes in cochlear function compared with animals receiving amikacin alone.5

Since the preliminary research on this topic has involved animals and not human patients no conclusive recommendations can be offered. However, a diverse set of clinical studies have demonstrated alpha-lipoic acid's role as a potent anti-oxidant and its ability to enhance protective systems in the liver and kidney in a variety of situations. Therefore, while supplementation with alpha-lipoic acid might be advisable for individuals using aminoglycosides, the available research literature provides no specific indications as to the appropriate dosage for this particular situation. However, any individual using alpha-lipoic acid in relation to gentamicin should do so only under supervision of a the prescribing physician and a nutritionally-trained healthcare professional.6

During the course of eliminating disease-causing bacteria, antibiotics also usually destroy normally-occurring beneficial bacterial flora that form an integral part of the healthy intestinal ecology and assist digestive and immune functions. Diarrhea and yeast infections, including vaginal yeast, are common side-effects of the disruption of intestinal ecology and the creation of an environment more susceptible to proliferation of pathogenic levels of opportunistic yeast. nutritional support: Supplementation of beneficial "probiotic" bacterial flora, such as Lactobacillus acidophilus, Bifidobacterium bifidus and Lactobacillus cassei, preferably in the form of a varied, vigorous and abundant culture, will restore the healthy intestinal ecology and stabilize the mucosal lining of the gut. A supplemental dosage of at least one billion organisms per day is necessary to achieve the critical mass of bacterial restoration and successfully reinvigorate healthy intestinal ecology.7

Hypomagnesaemia in children with cystic fibrosis (CF) is under-recognized. We report a child with CF who developed significant hypomagnesaemia following intravenous (i.v.) treatment with aminoglycosides for exacerbations of Pseudomonas aeruginosa infection. Three additional cases have also been observed. Investigations in two patients have revealed excessive renal loss of magnesium. It is postulated that renal tubular damage secondary to the cumulative effects of repeated courses of aminoglycosides resulted in hypomagnesaemia, and we suggest screening for this problem by monitoring serum magnesium regularly in all patients with CF receiving multiple courses of aminoglycosides.8

: Free radical generation is increasingly implicated in a variety of pathological processes, including drug toxicity. Recently, a number of studies have demonstrated the ability of gentamicin to facilitate the generation of radical species both in vivo and in vitro, which suggests that this process plays an important role in aminoglycoside-induced ototoxicity. Free radical scavengers are compounds capable of inactivating free radicals, thereby attenuating their tissue damaging capacity. In this study we have determined the ability of the powerful free radical scavenger alpha-lipoic acid (100 mg/kg/day) to attenuate the cochlear damage induced by a highly ototoxic regimen of the aminoglycoside amikacin (450 mg/kg/day, i.m.). Experiments were carried out on pigmented guinea pigs initially weighing 200-250 g. Changes in cochlear function were characterized as shifts in compound action potential (CAP) thresholds, estimated every 5 days, by use of chronic indwelling electrodes implanted at the round window, vertex, and contralateral mastoid. Results showed that animals receiving alpha-lipoic acid in combination with amikacin demonstrated a significantly less severe elevation in CAP thresholds compared with animals receiving amikacin alone (P < 0.001; t-test). These results provide further evidence of the recently reported intrinsic role of free radical generation in aminoglycoside ototoxicity, and highlight a potential clinical therapeutic use of alpha-lipoic acid in the management of patients undergoing aminoglycoside treatment.9

Gentamicin causes isolated, reversible calciuria in rats by an unknown mechanism. We hypothesized that gentamicin calciuria is related to nonantibacterial properties that may interfere with transtubular calcium transport (calcium channel blockade, Na,K-ATPase inhibition or competition with calcium for binding to the brush-border membrane). The calciuric effect of gentamicin was compared to the calcium channel blockers lanthanum and cobalt, the Na,K-ATPase inhibitor ouabain and the polycation aprotinin (which competes with gentamicin for brush-border membrane binding). Although gentamicin 0.02 mmol/kg caused a 6-8-fold increase in urine calcium concentration, none of the other agents was calciuric. We also found that the calciuric effects of gentamicin and furosemide were additive, whereas the noncalciuric diuretic chlorothiazide had no effect on gentamicin calciuria. We also determined the effect of poly-L-aspartic acid (PAA), which binds gentamicin and prevents nephrotoxicity. PAA caused isolated calciuria similar in magnitude and character to gentamicin. However, PAA pretreatment decreased the magnitude of gentamicin calciuria to insignificance. PAA pretreatment did not prevent furosemide calciuresis. These results indicate that: 1) gentamicin and furosemide calciuria are caused by different mechanisms; 2) gentamicin calciuria is probably not mediated by calcium channel blockade, Na,K-ATPase inhibition or displacement of brush-border membrane-bound calcium; 3) gentamicin and PAA calciuria may reflect interference with intracellular events related to transtubular calcium transport.10

Two independent techniques were used in anesthetized rats in an attempt to locate the nephron site of the reduced tubular calcium reabsorption accompanying acute gentamicin infusion. The first technique was that of lithium clearance used to assess proximal sodium (and secondarily calcium) handling. Observations that lithium clearance was comparable in control and gentamicin-treated animals (1.83 +/- 0.39 vs. 1.46 +/- 0.14 ml.min-1 for first experimental period) suggests a lack of proximal effect of the drug. The second technique was that of tracer microinjection whereby superficial nephrons were injected with 45Ca and tubule calcium transport was assessed from the recovery of radioactivity in the final urine. 45Ca recovery values from distal microinjections were comparable in control and gentamicin-treated groups (81.1 +/- 2.0 vs. 77.7 +/- 4.6%). However, 45Ca recovery values from proximal microinjections were significantly higher in the gentamicin group (9.4 +/- 1.0 vs. 3.5 +/- 0.8%; P < .001). These data suggest that the effects of gentamicin on renal calcium handling are mediated at a nephron site proximal to the distal tubule (i.e., loop of Henle or proximal tubule itself). Closer examination of individual proximal micropuncture data may point to an effect occurring predominantly in the pars recta of the proximal tubule or loop of Henle. Taken together, the results of both parts of the present study suggest that the early physiological effects of gentamicin on the kidney occur in a different nephron segment from any subsequent nephrotoxicity.11

Seven patients (3 females, 4 males) developed symptomatic hypomagnesemia, hypocalcemia, and hypokalemia following gentamicin therapy. The excessive and inappropriate urinary excretion of magnesium and potassium in the presence of subnormal serum concentrations was noted. A significant correlation was found between the total cumulative dose of gentamicin and serum Mg concentration (r = 0.76, p less than 0.05), as well as between the renal wasting of Mg and the total cumulative dose of gentamicin administered (r = 0.89, p less than 0.01). The gentamicin-induced Mg depletion is a very rare but important complication which is most likely to occur when the drug is given to older patients in large doses over extended periods of time12

1. Standard renal clearance techniques were used to assess the dose-response relationship between acute gentamicin infusion and the magnitude of hypercalciuria and hypermagnesiuria in the anaesthetized Sprague-Dawley rat. Also investigated were whether these effects occurred independently of renal tubular cell injury. 2. Acute gentamicin infusion was associated with a significant hypercalciuria and hypermagnesiuria evident within 30 min of drug infusion. The magnitude of these responses was related to the dose of drug infused (0.14-1.12 mg kg(-1) min[-1]). Increased urinary electrolyte losses resulted from a decreased tubular reabsorption of calcium and magnesium. 3. A rapid dose-related increase in urinary N-acetyl-beta-D-glucosaminidase (NAG) excretion was also observed in response to gentamicin infusion. However, there was no evidence of renal tubular cell injury and no myeloid bodies were observed within the lysosomes of the proximal tubular cells. Gentamicin may thus interfere with the mechanisms for cellular uptake and intracellular processing of NAG causing increased NAG release into the tubular lumen. 4. The absence of changes in renal cellular morphology indicates that the excessive renal losses of calcium and magnesium were an effect of gentamicin per se and not the result of underlying renal tubular injury. The renal effects described in this paper were apparent after administration of relatively low total drug doses, and with plasma concentrations calculated to be within the clinical range. These findings suggest that disturbances of plasma electrolyte homeostasis could occur in the absence of overt renal injury in patients receiving aminoglycoside antibiotics.13

Because calcium has been reported to modify gentamicin binding to its proximal tubular brush border membrane receptor, we studied the effects of dietary calcium loading and subsequent hypercalciuria on experimental gentamicin nephrotoxicity. Male Fischer 344 rats were fed one of two diets that were identical except for calcium carbonate content: normal (0.5%) and high (4%). The high-calcium diet made rats hypercalciuric but there were no differences between the two groups in inulin clearance, sodium or osmolar excretion, or serum calcium prior to gentamicin administration. Animals on both diets were treated with gentamicin, 20 mg/kg b.i.d., for periods of 3 to 21 days. Both groups developed acute renal failure, but animals on the high-calcium diet had less severe acute toxic injury, as evidenced by studies of inulin clearance, renal histology, and in vitro cortical uptake of NMN and PAH. Furthermore, calcium-loaded animals tended to have lower peak renal cortical gentamicin levels during the period of acute toxicity. The mechanism by which increased dietary calcium protects against gentamicin nephrotoxicity remains speculative. Calcium and gentamicin may compete for the same brush border receptor or alternatively parathyroid suppression may result in diminution in tubular cell membrane drug binding sites. The possibility that high-calcium diets exert a nonspecific salutory effect on proximal tubular cell integrity has not been excluded.14

The intraperitoneal administration of gentamicin (100 mg kg[-1] day[-1]) to rats is associated with an increased production of malondialdehyde (MDA), which is an end product of lipid peroxidation in the kidney. The level of glutathione (GSH) and the activity of three antioxidant systems--superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx)--were also decreased in the kidney. The liver, however, did not show any such alterations. Gentamicin (100 mg kg[-1] day[-1]) plus lipoic acid administration (25 mg kg[-1] day[-1]) by gastric intubation brought about a decrease in the degree of lipid peroxidation. An increase in the GSH level and in the activity of SOD, CAT and GPx was also observed. From these observations it can be concluded that administration of DL-alpha-lipoic acid prevents lipid peroxidation, which may, at least partly, play an important role in the injury cascade of gentamicin-induced nephrotoxicity15

The effect of the nephrotoxic aminoglycoside antibiotic, gentamicin, on calcium uptake by renal cortical mitochondria was assessed in vitro. Gentamicin was found to be a competitive inhibitor of mitochondrial Ca++ uptake. This effect displayed a dose response with a Ki of 233 microM and occurred at gentamicin concentrations below those that inhibit mitochondrial electron transport. These results further demonstrate the potential for gentamicin to alter membrane function and thereby contribute to toxic cell injury via its interactions with divalent cations.16

A retrospective study in coronary artery bypass graft patients was undertaken to assess the effect of gentamicin and a bypass prime with a high calcium on the incidence of renal failure. Patients who received both Haemaccel (polygeline, Hoechst Marion Roussel) (calcium concentration 6.25 mmol/l) in the bypass prime and gentamicin perioperatively had a higher incidence of renal failure compared with those who received only Haemaccel (P = 0.005), only gentamicin (P = 0.002) or neither (P = 0.0001). We suggest that the combination be avoided in this group of patients.17

There are no Herbal considerations at this time18



References

1 Mazze RI, Cousins MJ. Br J Anaesth. 1973 Apr;45(4):394-398; Valdivieso A, et al. Rev Med Chil. 1992 Aug;120(8):914-919; Kes P, et al. Magnes Trace Elem. 1990;9(1):54-60; Parsons PP, et al. Br J Pharmacol 1997 Oct;122(3):570-576.)

1 Conlon BJ, Aran JM, Erre JP, Smith DW. Attenuation of aminoglycoside-induced cochlear damage with the metabolic antioxidant alpha-lipoic acid. Hear Res. 1999 Feb;128(1-2):40-44.

2 Akbar A, et al. Acta Paediatr. 1999 Jul;88(7):783-785

3 Reference not Available

4 Tran Ba Huy P, Deffrennes D. Acta Otolaryngol [Stockh] 1988;105:511-515

5 Sandhya P, et al. J Appl Toxicol 1997 Nov-Dec;17(6):405-408; Conlon BJ, et al. Hear Res. 1999 Feb;128(1-2):40-44

6 Sandhya P, et al. J Appl Toxicol 1997 Nov-Dec;17(6):405-408; Conlon BJ, et al. Hear Res. 1999 Feb;128(1-2):40-44

7 Akbar A, Rees JH, Nyamugunduru G, English MW, Spencer DA, Weller PH. Aminoglycoside-associated hypomagnesaemia in children with cystic fibrosis. Acta Paediatr. 1999 Jul;88(7):783-785

8 Bolsin S, Jones S. Acute renal failure potentiated by gentamicin and calcium. Anaesth Intensive Care 1997 Aug;25(4):431-432. (Letter)

9 Elliott WC, Patchin DS. Effects and interactions of gentamicin, polyaspartic acid and diuretics on urine calcium concentration. J Pharmacol Exp Ther 1995 Apr;273(1):280-284.

10 Garland HO, Phipps DJ, Harpur ES. Gentamicin-induced hypercalciuria in the rat: assessment of nephron site involved. J Pharmacol Exp Ther. 1992 Oct;263(1):293-297

11 Humes HD, Sastrasinh M, Weinberg JM. Calcium is a competitive inhibitor of gentamicin-renal membrane binding interactions and dietary calcium supplementation protects against gentamicin nephrotoxicity. J Clin Invest 1984 Jan;73(1):134-147.

12 Kosek JC, Mazze RI, Cousins MJ. Nephrotoxicity of gentamicin. Lab Invest. 1974 Jan;30(1):48-57.

12 Mazze RI, Cousins MJ. Combined nephrotoxicity of gentamicin and methoxyflurane anaesthesia in man. A case report. Br J Anaesth. 1973 Apr;45(4):394-398.

12 McLean, R. Magnesium and its therapeutic uses: A review. Am J Med 1994 Jan;96(1):63-76. (Review)

12 Montie T, Patamasucon P. Aminoglycosides: the complex problem of antibiotic mechanisms and clinical applications. Eur J Clin Microbiol Infect Dis 1995;14:85-87. (Editorial)

12 Parsons PP, Garland HO, Harpur ES, Old S. Acute gentamicin-induced hypercalciuria and hypermagnesiuria in the rat: dose-response relationship and role of renal tubular injury. Br J Pharmacol 1997 Oct;122(3):570-576

13 Quarum ML, Houghton DC, Gilbert DN, McCarron DA, Bennett WM. Increasing dietary calcium moderates experimental gentamicin nephrotoxicity. J Lab Clin Med 1984 Jan;103(1):104-114.

14 Sandhya P, Varalakshmi P. Effect of lipoic acid administration on gentamicin-induced lipid peroxidation in rats. J Appl Toxicol 1997 Nov-Dec;17(6):405-408.

15 Sastrasinh M, Weinberg JM, Humes HD. The effect of gentamicin on calcium uptake by renal mitochondria. Life Sci. 1982 Jun 28;30(26):2309-2315

16 Schneider M, Valentine S, Clarke GM, Newman MA, Peacock J. Acute renal failure in cardiac surgical patients, potentiated by gentamicin and calcium. Anaesth Intensive Care 1996 Dec;24(6):647-650.

17 Tran Ba Huy P, Deffrennes D. Aminoglycoside ototoxicity: influence of dosage regimen on drug uptake and correlation between membrane binding and some clinical features. Acta Otolaryngol [Stockh] 1988;105:511-515.

17 Valdivieso A, Mardones JM, Loyola MS, Cubillos AM. [Hypomagnesemia associated with hypokalemia, hyponatremia and metabolic alkalosis. Possible complication of gentamycin therapy]. Rev Med Chil. 1992 Aug;120(8):914-919. [Article in Spanish]

18 N/A



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The information in Drug Watch is provided as a courtesy to NewsTarget readers by Applied Health Solutions in cooperation with Healthway Solutions. Although the information is presented with scientific references, we do not wish to imply that this represents a comprehensive list of considerations about any specific drug, herb or nutrient. Nor should this information be considered a substitute for the advice of your doctor, pharmacist, or other healthcare practitioner. Please read the disclaimer about the intentions and limitations of the information provided on these pages. It is important to tell your doctor and pharmacist about all other drugs and nutritional supplements that you are taking if they are recommending a new medication. Copyright © 2007 by Applied Health Solutions, Inc. All rights reserved.

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