Adverse Effects of Sodium Colistimethate

Koch‐Weser, Jan

doi:10.7326/0003-4819-72-6-857

Cited by 399 publications

(123 citation statements)

References 27 publications

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“…However, there have also been some reports that this nephrotoxicity is irreversible after the cessation of colistin treatment [7]. In addition, based on our clinical experience, we thought that it takes a shorter time to develop AKI after colistin use than that reported in the previous studies.…”

Section: Introductioncontrasting

confidence: 52%

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Early Acute Kidney Injury Is a Risk Factor That Predicts Mortality in Patients Treated with Colistin

Jeon²,

Choo³

et al. 2010

Nephron Clin Pract

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The nephrotoxicity of colistin has been reported in the literature. A previous report has shown that acute kidney injury (AKI) occurred after an average of 13.5 days, but we have experienced that AKI developed with colistin administration earlier. We investigated clinical features of patients who developed AKI according to the time of AKI development after colistin use. We retrospectively collected the data of the patients who were admitted to 4 hospitals between January 2007 and May 2009. This study included 119 patients who had received intravenous colistin for over 72 h. We compared the early AKI group (AKI developed within 7 days) with the late AKI group. The patients’ age was 64.1 ± 14.0 years. AKI occurred in 65 of the 119 patients (54.6%). The duration of colistin use was 7.7 ± 6.4 days. AKI occurred in 46 patients within 7 days after colistin treatment and in 19 patients after 7 days. The patients with early AKI had a higher mortality rate than those with late AKI (OR: 4.37, 95% CI: 1.34, 14.18). In conclusion, clinicians might be cautioned that the mortality rate is higher for the patients with early occurrence of AKI than that for the patients with late occurrence of AKI.

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Section: Introductioncontrasting

confidence: 52%

“…The most common adverse effects of colistin treatment are known to be neurotoxicity and nephrotoxicity [7]. Neurotoxicity is associated with dizziness, weakness, facial and peripheral paresthesia, vertigo, visual disturbances, confusion, ataxia and respiratory failure induced by neuromuscular blockade.…”

Section: Discussionmentioning

confidence: 99%

Early Acute Kidney Injury Is a Risk Factor That Predicts Mortality in Patients Treated with Colistin

Jeon²,

Choo³

et al. 2010

Nephron Clin Pract

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“…This analysis found that excessive CMS dosing was frequent and that use of the ABW to calculate doses was associated with a higher rate of NTX. Other published literature including nonoverweight or nonobese populations has shown multiple potential risk factors associated with CMS use to include male sex, age, hypoalbuminemia, hyperbilirubinemia, long durations of therapy, higher cumulative CMS doses, receipt of concomitant nephrotoxins, and concomitant vancomycin, rifampin, or calcineurin inhibitors (12,(15)(16)(17)23). Furthermore, NTX has been shown to independently predict fewer cures of infection and to increase the mortality rate (26).…”

mentioning

confidence: 99%

Incidence and Predictors of Nephrotoxicity Associated with Intravenous Colistin in Overweight and Obese Patients

Gauthier

Wolowich

Reddy

et al. 2012

Antimicrob Agents Chemother

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Intravenous colistin is used to treat resistant Gram-negative infections and is associated with nephrotoxicity. In overweight and obese adults, a paucity of data exists regarding the incidence and predictors of such toxicity. A retrospective nested case-control study was performed over 35 months for patients receiving intravenous colistin for >72 h with a body mass index (BMI) of >25 kg/m 2 . The objective was to investigate the incidence and predictors of nephrotoxicity. Severity of acute kidney injury was defined by RIFLE (risk, injury, failure, loss, and end-stage kidney disease) criteria. Dosing and mortality were secondarily investigated. Forty-two patients met the inclusion criteria, and 20 (48%) developed nephrotoxicity. Patients with toxicity were in the risk (15%), injury (5%), and failure (80%) categories based on RIFLE criteria. A logistic regression model identified four predictors of colistin-associated nephrotoxicity: a BMI of >31. . Among all of the patients, dosing based on the actual body weight and excessive dosing due to the use of the actual body weight were frequent at 64% and 92%, respectively. The 30-day all-cause in-hospital mortality rate was 40% in the toxicity group and 14% in the nontoxicity group (P ‫؍‬ 0.14). Patients receiving intravenous colistin should be monitored for nephrotoxicity, especially when the BMI exceeds 31.5 kg/m 2 . Prospective, randomized, controlled trials are warranted to further examine nephrotoxicity incidence and predictors and appropriate dosing strategies in this population. Intravenous colistimethate sodium (CMS, colistin) is a polymyxin-type antimicrobial currently used to treat multidrug-resistant (MDR) Gram-negative infections caused by bacteria such as Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumoniae (19). Although it was first used in the 1950s, CMS fell into disuse primarily due to significant associated nephrotoxicity (NTX), with incidence reports now ranging from 0% to 53.5% (8). Its unique history has been described in multiple reviews (8,18,21,24), and there is a notable lack of definitive recommendations regarding the most efficacious and least toxic way to administer CMS, including in overweight and obese patients (for whom the ideal body weight [IBW] is recommended by the package insert [13,28]). As the obesity epidemic continues within the United States, at a rate of Ͼ33% among adults (10), the questions of what the risk factors for NTX are and how clinicians should administer CMS to these patients remain critical.Limited data are available regarding NTX in overweight or obese patients receiving intravenous CMS. Following a thorough review of the literature, the only previously published evaluation of more than one overweight or obese individual receiving intravenous CMS included 10 obese patients (defined as those with an actual body weight [ABW] that is Ͼ140% of the IBW) (4). This analysis found that excessive CMS dosing was frequent and that use of the ABW to calculate doses was associated with a higher rate of N...

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“…Polymyxin B, a cationic detergent with antiendotoxin activity, has been shown to be protective in animals with gram-negative sepsis (12,17). This drug, a readily available antibiotic, is rarely administered parenterally because of its marked nephrotoxicity and neurotoxicity (13,23,47,50). We demonstrated in this study that a derivative of polymyxin B, polymyxin B nonapeptide, retains the anti-LPS activity of the parent compound but is less toxic.…”

Section: Discussionmentioning

confidence: 99%

“…In some models of endotoxin-induced tissue injury (21) and experimental gram-negative septicemia (17), polymyxin B has been found to be more protective than antibodies to core LPS. Unfortunately, the toxicity of polymyxin B (13,23,47,50) limits its potential as a therapeutic agent in septic shock. Furthermore, the broad antimicrobial spectrum of polymyxin B complicates specific evaluation of its anti-LPS effects during sepsis (12).…”

mentioning

confidence: 99%

Purification, toxicity, and antiendotoxin activity of polymyxin B nonapeptide

Danner

Joiner

Rubin

et al. 1989

Antimicrob Agents Chemother

147

110

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Polymyxin B, a relatively toxic antibiotic, has potent endotoxin-neutralizing properties that may be beneficial as adjunctive therapy in gram-negative sepsis. Polymyxin B nonapeptide (deacylated polymyxin B) is devoid of antibiotic activity but retains the capacity to disorganize the outer membrane of gram-negative bacteria. To evaluate the potential therapeutic usefulness of this derivative, we produced purified polymyxin B nonapeptide, tested its in vivo toxicity in animals, and evaluated its in vitro antiendotoxin activity. Effectiveness as an antiendotoxin agent was assessed by examining the ability of polymyxin B nonapeptide to block the enhanced release of toxic oxygen radicals induced by lipopolysaccharide in human neutrophils (priming). In vivo, at doses of 1.5 and 3.0 mg/kg, polymyxin B nonapeptide did not exhibit the neuromuscular blocking, neurotoxic, or nephrotoxic effects that were observed with polymyxin B sulfate. Both polymyxin B and polymyxin B nonapeptide inhibited lipopolysaccharide-induced neutrophil priming in a concentration-dependent manner, but the parent compound, polymyxin B, was 63 times more effective on a weight basis. The inhibitory activity of both compounds, however, diminished rapidly when they were added after the start of the lipopolysaccharide-neutrophil incubation. We conclude that polymyxin B nonapeptide is less toxic than polymyxin B and, at the doses tested, lacks the neurotoxicity and nephrotoxicity of the parent compound. Polymyxin B nonapeptide retains the antiendotoxin activity of polymyxin B but is much less potent. The findings suggest that these compounds block an early step in the neutrophil priming process, possibly lipopolysaccharide attachment to or insertion into the neutrophil membrane.

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Adverse Effects of Sodium Colistimethate

Cited by 399 publications

References 27 publications

Early Acute Kidney Injury Is a Risk Factor That Predicts Mortality in Patients Treated with Colistin

Early Acute Kidney Injury Is a Risk Factor That Predicts Mortality in Patients Treated with Colistin

Incidence and Predictors of Nephrotoxicity Associated with Intravenous Colistin in Overweight and Obese Patients

Purification, toxicity, and antiendotoxin activity of polymyxin B nonapeptide

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