Ciprofloxacin-induced Q-T interval prolongation

Knorr, John P.; Moshfeghi, Mersedeh; Sokoloski, Mary C.

doi:10.2146/ajhp070081

Cited by 33 publications

(19 citation statements)

References 17 publications

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“…In this experiment, the damaged myocardial cells affect the scalability of the heart, which finally result in slowing of the heart rate. It was first reported by Knorr et al [33] that ciprofloxacin could induce the prolongation of the Q-T interval. Later, many fluoroquinolone antibiotics were shown to prolong, the Q-T interval [34], which triggered an arrhythmia.…”

Section: Discussionmentioning

confidence: 95%

Toxicological Assessment of Trace β-Diketone Antibiotic Mixtures on Zebrafish (Danio rerio) by Proteomic Analysis

et al. 2014

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β-Diketone antibiotics (DKAs) can produce chronic toxicity in aquatic ecosystems due to their pseudo-persistent in the environment. In this study, after long-term DKA exposure to zebrafish (Danio rerio), 47 protein spots had greater than 2-fold differential expression as compared to the control; there were 26 positive proteins with 14 up-regulated and 12 down-regulated. The main functions of the differentially expressed proteins were related to signal transduction mechanisms and the cytoskeleton. Of the 26 target genes, 11 genes were consistent between their transcriptional and translational levels. Low dose DKA exposure (4.69 and 9.38 mg/L) stimulated spontaneous movement in zebrafish. Changes in both creatine kinase activity and creatine concentration showed a similar trend to zebrafish activity. There was no obvious change in SV-BA after DKA exposure, while a reduction of heart rate was concomitant with increasing DKA concentrations. DKAs also induced severe histopathological changes in zebrafish heart tissue, such as dissolution of cristae and vacuolation of mitochondria. These results demonstrated that trace-level DKA exposure affects a variety of cellular and biological processes in zebrafish.

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Section: Discussionmentioning

confidence: 95%

Toxicological Assessment of Trace β-Diketone Antibiotic Mixtures on Zebrafish (Danio rerio) by Proteomic Analysis

et al. 2014

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“…21 We anticipated no association between sudden death and norfloxacin, because it has no direct cardiac effects and does not interact with spironolactone. In contrast, we anticipated an association with ciprofloxacin and with nitrofurantoin, because the former tends to be used for more serious infections and can independently cause prolongation of the QT interval, 22,23 and the latter was associated with an increased risk of hyperkalemia in patients receiving spironolactone in our earlier study. 9 To prevent model overfitting, we adjusted our analysis for an extensive array of covariates associated with sudden death using a disease risk index.…”

Section: Discussionmentioning

confidence: 96%

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Antoniou

Hollands

Macdonald

et al. 2015

CMAJ

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T he use of spironolactone increased considerably following publication of the Randomized Aldactone Evaluation Study, which showed that the drug improved morbidity and mortality in carefully selected patients with severe systolic heart failure.1,2 Although spironolactone is generally well tolerated, hyperkalemia is a potentially life-threatening adverse effect of the drug in clinical practice.3-5 Strategies for mitigating the risk of serious hyperkalemia include cautious dosing of spironolactone, close monitoring of electrolyte levels and avoidance of other drugs that cause hyperkalemia.The widely used antibiotic trimethoprim has pharmacologic similarities to the potassium-sparing diuretic amiloride. It reduces urinary potassium excretion by about 40% and can increase the risk of life-threatening hyperkalemia in susceptible individuals, including those taking spironolactone.6,7 In combination with sulfamethoxazole, trimethoprim is most often used for the treatment of urinary tract infections. More than 20 million prescriptions are written for the combination each year in the United States. 8 We have previously shown that the use of trimethoprim-sulfamethoxazole in patients receiving spironolactone increased the risk of hospital admission with hyperkalemia more than 12-fold relative to amoxicillin.9 However, we did not examine whether the drug interaction was associated with an increased risk of sudden cardiac death, a predictable consequence of severe hyperkalemia. 10,11 This is important because sudden death in patients taking spironolactone may erroneously be attributed to intrinsic heart disease.Because treatment with trimethoprimsulfamethoxazole can precipitate life-threatening hyperkalemia in patients receiving spironolactone, we conducted a study to determine whether

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“…However allergic reactions to this drug have been reported rarely and some of them have affected the heart. Anaphylactoid reaction characterized by severe hypotension, wheezing, tachypnea, tachycardia, and pruritus [14] as well as prolongation of Q-T interval together with bradycardia [15] have been reported.…”

Section: Discussionmentioning

confidence: 99%

Kounis syndrome: Two extraordinary cases

Almpanis

Siahos

Karogiannis

et al. 2011

International Journal of Cardiology

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Ciprofloxacin-induced Q-T interval prolongation

Abstract: A pediatric patient with Crohn's disease and colitis with cryptitis developed a prolonged Q-T interval within 48 hours of treatment with ciprofloxacin.

Cited by 33 publications

References 17 publications

Toxicological Assessment of Trace β-Diketone Antibiotic Mixtures on Zebrafish (Danio rerio) by Proteomic Analysis

Toxicological Assessment of Trace β-Diketone Antibiotic Mixtures on Zebrafish (Danio rerio) by Proteomic Analysis

Trimethoprim–sulfamethoxazole and risk of sudden death among patients taking spironolactone

Kounis syndrome: Two extraordinary cases

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