Quinolone-induced arthropathy: an update focusing on new mechanistic and clinical data

Sendzik, Judith; Lode, H.; Stahlmann, Ralf

doi:10.1016/j.ijantimicag.2008.08.004

Cited by 94 publications

(52 citation statements)

References 46 publications

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“…Ciprofloxacin has a complex safety profile. A range of adverse drug reactions, including arthropathies, without identified long-term effects, need to be balanced with its efficacy (14)(15)(16). Potential neuroprotective effects were demonstrated in a juvenile animal model subjected to Escherichia coli sepsis (17).…”

Section: Discussionmentioning

confidence: 99%

Population Pharmacokinetics of Ciprofloxacin in Neonates and Young Infants Less than Three Months of Age

Zhao

Hill

Guellec

et al. 2014

Antimicrob Agents Chemother

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Ciprofloxacin is used in neonates with suspected or documented Gram-negative serious infections. Currently, its use is off-label partly because of lack of pharmacokinetic studies. Within the FP7 EU project TINN (Treat Infection in NeoNates), our aim was to evaluate the population pharmacokinetics of ciprofloxacin in neonates and young infants <3 months of age and define the appropriate dose in order to optimize ciprofloxacin treatment in this vulnerable population. Blood samples were collected from neonates treated with ciprofloxacin and concentrations were quantified by high-pressure liquid chromatography-mass spectrometry. Population pharmacokinetic analysis was performed using NONMEM software. The data from 60 newborn infants (postmenstrual age [PMA] range, 24.9 to 47.9 weeks) were available for population pharmacokinetic analysis. A two-compartment model with first-order elimination showed the best fit with the data. A covariate analysis identified that gestational age, postnatal age, current weight, serum creatinine concentration, and use of inotropes had a significant impact on ciprofloxacin pharmacokinetics. Monte Carlo simulation demonstrated that 90% of hypothetical newborns with a PMA of <34 weeks treated with 7.5 mg/kg twice daily and 84% of newborns with a PMA >34 weeks and young infants receiving 12.5 mg/kg twice daily would reach the AUC/MIC target of 125, using the standard EUCAST MIC susceptibility breakpoint of 0.5 mg/liter. The associated risks of overdose for the proposed dosing regimen were <8%. The population pharmacokinetics of ciprofloxacin was evaluated in neonates and young infants <3 months old, and a dosing regimen was established based on simulation.

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Section: Discussionmentioning

confidence: 99%

Population Pharmacokinetics of Ciprofloxacin in Neonates and Young Infants Less than Three Months of Age

Zhao

Hill

Guellec

et al. 2014

Antimicrob Agents Chemother

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“…For example, there is growing evidence that these drugs sequester magnesium ions essential for integrins responsible for cell-cell adhesion (84). This has been further substantiated by the work of Pfister et al, who demonstrated that administration of magnesium and vitamin E has a protective effect for fluoroquinolone-induced chondrotoxicity in a rat model (66).…”

Section: Fluoroquinolones and Chondrotoxicitymentioning

confidence: 96%

“…In vitro toxicity has been demonstrated in tenocytes and chondrocytes (11,84,101), and the chondrotoxicity has been associated with reactive oxygen species (51). Osteoblasts are also sensitive to fluoroquinolones, since these cells produce excess lactate in the presence of therapeutically relevant concentrations of the drug (13).…”

Section: Fluoroquinolones and Chondrotoxicitymentioning

confidence: 99%

Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components

Barnhill

Brewer

Carlson

2012

Antimicrob Agents Chemother

106

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This minireview explores mitochondria as a site for antibiotic-host interactions that lead to pathophysiologic responses manifested as nonantibacterial side effects. Mitochondrion-based side effects are possibly related to the notion that these organelles are archaic bacterial ancestors or commandeered remnants that have co-evolved in eukaryotic cells; thus, this minireview focuses on mitochondrial damage that may be analogous to the antibacterial effects of the drugs. Special attention is devoted to aminoglycosides, chloramphenicol, and fluoroquinolones and their respective single side effects related to mitochondrial disturbances. Linezolid/oxazolidinone multisystemic toxicity is also discussed. Aminoglycosides and oxazolidinones are inhibitors of bacterial ribosomes, and some of their side effects appear to be based on direct inhibition of mitochondrial ribosomes. Chloramphenicol and fluoroquinolones target bacterial ribosomes and gyrases/topoisomerases, respectively, both of which are present in mitochondria. However, the side effects of chloramphenicol and the fluoroquinolones appear to be based on idiosyncratic damage to host mitochondria. Nonetheless, it appears that mitochondrion-associated side effects are a potential aspect of antibiotics whose targets are shared by prokaryotes and mitochondria-an important consideration for future drug design. SIDE EFFECTS OF ANTIBACTERIAL DRUGST he desired activity of an antibiotic is to kill or prevent the growth of offending pathogenic bacteria, and yet these drugs may impact the host in an injurious manner. Generalized adverse events are common to most antibiotics (e.g., gastrointestinal distress with any oral antibacterial drug), but certain antibiotics are associated with specific effects (Table 1). Some adverse events are mild, e.g., yellowing of the teeth for tetracyclines (77, 79), increased intestinal peristalsis related to erythromycin therapy (7, 67), and reversible orange discoloration of skin and body fluids as observed with rifampin treatment (23, 31). Altered drug metabolism (106) is a common side effect that, in the absence of co-drug therapy, could also be considered mild. More serious side effects include photosensitivity (44) and anaphylactoid reactions (34) observed with many agents, ototoxicity (27, 83) following aminoglycoside therapy, chondrotoxicity (85, 88) and retinopathy (95) with fluoroquinolones, neuropathies associated with metronidazole (30, 107) and linezolid (15), and lactic acidosis and serotonin syndrome attributed to linezolid (21, 61). Other consequences can be severe or even devastating such as: the dermonecrolytic Stevens-Johnson syndrome associated with sulfonamide antimicrobial agents (74, 81); nephrotoxicity related to aminoglycosides (63, 73); aplastic anemia due to chloramphenicol (9, 91); hepatitis caused by many drugs, including isoniazid (72, 89); neuromuscular blockade related to aminoglycoside (64, 65) or lincosamide (4, 70) therapy; myopathies due to ionophores (5, 28, 75); and neoplasia related to metronidazole (19)....

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“…The use of quinolones has increased during recent years because of the increasing resistance of pneumococci and other bacteria tolactams and macrolides [1]. Tendinopathies are rare but severe side effects that have been observed for both classes of drugs [2][3][4][5][6][7][8][9][10]. The term 'tendinopathy' comprises several forms of tendon damage from a reversible inflammation (tendinitis) up to tendon rupture requiring surgical intervention.…”

Section: Introductionmentioning

confidence: 99%

Synergistic effects of dexamethasone and quinolones on human-derived tendon cells

Sendzik

Shakibaei

Schäfer‐Korting

et al. 2010

International Journal of Antimicrobial Agents

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Quinolones and glucocorticoids are frequently used drugs that may cause tendinopathy as a rare adverse effect. We exposed human tenocyte cultures to the steroid dexamethasone alone or in combination with either ciprofloxacin or levofloxacin at concentrations of 3 mg/L and 10 mg/L. At concentrations corresponding to peak levels in plasma and tissues during therapy (ca. 3-10 mg/L), ciprofloxacin caused a significant decrease in collagen type I and the 1 -integrin receptor. In contrast, no corresponding effect was induced by 3 mg/L levofloxacin.With both quinolones at 3 mg/L and 10 mg/L, the amount of matrix metalloproteinase-1 (MMP-1) and MMP-13 was increased. In addition, 3 mg/L ciprofloxacin and 10 mg/L levofloxacin activated caspase-3. Apoptotic changes were confirmed by electron microscopy. Incubation of human tenocytes with dexamethasone decreased the main matrix protein collagen type I, the

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Quinolone-induced arthropathy: an update focusing on new mechanistic and clinical data

Cited by 94 publications

References 46 publications

Population Pharmacokinetics of Ciprofloxacin in Neonates and Young Infants Less than Three Months of Age

Population Pharmacokinetics of Ciprofloxacin in Neonates and Young Infants Less than Three Months of Age

Adverse Effects of Antimicrobials via Predictable or Idiosyncratic Inhibition of Host Mitochondrial Components

Synergistic effects of dexamethasone and quinolones on human-derived tendon cells

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