Effects of Paracetamol on the Pharmacokinetics of Ciprofloxacin in Plasma Using a Microbiological Assay

Issa, Mohamed; Nejem, R’afat Mahmoud; El-Abadla, Naser S.; El-Naby, Mohamed Khamis; Roshdy, Abeer A; Kheiralla, Zainab A

doi:10.2165/00044011-200727070-00003

Cited by 14 publications

(7 citation statements)

References 13 publications

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“…In a randomized crossover study, the concentration of ciprofloxacin was found to be 3 µg·mL −1 (C max) or 14 µg·h −1 ·mL (area under the serum concentration time curve from 0 to 12 h) in the serum of a patient who had been given a single oral dose of 500 mg (Issa et al ., 2007; van Zanten et al ., 2008), which is within the range of the concentrations used in the present study. Recently, we reported that CIP increased the expression of COX‐2 and the production of PGE 2 in human monocytes (Takahashi et al ., 2005).…”

Section: Discussionmentioning

confidence: 99%

Ciprofloxacin inhibits advanced glycation end products‐induced adhesion molecule expression on human monocytes

Mori

Takahashi²,

Liu³

et al. 2010

British J Pharmacology

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Advanced glycation end products (AGEs) subtypes, proteins or lipids that become glycated after exposure to sugars, can induce complications in diabetes. Among the various AGE subtypes, glyceraldehyde-derived AGE (AGE-2) and glycolaldehyde-derived AGE (AGE-3) are involved in inflammation in diabetic patients; monocytes are activated by these AGEs. Ciprofloxacin (CIP), a fluorinated 4-quinolone, is often used clinically to treat infections associated with diabetis due to its antibacterial properties. It also modulates immune responses in human peripheral blood mononuclear cells (PBMC) therefore we investigated the involvement of AGEs in these effects. EXPERIMENTAL APPROACHExpression of intercellular adhesion molecule (ICAM)-1, B7.1, B7.2 and CD40 was examined by flow cytometry. The production of tumour necrosis factor (TNF)-a, interferon (IFN)-g, prostaglandin E2 (PGE2) and cAMP were determined by enzyme-linked immunosorbent assay. Cyclooxygenase (COX)-2 expression was determined by Western blot analysis. Lymphocyte proliferation was determined by [ 3 H]-thymidine uptake. KEY RESULTSCIP induced PGE2 production in monocytes, irrespective of the presence of AGE-2 and AGE-3, by enhancing COX-2 expression; this led to an elevation of intracellular cAMP in monocytes. Non-selective and selective COX-2 inhibitors, indomethacin and NS398, inhibited CIP-induced PGE2 and cAMP production. In addition, CIP inhibited AGE-2-and AGE-3-induced expressions of ICAM-1, B7.1, B7.2 and CD40 in monocytes, the production of TNF-a and IFN-g and lymphocyte proliferation in PBMC. Indomethacin, NS398 and a protein kinase A inhibitor, H89, inhibited the actions of CIP.

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Section: Discussionmentioning

confidence: 99%

Ciprofloxacin inhibits advanced glycation end products‐induced adhesion molecule expression on human monocytes

Mori

Takahashi²,

Liu³

et al. 2010

British J Pharmacology

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“…The effects of single-dose acetaminophen coadministration on single-dose ciprofloxacin pharmacokinetics were non-significant [269]. Single-dose chloroquine coadministration produced mean reductions in single-dose ciprofloxacin C max and AUC of 18% and 43%, respectively, and a mean increase in cumulative urinary excretion as a percentage of the dose of 1,000% (all p < 0.05) [270,271].…”

Section: Metabolism Interactionsmentioning

confidence: 88%

Quinolones

Guay¹

2011

Drug Interactions in Infectious Diseases

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Fluoroquinolone (FQ) antimicrobials are among the most commonly used agents in the outpatient and institutional patient care environments. Due to this high frequency of utilization, the potential for deleterious drug-drug interactions with nonantimicrobials is also high. The majority of interactions with the FQs involve deleterious effects on the FQ component. These are also the most clinically-important interactions with these agents. Multivalent cations such as Mg , and other minerals as well as drugs such as sucralfate, lanthanum, sevelamer, and didanosine (the cation-supplemented version of the latter) can substantially reduce FQ bioavailability, leading the subtherapeutic drug concentrations at the infection site and clinical failure. Separation of dose administrations may or may not reduce the magnitude of these interactions. Ciprofloxacin, norfloxacin, and two experimental FQs in clinical trials (pazufloxacin and prulifloxacin) act as moderate cytochrome P450 enzyme inhibitors and may increase serum concentrations of theophylline and caffeine. Warfarin pharmacodynamics are variably affected by the FQs. The pharmacodynamic interactions between NSAIDs and FQs are only relevant if fenbufen is used concurrently with enoxacin or, possibly, prulifloxacin. Caution is warranted if sparfloxacin or moxifloxacin is used concurrently with other medications prolonging the QTc interval or if patients have other risk factors for prolongation of the QTc interval (e.g. abnormal QTc interval pre-treatment, electrolyte abnormalities, use of starvation-liquid diets, or history of heart disease). Fluoroquinolone antimicrobials can be used effectively and safely in the vast majority of patients if the clinician remembers those few drug-drug interactions that are clinically-important.

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“…The most extensively studied drug-drug interactions with Cipro are those with metal ions [5][6][7]. However, there are a few other studies documenting potentially significant interactions between Cipro and other drugs, e.g., paracetamol, phenazopyridine and zolpidem [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Studies on the interaction between ciprofloxacin hydrochloride and diclofenac sodium

El-Sabawi¹,

Abu-Dahab²,

Bakri³

et al. 2019

Trop. J. Pharm Res

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Purpose: To study the interaction between ciprofloxacin hydrochloride (Cipro) and diclofenac sodium (DS) in the presence and absence of metal ions. Methods: Complexes were prepared in the aqueous phase at different molar ratios (r) of Cipro:DS (ranged from 0.2-2.0). The complexes were characterized by Fourier transform-infrared spectroscopy (FTIR), nuclear magnetic resonance (NMR), and high pressure liquid chromatography (HPLC). Their properties, i.e., solubility, dissolution and partition coefficient (log P), were studied along with their permeability across Caco-2 cells. Furthermore, the antimicrobial activity of Cipro and its complexes was determined using standard broth dilution method and expressed as minimum inhibitory concentration (MIC). Results: Cipro formed an ion pair with DS. The product was confirmed to be a combination of the two drugs, DS and Cipro, but in a ratio that is dependent on the added amounts of each component (r = 1:1 or 1:2). The 1:1 product was more lipophilic than the individual components leading to a lower aqueous solubility and a higher octanol/water partition coefficient log P (6.7 vs. 0.77). The presence of DS within the dissolution medium appeared to modify the dissolution of Cipro depending on the concentration. Moreover, ternary complexes involving Cipro, DS and metal ions (iron and/or calcium) exhibited improved antimicrobial effect (MIC, 0.016 µg/ml compared to 0.258 µg/ml for Cipro). Caco-2 cell permeation data indicate that the presence of DS significantly improved the apparent permeability coefficient (Papp) of Cipro (20.6 × 10-6 cm/s) which was three times higher than that of free Cipro (p < 0.05). DS also appeared to counteract the well-known negative effect of metal ions on the bioavailability of Cipro. Conclusion: There is a clinically relevant interaction between DS and Cipro at the absorption level as a result of ion pair formation, which might even counteract the negative effect of metals on the absorption of Cipro. These findings should aid the design of new Cipro ion pairs that provide higher bioavailability than free Cipro.

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Effects of Paracetamol on the Pharmacokinetics of Ciprofloxacin in Plasma Using a Microbiological Assay

Abstract: The results confirm an increased concentration-time profile of ciprofloxacin when the latter is co-administered with paracetamol. We believe that a pharmacokinetic interaction may have occurred.

Cited by 14 publications

References 13 publications

Ciprofloxacin inhibits advanced glycation end products‐induced adhesion molecule expression on human monocytes

Ciprofloxacin inhibits advanced glycation end products‐induced adhesion molecule expression on human monocytes

Quinolones

Studies on the interaction between ciprofloxacin hydrochloride and diclofenac sodium

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