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High-Performance Liquid Chromatography
Published in Adorjan Aszalos, Modern Analysis of Antibiotics, 2020
Joel J. Kirschbaum, Adorjan Aszalos
Concentrations in plasma and urine were determined using an octadecylsilane column and a mobile phase of 0.1 M phosphate buffer, pH 7. 5-acetonitrile (85:15) flowing at 1.5 ml/min through a 254 nm detector. Using cephaloridine as internal standard, calibration curves were constructed using concentrations of 2–250 µg/ml to investigate pharmacokinetics [218]. Cephapirin in plasma was quantified using an octadecylsilane column with a mobile phase of acetonitrile-dilute acetic acid, pH 2.8 (13:87), flowing at 1.5 ml/min into a detector set to 270 nm [219]. Recoveries averaged 100% between 200 and 1 µg/ml. Cefotaxime and cefoxitin could also be quantified by this method.
Cefadroxil, Cephaloridine, Cephacetrile, Cephapirin, Cephradine, and Other Rarely Used First-Generation Cephalosporins
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Cephaloridine use was associated with dose-dependent nephrotoxicity (Foord, 1975; Appel and Neu, 1977). This toxicity was not seen to such a degree with other first-generation cephalosporins and has led to the curtailment of use of cephaloridine.
Role of Transport in Chemically-Induced Nephrotoxicity *
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Although cephaloridine is no longer used as a therapeutic agent, it was the first cephalosporin studied with respect to nephrotoxicity and the compound for which there are the most data. Several experiments were undertaken by Tune and colleagues to demonstrate the mechanism by which cephalosporin entered proximal tubular cells as a prelude to the nephrotoxic response (for a summary of these data see Tune and Hsu, 1990 and Tune, 1986,1975). First, a large interspecies variation was observed in the accumulation of cephaloridine. The species which showed a high accumulation of cephaloridine also showed a high potential for nephrotoxicity. Those species which did not show a significant accumulation of the compound showed virtually no nephrotoxic response. Secondly, in newborn rabbits little or no cephaloridine toxicity was observed. This absence of a nephrotoxic response was correlated precisely with the absence of the organic anion transport system. However, an increase in toxicity was observed with cephaloridine as the animals grew and the organic anion secretory system developed. It was well established by Hook and colleagues (Hirsch and Hook, 1970a; Kim et al., 1972) that newborn animals lack the ability to secrete organic anions, and as these animals mature the organic anion secretory process made its presence known. Although it is known that the organic anion transport system is inducible in the newborn by treatment of the pregnant dam with organic anion substrates, e.g., penicillin (Hirsch and Hook, 1970b), no experiments have been undertaken to induce the system and then examine cephaloridine transport. Nonetheless, it is very likely that an enhanced cephaloridine transport would occur under these circumstances. Finally, it is possible to demonstrate that inhibition of organic anion transport can block or dramatically reduce the toxicity produced by cephaloridine. If animals are pretreated with probenecid or large doses of PAH, the accumulation of cephaloridine by renal tissue is reduced, and along with that reduction there is diminished renal toxicity. The toxic response could be restored by the administration of very large doses of cephaloridine even in probenecid-treated animals. This suggests that the effect of probenecid was simply to produce a competitive blockade of cephaloridine transport.
A review of antibiotics and psoriasis: induction, exacerbation, and amelioration
Published in Expert Review of Clinical Pharmacology, 2019
Guttate psoriasis: an early preliminary study (n = 9) showed penicillin or erythromycin for 10–14 days plus rifampin in the last 5 days markedly improved psoriasis in chronic streptococcal carriers [47], but later a randomized controlled trial (n = 20) failed to reveal benefit from the combination treatment for guttate psoriasis [48].Plaque psoriasis: another age and gender-matched control trial (n = 80) evaluated the efficacy of penicillin V 250 mg, every 6 hours plus rifampin 600 mg per day for chronic plaque-type psoriasis. The result demonstrated no change of mean PASI score (15.92 vs. 15.19) pre- and post-antibiotics treatment. However, antibiotics use duration given in this study maybe too limited (only 10 days) to observe the differences. It could only be concluded that short-term combination of antibiotics played no role for plaque-type psoriasis in routine use [49].GPP: a case series (n = 7) showed six out of seven patients with GPP successfully treated by cloxacillin plus cephaloridine for 6 weeks. In this study, all patients had positive coagulase positive staphylococci in blood culture [50].
The effect of aspirin on antibiotic susceptibility
Published in Expert Opinion on Therapeutic Targets, 2018
Petra Zimmermann, Nigel Curtis
SAL influences all three of these mechanisms: it increases or decreases expression of OMPs and efflux pumps and increases the membrane potential. Consequently, intracellular concentrations of both hydrophilic and lipophilic antibiotics are altered with resulting marked increases or decreases in minimal inhibitory concentrations (MICs). These changes in MICs can occur at regular therapeutic plasma concentrations of SAL (1.1–2.2 mmol/L). For example, in Serratia marcescens, the MICs of ampicillin, cefotaxime and cephaloridine rise by 2–4 fold when grown in the presence of SAL at 1 mmol/L and the MIC of cefoxitin rises by 20-fold [7]. The MICs of other bacteria to a range of antibiotics are similarly increased when grown in the presence of therapeutic or supratherapeutic concentrations of SAL (summarized in Table 1) [8–14].
An update on adverse drug reactions related to β-lactam antibiotics
Published in Expert Opinion on Drug Safety, 2018
Konstantinos Z. Vardakas, Georgios D. Kalimeris, Nikolaos A. Triarides, Matthew E. Falagas
Although the currently available β-lactams are considered very safe from the renal point of view, serum β-lactam levels seem to be related to nephrotoxicity [20]. β-Lactams were associated with 55% of antibiotic-induced interstitial nephritis in a series of 133 cases of drug-induced interstitial nephritis; amoxicillin was the commoner cause of them [80]. Cases of interstitial nephritis had been described with methicillin and cephaloridine, both of which are no longer used in clinical practice or are not available in the market [6]. Dose-dependent interstitial nephritis has been reported with ampicillin, but the frequency is much lower than that of methicillin [6]; a rash usually accompanied the renal injury, suggesting an allergic reaction [81]. Nafcillin-treated patients had more adverse events than oxacillin-treated ones, especially hypokalemia and acute kidney injury; nafcillin was also discontinued more often than oxacillin [62]. Case reports attributing the development of interstitial nephritis to nafcillin [82], piperacillin/tazobactam [83–87], meropenem [84], ertapenem [88], cefepime [89], ceftazidime [90], ceftriaxone [91,92], and ceftaroline have been published [93]. Cases of nephritis have been reported even after prophylactic antibiotics, usually at high doses and coadministered with aminoglycosides [94].