Myoclonus induced by amoxicillin-clavulanic acid

Viloria-Alebesque, Alejandro; Povar-Echeverría, Marina; Bruscas-Alijarde, María Jesús; Gracia-Gutiérrez, Anyuli; Royo-Trallero, Leticia; Al-Cheikh-Felices, P.

doi:10.1016/j.ebr.2020.100367

Cited by 2 publications

(1 citation statement)

References 9 publications

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“…Clinical symptoms related to AMX or ampicillin have already been described in clinical studies, such as myoclonia [ 12 ], delirium onset [ 13 ] (with a 95% confidence interval odds ratio of 2.13–9.45 for the ampicillin sulbactam combination), convulsions [ 14 ], and behavioral changes [ 15 ]. These data are supported by animal models with evidence for epileptogenicity and a depression-like response following direct intraventricular injections [ 4 ].…”

Section: Discussionmentioning

confidence: 99%

Amoxicillin-Induced Neurotoxicity: Contribution of a Healthcare Data Warehouse to the Determination of a Toxic Concentration Threshold

et al. 2023

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Background: Amoxicillin (AMX)-induced neurotoxicity is well described and may be associated with AMX overexposure. No neurotoxic concentration threshold has been determined thus far. A better knowledge of maximum tolerable AMX concentrations is of importance to improve the safety of high doses of AMX. Methods: We conducted a retrospective study using the local hospital data warehouse EhOP® to generate a specific query related to AMX neurotoxicity symptomatology. All patient medical reports containing a mention of neurotoxicity clinical symptoms coupled with AMX plasma concentration measurements were explored. Patients were classified into two groups according to the imputability of AMX in the onset of their neurotoxicity, on the basis of chronological and semiological criteria. A receiver-operating characteristic curve was performed to identify an AMX neurotoxic steady-state concentration (Css) threshold. Results: The query identified 101 patients among 2054 patients benefiting from AMX TDM. Patients received a median daily dose of 9 g AMX, with a median creatinine clearance of 51 mL/min. A total of 17 of the 101 patients exhibited neurotoxicity attributed to AMX. The mean Css was higher for patients with neurotoxicity attributed to AMX (118 ± 62 mg/L) than those without 74 ± 48 mg/L (p = 0.002). A threshold AMX concentration of 109.7 mg/L predicted the occurrence of neurotoxicity. Conclusions: This study identified, for the first time, an AMX Css threshold of 109.7 mg/L associated with an excess risk of neurotoxicity. This approach needs to be confirmed by a prospective study with systematic neurological evaluation and TDM.

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Section: Discussionmentioning

confidence: 99%

Amoxicillin-Induced Neurotoxicity: Contribution of a Healthcare Data Warehouse to the Determination of a Toxic Concentration Threshold

et al. 2023

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Amoxicillin/clavulanic-acid

2020

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Previous studies have demonstrated that Nocardia brasiliensis is susceptible to amoxicillin-clavulanic acid and that its I8-lactamases are inhibited in vitro by, clavulanic acid. A cardiac transplant patient with disseminated infection caused by N. brasiliensis was treated with this drug combination with good response, but relapsed while still on therapy. The relapse isolate was found to be identical to the initial isolate by using genomic DNA restriction fragment patterns obtained by pulsed field gel electrophoresis, but it was resistant to amoxicillin-clavulanic acid. On isoelectric focusing, the ,I-lactamase from the relapse isolate exhibited a shift in the isoelectric point (pl) of its major band from 5.10 to 5.04 compared with the enzyme from the pretreatment isolate. As determined by using values of the amount of ,-lactamase inhibitor necessary to give 50 5% inhibition of P-lactamase-mediated hydrolysis of 50 FM nitrocefin, the I8-lactamase of the relapse isolate was also 200-fold more resistant than the enzyme from the pretreatment isolate to clavulanic acid and was more resistant to sulbactam, tazobactam, cloxacillin, and imipenem. The I-lactamase of the relapse isolate exhibited a 10-fold decrease in hydrolytic activity for cephaloridine and other hydrolyzable cephalosporins compared with that for nitrocefin. Acquired resistance to amoxicillin-clavulanic acid in this isolate of N. brasiliensis appears to have resulted from a mutational change affecting the inhibitor and active site(s) in the

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Myoclonus induced by amoxicillin-clavulanic acid

Cited by 2 publications

References 9 publications

Amoxicillin-Induced Neurotoxicity: Contribution of a Healthcare Data Warehouse to the Determination of a Toxic Concentration Threshold

Amoxicillin-Induced Neurotoxicity: Contribution of a Healthcare Data Warehouse to the Determination of a Toxic Concentration Threshold

Amoxicillin/clavulanic-acid

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