The Identification of Mivacurium and Metabolites In Biological Samples

Montgomery, Madeline A.; LeBeau, Marc A.; Miller, Mark L.; Jufer, Rebecca A.

doi:10.1093/jat/29.7.637

Cited by 5 publications

(1 citation statement)

References 12 publications

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“…29 It has a short duration of action ranging from 10 to 15 min in normal patients, because it undergoes rapid metabolism and deactivation via hydrolysis of its ester linkage by plasma cholinesterase enzyme (PChE). 30 Although it is well-established that mivacurium has a limited duration of action that allows patients to recover rapidly after the surgery and begin to breath normally, many reported cases have suffered from a prolonged action reaching up to 16 h. 31,32 It was found -after various investigations-that those people (poor metabolizers) have either genetically or acquired deficiency in PChE which is solely responsible for mivacurium metabolism. This prolonged action is a lifethreatening problem as mivacurium still causing respiratory muscles' paralysis and apnea, therefore, mechanically-assisted breathing must be carried out immediately.…”

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confidence: 99%

A Companion Diagnostic for Personalizing Mivacurium at the Point-of-Care

Abdel-Moety

Al-Alamein

Fawaz

et al. 2020

J. Electrochem. Soc.

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Mivacurium chloride is envisioned as the "gold-adjunct" in anesthesia and emergency medicine. People across the world are administered mivacurium in emergency situations as clinicians prefer it among the frequently used neuromuscular blockers thanks to its rapid action and short duration. Mivacurium is promptly degraded and deactivated by plasma cholinesterase enzyme (PChE), however during emergency situations, some individuals were found to be unable to metabolize mivacurium shortly after its injection, resulting in prolonged paralysis and potentially lethal respiratory apnea. The most clinically significant cause of this residual paralysis and apnea is the reduced cholinesterase ability to effectively hydrolyze mivacurium. Hitherto, monitoring of mivacurium enzymatic degradation has been remaining a long-standing challenge for analytical chemists as well as anesthesiologists. Firstly, it undergoes rapid hydrolysis by the PChE-enzyme 8 min post-injection, therefore, frequent sampling all through the first minutes after mivacurium administration is mandatory. Secondly, its isolation from biological specimens is extremely difficult due to its chemical properties which involves both hydrophilic and lipophilic characteristics. These challenges impede the development of a universal protocol to be established for screening of PChE-activity towards mivacurium and which clearly identifies patients susceptible to prolonged paralysis. In this study, we designed a point-of-care (PoC) potentiometric sensor that can perform tracking of mivacurium enzymatic degradation kinetics with high accuracy and rapidly. Real serum samples were utilized for in vitro estimation of the rate of mivacurium metabolism, where values of 227 μmol l −1 and 62 μM min −1 were obtained for the characteristic parameters of the enzymatic reaction, K m and V max , respectively. Correlation of the results obtained using the proposed approach and earlier LC-MS/MS study is shown.

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confidence: 99%