Gough A W, Kasali O B, Sigler R E, Baragi V
Department of Pathology and Experimental Toxicology, Parke-Davis Pharmaceutical Research Division, Warner-Lambert Company, Ann Arbor, Michigan 48105.
Toxicol Pathol. 1992;20(3 Pt 1):436-49; discussion 449-50. doi: 10.1177/019262339202000313.
A class effect of quinolone antibacterial agents observed during animal toxicity testing is a specific arthropathy (QAP). Despite the growing list of laboratory animals susceptible to QAP and reports of arthralgia in patients treated with quinolones, the potential for QAP development in humans remains unknown. This review discusses current concepts in the biology of articular cartilage and how these concepts elucidate QAP pathogenesis. Biomechanical forces within synovial joints and toxicokinetic properties of quinolones contribute to QAP induction. Since a limited number of mechanistic pathways exist for acute articular damage, QAP may serve as a research tool to probe the pathobiology of injury to articular cartilage.
喹诺酮类抗菌药物在动物毒性试验中观察到的一种类效应是特定的关节病（喹诺酮类相关关节病，QAP）。尽管对喹诺酮类相关关节病易感的实验动物种类不断增加，且有使用喹诺酮类药物治疗的患者出现关节痛的报告，但喹诺酮类相关关节病在人类中发生的可能性仍不明确。本综述讨论了关节软骨生物学的当前概念，以及这些概念如何阐明喹诺酮类相关关节病的发病机制。滑膜关节内的生物力学力和喹诺酮类药物的毒代动力学特性促成了喹诺酮类相关关节病的诱发。由于急性关节损伤存在的机制途径有限，喹诺酮类相关关节病可能作为一种研究工具来探究关节软骨损伤的病理生物学。
