Juvenile canine drug-induced arthropathy: Clinicopathological studies on articular lesions caused by oxolinic and pipemidic acids
References (11)
Primary lesion in osteoarthrosis
Lancet
(1977)- et al.
Arthropathy induced by antibacterial fused n-alkyl-4-pyridone-3-carboxylic acids
Toxicol. Lett.
(1977) - et al.
Antibacterial drugs today. I
Drugs.
(1975) - et al.
Cinoxacin induced arthropathy in juvenile beagle dogs
Toxicol. Appl. Pharmacol.
(1979) The reaction of articular cartilage to injury and osteoarthritis
N. Engl. J. Med.
(1974)
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Cutaneous infectious diseases: Kids are not just little people
2015, Clinics in DermatologyCitation Excerpt :Fluoroquinolones are an important class of antimicrobials, given their broad spectrum of activity (including gram-negative, gram-positive, and atypical organisms), good tissue penetration, and oral bioavailability42,43; however, their use in children is generally discouraged ,given the arthropathy seen in juvenile animals in experimental trials.44 Preclinical studies of quinolones in juvenile beagle dogs revealed articular cartilage damage in weight-bearing joints.45–47 There have been reports of elderly patients developing quinolone-associated tendinitis and tendon rupture, most commonly in the Achilles tendon.46,48
TNF/TNFR<inf>1</inf> pathway and endoplasmic reticulum stress are involved in ofloxacin-induced apoptosis of juvenile canine chondrocytes
2014, Toxicology and Applied PharmacologyCitation Excerpt :Therefore, research on QN chondrotoxicity is helpful for clinical risk evaluation of QNs or for strategies to prevent adverse effects associated with these valuable antimicrobials. In regard to the chondrotoxicity of QNs, some researchers believed that QNs suppressed the activities of DNA topoisomerase of chondrocytes, and interfered with the synthesis and decomposition of cartilage substances such as glycosaminoglycan, collagen and protein (Gough et al., 1979). Later, studies showed that QN-induced chondrotoxicity was characterized by chondrocyte apoptosis (Lim et al., 2008; Sheng et al., 2007).
Ofloxacin induces apoptosis via β1 integrin-EGFR-Rac1-Nox2 pathway in microencapsulated chondrocytes
2013, Toxicology and Applied PharmacologyCitation Excerpt :Among the toxicities of QNs, one major disadvantage is their chondrotoxicity potential in juvenile animals, such as rats (Kato and Onodera, 1988), dogs (Burkhardt et al., 1992), rabbits (Machida et al., 1990), nonhuman primates (Stahlmann et al., 1990), and others (Gough et al., 1992). This toxicity is manifest as lameness, blistering, ulcerative erosion, or cavitation of the articular cartilage of the weight-bearing joints and chondrocyte loss and matrix degeneration (Gough et al., 1979; Kato and Onodera, 1988). Dosage needed to induce cartilage damage in juvenile dogs falls in the therapeutic range.
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