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Abstract
Objectives The aim of this study was to evaluate the effect of amikacin (AK) and enrofloxacin (EF) at concentrations consistent with those obtained by intra-articular and intravenous regional limb perfusion on both cytotoxicity and prostaglandin E2 (PGE2) production by equine chondrocytes. This study also determines if PGE2 production could be reduced by avocado/soybean unsaponifiables (ASU), glucosamine (GLU) and chondroitin sulphate (CS). Study Design Chondrocytes were grown in monolayer from the articular cartilage of 12 horses and treated with clinically relevant concentrations of AK and EF, with or without the combination of ASU + GLU + CS. Positive controls consisted of chondrocytes that were activated with lipopolysaccharide (LPS). Chondrocyte response was evaluated using both MTT cytotoxicity assay and immunoassay for PGE2 production. Results Amikacin and EF generated a dose-dependent cytotoxicity. Amikacin induced 90% cell death at a concentration of 25 mg/mL. Enrofloxacin induced 90% cell death at 1.0 mg/mL and 98% cell death at 10 mg/mL (p < 0.05). Amikacin failed to induce PGE2 production at any of the concentrations studied. In contrast, EF and the positive control (LPS) induced PGE2 production at all concentrations. Induction of PGE2 by EF at all concentrations was significantly reduced (p < 0.05) by pre-treatment with ASU + GLU + CS. Conclusions and Clinical Relevance Horses receiving commonly used dosages of AK and EF may benefit from administration of ASU + GLU + CS.
Highlights
Horses often receive antibiotic medications via intra-articular administration and intravenous regional limb perfusion (IVRLP) for the prevention and treatment of septic arthritis.[1]
Relevance Horses receiving commonly used dosages of AK and EF may benefit from administration of avocado/soybean unsaponifiables (ASU) þ GLU þ chondroitin sulphate (CS)
Taintor and colleagues demonstrated that 500 mg of AK administered into a normal joint ($50 mg AK per mL joint fluid at onset) maintains the AK concentration above the minimum inhibitory concentration (MIC) for most equine pathogens (i.e. 4 μg/mL) for 72 hours, but when the same dose is administered into an inflamed joint, the concentration is maintained above MIC for only 48 hours.[6]
Summary
Horses often receive antibiotic medications via intra-articular administration and intravenous regional limb perfusion (IVRLP) for the prevention and treatment of septic arthritis.[1] The effect of the higher antibiotic concentrations achieved by these routes has been associated with chondrocyte death.[2] Chondrocyte death from antibiotic medication use in cartilage explants has been reduced with simultaneous corticosteroid administration.[2] The use of nutraceuticals to minimize the negative impact of antibiotic medications at these higher concentrations has not been studied. One study demonstrated a median Cmax for AK by IVRLP of the distal interphalangeal joint of 600 μg/mL with a range of 37 to 2,400 μg/mL.[9] AK appears to have no gross inflammatory effect when administered via regional limb perfusion,[8] this is not true when the AK is repetitively administered via multiple intra-articular injections.[10] treatment of cartilage explants with AK results in an increase in chondrocyte death.[2]
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