关节内反复给药阿米卡星对健康马滑液血清淀粉样蛋白A、总蛋白和有核细胞计数的影响。

A F Sanchez Teran, L M Rubio-Martinez, N F Villarino, M G Sanz
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引用次数: 41

摘要

进行研究的原因:滑液中的血清淀粉样蛋白A (SAA)最近被用作马脓毒性关节炎的标志物,但反复关节内(IA)给药阿米卡星对滑液中SAA浓度的影响尚不清楚。目的:观察阿米卡星反复注射对正常马关节滑液SAA、总蛋白(TP)、有核细胞计数(NCC)及差异NCC的影响。方法:对5匹临床健康马进行对照、2期交叉研究。每个腕间关节每48 h接受2种治疗中的1种,连续5次:单独关节穿刺(对照组)或关节穿刺联合阿米卡星500 mg(治疗组)。每日进行临床及跛行检查。测定血清SAA、滑膜SAA、TP、NCC及差异NCC,并进行统计学比较。P < 0.05为显著性水平。结果:在整个研究过程中,马保持健康和无跛足。各组间所有变量的基线值无显著差异。第一个样品后,治疗组TP值显著高于对照组(P < 0.05)。第一次取样后,两组NCC均显著升高(P < 0.05)。差异性NCC未发现显著变化。在两组中,所有滑膜和大部分血清SAA浓度均低于定量下限。结论:反复服用阿米卡星引起滑液中TP和NCC值升高,其中一些TP浓度在脓毒性关节炎的范围内。相比之下,两组滑膜SAA浓度均未增加。潜在相关性:在评估先前取样或使用阿米卡星治疗的关节时,滑膜SAA可作为比TP和NCC更可靠的标志物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effects of repeated intra-articular administration of amikacin on serum amyloid A, total protein and nucleated cell count in synovial fluid from healthy horses.

Reasons for performing study: Serum amyloid A (SAA) in synovial fluid has recently been used as a marker for septic arthritis in horses but the effects of repeated intra-articular (IA) administration of amikacin on synovial SAA concentrations are unknown.

Objectives: To report the effect of repeated IA administration of amikacin on SAA, total protein (TP), nucleated cell count (NCC) and differential NCC in synovial fluid of healthy equine joints.

Methods: A controlled, 2 period crossover study was performed on 5 clinically healthy horses. Each intercarpal joint received one of 2 treatments every 48 h for 5 consecutive times: arthrocentesis alone (control group) or arthrocentesis combined with IA administration of 500 mg of amikacin (treatment group). Clinical and lameness examinations were performed daily. Serum SAA and synovial SAA, TP, NCC and differential NCC were measured and statistically compared. Significance level was set at P < 0.05.

Results: Horses remained healthy and nonlame throughout the study. Baseline values for all variables were not significantly different between groups. Values for TP in the treatment group were significantly higher than in the control group after the first sample (P < 0.05). In both groups NCC increased significantly (P < 0.05) after the first sample. No significant changes were identified in differential NCC. In both groups, all synovial and most serum SAA concentrations remained below the lower limit of quantification.

Conclusions: Repeated IA administration of amikacin caused increased values of TP and NCC in synovial fluid, with some TP concentrations falling within the range reported for septic arthritis. In contrast, synovial SAA concentrations did not increase in either group.

Potential relevance: Synovial SAA could serve as a more reliable marker than TP and NCC when evaluating a joint previously sampled or treated with amikacin.

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