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Pharmacokinetics of intra-articular, intravenous, and intramuscular administration of triamcinolone acetonide and its effect on endogenous plasma hydrocortisone and cortisone concentrations in horses

Lawrence R. Soma, VMD; Cornelius E. Uboh, PhD; Yowen You, PhD; Fuyu Guan, PhD; Raymond C. Boston, PhD American Journal of Veterinary Research September 2011 72 9 1234-1242
Objective—To compare pharmacokinetics of triamcinolone acetonide (TA) following IV, intra-articular (IA), and IM administration and determine its effect on plasma concentrations of hydrocortisone and cortisone. Animals—6 Thoroughbreds. Procedures—TA (0.04 mg/kg) was administered IV, IM, or IA, and plasma TA, hydrocortisone, and cortisone concentrations were determined. Results—IV administration of TA was fitted to a 2-compartment model. Median distribution half-life was 0.50 hours (range, 0.24 to 0.67 hours); elimination half-life was 6.1 hours (range, 5.0 to 6.4 hours). Transfer half-life of TA from joint to plasma was 5.2 hours (range, 0.49 to 73 hours); elimination half-life was 23.8 hours (range, 18.9 to 32.2 hours). Maximum plasma concentration following IA administration was 2.0 ng/mL (range, 0.94 to 2.5 ng/mL), and was attained at 10 hours (range, 8 to 12 hours). Maximum plasma concentration following IM administration was 0.34 ng/mL (range, 0.20 to 0.48 ng/mL) and was attained at 13.0 hours (range, 12 to 16 hours); concentration was still quantifiable at 360 hours. Hydrocortisone plasma concentrations were significantly different from baseline within 0.75, 2, and 1 hours after IV, IA, and IM administration, respectively, and remained significantly different from baseline at 96 and 264 hours for IV and IA administration. Following IM administration of TA, plasma concentrations of hydrocortisone did not recover to baseline concentrations by 360 hours. Conclusions and Clinical Relevance—Pharmacokinetics of TA and related changes in hydrocortisone were described following IV, IA, and IM administration. A single administration of TA has profound effects on secretion of endogenous hydrocortisone.

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