"Dec. 24, 2012 -- Colorado Springs high school junior Morgan Smith can't remember a time when he didn't have life-threatening food allergies.
The 16-year-old had his first reaction to peanut butter at 9 months of age when he broke out in hiv"...
Triamcinolone acetonide is a more potent derivative of triamcinolone. Triamcinolone acetonide is approximately eight times more potent than prednisone in animal models of inflammation. The clinical significance of this is unclear.
Although the precise mechanism of corticosteroid antiallergic action is unknown, corticosteroids have been shown to have a wide range of effects on multiple cell types (e.g. mast cells, eosinophils, neutrophils, macrophages, and lymphocytes) and mediators (e.g. histamines, eicosanoids, leukotrienes, and cytokines) involved in inflammation.
The pharmacokinetics of triamcinolone acetonide solution was evaluated in a single-dose study conducted in 24 patients with perennial allergic rhinitis. Following a single intranasal dose of 400 mcg of triamcinolone acetonide (twice the recommended starting dose of triamcinolone acetonide solution), the mean Cmax of the drug was 1.12 ng/mL (SD =0.38) with a median Tmax of 0.5 hours (range: 0.08 - 1.0).
A pharmacokinetic study to demonstrate dose proportionality was conducted in patients with perennial allergic rhinitis. The Cmax and AUC of the 200 and 400 mcg doses increased less than proportionally when compared to the 100 mcg dose. Following multiple dosing (100 or 200 or 400 mcg QD for 7 days), there was no evidence of drug accumulation.
The volume of distribution (Vd) reported was 99.5 L (SD =27.5).
In animal studies using rats and dogs, three metabolites of triamcinolone acetonide have been identified. They are 6βhydroxytriamcinolone acetonide, 21-carboxytriamcinolone acetonide and 21-carboxy-6β-hydroxytriamcinolone acetonide. All three metabolites are expected to be substantially less active than the parent compound due to (a) the dependence of anti-inflammatory activity on the presence of a 21-hydroxyl group, (b) the decreased activity observed upon 6-hydroxylation, and (c) the markedly increased water solubility favoring rapid elimination. There appeared to be some quantitative differences in the metabolites among species. No differences were detected in metabolic pattern as a function of route of administration.
After a single intranasal dose of 400 mcg of triamcinolone acetonide (twice the recommended starting dose of triamcinolone acetonide solution), the mean observed elimination half-life was 2.26 hours (SD=0.77). Based upon intravenous dosing of triamcinolone acetonide phosphate ester, the half-life of triamcinolone acetonide was reported to be 88 minutes. The reported clearance was 45.2 L/hour (SD=9.1) for triamcinolone acetonide.
The effect of age, specifically in geriatric and pediatric patients, on the pharmacokinetics of triamcinolone acetonide has not been studied.
Gender did not significantly influence the pharmacokinetics of triamcinolone acetonide solution.
The effect of race on the pharmacokinetics of triamcinolone acetonide solution has not been studied.
No specific pharmacokinetic studies have been conducted in renally or hepatically impaired subjects.
No specific drug-drug interactions have been investigated.
A small (approximately 5 to 7 patients per treatment group), parallel trial was conducted to assess the effect of triamcinolone acetonide solution on the Hypothalamic-Pituitary-Adrenal (HPA) axis. Patients with allergic rhinitis were treated for six weeks with 400 mcg, 800 mcg, or 1600 mcg total daily doses of triamcinolone acetonide solution, 10 mg oral prednisone once daily, or placebo. Adrenal response to a six-hour cosyntropin stimulation test suggests that intranasal triamcinolone acetonide solution 400 mcg/day for
six weeks did not measurably affect adrenal activity. Triamcinolone acetonide solution treatment arms using doses of 800 and 1600 mcg/day demonstrated a trend toward dose-related suppression of HPA response. However, this decrease did not reach statistical significance, whereas 10 mg daily oral prednisone did.
The efficacy of triamcinolone acetonide solution has been evaluated in 746 patients with seasonal or perennial allergic rhinitis who completed 8 controlled clinical trials.
In total, 1187 patients have been treated with triamcinolone acetonide solution in the clinical development program. Three adequate and well controlled multi-center trials involving 541 patients with seasonal allergic rhinitis who received doses of triamcinolone
acetonide solution ranging from 50 mcg to 400 mcg once daily were conducted. These trials evaluated the total nasal symptom scores that included stuffiness, rhinorrhea, itching, and sneezing. The results showed that patients who received ≥ 200 mcg daily of the active drug had statistically significant relief in the total nasal symptom score compared to those receiving placebo.
In one clinical trial that examined efficacy after 2 days of 200 or 400 mcg triamcinolone acetonide solution treatment, only the 400 mcg dose showed statistically significant improvement over placebo in the nasal symptoms of seasonal allergic rhinitis.
Last reviewed on RxList: 2/24/2009
This monograph has been modified to include the generic and brand name in many instances.
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