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At least 19 recordsLinked to original sources
PubMed1992

Synovial and serum levels of triamcinolone following intra-articular administration of triamcinolone acetonide in the horse.

Seven mature thoroughbred horses, weighing between 400 and 541 kg, were each injected intra-articularly into three joints with 6 mg/joint of triamcinolone acetonide (Vetalog). The fourth joint, the control, was injected with saline. Synovial fluid was taken from all four legs of the horses on days 1, 2, 3, 4, 5, 6, 7, 8, 11, and 15 following the injections. Triamcinolone acetonide was assayed by a radioimmunoassay. Blood was collected at 1, 2, 4, 6, 12 h and on days 1, 2, 3, 4, 5, 6, 7, 8, 11, and 15 following injection of either triamcinolone or saline. Both cortisol and triamcinolone were assayed. The results show that the synovial fluid level of triamcinolone was 7.5 micrograms/ml 1 day following treatment and decreased to 10 ng/ml by the 4th day. These low levels were maintained for approximately 14 days. By the 15th day, the triamcinolone was below a detectable level. Serum levels of triamcinolone increased to 3 ng/ml within 1 h and further increased to a peak of 4.3 ng/ml at 4th h. The level then decreased to 2 ng/ml at 24 h and to nearly an undetectable level in 48 h. The mean level of serum cortisol, on the other hand, gradually decreased as the serum level of triamcinolone increased. As the serum level of triamcinolone reached an undetectable level on the 2nd day, the serum cortisol level gradually increased and returned to the pre-administration level by the 5th day. These results showed that the intra-articular administration of triamcinolone maintained triamcinolone in the synovial fluid for 4-14 days and that the triamcinolone reached the blood within 1 h. The serum level of triamcinolone was maintained for 2 days and resulted in the inhibition of adrenal function for 4 days.

Animals↗
PubMed1983

Comparative teratogenicity of triamcinolone acetonide, triamcinolone, and cortisol in the rat.

Pregnant rats were injected im with 0.5 mg/kg triamcinolone acetonide (TAC) on day 12, 13, or 14 of gestation and the fetuses were examined for cleft palate on day 20. All three TAC-treated groups showed an increased proportion of fetuses with cleft palate compared to an untreated control group. Only the group treated on day 13 showed a significant increase in the proportion of litters affected. This indicates that day 13 of gestation is the most sensitive day for cleft palate induction by TAC in the rat. Pregnant rats were then treated on day 13 of gestation with either TAC, triamcinolone (TA), or cortisol. TAC was 59 times as potent as TA in inducing cleft palate, with ED50 values of 1.1 mg/kg and 65 mg/kg respectively. Cortisol induced a significant increase in cleft palates at 500 mg/kg, but the efficacy of this compound was too low to calculate an ED50 and relative teratogenic potency value. Other developmental abnormalities including umbilical hernias, resorption, and fetal death resulted from TAC treatment. Fetal growth retardation was produced by all three compounds. The rank order of teratogenic potency was determined to be TAC greater than TA greater than cortisol.

Animals↗
PubMed1986

The effect of preoperative subconjunctival triamcinolone administration on glaucoma filtration. I. Trabeculectomy following subconjunctival triamcinolone.

Trabeculectomies were performed on 15 eyes because of uncontrolled glaucoma despite the maximum use of tolerated antiglaucoma medication. We considered all of these eyes to be at increased risk for episcleral cicatricial closure for one of the following reasons: neonatal glaucoma, a patient of age 40 years or less, previously failed glaucoma filtration surgery, or aphakia. A standard operation was performed except that triamcinolone acetonide (4 mg) was injected subconjunctivally at the intended trabeculectomy site one week before surgery in 12 eyes, the day of surgery in two eyes, and two days prior to surgery in one eye. During the follow-up period of six to 16 months, 14 of 15 eyes had an intraocular pressure (IOP) of 18 mm Hg or less. The average IOP for these 14 eyes was 12.4 +/- 4.6 (mean +/- 1 SD), and only three of the 14 required any antiglaucoma medication. One eye was a surgical failure. All eyes with controlled IOP had diffuse microcystic filtration blebs by slitlamp examination. The postoperative visual acuity was within one line of the preoperative level in all eyes, except for the one failure. The use of triamcinolone did not appear to add any additional risks to the surgical procedure or to the postoperative period.

Adult↗
PubMed2003

Comparison of intra-articular triamcinolone hexacetonide and triamcinolone acetonide in oligoarticular juvenile idiopathic arthritis.

OBJECTIVE: To compare the efficacy and safety of intra-articular triamcinolone hexacetonide (TH) and triamcinolone acetonide (TA) in children with oligoarticular juvenile idiopathic arthritis (JIA). METHODS: One hundred and thirty joints of 85 patients undergoing intra-articular injections were randomly treated with either TH or TA depending on the availability of the drug. The efficacy of both treatments was evaluated prospectively in a blinded fashion. A good response was defined as a decrease in the articular score of > or =60% from baseline. Clinical, laboratory and immunological variables were noted in order to examine possible factors, other than treatment, predictive of the result. RESULTS: Seventy injections were performed using TH and 60 with TA. The two groups were comparable for clinical, immunological and laboratory characteristics. The rate of response was significantly higher with TH than with TA: 81.4% vs 53.3% (P = 0.001) at 6 months, 67.1 vs 43.3% (P = 0.006) at 12 months, and 60 vs 33.3% (P = 0.002) at 24 months. CONCLUSION: At comparable doses TH appeared to be much more effective than TA for intra-articular use, in both short- and long-term follow-up. This result was not affected by disease duration or degree of local and systemic inflammation.

Administration, Topical↗
PubMed2003

Submacular deposition of triamcinolone acetonide after triamcinolone-assisted vitrectomy.

PURPOSE: We describe a case demonstrating a submacular deposition of triamcinolone acetonide (TA) after a TA-assisted vitrectomy for retinal detachment. DESIGN: Interventional case report. METHODS: A 48-year-old Japanese man with rhegmatogenous retinal detachment in his left eye underwent a TA-assisted vitrectomy, endolaser photocoagulation, and sulfur hexafluoride (SF(6)) gas tamponade. RESULTS: At the end of the surgery and the day after undergoing vitrectomy, the deposition of TA was observed between the retinal pigment epithelium and neurosensory retina in the submacular area. These TA granules disappeared after 2 weeks. Two months after the operation, the retina was observed to be successfully attached and no abnormality was observed in the macula. The patient's visual acuity improved to 20/16, and no ophthalmoscopic or functional damage was observed. CONCLUSION: No apparent adverse effect was found in this case demonstrating a submacular deposition of TA.

Fluorescein Angiography↗
PubMedDate not supplied

Tri-Nasal triamcinolone acetonide nasal spray 200 and 400 micrograms qd versus placebo and Nasacort triamcinolone acetonide nasal aerosol 440 micrograms qd in patients suffering from seasonal allergic rhinitis during the grass season.

Tri-Nasal Nasal Spray is an investigational solution of triamcinolone acetonide (TAA) currently being evaluated as a treatment for allergic rhinitis. The safety and efficacy of 200 and 400 micrograms once daily doses of Tri-Nasal Nasal Spray, an active control (440 micrograms once daily of Nasacort Nasal aerosol), and Tri-Nasal Nasal Spray placebo were compared over a 2-week treatment period in a double-blind (the Nasacort treatment was not blinded), parallel design trial. A total of 377 adult patients in 13 centers were enrolled during the grass pollen season. The primary efficacy variable was the weekly average of the SSI (Symptom Severity Index), the sum of daily nasal congestion, rhinorrhea, and sneezing severity scores from the patient diary. A total of 355 patients completed the study. All active treatments were significantly more effective than placebo in relieving nasal symptoms at each treatment week. The 400 micrograms Tri-Nasal Nasal Spray and Nasacort treatments had a rapid onset of action, demonstrating significant improvement in the SSI versus placebo by the second day of treatment. Results for the individual nasal symptoms and other secondary efficacy measures paralleled those of the primary efficacy variables. Tri-Nasal Nasal Spray and Nasacort were comparable in safety, and in treating the nonocular symptoms of seasonal allergic rhinitis.

Administration, Intranasal↗
PubMed2000

A mass balance study to evaluate the biotransformation and excretion of [14C]-triamcinolone acetonide following oral administration.

The principle objective of this study was to characterize the absorption, metabolism, and disposition of orally administered [14C]-triamcinolone acetonide. Six healthy male subjects each received a single 100 microCi (approximately 800 micrograms) oral dose of [14C]-triamcinolone acetonide. Plasma, urine, and fecal samples were collected at selected times and analyzed for triamcinolone acetonide and [14C]-derived radioactivity. Plasma protein binding of triamcinolone acetonide was also determined. Metabolite profiling and identification were carried out in plasma and excreta. Principle metabolites were assessed for activity with in vitro anti-inflammatory models. [14C]-triamcinolone acetonide was found to be systemically absorbed following oral administration. The presystemic metabolism and clearance of triamcinolone acetonide were extensive, with only a small fraction of the total plasma radioactivity being made up of triamcinolone acetonide. Little to no parent compound was detected in the plasma 24 hours after administration. Most of the urinary and fecally [14C]-derived radioactivity was also excreted within 24 and 72 hours postdose, respectively. Mean plasma protein binding of triamcinolone acetonide was constant, predictable, and a relatively low 68% over a 24-fold range of plasma concentrations. Three principle metabolites of triamcinolone acetonide were profiled in plasma, urine, and feces. These metabolites were identified as 6 beta-hydroxy triamcinolone, 21-carboxylic acid triamcinolone acetonide, and 6 beta-hydroxy-21-oic triamcinolone acetonide. All three metabolites failed to show any concentration-dependent effects in anti-inflammatory models evaluating IL-5-sustained eosinophil viability and IgE-induced basophil histamine release.

Administration, Oral↗
PubMed1997

Triamcinolone acetonide. A review of its pharmacological properties and therapeutic efficacy in the management of allergic rhinitis.

Triamcinolone acetonide is a synthetic glucocorticoid which has been formulated as both an aerosol and an aqueous metered-dose pump spray for nasal inhalation in the treatment of allergic rhinitis. Nasally administered triamcinolone acetonide is not significantly absorbed into the systemic circulation and does not suppress hypothalamic-pituitary-adrenal (HPA) axis function at therapeutic dosages. Clinical trials with either formulation have shown that once-daily triamcinolone acetonide 110 to 220 micrograms reduces symptoms of allergic rhinitis within the first day of administration. Once symptoms are under control, the dosage of aqueous triamcinolone acetonide may be reduced from 220 to 110 micrograms/day without loss of effect. Both aqueous and aerosol formulations of triamcinolone acetonide are significantly more effective in relieving symptoms and reducing nasal eosinophil influx than placebo. Once-daily intranasal triamcinolone acetonide 220 micrograms/day produced similar reductions from baseline in nasal symptoms of allergic rhinitis, when measured both subjectively (visual analogue scales) and objectively (anterior rhinomanometry), to those seen with beclomethasone 84 to 168 micrograms twice daily, fluticasone 200 micrograms once daily or flunisolide 100 micrograms twice daily for 3 to 12 weeks. Furthermore, triamcinolone acetonide aerosol 220 micrograms/day was significantly more effective at reducing the nasal symptoms of allergic rhinitis than the oral antihistamines loratadine and astemizole (both 10mg daily) and was equally as effective in reducing the associated ocular symptoms. The use of intranasal triamcinolone acetonide and oral loratadine in combination did not confer any additional advantage over triamcinolone acetonide alone. Triamcinolone acetonide [110 to either 220 micrograms/day (aqueous) or 440 micrograms/day (aerosol)] was well tolerated in clinical trials; headache and epistaxis were the only adverse events considered possibly or probably related to aerosol therapy in a 1-year study (110 to 440 micrograms/day). Therefore, in accordance with the recommendations from the International Rhinitis Management Working Group regarding the use of nasal glucocorticoids, triamcinolone acetonide may be considered a first-line therapy option in adults with moderately severe seasonal allergic rhinitis with predominantly nasal symptoms and also in children and adult patients with perennial allergic rhinitis.

Adult↗
PubMed2003

[Treatment of oedematous, proliferative and neovascular diseases by intravitreal triamcinolone acetonide].

BACKGROUND: Recent studies have suggested that intravitreal triamcinolone acetonide may be a therapeutical possibility for treating of various intraocular neovascular, oedematous and proliferative diseases. METHODS AND RESULTS: Gain in visual acuity was relatively highest for eyes with intraretinal oedematous diseases such as diffuse diabetic macular oedema and various types of cystoid macular oedema due to reasons such as retinal venous occlusions and uveitis. Intravitreal triamcinolone may be useful as angiostatic therapy in eyes with iris neovascularisation and proliferative ischaemic retinopathies. Possibly, intravitreal triamcinolone may be helpful for exudative age-related macular degeneration. In eyes with chronic therapy resistant ocular hypotony, intravitreal triamcinolone can induce an increase in intraocular pressure. The role of intravitreal triamcinolone as adjunctive treatment of proliferative vitreoretinopathy has not been determined so far. Complications of intravitreal triamcinolone include secondary ocular hypertension in about 50 % of the eyes injected, with one per cent of the eyes necessitating antiglaucomatous filtrating surgery; a cataractogenic effect; and postoperative infectious endophthalmitis. Long-term studies of more than 3 years follow-up have been missing so far, so that there is no reliable information on long-term complications. The injection can be combined with cataract surgery. Cataract surgery performed some months after the injection did not show a markedly elevated rate of complications. If vision increases after the intravitreal triamcinolone injection, the injection can be repeated. The duration of the effect of a single intravitreal injection of triamcinolone ranges between 2 and 9 months. Triamcinolone acetonide was detected in the aqueous humour nine months after an intravitreal injection of 25 mg. CONCLUSIONS: Intravitreal triamcinolone acetonide may offer a possibility for adjunctive treatment of intraocular oedematous, neovascular and proliferative diseases.

Angiogenesis Inhibitors↗
PubMed1994

Effect of triamcinolone on parathyroid hormone-stimulated second messenger systems and phosphate transport in opossum kidney cells.

Although PTH is known to stimulate both the adenylate cyclase/protein kinase-A system and the phospholipase-C/protein kinase-C second messenger systems, the relative roles of these second messenger pathways remain unclear. The present studies were designed to examine the effect of triamcinolone on PTH-stimulated second messenger systems and phosphate transport in confluent cultures of opossum kidney cells. Triamcinolone was added to these cultures at a concentration of 10 nM for 24-48 h. Neither cell number nor protein content was changed by this treatment. The addition of triamcinolone did not alter PTH receptor binding or competitive displacement radioligand binding assay curves. PTH-stimulated cAMP generation and activation of protein kinase-A were not altered by triamcinolone. The glucocorticoid, however, increased basal phosphate uptake from 1.0 +/- 0.1 to 1.28 +/- 0.1 pmol/5 min.culture (P < 0.01). Phosphate transport was significantly decreased by PTH (0.01 nM) in the triamcinolone-treated cultures, but not in control cultures. Phosphate uptake in the presence of maximal doses of PTH was similar in both control and triamcinolone-treated cultures. Thus, the PTH-responsive component of phosphate transport was preserved, and the threshold dose for the effect of PTH was reduced after treatment with triamcinolone. Studies were then performed to evaluate the alternate second messenger pathway. In control cultures, PTH rapidly increased the level of diglyceride mass, as measured by diglyceride kinase assay, from 0.18 +/- 0.01 to a peak of 0.26 +/- 0.02 mol/100 mol total phospholipid (P < 0.002), 1 min after addition of the hormone. Triamcinolone pretreatment for 48 h, however, elevated the basal diglyceride levels, but the increase after the addition of PTH was totally abolished. The absence of an increase in diglyceride upon stimulation with PTH correlated with elimination of the PTH-stimulated increase in the activity of particulate protein kinase-C. Thus, in triamcinolone-treated cells, the effect of PTH on phosphate transport was preserved, and the threshold dose of PTH-induced alteration in phosphate transport was reduced in the absence of stimulation of this alternate second messenger pathway. These data show that triamcinolone in opossum kidney cells does not alter PTH activation of the cAMP/protein kinase-A system, but eliminates the increase in diglyceride and the activation of protein kinase-C in response to PTH. These studies emphasize the major role of the protein kinase-A system in the regulation of phosphate transport by PTH.

1-Methyl-3-isobutylxanthine↗
PubMed1985

Triamcinolone acetonide regulates glucocorticoid-receptor levels by decreasing the half-life of the activated nuclear-receptor form.

Glucocorticoid-receptor activation in GH1 cells results from the conversion of a 10 S oligomeric cytosolic form to a 4-5 S nuclear-binding species (Raaka, B. M., and Samuels, H. H. (1983) J. Biol. Chem. 258, 417-425). In this study, we report that triamcinolone acetonide (9 alpha-fluoro-11 beta, 16 alpha, 17 alpha, 21-tetrahydroxypregna-1,4-diene-3,20-dione 16,17-acetonide) elicits a time- and dose-dependent reduction of total-cell (nuclear + cytoplasmic) receptor. The mechanism of receptor regulation was studied by dense amino acid labeling of receptor using media containing 2H, 13C, and 15N-labeled amino acids. Total cell receptor was extracted with 0.4 M KCl and newly synthesized dense receptor was separated from pre-existing receptor of normal density by centrifugation in gradients of 15-30% sucrose (w/v) in D2O. Receptor levels in cells grown without [3H]triamcinolone acetonide was 260 +/- 19 fmol/100 micrograms of DNA (16,000 molecules/cell), and, with 10 nM [3H]triamcinolone acetonide, this decreased to 130 +/- 14 fmol/100 micrograms of DNA after 30 h. Receptor half-life was 19 +/- 1.9 h in the absence and 9.5 +/- 0.3 h in the presence of triamcinolone acetonide and accounted for the decrease in steady-state receptor levels. Receptor synthesis was 9.7 +/- 0.3 fmol/100 micrograms of DNA/h (580 molecules/cell/h) both in the presence and absence of 10 nM [3H]triamcinolone acetonide. Triamcinolone acetonide reduced the half-life in proportion to the extent of receptor occupancy and activation. During the approach to steady-state conditions, 10 nM [3H]triamcinolone acetonide shortened receptor half-life almost immediately to the value in cells grown with [3H]triamcinolone acetonide for 24 h or longer. Cycloheximide did not prevent the triamcinolone acetonide-mediated decrease in receptor half-life and the shortening of receptor half-life is rapidly reversed by removal of hormone. These studies support a model of receptor regulation in which triamcinolone acetonide converts the unactivated 10 S receptor to the activated 4-5 S form which is degraded at an increased rate by the cell.

Animals↗