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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↗
PubMed2004

Regression of optic nerve head neovascularization in proliferative diabetic retinopathy after intravitreal triamcinolone. Regression of diabetic optic disc neovascularization after intravitreal triamcinolone.

The aim of this study is to report the clinical outcome of a diabetic patient with optic nerve head neovascularization treated with an intravitreal injection of triamcinolone acetonide. A 52-year-old patient presented with clinically significant diffuse macular edema and optic nerve head neovascularization due to proliferative diabetic retinopathy in her right eye. Despite grid laser photocoagulation in the macular region macular edema progressed and visual acuity declined. The patient received a single intravitreal injection of 4 mg triamcinolone acetonide with topical anesthesia. After injection of triamcinolone acetonide visual acuity increased and macular edema decreased. Furthermore optic nerve head neovascularization had markedly regressed. No complication was observed during follow-up period. Intravitreal injection of triamcinolone acetonide may be useful for treatment of optic nerve head neovascularization in patients with proliferative diabetic retinopathy.

Diabetic Retinopathy↗
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↗
PubMed2004

Comparison of the intraarticular effectiveness of triamcinolone hexacetonide and triamcinolone acetonide in treatment of juvenile rheumatoid arthritis.

OBJECTIVE: To compare patients with juvenile rheumatoid arthritis (JRA) injected with triamcinolone hexacetonide (TH) or triamcinolone acetonide (TA) with respect to time to relapse. METHODS: This was a retrospective chart review of 85 patients: 51 patients with JRA who had received a joint injection with TH during the period June 2000-April 2001 and 48 patients who had received a joint injection with TA during the period May 2001-March 2002 who were followed for a minimum of 15 months, after an intraarticular steroid injection. RESULTS: The primary endpoint variable for the study was the time to relapse of the arthritis in the affected joint following an intraarticular injection. A total of 227 joints were injected, 114 with TH and 113 with TA. In the TH group the mean time to relapse (+/- SE) was 10.14 +/- 0.49 months compared to the TA group at 7.75 +/- 0.49 months (p < 0.0001) using the log-rank test. A proportional hazards (Cox) regression analysis revealed no statistical association between sex, duration of illness, or type of arthritis and relapse time. An analysis was performed on the first intraarticular injection for each patient, with the average time to relapse for all joints injected of 10.36 +/- 0.72 months for TH compared to 8.45 +/- 0.78 months for TA (p < 0.02). A further analysis of the first knee injections showed a relapse time in the TH group of 11.11 +/- 0.81 months compared to 7.95 +/- 0.95 months for TA (p < 0.008). CONCLUSION: TH offers an advantage to TA, as there is a longer duration of action leading to an improved prolonged response rate in weight-bearing joints, particularly the knees. The results suggest that TH should be the intraarticular steroid of choice, particularly for the knee joint, in patients with JRA.

Adolescent↗
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↗
PubMed2006

Toxicity of triamcinolone acetonide on retinal neurosensory and pigment epithelial cells.

PURPOSE: To study the toxicity of triamcinolone acetonide (Kenalog; Bristol-Meyers Squibb, Princeton, NJ) on retinal pigment epithelial (ARPE-19) and retinal neurosensory (R28) cells. METHODS: ARPE-19 and R28 were grown in tissue culture in Dulbecco's modified Eagle's medium (DMEM) containing 10% fetal bovine serum. Cells were treated with 50, 100, and 200 microg/mL concentration of triamcinolone acetonide for 2, 6, and 24 hours. The cells were also treated with the steroid without the vehicle and with the vehicle alone, in which triamcinolone acetonide was suspended. Toxicity was determined by trypan blue dye-exclusion and WST-1 mitochondrial dehydrogenase assays. RESULTS: Vehicle alone did not reduce the viability of ARPE-19 or R28 cells and also did not affect the mitochondrial dehydrogenase activity of the cells. The mean cell viability of ARPE-19 and R28 cells after exposure to triamcinolone acetonide with vehicle 200 microg/mL for 24 hours was 70.7% +/- 10.61% and 75.35% +/- 12.42%, respectively compared with the untreated ARPE-19 (92.7% +/- 6.24%, P < 0.01) and R28 cells (90.63% +/- 5.62%, P < 0.001). The mean cell viability of ARPE-19 cells after exposure to triamcinolone acetonide (200 microg/mL) alone without the vehicle was 84.96% +/- 0.32%, 85.2% +/- 3.26%, and 84.73% +/- 2.71% at 2, 6, and 24 hours, respectively, compared with the untreated ARPE-19 cells (P < 0.001). The R28 cells exposed to triamcinolone acetonide (200 microg/mL) without the vehicle also had a significant reduction in the mean cell viability at 24 hours (86.42% +/- 3.87%, P < 0.001) and 6 hours (89.03% +/- 1.01%, P < 0.01). There was a significant reduction in the mitochondrial dehydrogenase activity in the ARPE-19 cells when treated with both triamcinolone acetonide, with or without the vehicle at a concentration of 200 microg/mL at all time points (P < 0.01). R28 cells did not have any significant reduction in mitochondrial dehydrogenase activity when treated with triamcinolone acetonide without the vehicle at any of the doses, but there was a significant reduction when the R28 cells were treated with triamcinolone acetonide with vehicle (200 microg/mL) for 24 hours (P < 0.05). Triamcinolone acetonide with vehicle caused a greater reduction in cell viability and mitochondrial dehydrogenase activity than did triamcinolone without vehicle, in both cell lines, although the difference was not statistically significant. CONCLUSIONS: Triamcinolone acetonide is toxic to proliferating cells of retinal origin in vitro at doses normally used in clinical practice. The vehicle by itself appears to be nontoxic to the cells, but may have a potentiating effect on the cytotoxicity of triamcinolone acetonide. The results of this in vitro study cannot be directly extrapolated to clinical practice, but, based on these data, further studies may be warranted.

Cell Culture Techniques↗
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↗