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Effects of triamcinolone on brain and cerebrospinal fluid apolipoprotein E levels in rats.

Chiba H, Akita H, Hui SP, Takahashi Y, Nagasaka H, Fuda H, Kobayashi K.

Department of Laboratory Medicine, Hokkaido University School of Medicine, Sapporo, Japan. chibahit med.hokudai.ac.jp

The effects of the short term administration of triamcinolone (0.5 mg per 100 g body weight, 5 days) on apolipoprotein E and A-I concentrations in cerebrospinal fluid (CSF), brain extract and serum were studied in male Wistar rats using enzyme immunoassays. ApoE was significantly increased by triamcinolone in apoE-rich HDL1 in serum; 40+/-13 (mean+/-SD) vs. 68+/-23 mg/dl (15 saline-treated rats vs. 11 triamcinolone-treated rats)(P<0.01), which was paralleled by an increase in serum apoA-I (76+/-21 vs. 184+/-24 mg/dl), while serum lipids also increased significantly. No significant difference was observed in the apoE concentrations in CSF (296+/-170 vs. 269+/-67 microg/dl) or brain extract (5.0+/-1.6 vs. 5.7+/-1.8 microg/g wet weight). The apoA-I concentrations found in CSF and brain extract were much lower than those for apoE and were not appreciably affected by triamcinolone: 7.7+/-5.5 vs. 4.5+/-3.1 microg/dl for CSF and <0.5 vs. <0.5 microg/g wet weight for brain extract. The apo E metabolism in the rat central nervous system appears to be refractory to the short term administration of triamcinolone and to changes in the serum lipoprotein metabolism. ApoA-I appears unlikely to play a significant role in the rat central nervous system.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9150415&dopt=Abstract triamcinolone Kenalog



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Prospective use of intramuscular triamcinolone acetonide in pseudogout.

Roane DW, Harris MD, Carpenter MT, Finger DR, Jarek MJ, Alloway JA, Erickson AR, Venanzi WE, Drehmer TJ.

Department of Medicine, David Grant Medical Center, Travis Air Force Base, CA, USA.

OBJECTIVE: To prospectively assess the efficacy of intramuscular (i.m.) triamcinolone acetonide in the treatment of pseudogout. METHODS: Fourteen patients with crystal proven pseudogout presenting with an acute attack within 5 days of onset were treated with intramuscular triamcinolone acetonide 60 mg and followed for 30 days. Patients with inadequate response were eligible for a 2nd triamcinolone acetonide injection on Day 1-2. RESULTS: Twelve patients had contraindication to nonsteroidal antiinflammatory agents (NSAID). Acute arthritis was monoarticular in 10 patients, and involved 2 or more joints in 4 patients. All patients had good clinical response to triamcinolone acetonide based on restoration of near baseline joint range of motion and joint circumference, and at least 50% improvement in patient and physician global assessment. Major clinical improvement occurred by Day 1-2 (2 patients), Day 3-4 (11 patients), and Day 10-14 (one patient). Six patients required a 2nd triamcinolone acetonide injection on Day 1-2. Toxicities were not observed. CONCLUSION: I.m. triamcinolone acetonide appears to be safe, well tolerated, and effective in the treatment of pseudogout. It may be a reasonable alternative therapy when NSAID are contraindicated, and for polyarticular attacks where intraarticular corticosteroids are impractical.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9195527&dopt=Abstract triamcinolone Kenalog



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Determination of triamcinolone, triamcinolone acetonide and fluocinonide in dosage forms.

Agbaba D, Zivanov-Stakic D, Vladimirov S, Zubac K.

Department of Pharmaceutical Chemistry, Faculty of Pharmacy, Belgrade, Yugoslavia.

The colorimetric method for determination of triamcinolone, triamcinolone acetonide and fluocinonide in tablets, ointments and cream using isonicotinic acid hydrazide is proposed. This method provides a precise and reproducible results (recovery ranged within 97.42-101.75%, variation coefficient ranged within 0.99-2.56%).

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12959252&dopt=Abstract triamcinolone Kenalog



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Evidence that the transit of glucose into liver microsomes is not required for functional glucose-6-phosphatase.

Annabi B, van de Werve G.

Laboratoire d'Endocrinologie Metabolique, Department of Nutrition, Universite de Montreal, Quebec, Canada.

We show that the production of glucose from glucose-6-phosphate hydrolysis outside microsomes is a function of glucose-6-phosphatase independent of its property to form glucose inside microsomes. Indeed, during development (before 1 day of age), mouse liver microsomes had glucose-6-phosphatase producing glucose solely outside microsomes. Furthermore, in vivo treatment of rats with the glucocorticoid analogue triamcinolone resulted in increased glucose-6-phosphatase activity outside but not inside microsomes and without change in the catalytic subunit 40 kDa glucose-6-phosphatase mRNA abundance or protein level, indicating that other factors induced by triamcinolone (e.g., altered membrane lipid environment and/or a regulatory protein) were responsible for the activity change. Triamcinolone treatment also lessened the inhibition of glucose-6-phosphatase by pyridoxal 5'-phosphate (PLP), but this effect was not due to an interaction of PLP with the active site. Accordingly, reversal of the inhibition was observed after permeabilization of the microsomes. The two distinct orientations of liver microsomal glucose-6-phosphate phosphohydrolase suggest different physiological roles played by this enzyme in the endoplasmic reticulum membrane.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9245738&dopt=Abstract triamcinolone Kenalog



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Noninfectious endophthalmitis associated with intravitreal triamcinolone injection.

Roth DB, Chieh J, Spirn MJ, Green SN, Yarian DL, Chaudhry NA.

Retina Vitreous Center, Department of Ophthalmology, University of Medicine and Dentistry of New Jersey, New Brunswick 08901, USA. rothretina aol.com

BACKGROUND: Intravitreal injection of triamcinolone has been advocated to treat exudative macular diseases such as macular edema and choroidal neovascularization. OBJECTIVE: To describe 7 patients who developed a clinical picture simulating endophthalmitis after intravitreal triamcinolone injection. METHODS: Intravitreal triamcinolone injections were performed to treat refractory cystoid macular edema or diffuse macular edema associated with diabetic retinopathy, macular pucker, branch retinal vein occlusion, or pseudophakia. One patient received an injection in an attempt to treat exudation associated with occult choroidal neovascularization. RESULTS: Preinjection visual acuity ranged from 20/50 to 20/400. An extensive inflammatory response developed 1 to 2 days after injection in all 7 eyes. Five eyes had previously undergone vitrectomy. Four eyes had a layered hypopyon. All 7 eyes had an anterior chamber cellular reaction and vitritis. Visual acuity ranged from 20/400 to hand movements. The first 6 patients were treated for presumed endophthalmitis with vitreous cultures and intravitreal injections of antibiotics. All 6 cultures were negative for any organisms, and the eyes resolved their inflammatory response, with recovery to preinjection visual acuity or better. The seventh patient was treated with topical prednisolone without antibiotic therapy, and the inflammation resolved, with resolution of the macular edema seen before the intravitreal triamcinolone injection. CONCLUSION: It may be appropriate to closely observe noninfectious, toxic endophthalmitis in patients treated with intravitreal triamcinolone before assuming it to be infectious, especially in the absence of eye pain.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12963610&dopt=Abstract triamcinolone Kenalog



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An intravitreal sustained-release triamcinolone and 5-fluorouracil codrug in the treatment of experimental proliferative vitreoretinopathy.

Yang CS, Khawly JA, Hainsworth DP, Chen SN, Ashton P, Guo H, Jaffe GJ.

Department of Ophthalmology, Duke University, Durham, NC 27710, USA.

OBJECTIVE: To determine the efficacy and pharmacokinetics of an intravitreal sustained-release triamcinolone acetonide and 5-fluorouracil (TA/5-FU) codrug in the treatment of experimental proliferative vitreoretinopathy (PVR). METHODS: The therapeutic efficacy of the TA/5-FU codrug was determined in a rabbit model that simulates human PVR. Intravitreal levels of triamcinolone and 5-fluorouracil were measured at different time points and drug release in vitro was tested. Toxic effects were evaluatedby electroretinograpy, clinical examination, and light microscopy. RESULTS: Both the severity of PVR grade and the percentage of eyes with moderate or worse tractional detachment were significantly less in eyes treated with the codrug. The therapeutic effect of the intravitreal codrug was paralleled by sustained intravitreal levels of triamcinolone and 5-fluorouracil. There were no drug-related toxic effects evident on clinical or histopathologic examination of eyes containing the TA/5-FU codrug. CONCLUSIONS: The intravitreal sustained-release TA/5-FU codrug effectively inhibits the progression of PVR in a rabbit model that closely resembles PVR in humans. The TA/5-FU codrug may simultaneously target different components of the wound-healing response.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9445210&dopt=Abstract triamcinolone Kenalog