Kenalog
Rate of urinary urea output correlates to degree of muscular atrophy induced by triamcinolone acetonide.

Shoji S.

Department of Medicine, Shinshu University School of Medicine, Matsumoto, Japan.

1. The effect of administering triamcinolone acetonide (10 mg kg-1 day-1) as seven consecutive single daily subcutaneous injections on urinary urea output and muscular atrophy was studied in rabbits. 2. The ratio of the wet weight of the lateral vastus of the quadriceps muscle to body weight (MI) varied greatly among the rabbits. 3. The ratio of urinary urea output after to before triamcinolone injection correlated significantly to MI. 4. These findings suggest that the ratio of urinary urea output can be used as a predictive index for steroid myopathy.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1814684&dopt=Abstract triamcinolone Kenalog



Kenalog
Effect of adaptive steroids on the impairment of hepatic drug metabolic activity caused by hepatotoxic agents.

Kourounakis PN, Rekka E.

Department of Pharmaceutical Chemistry, School of Pharmacy, University of Thessaloniki, Greece.

Hepatic disfunction was produced in female rats by ethanol, carbon tetrachloride, dimethyl mercury or Freund's Adjuvant. This disfunction was expressed by increased SGPT, liver triglycerides level, and reduced resistance to zoxazolamine, digitoxin and indomethacin. Treatment with spironolactone, pregnenolone-16_-carbonitrile or triamcinolone reduced only slightly SGPT and triglycerides, but restored the reduced resistance to drugs, and the impairment of the liver drug metabolism in vitro. Triamcinolone was the least effective. Spironolactone, pregnenolone-16_-carbonitrile and triamcinolone were most active in preventing the hepatotoxicity of dimethyl mercury, of carbon tetrachloride and of Freund's Adjuvant respectively. Restoration of drug metabolism is attributed to the microsomal enzyme induction in general. Triamcinolone, when potent in rats with adjuvant induced disease (AID), acted by a glycocorticoid mediated mechanism. In AID, treatment of inflammation restored liver drug metabolism, but restoration of the hepatic drug metabolic activity in AID rats only slightly ameliorated inflammation. None of the tested steroids demonstrated any activity against lipid peroxidation, thus excluding any mediation of a free radical mechanism in spironolactone, PCN or triamcinolone involvement in drug response and metabolism of the damaged liver by the hepatotoxic agents used.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1820873&dopt=Abstract triamcinolone Kenalog



Kenalog
Endogenous excitatory amino acid regulation of the progesterone-induced LH and FSH surge in estrogen-primed ovariectomized rats.

Brann DW, Mahesh VB.

Department of Physiology and Endocrinology, Medical College of Georgia, Augusta.

The role of endogenous excitatory amino acid neurotransmission in the regulation of progesterone and triamcinolone acetonide-induced LH and FSH release was examined. Estrogen-primed ovariectomized rats were utilized in this study. Progesterone or triamcinolone acetonide (1 mg/kg body weight) treatment led to a highly significant elevation of serum LH and FSH levels 5 h later. Treatment with the selective noncompetitive NMDA receptor antagonist, MK801, had no effect on serum LH and FSH levels when compared to estrogen controls. However, MK801 administered 1 h prior to progesterone or triamcinolone acetonide administration completely blocked their ability to induce LH and FSH surges. These studies demonstrate for the first time the involvement of endogenous excitatory amino acid neurotransmission in the mediation of progesterone and corticosteroid-induced LH and FSH surges.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1828545&dopt=Abstract triamcinolone Kenalog



Kenalog
Enhancing effect of pyrrolidone derivatives on transdermal penetration of 5-fluorouracil, triamcinolone acetonide, indomethacin, and flurbiprofen.

Sasaki H, Kojima M, Mori Y, Nakamura J, Shibasaki J.

Faculty of Pharmaceutical Sciences, Nagasaki University, Japan.

The enhancing effects of pyrrolidone derivatives on the transdermal penetration of 5-fluorouracil, triamcinolone acetonide, indomethacin, and flurbiprofen were studied by using an in vitro technique and full-thickness rat skin. The enhancers included 1-methyl (1), 1-hexyl (2), and 1-lauryl-2-pyrrolidone (3). Penetrants with various physicochemical properties were used. Flurbiprofen penetrated through skin rapidly after application alone. 5-Fluorouracil, triamcinolone acetonide, and indomethacin showed little penetration. Pyrrolidone derivatives enhanced the penetration of penetrants, especially the lipophilic compounds 2 and 3, which showed a great enhancing effect on the penetration of 5-fluorouracil and indomethacin. Pyrrolidone derivatives also enhanced the solubility of these penetrants in isopropyl myristate. Compounds 2 and 3 showed greater enhancing effects on the solubility and penetration of hydrophilic penetrants than those of lipophilic penetrants. These results suggest that the pyrrolidone derivatives enhance the flux of penetrants in skin by increasing the solubility of penetrants in the stratum corneum. Compounds 1 and 2 were detected in the receptor phase. All enhancers accumulated to a great extent in the skin. These derivatives also enhanced the skin retention of drug. It is concluded that these pyrrolidone derivatives are useful for transdermal drug delivery, although further studies are necessary before they could be used clinically.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1941542&dopt=Abstract triamcinolone Kenalog



Kenalog
Intravitreal triamcinolone acetonide for the treatment of chronic pseudophakic cystoid macular oedema.

Karacorlu M, Ozdemir H, Karacorlu S.

Istanbul Retina Institute, Istanbul, Turkey. retina pobox.com

PURPOSE: To evaluate the effect of intravitreal triamcinolone acetonide for chronic pseudophakic cystoid macular oedema (CME) resistant to medical treatment. METHODS: Six eyes of six patients with chronic pseudophakic CME, aged 58-74 years (average 66 years), made up the study population. All eyes had persistent CME despite having received medical treatment for at least 3 months. Intravitreal injection of 4 mg (0.1 ml) triamcinolone acetonide was offered to treat macular oedema. The visual and anatomic responses were observed as well as potential complications related to the injection procedure and corticosteroid medication. RESULTS: The follow-up period was between 6 and 10 months (mean 8.5 months). Baseline central macular thickness averaged 504 microm. At 1 month, a reduction in the mean central macular thickness of 52% from 504 microm to 264 microm was obtained. At 3 and 6 months, the mean central macular thicknesses were 240 microm and 232 microm, respectively. Five of the six eyes maintained a visual gain of 15 or more letters from baseline at 6 months. During follow-up no patient had intraocular pressure (IOP) exceeding 21 mmHg. No injection-related complications were encountered. CONCLUSIONS: Intravitreal triamcinolone acetonide is a promising therapeutic method for chronic pseudophakic CME resistant to medical treatment. Further study with a longer follow-up period and larger series is warranted to assess the treatment's longterm efficacy and safety and the need for retreatment.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14641270&dopt=Abstract triamcinolone Kenalog



Kenalog
Interaction of rat liver glucocorticoid receptor with a newly synthesized antisteroid ZK98299.

Zakula Z, Moudgil VK.

Department of Biological Sciences, Oakland University, Rochester, MI 48309-4401.

Steroid receptor antagonists are important biochemical probes for understanding the mode of steroid hormone action. We have studied the interaction between rat liver glucocorticoid receptor and a newly synthesized antisteroid ZK98299 (13-antigestagen; [11-beta-(4-dimethylaminophenyl)-17a-hydroxy-17 beta-(3- hydroxypropyl)-13 alpha-methyl-4,9-gonadien-3-one]). Glucocorticoid receptor from freshly prepared hepatic cytosol bound [3H]ZK98299 with affinity approximately equal to that of [3H]triamcinolone acetonide. The binding of both steroids reached a maximum at 4 h at 0 degrees C. Both ligands were able to compete for the steroid binding site but progesterone, estradiol and dihydrotestosterone (DHT) failed to compete for the [3H]ZK98299 and [3H]triamcinolone acetonide binding. While [3H]ZK98299 binding to glucocorticoid receptor could occur in the presence of iodoacetamide and N-ethylmaleimide (NEM), [3H]triamcinolone acetonide binding capacity was completely abolished following such treatments. The [3H]ZK98299-receptor complexes sedimented as 9 S and 4 S molecules under control (4 degrees C) and receptor transforming (23 degrees C) conditions, and exhibited a faster rate of dissociation at 23 degrees C when compared with [3H]triamcinolone acetonide-receptor complexes. These results indicate that ZK98299 interacts with hepatic glucocorticoid receptor. The differential effects of iodoacetamide and NEM on the interaction of glucocorticoid receptor with ZK98299 and triamcinolone acetonide, and the faster rate of dissociation of [3H]ZK98299-receptor complexes suggest that treatment with these agents (NEM and iodoacetamide) results in distinct conformational changes in glucocorticoid receptor structure with respect to triamcinolone acetonide and ZK98299 binding. Alternatively, ZK98299 may be interacting with a site which is distinct from one which accepts triamcinolone acetonide.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2018785&dopt=Abstract triamcinolone Kenalog