Synalar
Hydroquinone 4%, tretinoin 0.05%, fluocinolone acetonide 0.01%: a safe and efficacious 12-month treatment for melasma.

Torok HM, Jones T, Rich P, Smith S, Tschen E.

HMT Dermatology Associates, Inc, Medina, Ohio, USA. helenmtorok aol.com

This article describes a long-term, multicenter, open-label, 12-month study of once-daily fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05% (Tri-Luma Cream, hereinafter called TC [triple combination]) application in the treatment of melasma. A total of 228 patients with facial melasma were enrolled and treated; 173 patients (76%) completed the study. Most patients had 1 to 2 courses of treatment lasting approximately 6 months in total. TC cream showed a favorable safety profile. only 3 patients (1%) withdrew from the study due to treatment-related adverse events (AEs). A total of 129 patients (57%) experienced at least one treatment-related AE. Most AEs were expected application-site reactions that were mild and transient in nature and did not require remedial therapy. There were no cases of skin atrophy or skin thinning and only 6 cases of telangiectasia (5 mild and 1 moderate), most of which had improved by the end of the study. Results of the efficacy assessments were positive, with both the patient and the physician assessing melasma to be either completely or nearly cleared by the end of the study in more than 90% of cases. In this study, a once-daily application of TC cream over an extended period of 12 months showed no notable safety concerns and offered an effective treatment for melasma.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=15732437&dopt=Abstract fluocinolone Synalar



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Stability of steroid ointments diluted with Compound Zinc Paste B.P.

Barnes AR, Nash S, Watkiss SB.

Pharmaceutical Sciences Institute, Aston University, Birmingham, U,K.

The chemical stability of a range of corticosteroid ointments diluted with Compound Zinc Paste B.P. was studied by high-performance liquid chromatography (HPLC). Betamethasone dipropionate degraded by first-order kinetics at both 25 degrees C and 32 degrees C. At 25 degrees C the mean first-order reaction rate constant was 9.58 x 10(-3)/day, with a t90 (time to reach 90% of the original concentration) of 11.0 days. At 32 degrees C the mean first-order reaction rate constant was 2.42 x 10(-2)/day, with a t90 of 4.4 days. Of the other steroids studied, Fluocinolone acetonide was the least stable, with 33.8% remaining after a 7-day storage period at 25 degrees C. Betamethasone-17-valerate and fluocinonide were of intermediate stability between betamethasone dipropionate and fluocinolone acetonide. None of the steroid ointments studied had adequate stability in Compound Zinc Paste B.P. to allow extemporaneous dilution with this base.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1856247&dopt=Abstract fluocinolone Synalar



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Pharmacokinetics of fluocinolone acetonide in patch versus cream formulations.

Broggini M, Benvenuti C, Botta V, Broccali G.

Medical Department, Filippo del Ponte Hospital, Varese.

The pharmacokinetics of the fluocinolone acetonide patch containing 8 mcg/cm2 and a 0.025% cream were studied in a cross-over trial in 12 healthy volunteers 6 male and 6 female mean age 24.9 years. Each subject was treated with 0.8 mg of both fluocinolone acetonide formulations for 12 h on non-consecutive days. The high performance liquid chromatography method was used to determine the plasma and urine levels of the drug. Minor fluctuations in the plasma profile after patch application were observed, even if no significant difference was found between the two formulations with regard to peak plasma concentration, time to reach peak levels, area under the concentration curve and half-life.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1874579&dopt=Abstract fluocinolone Synalar



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Inhibition of microcystin-induced release of cyclooxygenase products from rat hepatocytes by anti-inflammatory steroids.

Naseem SM, Hines HB, Creasia DA.

United States Army Medical Research Institute, Fort Detrick, Frederic, Maryland 21701-5001.

We showed previously that exposure to microcystin causes eicosanoid release. That study was extended further to test the effect of glucocorticoids on microcystin-induced release of [14C]arachidonic acid and its metabolites from rat hepatocytes previously treated with [14C]arachidonic acid. Release of total radioactivity was 4-fold greater from hepatocytes after 2-hr incubation with 1 microM microcystin than after incubation with control medium. Fluocinolone pretreatment decreased the microcystin-induced synthesis and release of prostacyclin by 24 +/- 2.6% (P less than 0.05) and thromboxane B2 by 39 +/- 3% (P less than 0.025). Treatment of hepatocyte cultures with either microcystin (1 microM) or steroids had no effect on cell viability or total cell protein. Total radioactivity released into the incubation medium was not affected by glucocorticoid alone. Under these conditions, the quantities of both prostaglandin F2 alpha and prostaglandin E2 released were not significantly different when control and microcystin-treated cultures were compared. The half-maximal inhibition (IC50) values obtained from the dose-response data for the inhibition of arachidonic acid release by steroids were comparable with normal cortisol levels in humans. Dose-response curves gave the following rank order of inhibitory potency: fluocinolone greater than dexamethasone greater than hydrocortisone. These results suggest that glucocorticoid therapy might be beneficial in microcystin toxicosis.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2124352&dopt=Abstract fluocinolone Synalar



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Effect of toxins on arachidonic acid metabolism in rat cultured pulmonary alveolar macrophages.

Naseem SM, Hines HB, Creasia DA.

U.S. Army Medical Research Institute of Infectious Diseases, Division of Pathophysiology, Fort Detrick, Frederick, Maryland 21701-5011.

The action of a trichothecene (T-2), microcystin-LR and saxitoxin on arachidonic acid metabolism in cultured rat alveolar macrophages was studied. Pulmonary macrophages exposed to T-2 trichothecene were stimulated to synthesize and release large amount of thromboxane B2 (TxB2) and 6-Keto F1 alpha. Microcystin-LR induced significant release of prostaglandins F2 alpha (140%), PGE2 (175%) and TxB2 (169%) compared to controls. Saxitoxin induced TxB2 release by 37%. Arachidonic acid release was stimulated by all three toxins. The release of arachidonic acid and its metabolites in alveolar macrophages exposed to T-2 toxin was partially blocked by fluocinolone (1 microM). These results suggest that macrophages synthesize and release inflammatory mediators in response to toxin exposure, and fluocinolone may protect against T-2 toxicosis.

Online source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2510727&dopt=Abstract fluocinolone Synalar