tretinoin and Telangiectasis

The clinical and histologic effects of a new emollient cream formulation of topical tretinoin at concentrations of 0.05% and 0.01% were examined in 251 subjects with mild to moderate photodamaged facial skin in a randomized, double-blind, vehicle-controlled, multicenter study. Seventy-nine percent of the subjects who received 0.05% tretinoin for 24 weeks showed overall improvement in photodamaged skin compared with improvement in 48% of the vehicle-treated control subjects. Significant reductions were found in fine wrinkling, mottled hyperpigmentation, roughness, and laxity after 0.05% tretinoin therapy when compared with controls. In addition, histologic changes of increased epidermal thickness, decreased melanin content, and stratum corneum compaction provide independent evidence supporting clinical improvement. Side effects of erythema, peeling, and stinging were usually mild and well tolerated.

Topics: Administration, Cutaneous; Adult; Dose-Response Relationship, Drug; Double-Blind Method; Face; Female; Humans; Lentigo; Male; Middle Aged; Pigmentation Disorders; Placebos; Skin; Skin Aging; Skin Diseases; Telangiectasis; Tretinoin

13-cis-Retinoic acid, retinyl-mthyl-ether, retinyl-phenyl-ether, retinyl-thio-ether and axerophthene each induced dose-dependent sister-chromatid exchanges (SCE) in human diploid fibroblasts. The functional relationship between retinoid concentration and SCE rate was similar in each of the 5 retinoids tested. The relationship reached a plateau at concentrations exceeding 8 micrograms/ml. alpha-Naphthoflavone (ANF), an inhibitor of P448-dependent mono-oxygenase, prevented the retinoid-induced increase of the SCE rate, but had no inhibitory effect in the presence of 4-nitroquinoline-1-oxide, an ultimate carcinogen. ANF did not reduce the spontaneously increased SCE rate in fibroblasts of patients with Bloom's syndrome. Retinoids failed to induce SCE in V79 Chinese hamster cells, which lack mono-oxygenase. Thus, we conclude that the retinoid-induced SCE rate increases independently of structural changes in the molecular side-chain ad that a metabolic activation of retinoids is required for SCE induction by cytochrome P448-dependent mono-oxygenase.

Topics: Abnormalities, Multiple; Animals; Benzoflavones; Biotransformation; Cell Line; Cricetinae; Cricetulus; Crossing Over, Genetic; Cytochrome P-450 CYP1A2; Cytochromes; Dose-Response Relationship, Drug; Fibroblasts; Humans; Isotretinoin; Mixed Function Oxygenases; Sister Chromatid Exchange; Skin; Structure-Activity Relationship; Telangiectasis; Tretinoin; Vitamin A