RESUMEN
Within their first days of life, newborns' skin undergoes various adaptation processes needed to accommodate the transition from the wet uterine environment to the dry atmosphere. The skin of newborns and infants is considered as a physiological fragile skin, a skin with lower resistance to aggressions. Fragile skin is divided into four categories up to its origin: physiological fragile skin (age, location), pathological fragile skin (acute and chronic), circumstantial fragile skin (due to environmental extrinsic factors or intrinsic factors such as stress) and iatrogenic fragile skin. Extensive research of the past 10 years have proven evidence that at birth albeit showing a nearly perfect appearance, newborn skin is structurally and functionally immature compared to adult skin undergoing a physiological maturation process after birth at least throughout the first year of life. This article is an overview of all known data about fragility of epidermis in 'fragile populations': newborns, children and adolescents. It includes the recent pathological, pathophysiological and clinical data about fragility of epidermis in various dermatological diseases, such as atopic dermatitis, acne, rosacea, contact dermatitis, irritative dermatitis and focus on UV protection.
Asunto(s)
Epidermis/fisiología , Adaptación Fisiológica , Adolescente , Células Cultivadas , Niño , Células Epidérmicas , Humanos , Recién Nacido , Queratinocitos/citologíaRESUMEN
Several studies have explained the influence of clofibrate on lipid metabolism, and the depressive effect of this drug on blood triglyceride and cholesterol levels is now well-known. Inhibition of triglyceride formation in the liver, and thus a reduced release of newly synthesized triglycerides coupled with increased fatty acid catabolism, might partially explain the lipid-lowering effect of clofibrate. These in vitro studies were designed to determine the effects of a new normolipemic product, procetofen, on hepatic microsomal synthesis of triglycerides and mitochondrial catabolism of oleic acid. These subcellular particles were isolated from normal rats or those treated for 8 days with clofibrate (250 mg/kg/day) or procetofen (100 mg/kg/day). Microsomal triglyceride synthesis from 3H oleate was not significantly changed in the clofibrate-treated group, while it decreased by 25 p. 100 in the procetofen-treated group. In the mitochondrial system, 14CO2 production from 10-14C oleate was small and unaffected by either drug. Therefore, the radioactivity of acid-soluble products was enhanced by 40 or 130 p. 100 when mitochondria were isolated from the livers of rats treated with clofibrate or procetofen, respectively. These data support the hypothesis that the plasma lipid-lowering effect of procetofen in vivo could be explained by increased hepatic fatty acid degradation which probably induced a reduction of triglyceride synthesis.