For recalcitrant or severe nodulocystic acne, oral isotretinoinmay be instituted. Isotretinoin, an oral analog of vitamin A,normalizes follicular keratinization, reduces sebum production,and decreases 5α-dihydrotestosterone formation and androgen receptor–binding capacity. A course of isotretinoin (0.5 to1 mg/kg/day to reach a cumulative dose of 120 mg/kg) is theonly medication that can permanently alter the course of acne and induce a durable remission. Because of the high incidenceof adverse effects, it should be used only by physicians familiar with this medication. Isotretinoin therapy requires carefulpatient selection, pretreatment counseling, and monthly laboratory monitoring. It is teratogenic and must not be used immediately before or during pregnancy.
Acne has significant and frequently devastating effects on an adolescent’s body image and self-esteem. There may be little correlation between severity and psychosocial impact. Scarring may result in permanent morbidity.
Classically, acne lasts 3 to 5 years, although some individuals may have disease for 15 to 20 years. Only early treatment with isotretinoin may alter the natural course of acne. Acne lesions often heal with temporary postinflammatory erythema and hyperpigmentation. Depending on the severity, chronicity, and depth of involvement, pitted, atrophic, or hypertrophic scars may develop. Cystic acne has the highest incidence of scarring because rupture of a deep cyst induces the greatest inflammation, though scarring may be caused by milder pustular or even comedonal acne.
Greasy hair and cosmetic preparations should be avoided becausethey exacerbate preexisting acne. There are no effective means forpreventing acne, and there is little evidence that diet is associated with acne. Repetitive cleansing with soap and water or useof astringents or abrasives removes only surface lipids. Their usemakes the skin appear less oily but does not prevent formation ofmicrocomedones and may paradoxically worsen acne.
Atopic dermatitis is a chronic inflammatory disease with no known cure. It is associated with significant psychosocial morbidity and decreased health-related quality of life. For many affected individuals, atopic dermatitis is the skin manifestation of atopy accompanied by asthma and allergic rhinitis.
Atopic dermatitis manifests with a defective skin barrier,reduced innate immune responses, and exaggerated immuneresponses to allergens and microbes. Both genetic predisposition and environmental factors play a role in the development of atopic dermatitis. Genes associated with skin barrier dysfunction and inflammation have been linked with atopicdermatitis. Inflammatory mediators involved include predominantly T helper cells, with the TH2 pathway implicated early in acute lesions and a TH1 predominance found in chroniclesions. Langerhans cells, IgE, and eosinophils play a prominent role, as well as many other inflammatory mediators. Environmental and contact allergens, infections, irritants, extremesof temperature, sweat, and lack of humidity can exacerbate thecondition, as can scratching or rubbing. Triggers are somewhatvariable from individual to individual.
Atopic dermatitis is the most common skin disease in children,with an estimated prevalence of up to 20% of children. Only1% to 2% of adults manifest disease. In addition to genetic factors, an environmental influence contributes. Atopic dermatitisoccurs more frequently in urban areas and in higher socioeconomic classes. Prevalence is lower in areas where industrial pollution is less and where eosinophil-mediated infectionssuch as helminthic infections are endemic.