DiagnosisandTreatmentofAcne.PDFVIP

acnes, which provokes an immune response through the production of numerous inflam- matory mediators. Inflammation is further enhanced by follicular rupture and subsequent leakage of lipids, bacteria, and fatty acids into the dermis. Diagnosis The diagnosis of acne is based on the history and physical examination. Lesions most com- monly develop in areas with the greatest con- centration of sebaceous glands, which include the face, neck, chest, upper arms, and back. Acne vulgaris may be defined as any dis- order of the skin whose initial pathology is the microscopic microcomedo.3 The micro- comedo may evolve into visible open com- edones (“blackheads”) or closed comedones (“whiteheads”). Subsequently, inflammatory papules, pustules, and nodules may develop. Nodulocystic acne consists of pustular lesions larger than 0.5 cm. The presence of excoria- tions, postinflammatory hyperpigmentation, and scars should be noted. Acne may be triggered or worsened by external factors such as mechanical obstruc- tion (i.e., helmets, shirt collars), occupational exposures, or medications. Common medi- cations that may cause or affect acne are listed in Table 1.4 Cosmetics and emollients may occlude follicles and cause an acneiform A cne is a disease of piloseba- ceous units in the skin. It is thought to be caused by the interplay of four factors. Excessive sebum production secondary to sebaceous gland hyperplasia is the first abnormality to occur.1 Subsequent hyperkeratinization of the hair follicle pre- vents normal shedding of the follicular kera- tinocytes, which then obstruct the follicle and form an inapparent microcomedo.2 Lipids and cellular debris soon accumulate within the blocked follicle. This microenvironment encourages colonization of Propionibacterium Acne can cause significant embarrassment and anxiety in affected patients. It is impor- tant for family physicians to educate patients about available treatment options and their expected outc