Powderma as compared to the main ingredients in most acne treatments.
Meta-analysis comparing efficacy of Clindamycin, Salicylic Acid, Benzoyl Peroxide and Powderma for treating mild, moderate or severe acne (acne vulgaris). In a well controlled clinical study of 87 patients; 15 used 1% Clindamycin, 19 used 2% Salicylic Acid, 18 used 5% Benzoyl Peroxide, 27 used Powderma, and 8 used a placebo. Patients were 15 years of age and older and treated once a day for three weeks. Patients were evaluated for face and upper body acne with lesions counted on day 7, 14, and 21. The primary efficacy measures were the lesion counts and the investigator's global assessment evaluation at week 3. Percent reductions in lesion counts during the clinical trial are shown below:
An evaluator's global score (EGS) of clear or almost clear at week 3 was achieved in significantly more patients treated with Powderma than the other treatment groups. Secondary outcomes measured the side effect profile using an application site scale for dryness, scaling, redness, and stinging/burning. Although the instances of irritation with Powderma were less than 10%, significantly less than the other medications included in this study, if a reaction suggesting sensitivity or chemical irritation occurs, use should be reduced or discontinued. Keep away from eyes, mouth, and mucous membranes.
Acne is a follicular disorder occurring in pilosebaceous units in the skin of the face, neck, and upper trunk. These sebaceous follicles have follicular channels and adjacent multiacinar sebaceous glands. In the lubrication process of normal skin, sebum travels through the follicular canal to the skin surface, carrying along with it desquamated cells from follicular epithelium. Acne develops when these specialized follicles undergo pathologic alterations that result in the formation of non-inflammatory lesions (comedones) and inflammatory lesions (papules, pustules, and nodules)1. The manifestations of acne are thought to be the product of four pathogenic events: 1) increased sebum production fueled by androgenic stimulation; 2) obstruction of the pilosebaceous unit due to an abnormal keratinization process; 3) proliferation of Propionibacterium acnes, an anaerobic diphtheroid normally residing in pilosebaceous follicles; and 4) inflammation that is mediated both by the action of chemotactic factors and various enzymes, and initiated in part by the interaction of P. acnes with toll-like receptors. Impaction of the pilosebaceous follicle gives rise to the microcomedo that is thought to be the precursor lesion of face and body acne.