Nonprescription acne vulgaris treatments: Their role in our treatment armamentarium—An international panel discussion

Background: Acne vulgaris (acne), a common inflammatory skin disorder, has its peak incidence between 14 and 19 years of age, with girls frequently developing acne earlier than boys. Over recent years, persistent acne is becoming more prevalent in adult women. Objectives: This review and panel discussion addresses challenges in acne management, particularly in adult women. The role which nonprescription acne treatment can play is explored when used as monotherapy or as an adjunctive treatment for acne of all severity. Methods: The best available evidence on nonprescription acne treatment was coupled with the opinion of an international expert panel of dermatologists to adopt statements and recommendations discussed in this review. Results: All severity of acne has a significant burden on patients. Addressing environmental factors that are important for the individual with acne may help to educate, prevent, effectively manage, and maintain acne, as per the panel. They agreed that the adult female acne population has unique needs because of their aging skin and social environment. Nonprescription acne treatment products may help to balance the efficacy and tolerability of prescription acne treatment. Currently, there are no specific guidelines for how to use nonprescription acne treatment products in these patients. Conclusion: The panel agreed that guidelines including nonprescription acne treatment either as monotherapy for mild acne or in combination with prescription treatments for more severe acne would address a significant unmet need

Treatment of seborrheic dermatitis: a comprehensive review

Seborrheic dermatitis (SD) is a chronic, recurring inflammatory skin disorder that manifests as erythematous macules or plaques with varying levels of scaling associated with pruritus. The condition typically occurs as an inflammatory response to Malassezia species and tends to occur on seborrheic areas, such as the scalp, face, chest, back, axilla, and groin areas. SD treatment focuses on clearing signs of the disease; ameliorating associated symptoms, such as pruritus; and maintaining remission with long-term therapy. Since the primary underlying pathogenic mechanisms comprise Malassezia proliferation and inflammation, the most commonly used treatment is topical antifungal and anti-inflammatory agents. Other broadly used therapies include lithium gluconate/succinate, coal tar, salicylic acid, selenium sulfide, sodium sulfacetamide, glycerin, benzoyl peroxide, aloe vera, mud treatment, phototherapy, among others. Alternative therapies have also been reported, such as tea tree oil, Quassia amara, and Solanum chrysotrichum. Systemic therapy is reserved only for widespread lesions or in cases that are refractory to topical treatment. Thus, in this comprehensive review, we summarize the current knowledge on SD treatment and attempt to provide appropriate directions for future cases that dermatologists may face

Seborrheic dermatitis—Looking beyond Malassezia

Seborrhoeic Dermatitis (SD) is a very common chronic and/or relapsing inflammatory skin disorder whose pathophysiology remains poorly understood. Yeast of the genus Malassezia has long been regarded as a main predisposing factor, even though causal relationship has not been firmly established. Additional predisposing factors have been described, including sebaceous activity, host immunity (especially HIV infection), epidermal barrier integrity, skin microbiota, endocrine and neurologic factors, and environmental influences. Genetic studies in humans and mouse models-with particularly interesting insights from examining the Mpzl3 knockout mice and their SD-like skin phenotype, and patients carrying a ZNF750 mutation-highlight defects in host immunity, epidermal barrier and sebaceous activity. After synthesizing key evidence from the literature, we propose that intrinsic host factors, such as changes in the amount or composition of sebum and/or defective epidermal barrier, rather than Malassezia, may form the basis of SD pathobiology. We argue that these intrinsic changes provide favourable conditions for the commensal Malassezia to over-colonize and elicit host inflammatory response. Aberrant host immune activity or failure to clear skin microbes may bypass the initial epidermal or sebaceous abnormalities. We delineate specific future clinical investigations, complemented by studies in suitable SD animal models, that dissect the roles of different epidermal compartments and immune components as well as their crosstalk and interactions with the skin microbiota during the process of SD. This research perspective beyond the conventional Malassezia-centric view of SD pathogenesis is expected to enable the development of better therapeutic interventions for the management of recurrent SD