0.5% Liposome-encapsulated 5-aminolevulinic acid (ALA) photodynamic therapy for acne treatment

Abstract

Background: Photodynamic therapy using topical 5-aminolevulinic acid (ALA) has been successful in treating acne vulgaris, but sun avoidance for at least 48 hours after treatment is necessary due to the risk of post-treatment photosensitivity. Recently, a lower concentration of liposome-encapsulated 5-ALA was introduced to minimize this risk. Objectives: To evaluate the efficacy and safety of liposome-encapsulated 0.5% 5-ALA in the photodynamic therapy of inflammatory acne and its effects on sebum secretion in Asian skin. Methods: Thirteen Korean subjects with inflammatory acne were administered 0.5% ALA spray before photoradiation treatment. Photoradiation was performed at 3.5–6.0 J/cm² three times during each of two visits, performed 2 weeks apart. Improvement of acne was evaluated subjectively and objectively based on the Korean Acne Grading System. Sebum secretion was measured quantitatively at each visit. Results: The mean reduction in acne grade at the end of the treatment was 43.2%. Of the patients, 69.2% reported improvements in subjective skin oiliness, but fewer showed objective reductions in sebum secretion as determined by the Sebumeter^® SM10. No serious adverse events were observed. Conclusion: Photodynamic therapy using liposome-encapsulated 0.5% 5-ALA improved inflammatory acne with minimal side effects in Asians.     

Salicylic acid treats acne vulgaris by suppressing AMPK/SREBP1 pathway in sebocytes

Acne vulgaris is a prevalent cutaneous disease characterized by a multifactorial pathogenic process including hyperseborrhea, inflammation, over‐keratinization of follicular keratinocytes and Propionibacterium acnes (P acnes) overgrowth. Salicylic acid (SA), a beta‐hydroxy acid, is frequently used in the treatment of acne. SA has been found to decrease skin lipids and to possess anti‐inflammatory properties. However, few studies have elucidated the mechanisms and pathways involved in such treatment of acne. In this study, we initially investigated the anti‐acne properties of SA in human SEB‐1 sebocytes. Treatment with SA decreased sebocyte lipogenesis by downregulating the adenosine monophosphate‐activated protein kinase (AMPK)/sterol response element‐binding protein‐1 (SREBP‐1) pathway and reduced inflammation by suppressing the NF‐κB pathway in these cells. Salicylic acid also decreased the cell viability of SEB‐1 by increasing apoptosis via the death signal receptor pathway. Subsequently, histopathological analysis of a rabbit ear acne model after application of SA for three weeks confirmed that SA suppressed the levels of cytokines and major pathogenic proteins around acne lesions, which supports the mechanisms suggested by our in vitro experiments. These results initially clarified that therapeutic activities of SA in acne vulgaris treatment could be associated with the regulation of SREBP‐1 pathway and NF‐κB pathway in human SEB‐1 sebocytes.     

A Retrospective Cohort Study and Clinical Classification System of Acne Keloidalis Nuchae

BACKGROUND: Although many treatments are available for acne keloidalis nuchae (AKN), no systematic classification scheme exists to evaluate the outcomes of these treatments. OBJECTIVE: This study aimed to propose an AKN classification scheme. METHODS: A retrospective data analysis of several parameters, including lesion distribution, lesion type, and scalp disease association, was conducted in 108 men diagnosed with AKN between July 2009 and November 2020 in an outpatient dermatology setting. A three-tier classification system was developed as follows: Tier 1, lesion distribution relative to an area demarcated by two horizontal lines on the occipital prominences and tips of the mastoid processes and lesion sagittal width defined using Classes I through IV; Tier 2, lesion types including papules/nodules (discrete/merged), plaques, and tumorous masses; and Tier 3, the presence or absence of folliculitis decalvans (FD) or dissecting cellulitis (DC). RESULTS: All patients were non-white men, with most being of African (58%) or Hispanic (37%) descent. The most prevalent Tier 1 AKN presentation was Class II (58%). The mean sagittal width for Classes I through III were 2.4cm (I), 4.5cm (II), and 8.0cm (III), with Class IV characterized by widespread scalp disease. Plaques were most common in Tier 2-type lesions. FD or DC was found in seven percent of the study participants. Patients of African descent had a greater tendency to develop tumorous masses (p<0.02). LIMITATIONS: The retrospective study design and possible selection bias. CONCLUSION: We proposed an AKN classification scheme as a tool for objectively describing AKN lesions and evaluating treatment outcomes.