The Journal of dermatology最新文献

Palisaded neutrophilic and granulomatous dermatitis (PNGD) is a reactive granulomatous dermatitis; the umbrella term includes interstitial granulomatous dermatitis and interstitial granulomatous drug reaction, in addition to PNGD. The histological findings of PNGD include leukocytoclastic vasculitis, neutrophilic infiltrates, and collagen degeneration with palisades of histiocytes and small granulomas. Clinically, the patients show symmetrical, smooth papules that are skin-colored to red, some with central umbilication or crusting, located mainly on the elbows and extremities. PNGD usually occurs with some systemic diseases, such as systemic lupus erythematosus, suggesting a cutaneous reaction pattern due to underlying internal inflammation. Although the present case was histologically diagnosed as PNGD, while excluding other granulomatous diseases, multiple indurated erythematous papules with a tendency to coalesce widely were seen, mimicking erythroderma without any underlying immunological diseases. In addition, the eruption coincided with fluctuating high fever. This was a rare case of PNGD with no underlying immunological disease that presented with severe manifestations such as fever and erythroderma.

Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by pruritus, barrier dysfunction, and complex immune dysregulation. Phototherapy with narrow-band ultraviolet B (NB-UVB) or 308 nm excimer devices is clinically effective for AD, but the underlying mechanisms remain incompletely understood. In this study, we investigated the therapeutic effects of a 308-nm excimer lamp using a murine model of AD induced by topical application of the vitamin D3 analog MC903. C57BL/6 mice were treated with MC903 for 13 consecutive days, with or without irradiation by a 308-nm excimer lamp at 100 mJ/cm² every other day. Clinical severity was assessed daily, and histological, immunohistochemical, and molecular analyses were performed on lesional skin. Excimer irradiation significantly alleviated MC903-induced dermatitis from days 4 to 12, with reduced clinical severity scores, epidermal thickness, and acanthosis compared with non-irradiated controls. Immunohistochemical analysis revealed a significant decrease in intraepidermal PGP9.5-positive nerve fibers in irradiated mice, suggesting that excimer therapy attenuates pruritus through neuroimmune modulation. Furthermore, excimer irradiation increased dermal infiltration of Foxp3-positive regulatory T cells and decreased plasma IgE levels, although no significant upregulation of IL-10 mRNA was detected. Importantly, quantitative PCR demonstrated that excimer irradiation reduced thymic stromal lymphopoietin (TSLP) expression in lesional skin, while levels of other Th2-related cytokines such as IL-4 and IL-13 remained unchanged. These findings indicate that 308-nm excimer lamp therapy ameliorates AD-like dermatitis through dual mechanisms: suppression of intraepidermal nerve fibers and downregulation of epithelial-derived TSLP, together with enhanced regulatory T-cell infiltration. This study provides new mechanistic insights into the immunological and neurocutaneous effects of excimer phototherapy, supporting its clinical use in AD and potentially other inflammatory skin diseases.

Atopic dermatitis (AD) essentially exhibits dysbiosis of skin fungal microbiome, mycobiome, characterized by depletion of Malassezia. The effects of recent systemic therapies for AD on skin mycobiome were not understood enough. We examined changes of skin mycobiome before and after systemic treatments with anti-IL-4Rα antibody (dupilumab: DUP) and calcineurin inhibitor (cyclosporine, CyA). Swab samples from postauricular areas in 19 AD patients treated with dupilumab (n = 13) and cyclosporine (n = 6) were collected before and 4-8 weeks after starting each treatment. Fungal DNA was amplified from the samples and sequenced with ITS1 metagenomic analysis, and taxonomic classification was performed. Fungi belonging to total 89 genera were detected. The share of the fungus was most occupied by Malassezia (81.3%), followed by Aspergillus (3.7%), and Trametes (1.1%) before DUP and CyA treatment, and occupied by Malassezia (87.3%), followed by Aspergillus (1.9%), and Candida (1.7%) after treatment. Three AD patients whose ratio of Malassezia in the skin mycobiome was under 50%, showed an exploratory increase of Malassezia after treatments (before 17.3%, after 67%). Analysis of the Malassezia species revealed an increase in M. restricta (before 70.5%, after 79.5%) and a decrease in M. globosa (before 23.9%, after 16.1%). No consistent patterns distinguishing DUP and CyA were observed. Systemic treatment with DUP and CyA was associated with shifts toward higher Malassezia abundance and modulation between M. restricta and M. globosa. These findings are exploratory and require validation in larger controlled studies.

This study aimed to evaluate the clinical efficacy of combination therapy with clindamycin and benzoyl peroxide in treating acne vulgaris. We assessed the antimicrobial susceptibility of Cutibacterium acnes isolates obtained from these patients. In addition, the potential risk of C. acnes developing resistance to clindamycin and benzoyl peroxide following exposure was investigated in vitro. We analyzed 182 C. acnes isolates from patients with acne to evaluate the clindamycin susceptibility and resistance determinants and to examine the association between topical clindamycin use and resistance. We also tested the resistance frequency of C. acnes to clindamycin monotherapy and clindamycin/benzoyl peroxide combination therapy in vitro. The clindamycin resistance rates in the clindamycin/benzoyl peroxide and clindamycin monotherapy groups were 22.9% and 46.7%, respectively. The combination group showed a significantly lower clindamycin resistance rate (p < 0.05). Under clindamycin monotherapy, resistant strains emerged at a frequency of 8.1 × 10^-8 to 8.7 × 10^-8, whereas no resistant strains were detected under clindamycin/benzoyl peroxide combination conditions. The combination of clindamycin and benzoyl peroxide effectively suppressed the emergence of clindamycin-resistant C. acnes.