Journal of Dermatology最新文献

Serizawa N, Okazaki S, Otsuka Y, Koto M, Okabe K, Ito M, et al. Dietary habits in Japanese patients with palmoplantar pustulosis. J Dermatol. 2021;48:366–375.

There were errors in Table 1 and Table 5. The correct Table 1 and Table 5 are shown below.

We apologize for these errors.

Prurigo chronica multiformis is a commonly used diagnostic designation for a peculiar subtype of prurigo in Japan, although the disease entity might not be well-recognized in other countries. Experts approved by the Japanese Dermatological Association attempted to build a common consensus on prurigo chronica multiformis, agreeing that it is a unique and important disease entity in elderly patients. Skin lesions are characterized by intensely pruritic, edematous, urticarial papules, or small macules, which gradually become solid papules/small nodules. The papules tend to aggregate and occasionally coalesce into polygonal lichenified plaques. The most commonly affected sites are the lower abdomen and lower back, although the chest, thighs, and upper back might also be involved. Common histopathological features of prurigo chronica multiformis include infiltration of lymphocytes and eosinophils in the upper dermis, with minimal epidermal changes. Basophil infiltration is also observed. The epidemiological incidence, differences in clinical manifestations by geographical location, and disease placement among other forms of prurigo and/or related skin diseases need to be further elucidated. Dermatologists should be aware of the clinical characteristics of prurigo chronica multiformis.

Kitano T, Koiwai T, Fujikawa K, Mori S,Matsumoto T, Sato T. Ozenoxacin suppresses sebum production by inhibiting mTORC1 activation in differentiated hamster sebocytes. J Dermatol. 2024;51:1187–98. https://doi.org/10.1111/1346-8138.17409

In the legend of Figure 2, the text “^$P < 0.05 compared with insulin (Tukey's multiple comparison test).” was incorrect. This should have read: “^$P < 0.05 compared with 5α-DHT (Tukey's multiple comparison test).”

In the legend of Figure 4, the text “^#P < 0.05 compared with insulin +10⁻³ N NaOH (Dunnett's multiple comparison test).” was incorrect. This should have read: “^#P < 0.05 compared with 5α-DHT +10⁻³ N NaOH (Tukey's multiple comparison test).”

In the legend of Figure 4, the text “^$P < 0.05 compared with insulin (Dunnett's multiple comparison test).” was incorrect. This should have read: “^$P < 0.05 compared with 5α-DHT (Tukey's multiple comparison test).”

In the legend of Figure 5, the text “^‡P < 0.05 compared with insulin + ozenoxacin 100 μmol/L, or 5α- DHT+ ozenoxacin 10 μmol/L (Tukey's multiple comparison test).” was incorrect. This should have read: “^‡P < 0.05 compared with insulin + ozenoxacin 30 μmol/L, or 5α- DHT+ ozenoxacin 10 μmol/L (Tukey's multiple comparison test).”

In the legend of Figure S1, the text “^#P < 0.05 compared with insulin + 10–3 N NaOH (Tukey's multiple comparison test).” was incorrect. This should have read: “^#P < 0.05 compared with 5α-DHT + 10⁻³ N NaOH (Tukey's multiple comparison test).”

We apologize for these errors.

Inflammatory diseases that are driven by several pro-inflammatory cytokines has resulted in in the development of targeted therapies across different disease settings. Interleukin (IL)-36 cytokines have been implicated in several inflammatory diseases. In this review we describe the scientific evidence surrounding the use of the IL-36 receptor (IL-36R)-targeting antibody, spesolimab, in IL-36-mediated skin diseases: generalized pustular psoriasis (GPP), palmoplantar pustulosis (PPP), hidradenitis suppurativa, and Netherton syndrome (NS). Spesolimab, a high affinity, specific, humanized, antagonistic immunoglobulin G1 antibody, targets the IL-36R at a binding site distinct from its agonists, IL-36α/β/γ, and at least one endogenous antagonist, IL-36R antagonist. In vitro and in vivo data for spesolimab show effective inhibition of IL-36R-mediated signaling pathways, and six Phase I studies in healthy volunteers presented a favorable safety and pharmacokinetic (PK) profile, leading to the development of a clinical trial program to evaluate spesolimab in the treatment of IL-36R-mediated diseases. Six studies (including an expanded access program) have evaluated the efficacy, safety, PKs, and pharmacogenomics of spesolimab in patients with GPP flares. Spesolimab treatment of GPP flares resulted in rapid and sustained improvements in pustular and skin clearance, and clinically significant improvements in patient-reported symptoms and quality of life. Spesolimab also significantly reduces the risk of GPP flares and flare occurrence, preventing disease worsening and has a favorable safety profile. There have been three trials of spesolimab in PPP; further evaluation is needed to better define those patients who might benefit from the treatment. A trial of spesolimab in NS is ongoing, while other spesolimab trials suggest that IL-36 may only play a secondary role in the pathogenesis of atopic dermatitis. In conclusion, research into spesolimab has provided much needed insight into the role of IL-36 in the human immune system and the mechanism behind IL-36-mediated inflammatory diseases. Spesolimab provides an efficacious targeted treatment for GPP, a disease with a high unmet medical need.

This post-hoc analysis of the ALLEGRO phase 2b/3 study (NCT03732807) evaluated the efficacy and safety of ritlecitinib, an oral Janus kinase 3/TEC family kinase inhibitor, in patients with alopecia totalis (AT) and alopecia universalis (AU). Patients aged ≥ 12 years with alopecia areata (AA) and ≥50% scalp hair loss received once-daily ritlecitinib 50 or 30 mg (± 4-week 200-mg loading dose) or placebo for 24 weeks. In a subsequent 24-week extension period, the ritlecitinib groups continued their doses and patients initially assigned to placebo switched to ritlecitinib (200/50 or 50 mg daily). In this analysis, clinician- and patient-reported hair regrowth outcomes were assessed at weeks 24 and 48 in four AA subgroups: AT/AU, AT, AU, and non-AT/AU. Safety was monitored throughout. Of the 718 randomized patients, 151 (21%) and 147 (20%) were defined as having AT or AU, respectively. At week 24, Severity of Alopecia Tool (SALT) score ≤20 (≤20% scalp hair loss) response rates were higher in the ritlecitinib-treated AT/AU, AT, and AU groups (7%–14%, 7%–21%, and 4%–10%, respectively) vs the placebo group (0% in the AT/AU, AT, and AU groups). The proportions of patients with a SALT score of ≤20 increased through week 48 (AT/AU, 13%–31%; AT, 11%–27%; AU, 6%–41%). Additionally, at week 24, 25%–43%, 32%–42%, and 12%–50% of patients with AT/AU, AT, and AU, respectively, who received ritlecitinib achieved a moderately or greatly improved response based on the Patient Global Impression of Change scale. Response rates generally increased through week 48 and were similar across AA subgroups. In patients with AT/AU, ritlecitinib was well tolerated with a safety profile consistent with that of the overall AA population. Ritlecitinib demonstrated clinical efficacy, patient-reported improvement, and an acceptable safety profile in patients with AT and AU through week 48. A plain language summary of this study is available at https://doi.org/10.25454/pfizer.figshare.26879161. Clinicaltrials.gov: NCT03732807.

Bimekizumab treatment has demonstrated significant improvements in clinical outcomes in patients with moderate to severe plaque psoriasis; however, studies so far have focused on predominantly White patient populations from North America and Europe, with one smaller study in a Japanese population. Here, clinical responses, safety, and tolerability of bimekizumab treatment in Korean patients are reported. Korean patients with moderate to severe plaque psoriasis were randomized to bimekizumab 320 mg every 4 weeks (Q4W) or placebo Q4W to week 16. Co-primary efficacy end points were achievement of ≥90% improvement from baseline in the Psoriasis Area and Severity Index (PASI 90) and Investigator's Global Assessment score of 0/1 (clear/almost clear) at week 16. Secondary efficacy end points included achievement of PASI 75 at week 4 and Dermatology Life Quality Index 0/1 at week 16. Safety outcomes were also assessed. Statistical analysis of the co-primary efficacy end points was performed using a type I error rate, at a two-sided α level of 0.05. Overall, 47 Korean patients were randomized to treatment (bimekizumab: 32, placebo: 15). At week 16, bimekizumab-treated patients had significantly higher clinical responses versus placebo-treated patients (PASI 90: 81.3% vs. 0%; IGA 0/1: 87.5% vs. 0%, p < 0.001 for both). Bimekizumab showed a rapid onset of clinical response, with 75.0% of patients achieving PASI 75 by week 4 (0% in placebo patients [nominal p < 0.001]). A higher proportion of bimekizumab-treated patients achieved DLQI 0/1 at week 16 (46.9% vs. 6.7% in placebo patients, nominal p = 0.007), indicating greater improvements in health-related quality of life (HRQoL) following bimekizumab treatment. Bimekizumab was well-tolerated in Korean patients, with no new safety signals identified. Treatment with bimekizumab led to rapid improvements in clinical responses and HRQoL versus placebo in Korean patients, consistent with responses in global populations. These findings suggest that bimekizumab is an effective and well-tolerated treatment option in Korean patients with psoriasis.

Tapinarof is a nonsteroidal, topical, aryl hydrocarbon receptor agonist. We evaluated the efficacy and safety of tapinarof cream 1% in Japanese patients aged ≥12 years with atopic dermatitis (AD) in two phase 3 trials, ZBB4-1 and ZBB4-2. ZBB4-1 (N = 216) consisted of an 8-week, double-blind, vehicle-controlled treatment period (period 1) and a 16-week extension treatment period (period 2). Patients were randomized 2:1 to tapinarof or vehicle in period 1; subsequently, all patients who enrolled in period 2 received tapinarof. ZBB4-2 (N = 291) was a 52-week, open-label, uncontrolled trial in which all patients received tapinarof. In period 1 of ZBB4-1, the proportion of patients who achieved an Investigator's Global Assessment (IGA) score of 0 (clear) or 1 (almost clear) with ≥2-grade improvement from baseline at week 8 (IGA treatment success, the primary end point) was 20.24% in the tapinarof group and 2.24% in the vehicle group (p = 0.0007). The proportion of patients with ≥75% improvement from baseline in Eczema Area and Severity Index (EASI) score at week 8 (EASI-75 response, the key secondary end point) was 40.3% in the tapinarof group and 4.3% in the vehicle group (p < 0.0001). In ZBB4-2, IGA treatment success rate was 28.1% at week 16, 32.3% at week 24, and 41.3% at week 52, and EASI-75 response rate was 53.3% at week 16, 63.7% at week 24, and 76.6% at week 52, indicating that efficacy responses improved over time and were maintained over 52 weeks. Across the two trials, most adverse events (AEs) were mild or moderate; common AEs included folliculitis, acne, and headache. In summary, tapinarof cream 1% was effective and generally safe for up to 52 weeks of treatment in Japanese patients with AD.