A 57-year-old Japanese man had been diagnosed with psoriasis vulgaris based on the presence of widespread erythema on his whole body at 5 years prior to his current presentation. He had persistent erythema on the upper back and lumbar areas that was resistant to the topical treatment of the strongest class of corticosteroid (clobetasol propionate 0.05%) and narrow-band ultraviolet B (UVB) therapy for 3 years. Oral apremilast was introduced but discontinued soon because of severe headaches. Then, because he refused to undergo expensive treatments, reactive administration of oral deucravacitinib (6 mg/day) was initiation, which resulted in the disappearance of skin eruptions 3 months later. Thereafter, topical betamethasone butyrate propionate 0.05% ointment and weekly or biweekly narrow-band UVB exposure prevented the development of exacerbations for 9 months. However, since severe erythema appeared on the elbow and knee, deucravacitinib was again started; 4 weeks later, the erythema disappeared. Finally, maintenance therapy with topical betamethasone butyrate propionate and narrow-band UVB well controlled his condition for 1 year. Together, the reactive administration of deucravacitinib was useful for patients with psoriasis who wish to reduce their treatment cost.

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A 77-year-old Japanese male was referred to our department for an often-blistering skin lesion on his left wrist, which had developed about 3 years ago. At the initial visit to our department, a clinical examination revealed a 16x18-mm erythematous nodule with a blistered surface on the left wrist. A histological examination showed mild acanthosis with acantholysis and dyskeratotic keratinocytes, especially in the lower layers of the epidermis. The upper dermis showed a moderately dense cell infiltrate containing numerous eosinophils. Based on these clinical and histological findings, we made a diagnosis of acantholytic dyskeratotic acanthoma (ADA). The topical application of difluprednate ointment reduced the erythematous areas, and blisters no longer formed. ADA is a rare form of acanthoma, which histologically presents with acantholysis and dyskeratosis. ADA usually presents as a solitary nodule on the trunk. There have been no reports of ADA with blister formation to date. In our case, since the acantholysis was mainly localized to the lower layers of the epidermis and the lesion was located in the wrist area, we hypothesized that the blistering may have been caused by external forces, such as rubbing in daily life.

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We report the characteristics and course of 10 cases of highly pruritic atopic dermatitis treated with nemolizumab (anti-interleukin-31 receptor antibody) in our hospital. The cohort comprised nine men and one woman, with age, eczema area and severity index (EASI), and pruritus numerical rating scale (pNRS) score ranging from 24–76 years (mean: 54.3 years), 0.6–24.6 (mean: 15.3), and 5–10 (mean: 6.8), respectively. Half the patients had previously used biologics or Janus kinase (JAK) inhibitors, of which four had used dupilumab. Three patients discontinued nemolizumab during the treatment course. The EASI improved gradually, but the pNRS scores of all patients decreased after the first dose; six of the seven continuing patients achieved a pNRS score of 0–1 by 24 weeks. Immunoglobulin E (IgE) levels mostly remained unchanged. The levels of thymus and activation–regulated chemokine (TARC) stably decreased in two patients, but repeatedly increased and decreased in the others. Three of the four patients previously using dupilumab achieved a pNRS score of 0 after the first dose, while the remaining patient achieved a pNRS score of 0 after the second dose. Symptoms of itching improved earlier in patients previously using dupilumab. Among the seven types of biologics and JAK inhibitors available, nemolizumab was more effective in patients with severe itching whose skin symptoms could be moderately controlled with topical steroids. The clinical assessment tools EASI and pNRS score can be considered more insightful measures of treatment efficacy than IgE and TARC levels.

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Japanese spotted fever is a rickettsial infection that is transmitted by ticks carrying Rickettsia japonica. Although most cases occur in western Japan, reports of infection have been increasing nationwide due to the expansion of tick activity caused by global warming.^1)-3) We diagnosed and treated 18 cases of Japanese spotted fever in our department between April 2020 and November 2024. Several new findings were observed in these 18 cases. We found that gastrointestinal symptoms such as diarrhea occasionally preceded skin rash, which could delay dermatology consultation and lead to life-threatening conditions such as disseminated intravascular coagulation (DIC). A rash on the palms could be an additional sign of the diagnosis, and a severe rash was observed on the skin of the hemilateral lymphedema leg in one case. Histopathologically, microthrombosis is often observed in both tick bites and erythema lesions. Additionally, a latent period between a tick bite and disease onset may be longer than previously thought. In this paper, we present the results of the 18 cases and discuss the above points.

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