Systemic inflammation plays a central role in the pathophysiology of psoriasis. This study examined accessible systemic inflammatory markers in patients with psoriasis vulgaris and psoriatic arthritis. We aimed to evaluate their association with psoriasis severity, the presence of arthritis, and drug continuation rates. The findings revealed that neutrophil, monocyte, and platelet count, neutrophil/lymphocyte ratio, monocyte/lymphocyte ratio, systemic inflammation response index, systemic immune/inflammation index (SII), and CRP were positively correlated with Psoriasis Area and Severity Index scores. Patients presenting with higher platelet/lymphocyte ratio (PLR) or CRP values were more likely to be diagnosed with psoriatic arthritis than with psoriasis vulgaris in the multivariate regression analysis. Importantly, patients with higher pretreatment neutrophil or platelet count, PLR, and SII were associated with lower treatment continuation rates of conventional systemic agents. Higher pretreatment scores of systemic inflammatory markers did not affect treatment retention rates of biologics. These findings suggest that several accessible systemic inflammatory markers may effectively assess underlying systemic inflammation and may provide an indication for a therapeutic approach in patients with psoriasis vulgaris and psoriatic arthritis.

Dear Editor, Circumscribed palmoplantar hypokeratosis (CPH), which was first reported in 2002 by P erez et al., 1 is typically identified as a well-circumscribed, solitary, long-standing and asymptomatic depressed annular erythema on the palmar or plantar surfaces that predominantly occurs in middle-aged to elderly women. Histopathologically, it is characterized by an abrupt decrease in the horny layer thickness, forming a sharp stair between normal and involved skin. Despite its distinct clinical and histopathological features, it is often misdiagnosed as Bowen's disease because of its rarity. We witnessed a case of pigmented CPH showing a parallel ridge pattern (PRP) under dermoscopy; it had to be differentiated from acral lentiginous melanoma (ALM) which is a common melanoma subtype in Asian patients. To our knowledge, this is the first report of pigmented CPH mimicking ALM. An 80-year-old Japanese woman presented at our hospital with a 1-year history of a brown patch on the right arch of her sole, 15 mm in diameter, depressed, with a partially irregular border and color variegation; she did not have plantar hyperhidrosis. Dermoscopic examination revealed PRP and pigmentation around the porus sudoriferus. On palpation, a dent suggestive of the loss of the stratum corneum was felt. Although CPH was the primary diagnosis, a partial biopsy was performed to exclude ALM. The biopsy specimen included

Bullous pemphigoid (BP) is an autoimmune disease characterized by autoantibody-mediated activation of immune cells and subepidermal blister formation. Excess amounts of extracellular DNA are produced in BP, however, it remains unclear how extracellular DNA contributes to BP pathogenesis. Here we show a possible mechanism by which interleukin (IL)-26 binds to extracellular DNA released from neutrophils and eosinophils to support DNA sensing. Patients with BP exhibited high circulating levels of IL-26, forming IL-26–DNA complexes in the upper dermis and inside the blisters. IL-26–DNA complexes played a dual role in regulating local immunity and blister formation. First, they enhanced the production of inflammatory cytokines in monocytes and neutrophils. Second, and importantly, the complexes augmented the production and activity of proteases from co-cultured monocytes and neutrophils, which induced BP180 cleavage in keratinocytes and dermal-epidermal separation in a modified human cryosection model. Collectively, we propose a model in which IL-26 and extracellular DNA synergistically act on immune cells to enhance autoantibody-driven local immune responses and protease-mediated fragility of dermal-epidermal junction in BP.