International Journal of Dermatology最新文献

Kidney transplant recipients (KTRs) are at increased risk of developing cutaneous squamous cell carcinoma (cSCC), particularly when treated with calcineurin inhibitors (CNI), which are strongly associated with tumorigenesis. In contrast, mTOR inhibitors such as sirolimus have demonstrated antitumor activity, but their role in secondary prevention of cSCC remains unclear. We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) to evaluate the impact of switching from a CNI-based to an mTOR inhibitor-based immunosuppressive regimen on the incidence of cSCC in KTRs with prior cSCC. MEDLINE, EMBASE, CENTRAL, and trial registries were searched through June 2025. Incidence rate ratios (IRRs) for cSCC and risk ratios (RRs) for adverse events (AEs) were pooled using a random-effects model. Risk of bias was assessed with Cochrane RoB2. The study was registered in PROSPERO prior to data extraction (CRD42024583966). The study was unfunded. Four RCTs (393 patients) were included. Sirolimus significantly reduced 2-year cSCC incidence (IRR 0.51, 95% CI 0.39-0.67). However, discontinuation was more frequent (RR 8.60, 95% CI 1.95-37.93) due to AEs. No significant differences in mortality or graft rejection were found. Certainty of evidence was high for cSCC incidence and low for adverse events due to heterogeneity and selective reporting. In conclusion, sirolimus reduces secondary cSCC risk but increases AEs; patient selection and monitoring are essential. Trial Registration: PROSPERO number: CRD42024583966.

Background: Enfortumab vedotin (EV) frequently causes cutaneous eruptions that can mimic erythema multiforme and Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN), complicating management decisions.

Objective: The aim of this study was to define reproducible clinicopathologic patterns and evaluate immunohistochemical markers that distinguish EV-induced cutaneous toxicity (EVICT) eruptions from histologic mimics.

Methods: This retrospective case series included nineteen patients receiving EV (twenty-four biopsies), compared with ten controls (erythema multiforme or SJS/TEN). Blinded review assessed histologic patterns and immunohistochemistry for immunoglobulin G (IgG), Nectin-4, and cytotoxic T-cells.

Results: All cases showed interface dermatitis fitting one of four patterns: classic vacuolar, cytotoxic with epidermal dysmaturation, necrolytic SJS/TEN-like, or spongiotic interface. Epidermal "ring" mitoses were frequent in EV-related biopsies and absent in controls. Intercellular IgG staining occurred in 83% of EV cases versus 20% of controls, yielding an area under the curve of 0.86; any intercellular staining provided 82% sensitivity and 80% specificity, while moderate or strong staining achieved 100% specificity. Cytotoxic T-cell density and Nectin-4 expression did not reliably discriminate groups.

Limitations: Retrospective design, modest sample size, and potential confounding by concomitant therapies.

Conclusion: Intercellular IgG on routine immunohistochemistry, together with characteristic "ring" mitoses, provides a practical framework to identify enfortumab vedotin-associated eruptions and differentiate them from erythema multiforme and SJS/TEN.

Acquired progressive kinking of the hair (APKH) is an underrecognized hair disorder characterized by a gradual change in hair texture, often manifesting as increased curliness, frizziness, and darkening of the shafts. While various systemic triggers and congenital conditions can induce similar phenotypes, a subset of cases-particularly those involving the frontal and temporal scalp in young males-appears to be linked to androgen-mediated mechanisms. This narrative review focuses on the androgen-dependent phenotype of APKH, integrating clinical, trichoscopic, and histopathological findings and presenting a representative case. We also propose a conceptual framework for distinguishing between androgen-dependent and non-androgen-dependent subtypes. A detailed analysis of all published cases meeting criteria for androgen-sensitive APKH is provided, highlighting patterns of progression, diagnostic clues, and therapeutic implications. Recognizing this presentation as a potential early manifestation of androgenetic alopecia may inform clinical decisions and prompt timely intervention.