Objective To investigate whether macrophage ferroptosis occurs in atopic dermatitis (AD) lesions and its role in AD, and to elucidate the mechanism by which 4-octyl itaconate (4-OI) alleviates AD inflammatory skin damage by inhibiting oxidative stress and macrophage ferroptosis. Methods A total of 40 male C57BL/6 mice were used. Fifteen mice were randomly assigned to 3 groups (n=5 each): the blank control group received no treatment, and the other two groups were treated with calcipotriol (MC903) to establish the AD model. Skin lesions were collected on days 0, 7, and 14 post-modeling to observe histopathological changes, mRNA expression of IL-4, IL-5, and IL-13, and macrophage infiltration. Another 10 mice were randomly divided into sham and MC903-model groups (n=5 each). The sham group received topical ethanol, while the MC903-model group received topical MC903 for 14 consecutive days. The levels of oxidative stress, macrophage ferroptosis, and markers of the endogenous itaconate/Nrf2 pathway (Acod1, GPX4, PTGS2, Nrf2, and HO-1) in skin lesions were compared between the two groups. A further 15 mice were randomly divided into sham, MC903-model, and MC903+4-OI treatment groups (n=5 each). Mice in the MC903+4-OI group received intraperitoneal injection of 4-OI (50 mg/kg) concurrently with MC903 application for 14 consecutive days to evaluate the therapeutic effect of 4-OI on AD skin lesions. Histopathological changes were assessed by H&E staining. The expression levels of type 2 inflammatory cytokines (IL-4, IL-5, IL-13), ferroptosis-related markers, and GPX4, PTGS2, Nrf2, and HO-1 were detected by real-time quantitative PCR and Western blotting. Macrophage infiltration was examined by immunofluorescence. Oxidative stress was evaluated by ELISA for malondialdehyde (MDA) levels and by flow cytometry for DCFDA+ macrophages in lesional skin. Results Over time following MC903 induction, the epidermis of lesional skin in the model group showed progressive thickening (P<0.05), along with elevated levels of type 2 inflammatory cytokines IL-4, IL-5, and IL-13 (P<0.01) and increased macrophage infiltration. Compared with the sham group, the ferroptosis marker GPX4 was downregulated and PTGS2 was abnormally upregulated (P<0.01), while Acod1, Nrf2, and HO-1 were upregulated (P<0.01). Concurrently, increased malondialdehyde (MDA) content and an elevated proportion of DCFDA+ macrophages in lesional skin were observed (P<0.01). In contrast, treatment with 4-OI significantly ameliorated skin lesions (P<0.01), reduced the levels of IL-4, IL-5, and IL-13 (P<0.01), suppressed macrophage ROS and MDA production, and reversed the abnormal expression of GPX4 and PTGS2 (P<0.05) compared with the MC903 model group. Conclusions Macrophage ferroptosis is present in AD skin lesions, and 4-OI attenuates skin inflammatory damage by suppressing oxidative stress and macrophage ferroptosis.
Objective To summarize the cutaneous histopathological features of patients with dermatomyositis (DM), identify histopathological clues in patients with concomitant malignancies, and investigate histopathological differences among subtypes of myositis antibodies. Methods A total of 38 patients diagnosed with DM who underwent skin biopsy from January 2017 to October 2025 were retrospectively enrolled. The results of hematoxylin-eosin (HE) staining and direct immunofluorescence (DIF) were collected. A histopathological evaluation system consisting of 13 binary variables and 5 ordinal variables was established. According to the presence of concomitant malignancy, patients were divided into the cancer-associated myositis (CAM) group (n=6) and the non-cancer-associated myositis (Non-CAM) group (n=32). Based on the myositis antibody profile, patients were further subclassified into transcription intermediary factor 1-γ (TIF1-γ), Mi-2, melanoma differentiation-associated protein 5 (MDA5), nuclear matrix protein 2 (NXP2), small ubiquitin-like modifier activating enzyme 1 (SAE1), myositis-associated antibody (MAA), and seronegative subgroups. The cutaneous histopathological features of each group were summarized, and intergroup differences were analyzed. Results HE staining revealed lymphocytic infiltration at the dermoepidermal junction in all patients (100%). Common histopathologic features included basal cell liquefactive degeneration (86.84%), spongiosis (81.58%), edema of superficial dermal collagen fibers (81.58%), and pigment incontinence (78.95%). Among the 32 patients who underwent DIF, 12 (37.50%) were negative for all tested markers, whereas 12 (37.50%) had at least two positive DIF findings. Immunoglobulin M (IgM) deposition along the basement membrane zone (BMZ) was the most frequent finding (50.00%), whereas immunoglobulin A (IgA) deposition was the least frequent (3.13%). Compared with the Non-CAM group, the CAM group had a higher frequency of intracellular edema within the spinous layer (66.67% vs. 12.50%, P=0.012), as well as higher dyskeratosis scores (1.5 vs. 0.0; P=0.048) and basal cell liquefactive degeneration scores (2.0 vs. 1.0; P=0.032). The cutaneous histopathology of all antibody subtypes was dominated by the interface injury shared by DM. Conclusions The core histopathologic features of DM skin lesions are lymphocytic infiltration at the dermoepidermal junction and basal cell liquefactive degeneration. IgM deposition along the BMZ is the most common DIF finding and may aid in diagnosis. Compared with the Non-CAM group, the CAM group more frequently exhibited intracellular edema and showed more severe dyskeratosis and basal cell liquefactive degeneration, suggesting that these histopathologic changes may be associated with an increased risk of malignancy.
Objective To evaluate the short-term efficacy and safety of xeligekimab in patients with severe plaque psoriasis based on real-world data, and to perform an exploratory comparison with patients treated with secukinumab during the same period. Methods The clinical data of eligible patients with severe plaque psoriasis treated at the Department of Dermatology, Kaifeng People's Hospital, between September 2024 and December 2025 were retrospectively analyzed. The xeligekimab group included 23 patients, while the control group comprised 23 patients selected from 52 patients who received secukinumab during the same period using propensity score matching with a caliper value of 0.02. A total of 46 patients were included in the final analysis. The psoriasis area and severity index (PASI) scores and PASI 75/90/100 response rates were compared between the groups at baseline and at weeks 4 and 12. Investigator global assessment (IGA) scores and adverse reactions were also recorded. Results After matching, baseline characteristics showed no statistically significant differences between the two groups (all P values >0.05). At weeks 4 and 12, PASI scores decreased significantly compared with baseline in both groups (xeligekimab group: t=20.75 and 24.23, respectively; secukinumab: t=20.85 and 23.01, respectively; all P<0.001). IGA scores also decreased significantly at week 12 in both groups (xeligekimab: Z=-4.28; secukinumab: Z=-4.26; both P<0.001). No significant between-group differences were observed in PASI 75/90/100 response rates at weeks 4 and 12 (all P values >0.05). The overall incidence of adverse events was 8.70% (2/23) in the xeligekimab group and 13.04% (3/23) in the secukinumab group, with no statistically significant difference (P=1.000). Conclusions Xeligekimab showed favorable short-term efficacy and acceptable safety in the treatment of severe plaque psoriasis. The secukinumab reference group showed a similar pattern of clinical improvement. However, given the non-randomized,exploratory nature of this study, these findings warrant further validation in prospective studies.
Objective To compare the clinical efficacy and safety of warm versus room-temperature saturated saline soaking for the treatment of multiple plantar warts. Methods Sixty patients with multiple plantar warts were randomly assigned to a room-temperature group and a warm-saline group (n=30 each). Both groups underwent foot soaking in saturated saline prepared with food-grade refined salt conforming to GB 2721-2015 for 30 minutes once daily for 8 consecutive weeks. The soaking temperature was maintained at 26-35 ℃ in the room-temperature group and at 41 ℃ in the warm-saline group. Clinical efficacy was evaluated at weeks 2, 4, 6, and 8; the time to complete wart clearance was recorded among patients who achieved complete clearance; local adverse reactions were observed; and all cured patients were followed up for 6 months to assess recurrence. Results At weeks 2, 4, and 6, there were no significant between-group differences in the complete clearance rate or overall response rate (all P>0.05). At week 8, the complete clearance rate was significantly higher in the warm-saline group than in the room-temperature group (86.67% vs. 60.00%, P<0.05); the overall response rates at all time points showed no statistically significant difference between groups (all P>0.05). The time to complete wart clearance was 4 (4-6) weeks in both groups, with no significant between-group difference (P>0.05). No local adverse reactions were observed in either group throughout treatment. At 6-month follow-up, no new warts developed at the original lesion sites or within 3 cm of the surrounding skin among patients who had achieved complete clearance, and no recurrences were recorded. Conclusions Warm saturated saline soaking resulted in a higher complete clearance rate in the long-term period for multiple plantar warts compared with room-temperature saturated saline. Short-term lesion improvement, wart regression speed, safety profile, and long-term recurrence risk were comparable between the two groups. This therapy is non-invasive, cost-effective, and easy to administer, making it a viable option for home-based management of multiple plantar warts.
Objective To analyze the results and distribution characteristics of four preoperative bloodborne infection markers among dermatology patients. Methods A retrospective analysis was conducted on the results of the four preoperative infectious disease markers (HBsAg, anti-HCV, anti-TP, and HIV Ag/Ab) from 21 406 dermatology patients treated at the Dermatology Hospital, Southern Medical University between 2022 and 2023. Systematic screening and statistical analysis were performed to compare differences in positive rates between outpatients and inpatients, and across sex and age groups, and to analyze pattern of multiple-marker positivity. Results The overall positivity rate for the four preoperative markers among the 21 406 patients was 10.57% (2 263/21 406). The positive rates for each individual marker were as follows: HBsAg 6.46% (1 382/21 406, highest in the 31-40-year age group), anti-TP 3.06% (655/21 406, highest in the 21-30-year age group), anti-HCV 0.80% (172/21 406; highest in the 41-50-year age group), and HIV-Ag/Ab screening reactivity 0.25% (54/21 406; highest in the 31-40-year age group), pending confirmatory testing. The differences in the positivity rates of these four markers between outpatients and inpatients were all statistically significant (all P<0.05). Except for anti-HCV, positivity rates for the other three markers differed significantly by sex (P<0.05). The age distribution of patients testing positive for each marker showed statistically significant differences. A total of 114 cases of co-infection were identified, with HBsAg combined with anti-TP being the most common (56 cases, 49.12%). Conclusions The positivity rate of preoperative bloodborne infection markers was relatively high among dermatology patients and exhibits specific demographic characteristics. The positivity rate was higher among inpatients than among outpatients. Routine preoperative infection screening is crucial for identifying high-risk populations, implementing targeted occupational safety measures, and reducing the risk of healthcare-associated transmission and medicolegal disputes.
We report a case of inverted follicular keratosis (IFK) with seborrheic keratosis (SK). A 69-year-old man presented with a black-brown nodular with ulceration and recurrent bleeding on the left cheek for more than six months. Dermatological examination revealed a black-brown nodule measuring approximately 1.5 cm×0.6 cm on the left cheek. The lesion was elevated, with a rough surfaced and focal verrucous changes. It was firm, non-tender, and without induration at the base. Histopathological examination of the excised specimen showed hyperkeratosis, acanthosis, and papillomatosis. The proliferating cells consisted of basaloid cells and squamous cells, with pseudohorn cysts and squamous eddies. Increased numbers of neutrophils and lymphocytes were observed around the hair follicles and blood vessels, along with neutrophilic infiltration in the interlobular septa of the subcutaneous fat. The final diagnosis was IFK coexisting with SK. The lesion was completely excised, with no recurrence during 1-year of follow-up.
We report three cases of acneiform eruption induced by EGFR-TKIs. Three middle-aged or elderly patients with lung cancer presented with acneiform eruptions of varying severity involving the face, neck, back and buttocks after treatment with icotinib or gefitinib. Dermatological examination revealed erythema and papules on the face in patient 1; erythema, pustules, desquamation on the face in patient 2; papules, erythema and pustules on the neck, back and buttocks in patient 3. Histopathological examination of skin lesions from patients 2 and 3 revealed neutrophilic infiltration in the dermis. Histopathological data were unavailable for patient 1. A diagnosis of acneiform eruption was made in all three patients. After treatment with oral doxycycline and other supportive therapies, the eruptions improved. EGFR-TKI was continued throughout dermatologic treatment in all three patients. The skin eruption continued to improve during 2~3 week's follow-up.
Psoriasis is a chronic inflammatory disease involving immune dysregulation, abnormal proliferation of keratinocytes (KCs), and neurogenic inflammation, with its molecular mechanisms not yet fully elucidated. Ion channels, as core components of cellular signal transduction, play a pivotal regulatory role in these pathological processes. This article systematically summarizes recent advances in the roles of transient receptor potential (TRP) channels, potassium channels, calcium channels, purinergic P2X receptors (P2XR), and mechanosensitive Piezo channels in the dysfunction of KCs, immune-mediated inflammation, and neuro-immune-skin interactions in psoriasis. For the first time, it proposes a “Ca2+ signaling pathway network-chronic inflammation loop-neural sensitization” cascade amplification integration model, illustrating how different types of ion channels synergistically drive disease progression within the psoriatic microenvironment. Additionally, this review summarizes advances in the clinical translation of ion channel-targeted therapies, with a focus on the development status and challenges of candidate agents such as Kv1.3 inhibitors, calcium release-activated calcium (CRAC) channel antagonists, and TRPV channel modulators, aiming to provide new insights for precision-targeted treatment of psoriasis.
Vitiligo is a chronic inflammatory skin disorder characterized by acquired depigmentation and involves complex interactions among oxidative stress, genetic susceptibility, immune dysregulation, and microenvironmental abnormalities. Emerging evidence indicates that innate immune activation plays a pivotal role in both the initiation and maintenance of disease activity in vitiligo. Oxidative stress-induced melanocyte promotes the release of damage-associated molecular patterns, which activate pattern recognition receptors, including Toll-like receptors, NOD-like receptors, and the receptor for advanced glycation end products. This process subsequently activates dendritic cells, natural killer cells, and innate lymphoid cells, thereby amplifying inflammatory cascades and promoting adaptive immune activation through the IFN-γ/CXCL9/CXCL10 axis. In addition, emerging mechanisms such as ferroptosis, cuproptosis, and exosome-mediated immune regulation have been implicated in melanocyte injury and amplification of inflammation. With advances in reflectance confocal microscopy, optical coherence tomography, multiphoton microscopy, and serum biomarker assays, evaluation of vitiligo activity has gradually shifted from conventional morphological assessment toward dynamic, and precision-oriented monitoring based on disease-mechanisms. This review summarizes the core mechanisms of innate immune activation in vitiligo and their interactions with adaptive immunity, with particular emphasis on recent advances in noninvasive imaging, molecular biomarkers, multi-omics approaches, and artificial intelligence-assisted monitoring strategies. Current limitations and future perspectives for clinical translation are also discussed to inform precision diagnosis and individualized management of vitiligo.
Acquired reactive perforating collagenosis (ARPC) is a refractory pruritic dermatosis closely associated with systemic diseases, and conventional treatments often have limited efficacy. Recent studies have suggested that type 2 inflammation and the key cytokines IL-4/IL-13 may be involved in its pathogenesis. As a monoclonal antibody targeting IL-4Rα, dupilumab can simultaneously block the IL-4/IL-13 signaling pathway, providing a potential therapeutic option for ARPC. This review summarizes the pathogenesis of ARPC, the mechanism of action, clinical efficacy and safety of dupilumab, analyzes the limitations of current evidence, and outlines future research directions, with the aim of informing the diagnosis and management of ARPC.
As an effective therapeutic strategy for malignant neoplasms, boron neutron capture therapy (BNCT) has demonstrated promising clinical outcomes across various cutaneous malignancies. Multicenter studies in melanoma have reported complete response rates of 73%-78%, an overall disease control rate of 88%, and a 5-year disease-specific survival of 58%, with manageable toxicities including cutaneous radiation injury. For genital melanoma and extramammary Paget disease, BNCT has shown promising efficacy. In the first-in-human phase Ⅰ trial for cutaneous angiosarcoma, BNCT achieved a best overall response rate of 70% and a 2-year overall survival rate of 90.0%. Additionally, BNCT has exhibited therapeutic potential in cutaneous metastases and soft tissue sarcomas with cutaneous or subcutaneous involvement. This review systematically summarizes clinical advances in BNCT for cutaneous malignancies and discusses its clinical feasibility, current limitations, and future prospects.
