BACKGROUND:Plantar warts are among the most common skin lesions caused by the human papillomavirus (HPV) and are highly resistant to treatment. Obesity is a well-established factor for skin disease, yet few studies have focused on its association with plantar warts. This study aimed to describe the clinical characteristics of plantar warts and their relationship with body mass index (BMI). METHODS:This retrospective case series included patients with plantar warts treated at the dermatology department of the Third People's Hospital of Hangzhou between May 2023 and March 2025. An electronic medical record system was used to collect participants' demographic and clinical data. Dermoscopy was used to evaluate wart dermatological features, focusing on two key aspects: vascularity and surface patterns. Patients were categorized into two groups based on BMI: BMI ≥ 24.0 kg/m2 and BMI < 24.0 kg/m2, to compare their dermatological characteristics. RESULTS:A total of 262 patients with plantar warts were included in the study (average age: 37 ± 12.75 years), with more females (55.73%) than males (44.27%). Most plantar warts were single lesions (66%) and appeared predominantly on the soles (49%) and toes (29%). Dermoscopically, the majority exhibited dotted blood vessels (79%) and a yellow or brown color, both for the background (74%) and surface pattern (68%). Among the 262 patients, 90 were in the BMI ≥ 24.0 kg/m2 group (34.25%), and 172 were in the BMI < 24.0 kg/m2 group (65.65%). Compared to the BMI< 24 kg/m2 group, the BMI≥24 kg/m2 group had a significantly higher proportion of males (61.11% vs. 35.47%, p < 0.001), frogspawn (35.56% vs. 19.77%, p = 0.012), and papilliform patterns (7.78% vs. 5.81%). No statistically significant differences were observed in age, number of warts, location, background color, and vascular characteristics between the two groups (p > 0.05). CONCLUSIONS:This case series demonstrate the utility of dermoscopy as a non-invasive and cost-effective tool for identifying and characterizing the features of plantar warts. Our descriptive findings revealed variations in the dermoscopic patterns of plantar warts across different BMI categories. Our findings offer preliminary insights into the clinical presentation of plantar warts, paving the way for future studies with more robust design and statistical analysis.

BackgroundCutaneous T-cell lymphoma (CTCL) is a heterogeneous group of T-cell lymphomas characterized with the presence of clonal malignant T cells. Mycosis fungoides (MF) is the most common type of CTCL. However, the pathogenesis of MF and the role of the tumor microenvironment (TME) remain unclear.MethodsWe performed single-cell RNA sequencing on tumor and adjacent normal tissues and peripheral blood mononuclear cell (PBMC) from patients with advanced MF and healthy control (HC). We compared skin lesions in different stages within the same patient to overcome inter-individual variability.ResultsThe malignant clones displayed dual phenotypes characterized with tissue-resident memory T cells (TRMs) and central memory T cells (TCMs). We supposed that the tumor cells transformed from TRM-dominant phenotype to TCM-dominant phenotype during MF progressed from early-stage to advanced-stage. The cancer-associated fibroblasts (CAFs) showed active role in TME. The occurrence of inflammatory CAFs (iCAFs) may represent the advanced-stage MF. There may be mutual positive feedback of the crosstalk between tumor cells and CAFs during the MF development. Tumor cells promote CAF generation, and the CAFs, in turn, improve the invasiveness and metastasis of the malignant T cells through the IL-6/JAK2/STAT3/SOX4 or IL-6/HIF-1α/SOX4 pathway. SOX4 may be a critical regulatory gene of this positive feedback loop. Target SOX4 may disrupt the interactions between tumor cells and CAFs.ConclusionOur study revealed the origin and evolution trajectory of MF and uncovered the intercellular interactions between malignant T cells and CAFs, providing new insights into the novel treatment targets of MF.

Mycosis fungoides (MF) is a low-grade malignant cutaneous T-cell lymphoma that originates from memory T cells. It typically follows a unique and relatively indolent disease course. MF is used to be characterized by a tissue-resident memory T cell (TRM) phenotype, although recent molecular research has revealed its complexity, casting doubt on the cell of origin and the TRM-MF paradigm. Recent clonal heterogeneity studies suggest that MF may originate from immature early precursor T cells. During development, the tumour microenvironment (TME) influences tumour cell phenotype. The exact origin and development trajectory of MF remains elusive. Clarifying the origin of MF cells is vital for accurate diagnosis and effective treatment.

Male obesity is a pandemic health issue and can disrupt testicular steroidogenesis. Here, we explored the mechanism by which High-fat diet (HFD)-induced steroidogenic inhibition. As expected, HFD induced lipid droplet accumulation and reduced the expression of StAR, P450scc, and 3β-HSD, three steroidogenic enzymes, in mouse testes. Palmitic acid (PA), a saturated fatty acid is usually used to trigger lipotoxicity in vitro, induced greater accumulation of lipid droplets and the downregulation of steroidogenic enzymes in TM3 cells. Mechanistically, both HFD and PA disturbed mitochondrial fusion/fission dynamics, and then induced mitochondrial dysfunction and mitophagy inhibition in mouse Leydig cells. Additionally, mitochondrial fusion promoter M1 attenuated PA-induced imbalance of mitochondrial dynamics, mitophagy inhibition, mitochondrial reactive oxygen species (ROS) production and mitochondrial dysfunction in TM3 cells. Mitofusin 2 (MFN2) knock-down further aggravated PA-induced imbalance of mitochondrial dynamics, mitochondrial ROS production and mitochondrial dysfunction in TM3 cells. Importantly, M1 rescued PA-induced downregulation of steroidogenic enzymes, whereas MFN2 knock-down further aggravated PA-induced downregulation of steroidogenic enzymes in TM3 cells. Overall, our results provide laboratory evidence that mitochondrial dysfunction and mitophagy inhibition caused by dysregulation of mitochondrial fusion may be involved in HFD-induced steroidogenesis inhibition in mouse Leydig cells.

Purpose:To summarize the clinical, histopathological and therapeutic features of senile gluteal dermatosis.Patients and Methods:Retrospective analysis of 230 cases who visited the outpatient clinic of Hangzhou No. 3 People's Hospital for skin lesions on the buttocks and hips from 2018.8-2023.8 were included in the study, basic clinical information was collected, and they were subjected to physical examination of the buttocks and hips, and 36 cases were senile gluteal dermatosis, of which 7 underwent histopathological biopsy.Results:A total of 230 patients were included, of which 36 were diagnosed with geriatric buttock dermatosis, with a mean age of (84.2±12.6) years, mean body mass index of (21.7±3.8) kg/m2, and a male to female ratio of 2:1. There was a significant correlation between the occurrence of the disease and age, gender, body mass index, sedentary time, type of chair used, and hypertension (P<0.05). The severity of the lesions may be associated with longer sitting time and prolonged use of bamboo chairs (P<0.05). Histopathologic changes were not specific. The skin lesions could subside after general treatment such as improvement of lifestyle, use of pressure-reducing air mattresses, salicylic acid cream, and moisturizing creams.Conclusion:Senile gluteal dermatosis is a common senile physical dermatosis, mainly manifested as brownish scaly plaques, erythema and crusted ulcers, which can often be cured under reasonable treatment.

The authors report no conflicts in this work. Data sharing is not applicable to this article as no new data were created or analyzed in this study.

The Journal of DermatologyEarly View LETTER TO THE EDITOR Oral abrocitinib in the treatment of refractory dissecting cellulitis of the scalp: A case report Sha Jin, Sha Jin orcid.org/0009-0008-8596-6133 Department of Dermatology, Hangzhou Third People's Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, ChinaSearch for more papers by this authorChao Yue, Chao Yue Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, ChinaSearch for more papers by this authorShiwen Wang, Shiwen Wang Department of Dermatology, Hangzhou Third People's Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, ChinaSearch for more papers by this authorPing Wang, Corresponding Author Ping Wang [email protected] Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China Correspondence Ping Wang, Department of Dermatology, Hangzhou Third People's Hospital, West Lake Road 38, Hangzhou 310009, China. Email: [email protected]Search for more papers by this author Sha Jin, Sha Jin orcid.org/0009-0008-8596-6133 Department of Dermatology, Hangzhou Third People's Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, ChinaSearch for more papers by this authorChao Yue, Chao Yue Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, ChinaSearch for more papers by this authorShiwen Wang, Shiwen Wang Department of Dermatology, Hangzhou Third People's Hospital Affiliated to Zhejiang Chinese Medical University, Hangzhou, ChinaSearch for more papers by this authorPing Wang, Corresponding Author Ping Wang [email protected] Department of Dermatology, Hangzhou Third People's Hospital, Hangzhou, China Correspondence Ping Wang, Department of Dermatology, Hangzhou Third People's Hospital, West Lake Road 38, Hangzhou 310009, China. Email: [email protected]Search for more papers by this author First published: 11 April 2024 https://doi.org/10.1111/1346-8138.17232Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat No abstract is available for this article. REFERENCES 1Badaoui A, Reygagne P, Cavelier-Balloy B, Pinquier L, Deschamps L, Crickx B, et al. Dissecting cellulitis of the scalp: a retrospective study of 51 patients and review of literature. Br J Dermatol. 2016; 174: 421–423. 10.1111/bjd.13999 CASPubMedWeb of Science®Google Scholar 2Wu Q, Bu W, Zhang Q, Fang F. Therapeutic options for perifolliculitis capitis abscedens et suffodens: a review. Dermatol Ther. 2022; 35:e15763. 10.1111/dth.15763 CASPubMedWeb of Science®Google Scholar 3Alavi A, Hamzavi I, Brown K, Santos LL, Zhu Z, Liu H, et al. Janus kinase 1 inhibitor INCB054707 for patients with moderate-tosevere hidradenitis suppurativa: results from two phase II studies. Br J Dermatol. 2022; 186: 803–813. 10.1111/bjd.20969 CASPubMedWeb of Science®Google Scholar 4De SK. Abrocitinib: first globally approved selective Janus Kinase-1 Inhibitorfor the treatment of atopic dermatitis. Curr Med Chem. 2023; 30: 4278–4282. 10.2174/0929867330666230216123419 CASPubMedWeb of Science®Google Scholar 5Islam Z, Toker M, Gandhi IM, Sher A, Campton K. Improvement of recalcitrant dissecting cellulitis of the scalp after a trial of Upadacitinib. Cureus. 2024; 16:e52377. PubMedWeb of Science®Google Scholar Early ViewOnline Version of Record before inclusion in an issue ReferencesRelatedInformation

PURPOSE:Autoimmune bullous diseases, connective tissue diseases, and vasculitis represent a group of severe rare skin diseases. While glucocorticoids and immunosuppressive agents serve as standard treatments for these diseases, their efficacy is limited due to adverse side effects, indicating the need for alternative approaches. Biologics have been used in the management of some rare skin diseases. However, the use of biologics is associated with concerns, such as infection risk and high costs, prompting the quest for efficacious and cost-effective alternatives. This study discusses the safety issues associated with tofacitinib and its potential in treating rare skin diseases.METHODS:This narrative review focuses on the pharmacodynamic properties of tofacitinib and its impact on the JAK/STAT pathway. In addition, we present a comprehensive discussion of the effects and mechanism of action of tofacitinib for each severe rare skin disease.RESULTS:This role of tofacitinib in treating severe rare skin diseases has been discussed, shedding light on its promising prospects as a treatment modality. Few reports of serious adverse events are available in patients treated with tofacitinib.CONCLUSION:We explored the mechanism of action, efficacy, and safety considerations of tofacitinib and found that it can be used as a treatment option for rare skin diseases. However, multicenter clinical studies are needed to confirm the efficacy and safety of JAK inhibitors.

Acral melanoma (AM) is a subtype of melanoma with high prevalence in East Asians. AM is characterized by greater aggressiveness and lower survival rates. However, there are still fewer studies on immune mechanisms of AM especially subungual melanoma (SM) versus non-subungual melanoma (NSM). In order to explore tumor heterogeneity and immune microenvironment in different subtypes of AM, we applied single-cell RNA sequencing to 24,789 single cells isolated from the SM and plantar melanoma (PM) patients. Aspects of tumor heterogeneity, melanocytes from PM and SM had significant differences in gene expression, CNV and pathways in which tumor-associated such as NF-kb and Wnt were involved. Regarding the immune microenvironment, PM contained more fibroblasts and T/NK cells. The EPHA3-EFNA1 axis was expressed only in cancer-associated fibroblast (CAF) and melanocytes of PM, and the TIGIT-NECTIN2 axis was expressed in both AM subtypes of T/NK cells and melanocytes. Altogether, our study helps to elucidate the tumor heterogeneity in AM subpopulations and provides potential therapeutic targets for clinical research.

Disulfidptosis is a novel mechanism underlying actin-cytoskeleton-associated cell death, but its function in colorectal cancer (CRC) is still elusive. In this study, we investigated the potential role of Disulfidptosis-Related Long Non-Coding RNAs (DRLs) as prognostic indicators in CRC. Through transcriptome data from TCGA CRC cases, we identified 44 prognosis-correlated DRLs by Univariate Cox Regression Analysis and observed a differential expression pattern of these DRLs between CRC and normal tissues. Consensus clustering analysis based on DRL expression led to subgroup classification of CRC patients with distinct molecular fingerprints, accompanied by a superior survival outcome in cluster 2. We are encouraged to develop a score model incorporating 12 key DRLs to predict patient outcomes. Notably, this model displayed more reliable accuracy than other predictive indicators since DRLs are intimately related to tumor immune cell infiltration, suggesting a considerable potential of our DRL-score model for tumor therapy. Our data offered a valuable insight into the prognostic significance of DRLs in CRC and broke a new avenue for tumor prognosis prediction.

A 55-year-old female presented with a gradually enlarged red plaque and ulceration on the right side of her nose, face and suborbital region for ten years. The histopathologic features indicated infectious granuloma. The results of the fungal culture of the tissue and DNA sequencing identified as Cladosporium halotolerans infection. The patient was diagnosed with phaeohyphomycosis due to Cladosporium halotolerans. In this case, it was unsuitable for surgical treatment since the lesion was located periorbital. Furthermore, the patient had a poor response to oral itraconazole (400 mg/d) for 9 months. Therefore, ALA-PDT was added to the treatment regimen. The patient received ALA-PDT irradiation 5 times at 2-week intervals and achieved significant clinical remission. We believe that ALA-PDT may be an effective and safe adjuvant therapy.

BackgroundFollicular mucinosis (FM) is generally divided into a primary benign idiopathic form and a secondary form associated with mycosis fungoides.ObjectiveTo analyze the clinical and pathological features of FM and explore the pathological significance of CD103 expression.MethodsIn this case series, we retrospective analysis the clinical, pathological, treatment and follow-up treatment of 15 cases of FM. The expression of CD103 in all cases was detected by immunohistochemistry.ResultA total of 15 patients were enrolled, 7 were primary follicular mucinosis (P-FM) and 8 were mycosis fungoides-associated follicular mucinosis (MF-FM). Lesions of both P-FM and MF-FM are difficult to distinguish, present with red or dark red plaques and follicular papules. Pathologically, MF-FM showed more significant infiltrates of folliculotropic lymphoid cells, and the amount and proportion of CD103+ cells were significantly higher than that in P-FM. Follow-up data were available for 13 patients. Three cases were resolved after surgical resection, two patients were marked improved after oral administration of hydroxychloroquine and three times ALA photodynamic therapy respectively. The rest patients showed only modest efficacy.ConclusionFM should be differentiated based on pathological characteristics and treatment response, CD103 is helpful in differential diagnosis of FM.

Dear Editor, Addison's disease (AD) is a potentially life-threatening endocrine disorder caused by adrenocortical insufficiency. A deficiency in Adrenocorticotropic Hormone (ACTH) diminishes the negative feedback to the hypothalamic-pituitary axis, leading the adenohypophysis to secrete elevated levels of plasma ACTH and melanocyte-stimulating hormone. This hormonal alteration results in skin and mucosal melanin pigmentation.1 A woman in her mid-forties presented with a four-month history of mucocutaneous pigmentation. The pigmentation, bronzed in appearance, initially appeared on her face and gradually spread across her entire body. It was particularly prominent on the sides of her joints and areas exposed to light. She also developed inhomogeneous grey-black longitudinal melanonychia in her fingernails and toenails, along with hyperpigmentation in her lips, tongue, and mucosal regions (Figure 1). As the pigmentation evolved, the patient reported a loss of appetite and weight, fatigue, anxiety, and muscular discomfort in the lower limbs. She had an overall good health history, with no oral medication intake for about a year. No individuals with similar symptoms were reported in her immediate family or local community. Upon investigation, we noted an elevated secretion of the patient's prolactin in sex hormones (46.25 ng/mL). Her ACTH level spiked at 8 a.m. (>278 pmol/l), more than twice the upper limit of the standard range, while her cortisol levels were low (2.92 ug/dL at 8 a.m.; 1.18 ug/dL at 4 p.m.;1.79 ug/dL at midnight). The patient's antinuclear antibody, rheumatoid factor, serum electrolyte, and thyroid function all appeared normal. Abdominal enhanced computed tomography scans revealed a left adrenal tumor of approximately 1.2 × 0.6 cm, suspected to be an adenoma. Hypophysis-enhanced magnetic resonance imaging did not reveal any pituitary abnormalities. Given the irregular hormone levels, we diagnosed the patient with AD. Following a course of oral hormone therapy, the patient's skin and mucosal pigmentation significantly improved. In this case, the patient exhibited an inhomogeneous longitudinal brown pigment band under the nails (subungual) and around the nails (periungual). However, a dermatoscopic examination of the nail fold presented normal results, indicating a negative Hutchinson's sign (Figure 2). Hutchinson's sign, characterized by the extension of brown-black pigment from the nail bed, matrix, and nail plate into the adjacent cuticle and proximal and lateral nail folds, is a diagnostic feature of subungual melanoma.2 In contrast, hyperpigmentation of the nail bed may be visible through the "transparent" nail folds, thus mimicking Hutchinson's sign. While melanonychia in AD has been reported in several studies, no identification of Hutchinson's sign in association with AD has been made.3, 4 The normal appearance of the nail folds in this patient suggests a pseudo-Hutchinson sign, a feature that can be associated with AD. Therefore, AD should be considered in cases of mucocutaneous pigmentation in conjunction with nail discoloration. Inhomogeneous longitudinal melanonychia accompanied by a pseudo-Hutchinson sign may serve as an indicator of nail changes in AD, assisting in its diagnosis. The patient in this manuscript has given written informed consent to the publication of his case details and photographs. This study was supported by grants from Zhejiang Natural Fund Project (grant number: LBZ22H160001). The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research reported. Zhejiang Natural Fund Project, Grant Number: LBZ22H160001 Data sharing is not applicable to this article as no datasets were generated or analyzed during the current study.

We present the case of a 37-year-old male diagnosed with Mycosis fungoides (MF) after gradually developing multiple skin tags and brownish lichenoid papules. The patient had pre-existing erythema over his entire body, especially his face, upper extremities, and trunk, for over 1.5 years. Microscopic examination of the papule and the skin tag (ST) exhibited similar features mainly characterized by superficial dense band-like lymphoid infiltrates and epidermotropism of atypical lymphocytes (Pautrier's micro-abscesses). Immunohistochemistry further revealed the lymphoid infiltrates predominantly expressed LCA, CD3, CD4, and CD45RO but lacked CD7, CD8, CD30, CD20, and CD79a. The finding of this study that reports MF characterized by unusual STs suggests that some causes and effects have not been previously described in MF.

Background Autophagy dysregulation and oxidative stress play critical pathophysiological roles in developing obesity-related metabolic health disorders. This study aims to investigate how autophagy modulation is related to resveratrol (RSV) antioxidant activities and preventive effects on steroidogenesis decline associated with a high-fat diet (HFD) and oxidative damage. Methods and results Eight-week-old C57BL/6 J male mice were fed with HFD with or without supplement RSV (400 mg/kg/day) by gavage for 16 weeks. The control group was fed with a standard diet with no RSV or the same amount of RSV. Mouse Leydig cell line TM3 cell was used for in vitro studies. Oxidative stress was induced in TM3 cells with H 2 O 2 , followed by RSV treatment plus autophagy activator rapamycin or autophagy inhibitor 3-methyladenine, respectively. RSV supplement could upregulate proteins level of StAR and mitochondrial proteins COX4 and mtTFA, indicating the amelioration of steroidogenesis decline and mitochondrial dysfunction caused by HFD. Antioxidants such as GPx4 and SOD2 were improved by RSV as well. The observation of autophagosomes and the changes in expressions of LC3II/I, Beclin1, and Atg7 indicated that RSV could reverse the autophagy defect associated with HFD. 3-methyladenine inhibition of autophagy partially abolished RSV protection on mitochondrial function and steroidogenesis in H 2 O 2 -challenged TM3 cells. However, the combination use of rapamycin and RSV did not improve protection on Leydig cells against oxidative damage. Conclusions The stimulation of autophagy by RSV is closely linked to its antioxidant actions and positive impact on steroidogenesis in HFD mice. The findings suggest RSV is protective against obesity-related Leydig cell impairment.

Primary localized cutaneous nodular amyloidosis (PLCNA) is rare and clinically noncharacteristic, presenting mostly as plaque-like lesions. We report a case of a progressively larger erythematous plaque following a contusion of the skin on the right zygomatic area, which was strangely covered with recurrent scattered 2 mm whiteish blisters to the extent that it was misdiagnosed as a herpesvirus infection several times over a decade. Pathology and special staining diagnosed nodular amyloidosis with milia.

Rowell syndrome is the occurrence of erythema multiforme-like lesions in patients with cutaneous lesions of lupus erythematosus.1 We present a young female patient with systemic lupus erythematosus (SLE), whose hand lesions exhibited both connective tissue disease–related periungual angiotelectasis and the typical erythema multiforme.