IntroductionRosacea is a chronic inflammatory skin disorder characterized by neurovascular instability and dysregulated innate immunity. Although mast-cell activation is increasingly recognized as a central pathogenic feature, the neuroimmune mechanisms linking neuropeptide signaling to mast cell-mediated inflammation remain incompletely defined. This study investigated whether calcitonin gene-related peptide (CGRP) promotes mast cell-mediated inflammation in rosacea and explored the underlying signaling mechanism.MethodsBioinformatic analyses of the GSE65914 dataset were performed to characterize rosacea-associated molecular pathways and mast-cell signatures. Serum and skin samples from patients with rosacea and healthy controls were analyzed by ELISA, histological staining, and immunofluorescence. In vitro, CGRP-induced mast-cell activation and CALCRL/RAMP1–JAK3–STAT1 signaling were investigated in LUVA cells using RT-qPCR, western blotting, immunofluorescence, degranulation assays, ELISA, and pharmacological approaches, while the potential CALCRL–JAK3 association was assessed by molecular docking and reciprocal co-immunoprecipitation. In vivo, ACK2-mediated mast-cell depletion and pharmacological blockade of the CGRP receptor or JAK3 were evaluated in CGRP-aggravated LL37-induced rosacea-like mouse models.ResultsRosacea lesions showed enrichment of immune-inflammatory pathways, JAK–STAT signaling, and mast cell-associated signatures. Serum CGRP levels were elevated in patients with rosacea and positively correlated with flushing and erythema severity. Lesional skin showed increased CGRP expression and enhanced localization of CALCRL, RAMP1, phosphorylated JAK3, and phosphorylated STAT1 in dermal CD117+ mast cells. In LUVA mast cells, CGRP upregulated CALCRL/RAMP1 expression, activated JAK3–STAT1 signaling, and promoted degranulation, histamine release, and inflammatory mediator production. Molecular docking and reciprocal co-immunoprecipitation supported a potential association between CALCRL and JAK3. Rimegepant or ritlecitinib attenuated CGRP-induced JAK3–STAT1 activation and mast-cell responses. Modulation of the canonical Gαs–cAMP–PKA pathway did not abolish CGRP-induced JAK3–STAT1 phosphorylation, indicating that this response is not primarily mediated by the cAMP–PKA cascade. In vivo, mast-cell lineage depletion attenuated CGRP-driven exacerbation of LL37-induced rosacea-like inflammation, while rimegepant or ritlecitinib alleviated inflammatory changes and reduced JAK3–STAT1 activation and mast-cell responses.ConclusionThese findings identify a CGRP-associated neuroimmune pathway in rosacea in which CALCRL/RAMP1-linked JAK3–STAT1 signaling promotes mast cell-mediated inflammatory amplification. Targeting the CGRP–CALCRL/RAMP1–JAK3–STAT1 axis may provide a mechanism-based therapeutic strategy for neurovascular-dominant or treatment-refractory rosacea.

IntroductionRosacea is a chronic inflammatory facial dermatosis with incompletely elucidated pathogenesis. LL37 is a key molecular mediator in rosacea development, and mast cells represent pivotal immune players in this process. However, the precise mechanism underlying LL37-induced mast cell degranulation remains undefined.MethodsA LL37-induced rosacea-like dermatitis mouse model was established with or without ruxolitinib treatment. Hematoxylin-eosin and toluidine blue staining were used to evaluate the pathological changes. Mice skin lesions were collected for transcriptome sequencing, Western blot and immunofluorescence. In vitro, the interaction between LL37 and TLR2 on the mast cell membrane surface was detected by co-immunoprecipitation and fluorescence staining. The activation of the TLR2/MyD88/JAK2/STAT3 signaling pathway was investigated using lentivirus-mediated TLR2 knockdown, MyD88 overexpression, combined with JAK2 inhibitor (ruxolitinib). Ten patients underwent VISIA skin analysis system and severity assessment following topical ruxolitinib treatment.ResultsLL37 induces activation of the TLR2/JAK2 pathway in mast cells of rosacea-like mice. Ruxolitinib ameliorated cutaneous erythema and reduced mast cell infiltration and degranulation. In vitro experiments demonstrated that LL37 directly binds to TLR2, triggering TLR2/MyD88 pathway activation and subsequent mast cell degranulation. Mechanistically, MyD88 directly interacts with JAK2 to modulate the JAK2/STAT3 signaling axis, which governs mast cell degranulation. Topical application of ruxolitinib exhibited clinical efficacy in rosacea patients.ConclusionThese findings collectively demonstrate that LL37 drives mast cell activation and degranulation in rosacea pathogenesis via TLR2/JAK2/STAT3 pathway activation, while ruxolitinib effectively suppresses this signaling axis. This study provides novel mechanistic insights and therapeutic strategies for rosacea management.

Purpose:Interleukin-17A (IL-17A) drives psoriasis and central nervous system neuroinflammation, but clinical research on whether IL-17A-targeted biotherapy modulates brain activity to improve neuropsychiatric outcomes in psoriasis is lacking. This study aims to investigate brain functional changes, cognitive impairment, and the effects of IL-17A monoclonal antibody therapy in psoriasis vulgaris. Patients and methods:Regular secukinumab treatment. Meanwhile, 20 healthy controls (HCs) matched in age and gender were enrolled. The patients underwent functional magnetic resonance imaging (fMRI) before treatment and 48 weeks after treatment. The healthy controls also had fMRI scans. It assessed clinical data, cognition/neuropsych status (MoCA, SDS, SAS), disease severity/quality of Life (PASI/DLQI), and brain function via rs-fMRI (ALFF/ReHo). Results:Compared to healthy controls, the psoriasis vulgaris patients showed increased ALFF in the frontal lobe, as well as increased frontal ReHo. The treatment group showed signal recovery in some brain regions. Patients before treatment had lower MoCA scores vs controls (P < 0.001)) and higher SAS/SDS scores (SAS, P < 0.0001; SDS, P < 0.05). Patients after treatment showed higher MoCA scores vs before treated (P < 0.05), similar to controls, with lower SAS scores (P < 0.0001) and reduced PASI/DLQI (P < 0.0001). Conclusion:Psoriasis is associated with brain dysfunction and neuropsychiatric symptoms. IL-17A antibody therapy improves skin symptoms, restores brain function, and alleviates neuropsychiatric issues vs untreated patients, supporting multidimensional treatment.

BACKGROUND:Rosacea is a chronic inflammatory skin disease characterized by persistent facial erythema and telangiectasia. The antimicrobial peptide LL37 is a key initiator in rosacea, with mast cells serving as critical inflammatory mediators. However, the precise mechanism underlying LL37-induced mast cell degranulation remains unclear. METHODS:The rosacea RNA-seq dataset GSE65914 was downloaded from the Gene Expression Omnibus (GEO) database and subjected to transcriptome analysis. DCFH-DA staining was performed to detect oxidative stress. Mitochondrial function was evaluated using MitoSOX and JC-1 staining. Calcein AM/Co2+ quencher staining was employed to assess mitochondrial permeability transition pore (mPTP) opening. Transmission electron microscopy was utilized to observe mitochondrial ultrastructure. Cytosolic mitochondrial DNA (mtDNA) was evaluated via immunofluorescence and qPCR. Western blotting and CUT&RUN assays were conducted to detect activation of the cGAS/STING/NF-κB axis. Mast cell degranulation was assessed using ELISA. N-acetylcysteine (NAC) was administered to scavenge reactive oxygen species (ROS). Cyclosporin A (CsA) was used to inhibit mPTP opening. SP23 was applied for chemical degradation of STING. A LL37-induced rosacea-like dermatitis mouse model was established and topically treated with applied CsA/SP23 cream. RESULTS:Transcriptomic profiling reveals significant enrichment of the cGAS/STING signaling pathway in rosacea lesions. LL37 induces oxidative stress-driven mitochondrial damage in mast cells, resulting in the leakage of mtDNA. Cytosolic mtDNA activates the cGAS/STING/NF-κB signaling pathway, inducing mast cell degranulation. ROS scavenging, blockade of mPTP or targeted degradation of STING significantly reduced mast cell activation. Animal experiments demonstrated that topical administration of CsA or SP23 suppressed cGAS/STING/NF-κB signaling in dermal mast cells and alleviated rosacea-like dermatitis. CONCLUSION:LL37 promotes mast cell-driven inflammation through mitochondrial stress and innate immune activation and suggest that targeting the mtDNA/cGAS/STING pathway may offer a promising therapeutic strategy for rosacea.

Acquired digital fibrokeratoma (ADF) is rare in clinical practice and is easily misdiagnosed. Herein, 5 cases of patients (3 males and 2 females) with ADF are reported. The mean age at onset was 42.6 years, and the mean disease duration was 3 years. Four patients had ADF on the hands, and 1 patient had ADF on the foot. The clinical manifestations were all solitary, skin-colored papules, with a firm texture and smooth surface, protruding from the skin surface. In 3 patients, ADF manifested as columnar protrusions, and in 2 patients, ADF manifested as dome-shaped protrusions. For all 5 patients, the diameters of the lesions were <1 cm. Clinically, all 5 patients were misdiagnosed (ie, eccrine poroma (EP), common warts, rudimentary polydactyly, pyogenic granuloma (PG), and acral fibroma). All cases of ADF were confirmed by histopathology. The histopathological manifestations of ADF were as follows: finger-like protrusions on the skin surface; collagen fiber bundles running vertically to the epidermis seen in the dermis; and thick red-stained collagen fibers connected with the normal dermal connective tissue below. All 5 patients underwent surgical resection; the distance between the incision margin and the edge of the tumor was 2-3 mm, and the surgical depth was the deep dermis. No recurrence was observed in more than half a year of follow-up after surgery.

Rosacea is a chronic inflammatory skin disease characterized by facial erythema and telangiectasia. Despite ongoing research, the pathogenesis of rosacea remains incompletely understood, and current therapies are not entirely satisfactory. The JAK/STAT signaling pathway plays an essential role in immunoregulation, inflammation, and neurovascular regulation. Inhibition of the JAK/STAT pathway appears to hold promise as a potential therapy for rosacea. This study aimed to investigate the effects of the JAK inhibitor tofacitinib on rosacea and to preliminarily explore its therapeutic mechanism. To this end, a rosacea-like mouse model was induced using LL37 and treated with a 2% tofacitinib emulsion. The results demonstrated that topical application of tofacitinib significantly ameliorated rosacea-like phenotype, reduced the infiltration of CD4+ T cells and mast cells, and suppressed dermal angiogenesis. RT-qPCR analysis revealed a reduction in mRNA expression levels of STAT1, STAT4, and STAT5a in skin lesions following topical tofacitinib treatment. Additionally, three patients diagnosed with erythematotelangiectatic rosacea (ETR) were included in the study and treated with oral tofacitinib, leading to a significant improvement in erythema and flushing symptoms. These findings collectively suggest that tofacitinib alleviates LL37-induced rosacea-like skin inflammation in mice and rosacea skin lesions by inhibiting the JAK/STAT signaling pathway.

OBJECTIVE:By presenting a case study on multiple instances of Bowen's disease and the consistent use of narrow-band ultraviolet B (NB-UVB) phototherapy over a three-year period, our aim is to enhance the comprehension of domestic clinicians regarding the disease. Additionally, we seek to review existing literature, encouraging dermatologists to consider clinical secondary primary lesion diagnoses.METHOD:Our approach involves analyzing a diagnosed case of multiple Bowen's disease, examining clinical manifestations, histopathology, imaging results, and treatment methods related to NB-UVB phototherapy. We aim to facilitate discussion and understanding through a comprehensive literature analysis.RESULTS:An elderly male with a 30-year history of psoriasis vulgaris initiated continuous NB-UVB therapy three years ago. A year later, he developed red patches and plaques with distinct borders and scaly surfaces on his face, trunk, lower extremities, and scrotum. Histopathological examination confirmed Bowen's disease. Treatment involved liquid nitrogen cryotherapy, with no recurrence observed during the one-year follow-up.CONCLUSION:This case highlights that Bowen's disease, typically solitary, can manifest as multiple instances, especially in individuals with a history of psoriasis vulgaris. While NB-UVB stands as the primary treatment for psoriasis vulgaris, caution is warranted due to the potential risk of skin tumor induction with prolonged high-dose usage. Clinicians should be vigilant in monitoring and assessing the long-term implications of such therapies.

Background Rosacea is a chronic inflammatory skin disease characterized by flushing, erythema, papules, and pustules on the central face. It affects patient appearance and is noted for its chronicity, recurrence, and resistance to treatment. Effective rosacea treatment requires repairing the skin barrier, reducing inflammation, and promoting vasoconstriction. Aims This study aims to evaluate the efficacy of topical ferulic acid in treating papulopustular rosacea and its impact on skin barrier function. Methods Sixty patients with mild to moderate papulopustular rosacea were selected from the Department of Dermatology at the Affiliated Hospital of Shandong Second Medical University between January 2023 and December 2023. Patients were randomly assigned to either a control group or an observation group, with 30 patients in each group. The observation group applied ferulic acid solution to the affected areas, while the control group used normal saline, both twice daily for 6 weeks. Both groups also received 0.1 g doxycycline hydrochloride tablets orally once daily. Skin lesions and skin barrier function were assessed using VISIA imaging and self-rating scales before and during treatment, and adverse reactions were recorded. Results After 6 weeks, both skin lesion assessments and self-assessment scores improved significantly from baseline, with greater improvement in the observation group compared to the control group (p < 0.05). Indicators of skin barrier function and VISIA imaging results demonstrated the efficacy of ferulic acid in treating rosacea. The total effective rate was significantly higher in the observation group (80.00%) compared to the control group (63.33%) (p < 0.05). In the observation group, nine patients (30.00%) experienced a greasy sensation initially, one patient (3.33%) reported tingling and itching, and no serious adverse reactions were observed. Conclusions Ferulic acid is effective as an adjuvant treatment for papulopustular rosacea, significantly improving skin lesions and repairing skin barrier function with minimal adverse reactions.

Background:Melanoma is an aggressive skin tumor with limited therapeutic options due to rapid proliferation, early metastasis, and poor prognosis. Baicalin (BA), a natural flavonoid, shows promise in inducing ferroptosis and apoptosis but faces challenges of poor solubility and bioavailability. To address these issues, we developed a multifunctional drug delivery system: manganese-doped ZIF-8 nanoparticles (ZIF(Mn)) loaded with BA and modified with folic acid (FA) and polyethylene glycol (PEG). FA targets melanoma cells by exploiting folate receptor overexpression, while PEG enhances biocompatibility and systemic circulation. Manganese enables magnetic resonance (MR) imaging for real-time, non-invasive therapy monitoring. Methods:BA-loaded ZIF(Mn)/FA-PEG nanoparticles were synthesized via a one-pot method, enabling drug encapsulation, Mn²+ incorporation, and surface modification. The nanoparticles were comprehensively characterized (particle size, Zeta potential, FTIR, and XRD). Cytotoxicity and cellular uptake were evaluated in B16-F10 melanoma cells, and in vivo experiments in C57BL/6J mice investigated MR imaging capability, antitumor efficacy, and biosafety. Results:BA@ZIF(Mn)/FA-PEG nanoparticles demonstrated excellent stability, a BA loading capacity of 33.50 ± 0.04%, and pH-responsive release, with accelerated drug release under acidic tumor conditions. Mn²+ provided strong T1-weighted MR imaging contrast. Cellular and animal studies showed enhanced uptake, reduced premature drug release, and improved compatibility. Mechanistically, the nanoparticles induced significant ferroptosis and apoptosis in melanoma cells, leading to potent antitumor effects. Conclusion:The BA@ZIF(Mn)/FA-PEG nanoplatform effectively integrates targeted delivery, imaging guidance, and dual ferroptosis-apoptosis induction, offering a promising strategy for improving melanoma treatment outcomes.

Purpose:Epidermal keratinocytes with an abnormal glucose metabolism have been identified in psoriasis. Hexokinase 2 (HK2) is a crucial enzyme involved in glycolytic metabolic pathways. However, the expression of HK2 and its potential therapeutic effects in psoriasis remains unclear. This study aimed to investigate the expression pattern of HK2 and evaluate its therapeutic effects in psoriasis.Patients and Methods:A gene expression dataset (GSE121212) downloaded from the Gene Expression Omnibus (GEO) database was used to examine the expression of HK2 in psoriasis. HK2 RNA and protein expression were investigated in psoriasis vulgaris (n=5) and healthy (n=5) samples. Immunohistochemistry for HK2 was performed on psoriasis vulgaris (n=22) and healthy skin (n=10) samples. Additionally, HaCaT cells were treated with M5 (interleukin [IL]-17A, tumor necrosis factor-α, IL-1α, IL-22, and Oncostatin-M) to induce a psoriatic inflammation cell model. A mouse model of psoriatic inflammation was established using topical 5% imiquimod cream. Psoriasis-like cells and mouse models were treated with the HK2 inhibitor 3-bromopyruvate (3-BrPA). Cell proliferation, glucose consumption, and lactate production were assessed. Furthermore, the activation of nuclear factor-kappa B (NF-Kb) and NOD-like receptor thermal protein domain associated protein 3 (NLRP3) was investigated using Western blot analysis.Results:According to the GEO dataset, HK2 expression was significantly elevated in psoriasis. Upregulation of HK2 in psoriatic tissues was confirmed by quantitative real-time polymerase chain reaction and Western blotting. The immunohistochemistry score for HK2 was higher in psoriatic lesions than in healthy skin. 3-BrPA inhibited the proliferation and glycolysis of M5-stimulated HaCaT cells. Topical 3-BrPA ameliorated imiquimod-induced psoriasis-like dermatitis. Activation of NF-kB and NLRP3 was downregulated by 3-BrPA treatment.Conclusion:Our study revealed that the glycolytic enzyme HK2 was upregulated in psoriasis and that the HK2 inhibitor 3-BrPA exhibited therapeutic effects in psoriasis cell and mouse models.

Chronic mucocutaneous candidiasis (CMC) is a rare infectious skin disease. This study reported a case of CMC in a child with clinical manifestations of oral mucosal leukoplakia and erythema and crust-like thick scabs on the skin of the face and upper limbs. Microscopic fungal examination revealed a large amount of pseudohyphae, and the fungal culture indicated Candida albicans. A drug sensitivity test indicated that it was sensitive to itraconazole and nystatin. Laboratory tests did not show significant immunodeficiency or endocrine abnormalities, and gene sequencing did not identify DNA gene mutations in the coiled-coil domain (CCD) or the DNA-binding domain (DBD) of signal transducer and activator of transcription 1 (STAT1). The skin lesions subsided after oral administration of itraconazole but relapsed 6 months later, and hypoparathyroidism occurred 1 year later. Patients with repeated superficial fungal infection should be alert to the possibility of CMC. CMC has numerous complications and a poor prognosis that requires the attention of clinicians. In this case, STAT1 mutation was not found, and parathyroid dysfunction was rare, providing reference for clinical diagnosis and treatment of CMC.

Mycobacterium marinum is an atypical bacterium, and skin infections caused by it are relatively rare, usually occurring in workers engaged in seafood processing and housewives who clean and prepare fish for consumption. The infection often occurs after the skin is punctured by fish scales, spines, etc. The JAK/STAT signaling pathway is closely related to the human immune response to infections. Therefore, JAK inhibitors may induce and exacerbate various infections in clinical practice. This article reports a case of mycobacterium marinum skin infection in the left upper limb of a female patient with chronic idiopathic myelofibrosis during treatment with ruxolitinib. The patient denied being punctured or scratched by fish scales or spines. Clinical manifestations included multiple infiltrative erythemas and subcutaneous nodules in the thumb and forearm. Histopathological examination showed infiltration of mixed acute and chronic inflammatory cells in the subcutaneous tissue. The diagnosis was ultimately confirmed by NGS sequencing. The patient was cured after taking moxifloxacin and clarithromycin for 10 months. Infection is a common adverse reaction of JAK inhibitors, but no literature has reported on mycobacterium marinum skin infections occurring during JAK inhibitor treatment, which is relatively rare. As the clinical application of JAK inhibitors becomes more widespread, the skin infections they cause may present in various forms and require the attention of clinicians.

Purpose: Melanomas are highly malignant and rapidly develop drug resistance due to dysregulated apoptosis. Therefore, proapoptotic agents could be effective for the management of melanoma. Hydrogen sulfide is ubiquitous in the body, and exogenous hydrogen sulfide has been reported to show inhibitory and pro-apoptotic effects on cancer cells. However, whether high concentrations of exogenous hydrogen sulfide have pro-apoptotic effects on melanoma and its mechanisms remain unknown. Hence, this study aimed to explore the pro-apoptotic effects and mechanisms of exogenous hydrogen sulfide on the A375 melanoma cell line treated with a hydrogen sulfide donor (NaHS).Methods: The cell proliferation test, flow cytometric analysis, Hoechst 33258 staining, and Western blotting of B-cell lymphoma 2 and cleaved caspase-3 were used to explore the pro-apoptotic effects of hydrogen sulfide on A375 cells. The transcriptional profile of NaHS-treated A375 cells was further explored via high-throughput sequencing. Western blotting of phosphorylated inositol-requiring enzyme 1 & alpha; (p-IRE1 & alpha;), phosphorylated protein kinase R-like ER kinase (p-PERK), phosphorylated eukaryotic translation initiation factor 2 & alpha; (p-eIF2 & alpha;), C/EBP homologous protein, glucose-regulating protein 78, IRE1 & alpha;, PERK, and eIF2 & alpha; was performed to verify the changes in the transcriptional profile.Results: NaHS inhibited A375 melanoma cell proliferation and induced apoptosis. The endoplasmic reticulum stress unfolded protein response and apoptosis-associated gene expression was upregulated in NaHS-treated A375 melanoma cells. The overactivation of the unfolded protein response and increase in endoplasmic reticulum stress was verified at the protein level.Conclusion: Treatment with NaHS increased endoplasmic reticulum stress, which triggered the overactivation of the unfolded protein response and ultimately lead to melanoma cell apoptosis. The pro-apoptotic effect of NaHS suggests that it can be explored as a potential therapeutic agent in melanoma.

Background:Condyloma cuminata (CA) is a sexually transmitted disease caused by human papillomavirus (HPV) infection, which is prone to recurrence and difficult to cure in the short term. CD207 is a C-type lectin receptor that is specifically expressed on the surface of Langerhans cells (LCs) and is considered as an LC-specific immunohistochemical marker. The main purpose of this study is to explore the correlation between the expression of CD207 in CA skin lesions and the duration of CA disease course and frequency of recurrence, in order to provide new prognostic markers for CA to clinicians.Materials and Methods:A total of 40 male patients with CA and their skin lesions were collected, as well as 40 healthy male penile tissue samples. The skin lesions of CA were clinically and histologically confirmed by acetic acid test. The expression of CD207 in epidermal tissues was detected using immunohistochemistry. The difference in the number of CD207 positive cells between CA skin lesions and healthy skin controls was compared, and the association between the number of CD207 positive cells in CA skin lesions and the duration of disease course and the frequency of recurrence was determined through Spearman correlation analysis.Conclusion:In CA skin lesions, CD207 positive cells were found to have morphological abnormalities and the number of cells was significantly reduced compared to healthy skin, suggesting that there may be antigen presentation dysfunction in CA skin lesions, which may be the reason for the prolonged and unresolved condition of the disease. The fewer CD207 positive cells in CA skin lesions, the longer the disease course and the more frequent the recurrence, therefore, the expression level of CD207 can be used as a new prognostic marker for predicting the outcome of CA.

Melanoma is a malignant tumor that originates from melanocytes. The incidence of melanoma is increasing worldwide, partially because of its insensitivity to radiotherapy or chemotherapy. Therefore, effective treatments for melanoma are urgently required. In this study, we employed folic acid-modified sulfasalazine long-circulating liposomes (FA-SSZ-Lips) to precisely target drug delivery to melanoma cells, eliciting ferroptosis effectively. The synthesized FA-SSZ-Lips were characterized as small spheres of a double-layer membrane, a particle size of 110.1 nm, and a zeta-potential of -22.8 +/- 0.66 mV. FA-SSZ-Lips are effective drug carriers with SSZ-loading ratio and SSZ release rate of 6.2 +/- 0.10%, and 72.63 +/- 1.40%, respectively. The liposomes enhanced SSZ solubility, and the folic acid modifications increased the liposome targeting to melanoma cells. Compared with SSZ alone, FA-SSZ-Lips more strongly inhibited B16F10 cell growth, significantly disrupted the intracellular redox balance, and induced ferroptosis. After treatment, considerable differences were observed in the tumor volumes between FA-SSZ-Lips and phosphate-buffered saline control groups. The tumor growth-inhibition value of the FA-SSZ-Lips group reached 70.09%. Thus, FA-SSZ-Lips exhibited favorable antitumor effects in vitro and in vivo and are a promising strategy for melanoma treatment.

1Department of Dermatology, Affiliated Hospital of Weifang Medical University, Weifang, Shandong, People’s Republic of China; 2Scientific Research Center, Anxi County Hospital, Quanzhou, Fujian, People’s Republic of China; 3Department of Dermatology, Yantai Yuhuangding Hospital, Yantai, Shandong, People’s Republic of China; 4Department of Dermatology, Liaocheng People’s Hospital, Liaocheng, Shandong, People’s Republic of China; 5Department of Dermatology, Weihai Municipal Hospital, Weihai, Shandong, People’s Republic of China; 6Department of Dermatology, Jinan Dermatosis Prevention and Control Hospital, Jinan, Shandong, People’s Republic of China; 7Department of Dermatology, Qilu Hospital of Shandong University, Jinan, Shandong, People’s Republic of China; 8Department of Otolaryngology, Qilu Hospital of Shandong University, Jinan, Shandong, People’s Republic of China

[This corrects the article DOI: 10.3892/etm.2015.2220.].

Purpose: The clinical and pathological data of patients with rhinofacial ulcers were retrospectively reviewed and analyzed to lay the foundation for standardized clinical treatment.Patients and Methods: We retrospectively analyzed the clinical data, etiology, pathological features, treatment methods, and prognosis of 243 patients with rhinofacial ulcers treated in the Departments of Otorhinolaryngology and Dermatology at six hospitals in Shandong Province, China from July 2014 to October 2021. The clinical characteristics and treatment methods of the rhinofacial ulcers were summarized to provide a basis for standardizing patients' diagnosis and treatment.Results: The male-to-female ratio of the 243 patients was 2.04:1, and their ages ranged from 25 to 91 years. The most common sites were the cheek, nasal dorsum, and upper lip. The common primary diseases were basal-cell carcinoma, squamous-cell carcinoma, and odontogenic fistula, but rare triggers played important roles in some cases, such as infection, autoimmune diseases, and adverse drug reactions. Surgical treatment was feasible for tumor ulcers; 71 patients with basal-cell carcinoma and 50 with squamous-cell carcinoma were treated with Mohs micrographic surgery. During the follow-up period of 1-84 months, most of the rhinofacial ulcers were cured, while natural killer/T-cell lymphoma, angiosarcoma, and melanoma were important causes of death. Conclusion: Various causes may lead to rhinofacial skin ulcers, and some cases lacking specificity of clinical manifestations are easily misdiagnosed in clinical practice. Histopathological biopsy is valuable for confirming the diagnosis, after which correct etiological treatment is very important.