Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Objectives: This study aimed to evaluate the correlation between mast cell (MC) density in rosacea-affected skin and the expression of key inflammatory mediators, including IL-6, TNF-α, and cathelicidin LL-37. By comparing lesions rich in MCs with those having fewer MCs, we sought to elucidate the role of MCs in the inflammatory mechanisms underlying rosacea pathogenesis.

Methods: Specimens were collected from 20 patients diagnosed with rosacea who attended the outpatient clinic between 2008 and 2013. Each specimen underwent staining using hematoxylin/eosin, Giemsa, IL-6, LL-37, and TNF-α for both histopathological and immunohistochemical analyses. The number of stained cells was counted across 10 randomly selected dermal layers at a magnification of ×400 using light microscopy. The results were categorized based on the number of MCs counted: more than 10 MCs were classified as MC-rich, and 10 or fewer MCs as MC-poor.

Results: Among the 20 patients (10 MC-rich and 10 MC-poor), the MC-rich group demonstrated significantly higher MC counts than the MC-poor group (P<0.001). However, there were no significant differences in the expression levels of IL-6, LL-37, or TNF-α between the two groups. Additionally, MC density did not show any significant associations with patient demographics, clinical characteristics, or systemic comorbidities.

Conclusion: Increased MC density was not associated with differences in IL-6, TNF-α, or LL-37 expression in rosacea lesions. These findings suggest that MC infiltration may not directly influence the inflammatory mediator profile in rosacea. Further research is required to identify distinctive pathological features or markers that can elucidate the mechanisms of rosacea.

Background: Occupational contact dermatitis (OCD) is prevalent among hairdressers due to frequent exposure to chemicals like hair dyes and bleaching agents. Despite the risks, awareness among hairdressers remains low, leading to underreporting and inadequate preventive measures. Objective: This study evaluated hairdressers’ awareness of harmful hair dye ingredients, their experiences with OCD, and the association with product usage patterns. Methods: A cross-sectional study involving 100 hairdressers in Korea examined the relationship between work experience, product usage, and OCD. Chi-square tests and multivariate regression identified significant correlations. Results: Among the participants, 51% reported experiencing adverse skin reactions, with the hands being the most commonly affected area. Longer work experience as a hairdresser was significantly associated with the occurrence of adverse effects ( p=0.046). Notably, shampoo was identified as a suspected causative material significantly more often by the severe group compared to the non-severe group (28.0% vs. 3.8%, p=0.04). Conclusion Chemical exposure and frequent wet work contribute to high rates of OCD among hairdressers. Poor glove usage, especially during shampooing due to inconvenience, is a major risk factor. Raising awareness, promoting proper glove use, and improving workplace safety training are essential for reducing these skin conditions.

Background: Nickel is a leading cause of allergic contact dermatitis. Patients with nickel allergy may suffer from persistent dermatitis not only through contact with nickel-plated items but also through ingestion of nickel-containing food. Objective: This study aimed to evaluate the current nickel content in Korean food products and provide more up-to-date Korean nickel-restricted diets that would increase patient compliance. Methods: The most frequently consumed food items were selected with replicates. Food samples were prepared according to the practices of normal consumers. The solid specimens were finely ground, and the liquid specimens were homogenized using a sterilized mixer. Tea bags were brewed in 100 mL of distilled water at 100 °C for 5 minutes. Solid (0.5 g) and liquid (2 g) specimens were subjected to microwave-assisted nitric acid digestion using inductively coupled plasma-mass spectrometry. Results: In total, 147 samples were collected from different food categories, including plant-based products, animal-based products, packaged foods, and drinks. Cocoa powder had the highest concentration of nickel (1.56 mg/kg), which is consistent with the results of previous studies. Soy products such as fermented soybean paste (Doenjang) (1.16 mg/kg), fermented soybean with red chili paste (Ssamjang) (0.67 mg/kg), and tofu (0.37 mg/kg) had elevated concentration of nickel. Moreover, nut-derived products such as chocolate (1.10 mg/kg), ground coffee (0.86 mg/kg), almond (0.84 mg/kg), and peanuts (0.64 mg/kg) contained elevated nickel concentration. Conclusion The nickel content in food constantly changes depending on the food processing procedures and place of origin. Therefore, revising the nickel-restricted diet is necessary to enhance patients’ understanding of it and help reduce dietary nickel intake.

Nivolumab is a checkpoint inhibitor monoclonal antibody, designed to interact with the programmed death cell receptor-1, preventing the inhibitory signaling on cytotoxic T cells. Immune checkpoint inhibitors can lead to severe cutaneous immune-related adverse events (irAEs). A 54-year-old female with a breast cancer metastasis was referred to our clinic due to diffuse cutaneous lesions of crusted erythematous patches and multiple blisters for 2 weeks. Five months before presentation, she started nivolumab/eribulin immunotherapy. Skin biopsy showed subepidermal blistering with perivascular lymphohistiocytic infiltration with eosinophils. Direct immunofluorescence showed linear deposition of immunoglobulin G and C3 along the dermoepidermal junction, consistent with bullous pemphigoid.Temporal relationship between initiation of nivolumab and skin lesion suggested the diagnosis of nivolumab-induced bullous pemphigoid. Dermatologic toxicity is the most common irAEs associated with nivolumab, but nivolumab-induced bullous pemphigoid is rare. Given the widespread use of immunotherapy, it is important to document this case to develop proper management strategies.

Nontuberculous mycobacterial infections, which are often acquired from environmental sources such as water and soil, exhibit a variety of cutaneous manifestations that frequently lead to misdiagnoses and delays in treatment. A 77-year-old woman presented with multiple skin lesions in a sporotricoid distribution on her right leg, which persisted despite standard antibiotic treatments. Based on the skin biopsy, revealing granulomatous inflammation with acid-fast bacilli, and PCR testing, a nontuberculous mycobacterial infection was diagnosed. Antimycobacterial drug combinations, including clarithromycin, isoniazid, and rifampicin for 4 months, complete the skin lesion's clearance. This case underscores the need for heightened suspicion and the use of appropriate diagnostic techniques, including tissue biopsies and molecular methods such as PCR.

Hepatic dysregulation of lipid metabolism exacerbates inflammation and enhances the progression of metabolic dysfunction-associated steatotic liver disease (MASLD). STAT3 has been linked to lipid metabolism and inflammation. Jolkinolide B (JB), derived from Euphorbia fischeriana, is known for its pharmacological anti-inflammatory and anti-tumor properties. Therefore, this study investigated whether JB affects MASLD prevention by regulating STAT3 signaling. JB attenuated steatosis and inflammatory responses in palmitic acid (PA)-treated hepatocytes. Additionally, JB treatment reduced the mRNA expression of de-novo lipogenic genes, such as acetyl-CoA carboxylase and stearoyl-CoA desaturase 1. Interestingly, JB-mediated reduction in inflammation and lipogenesis was dependent on STAT3 signaling. JB consistently modulated mitochondrial dysfunction and the mRNA expression of inflammatory cytokines by inhibiting PA-induced JAK/STAT3 activation. This study suggests that JB is a potential therapeutic agent to prevent major stages of MASLD through inhibition of JAK/STAT3 signaling in hepatocytes.