Heliotrope rash is a pathognomonic feature of dermatomyositis (DM); however, the molecular pathways implicated in cutaneous involvement have not been fully explored. Although the IL-23/Th17 axis has been implicated in inflammatory and autoimmune diseases, the clinical significance of circulating IL-23 across the idiopathic inflammatory myopathy (IIM) spectrum, particularly in cutaneous disease expression, remains insufficiently defined. In this cross-sectional study, we aimed to quantify serum IL-23 levels in patients with IIM and evaluate their association with cutaneous involvement, including overall skin disease activity assessed by the Cutaneous Dermatomyositis Disease Area and Severity Index (CDASI) and the presence of specific skin manifestations, particularly pathognomonic lesions, using a univariate analysis. Serum IL-23 levels were measured by Enzyme-Linked Immunosorbent Assay (ELISA) in patients with IIM and healthy controls (HCs), and their relationships with clinical and cutaneous variables were analyzed using univariable and multivariable approaches. Higher IL-23 levels were associated with cutaneous involvement, especially with pathognomonic skin manifestations and, most notably, heliotrope sign. IL-23 also showed a positive correlation with CDASI activity; the relationship with heliotrope sign remained consistent. Applying a multivariate model, heliotrope rash remained the only independent factor associated with IL-23 levels: in other words, IL-23 increases by 437.3 pg/mL when heliotrope is present. These findings suggest that IL-23 may be preferentially associated with a cutaneous phenotype characterized by heliotrope rash, rather than with global skin burden alone.
Vitamin D has long been recognized for its essential role in calcium and phosphorus homeostasis and skeletal maintenance. Over the past few decades, however, accumulating evidence has uncovered its pivotal nonskeletal function in orchestrating immune responses, sparking considerable interest in its association with various autoimmune disorders and inflammatory skin diseases. Chronic urticaria (CU) is a common skin disease with a complex etiology, and immune dysfunction is closely implicated in its pathogenesis. This narrative review systematically summarizes the epidemiological evidence, potential mechanisms of action, and clinical intervention studies regarding the relationship between vitamin D and CU. The available evidence, however, remains heterogeneous, and causality has not been firmly established owing to the predominance of cross-sectional designs and the presence of multiple confounding factors. Although most interventional studies report positive effects of vitamin D supplementation as an adjunct to standard therapy, findings are conflicting because of considerable heterogeneity in dosing regimens, treatment duration, and baseline vitamin D status. Based on the reviewed evidence, we propose a “threshold model,” which posits that vitamin D modulates the immune activation threshold rather than directly triggering disease. The deficiency of vitamin D lowers this threshold and increases CU susceptibility, whereas the clinical onset of CU requires additional triggering factors such as infections or autoantibodies. This model remains a theoretical framework requiring further clinical and mechanistic validation. This narrative review aims to provide an integrated perspective for understanding the complex relationship between vitamin D and CU and to offer a theoretical basis for the development of comprehensive treatment strategies.
Androgenetic alopecia (AGA) and seborrheic dermatitis (SD) are two common scalp disorders that frequently impair the quality of life and may coexist in a subset of patients across all genders. SD presents in 40%–50% of all patients diagnosed with AGA. Although these conditions are traditionally discussed separately, increasing evidence suggests that they may share overlapping pathogenic factors, including androgen-driven sebum hypersecretion, imbalance of the scalp microecology, barrier dysfunction, and inflammatory signaling. We propose an integrated framework for understanding SD–AGA coexistence, emphasizing the interplay among endocrine influences, sebum alterations, microbial imbalance, and inflammatory activation. Therefore, the management of patients with coexisting AGA and SD should move beyond single-target approaches and emphasize the restoration of scalp homeostasis, control of inflammatory cascades, and integration of antiandrogen therapy through comprehensive, individualized treatment strategies. This review may offer a new perspective for the combined management of these dual scalp disorders.
Background Keloid disease, marked by excessive fibrous tissue growth, is prevalent in dark‐skinned individuals. Mitochondrial integrity is essential for wound healing through cytoskeletal remodelling. Altered mitochondrial morphology and reactive oxygen species (ROS) signalling may underlie keloid pathology, which may be worsened by vitamin D insufficiency. Aim To investigate vitamin D status, mitochondrial function and oxidative stress in keloid disease. Methods Keloid tissue and whole blood were collected from 44 dark‐skinned patients (18–65 years). Plasma vitamin D levels were quantified by routine analysis. Plasma malondialdehyde (MDA), a lipid peroxidation marker, was measured using the thiobarbituric acid reactive substance assay. Mitochondrial DNA (mtDNA) integrity was assessed by quantitative PCR in keloid tissue, and mitochondrial morphology was examined with transmission electron microscopy (TEM). Results Among the 44 patients, 30 had normal vitamin D levels, 13 had low levels and 1 was deficient. Oxidative stress marker, MDA and mtDNA integrity were similar across vitamin D groups. No association was observed between vitamin D and plasma MDA levels. An inverse relationship emerged between mtDNA integrity and plasma MDA ( r = −0.5225, CI −0.751–−0.0182, p = 0.0036), while vitamin D positively correlated with mtDNA integrity ( r = 0.402, CI 0.052–0.665, p = 0.0224). TEM revealed subtle mitochondrial alterations in patients with low vitamin D, including reduced size, and double‐membrane outlines were visible in several micrographs, whereas others showed less pronounced boundary contrast. Conclusion Vitamin D insufficiency was uncommon in this cohort. While oxidative stress marker, MDA and mtDNA integrity did not differ by vitamin D status, structural mitochondrial changes were observed in dark‐skinned keloid patients with low vitamin D.
Objective:To investigate the prevalence and associated factors of steroid-induced diabetes mellitus (SDM) in dermatology inpatients receiving systemic glucocorticoid (GC) therapy, with particular focus on characterizing the dose-response relationship. Study Design:Retrospective observational cohort study. Place and Duration of Study:Department of Dermatology, The Affiliated Hospital of Xuzhou Medical University, Xuzhou, China, from August 2019 to October 2024. Methodology:A total of 293 patients treated with GCs were included, with 42 classified as having SDM and 251 as controls based on blood glucose monitoring. Data such as demographics, GC dosage, laboratory indices, and follow-up outcomes were analyzed by SPSS 26.0, R 4.4.1, and logistic regression analysis was applied to explore factors associated with the development of SDM. We modeled the nonlinear dose-response between average daily GC dose (methylprednisolone-equivalent) and SDM using multivariable logistic regression with restricted cubic splines, setting 0.6 mg/kg/day as the reference. All tests were two-sided, p < 0.05 indicates that the difference is statistically significant. Results:Among 293 patients, 42 (14.3%) developed SDM and 17 (5.8%) had impaired glucose regulation. SDM cases were older and had higher BMI, hypertension, family history of diabetes, higher average daily GC dose, and more frequent immunosuppressant use. Multivariate regression identified family history of diabetes (OR: 11.16), immunosuppressant use (OR: 3.48), average daily GC dose (OR: 29.13), and serum uric acid (OR: 1.007) as independent factors associated with SDM. The dose-response between average daily GC dose and SDM was significant (Wald χ 2 = 18.48, df = 3, p = 0.0004); risk rose steeply beyond 1.0 mg/kg/day (e.g., 1.2 mg/kg/day: OR: 3.94, 95% CI: 1.44-10.66). Conclusion:SDM is prevalent among dermatology inpatients receiving GCs. High-risk patients may benefit from closer glucose monitoring and individualized dose adjustment; prospective studies are warranted to confirm these associations.
