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Vitiligo, an acquired pigmentary disorder of unknown origin, is the most frequent cause of depigmentation worldwide, with an estimated prevalence of 1%. The disorder can be psychologically devastating and stigmatising, especially in dark skinned individuals. Vitiligo is clinically characterised by the development of white macules due to the loss of functioning melanocytes in the skin or hair, or both. Two forms of the disease are well recognised: segmental and non-segmental vitiligo (the commonest form). To distinguish between these two forms is of prime importance because therapeutic options and prognosis are quite different. The importance of early treatment and understanding of the profound psychosocial effect of vitiligo will be emphasised throughout this Seminar.

ABSTRACT Background Late‐onset vitiligo (LOV), generally defined as vitiligo that starts at age 30 or older, presents unique diagnostic and management challenges, reflecting an intricate interplay of genetic, environmental, and societal factors. Objectives This review aims to elucidate the distinct aspects of LOV such as epidemiology, clinical characteristics, and treatment outcomes thereby enhancing diagnostic precision and planning management strategies. Materials and Methods A comprehensive literature search was conducted across multiple databases including PubMed and EMBASE, adhering to PRISMA guidelines. Studies focused on adults (age 30 or older at the time of diagnosis) with LOV were included. Data on demographics, clinical features, and comorbidities were extracted. Results The literature search yielded five eligible articles with a total sample size of 1099 patients. LOV prevalence ranged from 6.5% to 14.7%, with a mean age of onset in the mid to late 50s. Vitiligo vulgaris was the most common form, with increased leukotrichia and the Koebner phenomenon. Associated autoimmune/endocrine disorders, including diabetes mellitus and thyroid diseases, were prevalent, suggesting systemic links. Treatment outcomes varied, with combination therapy and phototherapy showing promise. Conclusion Late‐onset vitiligo differs significantly from early‐onset vitiligo in its clinical traits, epidemiology, and treatment response, necessitating personalized care and targeted management strategies.

Background Patients with vitiligo experience reduced quality of life. Objective To comprehensively describe the available evidence for psychosocial burden in vitiligo. Methods A systematic review of observational studies and clinical trials identified using PubMed, EMBASE, Scopus, and the Cochrane databases was performed through 1 March, 2021, to assess psychosocial comorbidities in vitiligo. Two independent reviewers performed an assessment of articles and extracted data for qualitative synthesis. Results Included studies ( N = 168) were published between 1979 and 1 March, 2021; 72.6% were published since 2010. Disorders including or related to depression (41 studies, 0.1–62.3%) and anxiety (20 studies, 1.9–67.9%) were the most commonly reported. The most prevalent psychosocial comorbidities were feelings of stigmatization (eight studies, 17.3–100%), adjustment disorders (12 studies, 4–93.9%), sleep disturbance (seven studies, 4.6–89.0%), relationship difficulties including sexual dysfunction (ten studies, 2.0–81.8%), and avoidance or restriction behavior (12.5–76%). The prevalence of most psychosocial comorbidities was significantly higher vs healthy individuals. Factors associated with a significantly higher burden included female sex, visible or genital lesions, age < 30 years (particularly adolescents), and greater body surface area involvement, among others. The most commonly reported patient coping strategy was lesion concealment. Limitations Available studies were heterogeneous and often had limited details; additionally, publication bias is possible. Conclusions The results of this systematic review show that vitiligo greatly affects psychosocial well-being. The extent of psychosocial comorbidities supports the use of multidisciplinary treatment strategies and education to address the vitiligo-associated burden of disease. Protocol Registration PROSPERO (CRD42020162223). Graphic Abstract

Pigmentary network changes, and perifollicular and perilesional hyperpigmentation on polarized light examination, and a diffuse white glow on ultraviolet light examination were noted in evolving vitiligo lesions [4]. Figure 3 [See PDF] (a) Vitiligo showing loss of reticulate pigment network. (b) Ash leaf spots showing areas of faint reticular pigmentation and zones of total loss of any pigmentary pattern. Melanosomes are usually normal in size, shape, and internal structure, but can be diminished in number, heteromorphic, aggregated in melanocytes, or located in membrane bound aggregates [6].

Both alopecia areata (AA) and vitiligo are distinct, heterogenous, and complex disease entities, characterized by nonscarring scalp terminal hair loss and skin pigment loss, respectively. In AA, inflammatory cell infiltrates are in the deep reticular dermis close to the hair bulb (swarm of bees), whereas in vitiligo the inflammatory infiltrates are in the epidermis and papillary dermis. Immune privilege collapse has been extensively investigated in AA pathogenesis, including the suppression of immunomodulatory factors (e.g., transforming growth factor-β (TGF-β), programmed death-ligand 1 (PDL1), interleukin-10 (IL-10), α-melanocyte-stimulating hormone (α-MSH), and macrophage migration inhibitory factor (MIF)) and enhanced expression of the major histocompatibility complex (MHC) throughout hair follicles. However, immune privilege collapse in vitiligo remains less explored. Both AA and vitiligo are autoimmune diseases that share commonalities in pathogenesis, including the involvement of plasmacytoid dendritic cells (and interferon-α (IFN- α) signaling pathways) and cytotoxic CD8+ T lymphocytes (and activated IFN-γ signaling pathways). Blood chemokine C-X-C motif ligand 9 (CXCL9) and CXCL10 are elevated in both diseases. Common factors that contribute to AA and vitiligo include oxidative stress, autophagy, type 2 cytokines, and the Wnt/β-catenin pathway (e.g., dickkopf 1 (DKK1)). Here, we summarize the commonalities and differences between AA and vitiligo, focusing on their pathogenesis.

T-cells play a crucial role in progression of autoimmunity, including vitiligo, yet the initial steps triggering their activation and tissue damage remain unknown. Here we demonstrate increased presence of type-1 innate lymphoid cells (NK and ILC1)-producing interferon gamma (IFNγ) in the blood and in non-lesional skin of vitiligo patients. Melanocytes of vitiligo patients have strong basal expression of chemokine-receptor-3 (CXCR3) isoform B which is directly regulated by IFNγ. CXCR3B activation by CXCL10 at the surface of cultured human melanocytes induces their apoptosis. The remaining melanocytes, activated by the IFNγ production, express co-stimulatory markers which trigger T-cell proliferation and subsequent anti-melanocytic immunity. Inhibiting the CXCR3B activation prevents this apoptosis and the further activation of T cells. Our results emphasize the key role of CXCR3B in apoptosis of melanocytes and identify CXCR3B as a potential target to prevent and to treat vitiligo by acting at the early stages of melanocyte destruction. Tissue signals that prime autoreactive T cells at the onset of autoimmunity remain enigmatic. Here the authors show NK and ILC1 cells are increased in vitiligo patients, and induce melanocyte apoptosis via CXCR3B, which in turn leads to increased priming of T cell responses in cell culture.

Observation: Topical application of preparations containing superoxide dismutase and catalase in the treatment of vitiligo has a recent onset. Till the present time no such adverse reaction has been reported. In this article we present a case who developed pigmented macules with distant localization to depigmented patches during therapy with a plant extract containing superoxide dismutase and catalase (Vitix®). This is the first report of an adverse effect of Vitix® in the English language literature. Patients with facial vitiligo should be warned of this possibility.

ABSTRACT Background Clinical diagnosis and staging of vitiligo often rely on the patient's subjective recollection, physician's experience, or clinical evaluation methods. An objective, quantitative diagnostic approach is lacking. Aims This study was performed to compare the sensitivity and specificity of different lesion areas and full scanning of lesion areas using reflectance confocal microscopy (RCM) for diagnosis and staging of vitiligo. Methods Clinical and RCM data of patients diagnosed with vitiligo were collected. RCM data were gathered from three sites of a lesion: the center of the lesion, the margin of the lesion, and the perilesional normal skin. Scoring was conducted for each method, categorizing the results as either the progressive or stable stage of vitiligo. Results The sensitivity was significantly lower in the perilesional normal skin than at multiple sites (p < 0.001). The specificity was significantly lower in the center of the lesion and at the margin than at multiple sites and significantly higher in the perilesional normal skin than at multiple sites (p < 0.05 for all). Conclusions The results of RCM of different lesion areas of vitiligo showed that the rate of missed diagnosis of the progressive stage was lowest in the center of the lesion and comparable to that of multiple sites. The misdiagnosis rate for the stable stage was lowest in the perilesional normal skin, significantly differing from the other sites. Overall, scanning multiple sites yielded the most accurate results, offering flexibility in selection according to the patient's compliance.

Vitiligo is a T-cell mediated skin disorder characterized by progressive loss of skin color. In individuals genetically predisposed to the disease, various triggers contribute to the initiation of vitiligo. Precipitating factors can stress the skin, leading to T-cell activation and recruitment. Though hereditary factors are implicated in the pathogenesis of vitiligo, it is unknown whether precipitating, stressful events play a role in vitiligo. To understand this, we utilized a validated perceived stress scale (PSS) to measure this parameter in vitiligo patients compared to persons without vitiligo. Additionally, we probed a clinical database, using a knowledge linking software called ROCKET, to gauge stress-related conditions in the vitiligo patient population. From a pool of patients in an existing database, a hundred individuals with vitiligo and twenty-five age- and sex-matched comparison group of individuals without vitiligo completed an online survey to quantify their levels of perceived stress. In parallel, patients described specifics of their disease condition, including the affected body sites, the extent, duration and activity of their vitiligo. Perceived stress was significantly higher among vitiligo individuals compared to those without vitiligo. ROCKET analyses suggested signs of metabolic-related disease (i.e., 'stress') preceding vitiligo development. No correlation was found between perceived stress and the stage or the extent of disease, suggesting that elevated stress may not be a consequence of pigment loss alone. The data provide further support for stress as a precipitating factor in vitiligo development.

The International Journal of Molecular Sciences retracts the article, “Differential Expression of Nitric Oxide Synthase Isoforms nNOS and iNOS in Patients with Non-Segmental Generalized Vitiligo” [...]