Response Of Vitiligo Research Articles

The Effect of Ginkgo Biloba Extract on Oxidative Stress, Anti-Inflammatory and Antiapoptotic in Vitiligo Treated with Topical Desoxymethasone

Vitiligo is a progressive and multifactorial condition of skin, mucosa, and hair depigmentation. Loss of functional melanocytes leads to the appearance of white macules on the skin, often affecting the lips and genitalia. The impact extends to psychological stress, decreased quality of life, and risk of psychiatric morbidity. Various therapeutic strategies have been designed to inhibit the immune response in vitiligo to reduce melanocyte damage while increasing melanocyte repopulation. There is no standardized method of evaluating treatment outcomes in vitiligo patients. Herbal medicines several studies have shown that GB also has many benefits for health and healing skin diseases, one of which is used in treating vitiligo. Therefore, this study aimed to evaluate the potential of Ginkgo biloba extract as a therapeutic supplement in enhancing the positive effects of desoxymethasone on vitiligo. Using a double-blind randomized control trial clinical trial research design, 26 subjects were divided into treatment and control groups. The control group received standard vitiligo therapy with topical desoxymethasone and placebo, while the treatment group received topical desoxymethasone plus Ginkgo biloba extract. Melanin index, VASI score, MDA, TNF-α, CD8 expression, and caspase 3 were measured before and after treatment. The results showed that the administration of Ginkgo biloba extract had a significant effect in reducing MDA, TNF-α, CD8 expression, and caspase 3 levels, and improving melanin index and erythema in vitiligo patients who received topical desoxymethasone therapy. These findings demonstrate the positive potential of Ginkgo biloba extract as an adjunct to vitiligo therapy, resulting in favorable clinical and molecular impacts in patients undergoing combination treatments.

Membranal Expression of Calreticulin Induced by Unfolded Protein Response in Melanocytes: A Mechanism Underlying Oxidative Stress–Induced Autoimmunity in Vitiligo

Calreticulin (CRT), a damage-associated molecular pattern molecule, is reported to translocate from endoplasmic reticulum to membrane in melanocytes under oxidative stress. To investigate the potential role of CRT in the pathogenesis of vitiligo, we analyzed the correlation between CRT and ROS in serum and lesions of vitiligo, detected CRT and protein kinase RNA-like ER kinase (PERK) expression in vitiligo lesions, and studied the production of CRT and mediators of unfolded protein response (UPR) pathway, then tested the chemotactic migration of CD8+ T cells or CD11c+ CD86+ cells. Initially, we verified the overexpression of CRT in perilesional epidermis that was positively correlated with the disease severity of vitiligo. Furthermore, the PERK branch of UPR was confirmed to be responsible for the overexpression and membranal translocation of CRT in melanocytes under oxidative stress. We also found that oxidative stress-induced membranal translocation of CRT promoted the activation and migration of CD8+ T cells in vitiligo. Additionally, dendritic cells from vitiligo patients were also prone to maturation with the co-incubation of melanocytes harboring membranal CRT. CRT could be induced on the membrane of melanocytes via UPR and might play a role in oxidative stress-triggered CD8+ T cell response in vitiligo.

A meta-analysis of the placebo response in vitiligo: Causes and consequences for the interpretation of clinical trials.

The current understanding of the placebo response in vitiligo is limited. Nonetheless, it is difficult to compare the outcomes of vitiligo trials if the repigmentation rates in placebo patients vary significantly. We conducted a meta-analysis of the placebo response in vitiligo trials. Overall, repigmentation rates in patients receiving placebo were 22%, ranging substantially from 0 to 60%. Repigmentation (>25%) was still relatively common for placebo (9.35%), but fell to 5% when >50% improvement was analyzed. Higher frequencies of placebo responses correlated with more repigmentation in the intervention groups. Facial vitiligo and sunlight exposure was linked to higher placebo responses. Roughly estimating the amount of improvement using quartiles (0-25, 25%-50%, 50%-75%, 75%-100% repigmentation) resulted in higher placebo rates compared to other assessment methods. In clinical studies with older patients, the ratio of placebo reactions to treatment responses was higher. This is likely because clinical trials with older patients reported less repigmentation after treatment than studies with younger patients. The percentual difference in affected body surface area during the study period ranged from 6.2% worsening to 17.6% improvement in the placebo groups. This high variability in placebo responses illustrates the need for standardized outcome measures and more head-to-head trials in vitiligo.

063 Autoimmunity and disease outcomes of COVID-19, lessons from vitiligo patients

To date the COVID-19 pandemic is still ongoing with over 5 million registered deaths and over 1 million confirmed new cases daily Still limited information about the possible risks and protective factors for the severity and mortality of COVID-19 The initiation of the immune response in vitiligo is triggered by IFN-I production. Likewise, IFN-I and plasmacytoid dendritic cells (pDCs) play also an important role against SARS-CoV-2 virus including COVID-19 Patients with vitiligo have a genetic susceptibility profile that encodes for immune and apoptotic regulators A retrospective online questionnaire study (4 categories) was conducted in a cohort of vitiligo patients and healthy controls between November 2021 and January 2022. Categories: 1. Participant characteristics 2. COVID-19 risk factors 3. COVID-19 4. Vitiligo 209 participants completed the questionnaire 1. Do vitiligo patients clear a SARS-CoV-2 infection more efficiently compared to healthy controls? There was no significant relationship between vitiligo and developing COVID-19 [P=.930]. 35 [22%] vitiligo patients and 11 [22%] controls developed COVID-19. Univariate logistic regression models showed no confounding factors for developing COVID-19. 2. Do vitiligo patients have a higher risk of developing severe COVID-19 compared to healthy controls? There was a significant difference between having fever in vitiligo patients compared to healthy controls [p=.036], all other symptoms did not show a significant difference. 1 patient with vitiligo was admitted to the hospital, he was known with obesity and ITP. 10 vitiligo patients [28.6%] and 25 controls [45.5%] suffered from post-COVID-19 symptoms [P=.297]. The lingering symptoms between the two groups were similar: loss of smell, tiredness and shortness of breath were mostly reported. 3. Does a SARS-CoV-2 infection or COVID-19 increase the activity of vitiligo? 10 vitiligo patients reported that their vitiligo increased after COVID-19, all these patients already had an active vitiligo before or during COVID-19. 25 vitiligo patients reported that their vitiligo remained stable after COVID-19.

Evaluation of Combination of Microneedling with Tacrolimus in the Treatment of Stable Vitiligo

Introduction: Vitiligo is an amelanotic disorder that can manifest as localized patches to near total body depigmentation. It is considered a cosmetic disease but it is accompanied by extensive psychological effects. Multiple treatments have been tried until now but no single method has achieved the desired response. Tacrolimus is frequently used for vitiligo treatment with few adverse effects. Microneedling is a newer modality of therapeutic wounding that augments drug absorption. Combination of microneedling and tacrolimus have been tried to improve the repigmentation response in vitiligo. Our objective was to assess the safety and efficacy of this combined modality.
 Methods: Forty patients were subjected to combination of tacrolimus 0.1% ointment and microneedling at 2 week intervals for maximum 10 sessions with a follow-up period of 6 months. Assessment was based on grading of repigmentation and clinical improvement according to vitiligo noticeability scale.
 Results: Excellent repigmentation was observed in 30% cases. Improvement was significantly higher in lesions present on the head and neck. Mucosal vitiligo also showed good to excellent response. No severe side effects were reported. No complications or recurrences were observed during the follow-up period.
 Conclusion: Combination of microneedling and tacrolimus was found to be safe and efficacious in the treatment of stable vitiligo.

皮肤组织常驻记忆T细胞在白癜风炎症反应中的作用

皮肤组织常驻记忆T细胞在白癜风炎症反应中的作用

Clinical and Spectrophotometric Evaluation of Skin Photoadaptation in Vitiligo Patients after a Short Cycle of NB-UVB Phototherapy

Background: The phenomenon of photoadaptation to narrow-band ultraviolet B (NB-UVB) radiation has been previously described in vitiligo and has usually been clinically measured by the assessment of the minimal erythema dose (MED) after phototesting. Objectives: To assess the photoadaptive response in vitiligo and healthy skin after NB-UVB phototherapy not only clinically, but also by spectrophotometry. Materials and Methods: Fourteen patients affected by generalized vitiligo underwent NB-UVB phototherapy twice weekly for 12 weeks. Before and after phototherapy, a phototesting procedure was administered on vitiligo patches and adjacent healthy skin with a solar simulated radiation (SSR). Visual assessment of the MED took place after 24 h. A spectrophotometer was used to assess the a* value and the melanin index (MI*), as signs of skin erythema and pigmentation. The photoadaptation factor (MED-PF) and the a* photoadaptation factor (a*-PF) were calculated. Results: After NB-UVB phototherapy, both vitiligo and healthy skin showed an increase in MED and MI* values and a reduction of skin erythema compared to baseline (p < 0.05). MED-PF data showed a photoadaptation in 10 (71.4%) vitiligo lesions and in 12 (85.7%) healthy skin areas. The assessment of the a*-PF showed a negative mean percentage value in all affected and unaffected skin areas. Conclusions: A short cycle of NB-UVB phototherapy can induce photoadaptation in vitiligo by increasing the MED and reducing skin erythema after stimulation with SSR. This is most likely due to the physical filter function induced by ultraviolet radiation.

526 Autophagy is an adaptive stress response in Vitiligo

Evidence argue for some intrinsic metabolic defects in vitiligo cells inducing an oxidative stress that can activate the unfolded protein response (UPR) and eventually lead to activation of immune cells. A growing number of studies supports a dynamic interplay between cellular energy and autophagy balance and describes autophagy, which is a highly orchestrated process of recycling, as an adaptive response that restores energy demand under stress conditions. Indeed, its dysregulation would hinder the ability of cells to respond to stress and it might contribute to the onset and/or development of vitiligo. Here, we show that autophagy-related genes (Atg) are up-regulated in melanocytes and fibroblasts derived from non lesional skin of vitiligo patients. Moreover LC3-II, the most used biomarker of autophagosome formation, is significantly increased in vitiligo cells as demonstrated by western blot and immunofluorescence analyses. Autophagy occurrence can be ascribed to augmented intracellular ROS content since the expression of LC3-II decreased after treatment with the ROS scavenger N-acetyl-L-cysteine and, on the other hand, Atg mRNA level and LC3-II expression increased in normal cells following oxidative stress induced by tert-butyl hydroperoxide. A continuous intracellular ROS production and ATP depletion may converge to inducing autophagy through activation of the energy sensor pAMPK and inhibition of mTORC1 pathway. Herein, we show that pAMPK is upregulated and that the phosphorylation status of S6 kinase, a downstream target of mTORC1, is reduced in non lesional vitiligo melanocytes and fibroblasts compared to the control ones, as reported by western blot and immunofluorescent staining, thus confirming effective mTORC1 inhibition. In conclusion, autophagy is upregulated in vitiligo melanocytes and fibroblasts possibly as part of a broader metabolic program that promotes an adaptive response to restore energetic balance.

Pathogenesis and the emerging Therapy of Vitiligo

Vitiligo is a common and a disfiguring autoimmune disease, which has a negative impact on patients' self-esteem and quality of life. Pathogenesis of Vitiligo involves the interaction between defects of natural and extrinsic melanocytes, immune innate to swelling and destruction of T-cell-mediated melanocyte. Vitiligo affects about 1% of the general population. The risk of the disease was 6% for siblings and 23% for identical twins treatment is not only intended to stop the disease, but also to support repigmentation through the regeneration, proliferation and migration of melanocytes. Treatment strategies for dealing with all aspects of pathogenesis and pigmentation can be very effective, and this strategy may require a combination. Current treatments generally do not imply objective autoimmunity, and emerging treatments may use more specific methods based on a deep understanding of the pathogenesis of the disease, which can provide a good safety profile with a higher effectiveness. However, as with most medical treatments, careful patient selection and monitoring should enable us to normalize the pathogenic response of vitiligo in order to achieve the internal balance of healthy individuals.

Association of human leukocyte antigen-DRB1 with the response in patients with vitiligo

Background Vitiligo is a pigmentary disorder associated with the selective destruction of the skin melanocytes. Among the many human leukocyte antigen (HLA) alleles claimed to be incriminated in establishing vitiligo, HLA-DRB1 is included in many dermatological diseases and has been widely investigated in different studies worldwide. Aim To examine the susceptibility between HLA-DRB1 gene polymorphism and the therapeutic response of vitiligo. Patients and methods We performed a cohort study at Dermatology and Venereology Department, Zagazig Institution Hospitals from January 2018 to January 2019 on 80 patients with vitiligo who were subjected to treatment. Response to therapy was observed, and we followed up patients for 6 months. HLA-DRB1 genotyping using real-time PCR was performed once. Results The results showed that there was a significant statistical association regarding the therapeutic response in our study. Conclusion Our findings advise that DRB1 *0701 and *0413 are associated with good therapeutic response, whereas DRB1 *8 and *12 alleles are associated with worse therapeutic response among Egyptians.

A case of isomorphic response in vitiligo induced by inappropriate topical application of compound Kaliziran tincture

A case of isomorphic response in vitiligo induced by inappropriate topical application of compound Kaliziran tincture

HO-1 regulates the function of Treg: Association with the immune intolerance in vitiligo.

In vitiligo, cutaneous depigmentation is accompanied by increased T cell cytolytic activity targeting melanocytes, indicating that autoimmune tolerance is disrupted. The inhibited amount and function of Tregs have been indicated to be involved in the autoimmune intolerance in vitiligo, however, with the conclusion still controversial and the involved mechanism unknown. In this study, we explored the molecular and cellular alterations accounting for the impaired Treg response in vitiligo. Our results showed that the amount of Tregs was drastically reduced in peripheral blood of active vitiligo patients. Furthermore, the immunoregulatory function of Tregs was attenuated, with lower expression of CTLA4, IL‐10 and TGF‐β. Moreover, the expression of HO‐1, a functional modulator of Tregs, was decreased in vitiligo Tregs, and the concentrations of HO‐1 metabolites, including bilirubin, CoHb and iron, were correspondingly decreased in serum of vitiligo patients. In addition, we treated the Tregs from vitiligo patients with Hemin, an agonist of HO‐1, and found that enhanced HO‐1 expression restored the function of Tregs by up‐regulating IL‐10 expression. Our study demonstrates the essential role of HO‐1 in the impaired Treg response in vitiligo and indicates the potential of HO‐1 as a therapeutic target in vitiligo management.

High level of tumor necrosis alpha and serum interferon gamma as risk factors for progression of vitiligo disease

Vitiligo is an autoimmune disease that causes melanocyte of dysfunction. Cytokines played an important role in the pathogenesis of vitiligo. Interferon-gamma and TNF-µ were cytokines that induce apoptosis of melanocyte cell. The increase of cytokine levels affects the clinical course of vitiligo. The stable and progressive phase of vitiligo clinically is not easy to predict. Assessment of vitiligo stability could be used to determine treatment options, duration of therapy and prognosis. This study was a cross-sectional observational study which intended to prove high levels of TNF-? and IFN-g serum is a risk factor for vitiligo progression. The demographic, clinical, and laboratory data in active vitiligo subjects (n=30) were compared with stable vitiligo subjects (n=40). The relationship was analyzed with multivariate. Median of the subject age with active vitiligo was 44 years (8~60) and on the subject with stable vitiligo was 45 years (15~66). The most subjects were male (58.5%) and the most common type of vitiligo was non-segmental vitiligo (87.1%). Multivariate analysis showed a high level of TNF-µ serum increased the risk of vitiligo progressivity (Adjusted PR 390.89; CI 95 % 27.98-5460.12 ; p<0,001) and high level of IFN-g serum increased the risk of vitiligo progressivity (Adjusted PR 341.06; CI 95% 33.40-3482.26 ; p<0,001). The high level of TNF-µ and IFN-g serum as a risk factor for progression of vitiligo could be used to assess the activity of vitiligo disease. The further research about the association between TNF-µ and IFN-g to predict the therapeutic response in vitiligo.

Resistance to Narrowband Ultraviolet B Therapy Over Varicose Veins in Two Cases of Generalized Vitiligo

ABSTRACT Vitiligo is a difficult-to-control disease with a devastating impact in the lives of many patients. An association has been shown between the Koebner phenomenon and the occurrence of skin depigmentation in vitiligo. However, the medical literature contains very little information regarding the relationship between varicose veins, a common comorbidity for many patients, and vitiligo skin lesions. We present two cases of generalized vitiligo in which patients experienced delayed or absent repigmentation exclusively over varicose veins after narrowband ultraviolet B therapy, despite repigmentation over the rest of the body. In one case, repigmentation occurred after varicose vein treatment. These patients highlight potential and previously unexplored interactions between varicose veins and response to vitiligo phototherapy. The impact of varicose veins on vitiligo treatment may inform future research ideas into the pathogenesis of this skin disease. Furthermore, these cases suggest a possible mechanism of improving local treatment response in vitiligo by addressing underlying varicose veins.

Phototherapy for Vitiligo

References to the expected treatment response to phototherapy would be helpful in the management of vitiligo because phototherapy requires long treatment durations over several months. To estimate the treatment response of vitiligo to phototherapy. A comprehensive database search of MEDLINE, EMBASE, and the Cochrane library from inception to January 26, 2016, was performed for all prospective studies. The main keywords used were vitiligo, phototherapy, psoralen, PUVA, ultraviolet, NBUVB, and narrowband. All prospective studies reporting phototherapy outcome for at least 10 participants with generalized vitiligo were included. Of 319 studies initially identified, the full texts of 141 studies were assessed for eligibility, and 35 were finally included in the analysis. Of these, 29 studies included 1201 patients undergoing narrowband UV-B (NBUVB) phototherapy, and 9 included 227 patients undergoing psoralen-UV-A (PUVA) phototherapy. Two reviewers independently extracted the following data: study design, number and characteristics of the participants, phototherapy protocol, and rate of repigmentation based on the quartile scale. Single-arm meta-analyses were performed for the NBUVB and PUVA groups. Sample size-weighted means were calculated using a random-effects model for the repigmentation rates of the included studies. The primary outcomes were at least mild (≥25%), at least moderate (≥50%), and marked (≥75%) responses on a quartile scale. Response rates were calculated as the number of participants who showed the corresponding repigmentation divided by the number of all participants enrolled in the individual studies. The meta-analysis included 35 unique studies (1428 unique patients). For NBUVB phototherapy, an at least mild response occurred in 62.1% (95% CI, 46.9%-77.3%) of 130 patients in 3 studies at 3 months, 74.2% (95% CI, 68.5%-79.8%) of 232 patients in 11 studies at 6 months, and 75.0% (95% CI, 60.9%-89.2%) of 512 patients in 8 studies at 12 months. A marked response was achieved in 13.0% (95% CI, 2.1%-23.9%) of 106 patients in 2 studies at 3 months, 19.2% (95% CI, 11.4%-27.0%) of 266 patients in 13 studies at 6 months, and 35.7% (95% CI, 21.5%-49.9%) of 540 patients in 9 studies at 12 months. For PUVA phototherapy, an at least mild response occurred in 51.4% (95% CI, 28.1%-74.7%) of 103 patients in 4 studies at 6 months and 61.6% (95% CI, 20.2%-100%) of 72 patients in 3 studies at 12 months. In the subgroup analyses, marked responses were achieved on the face and neck in 44.2% (95% CI, 24.2%-64.2%), on the trunk in 26.1% (95% CI, 8.7%-43.5%), on the extremities in 17.3% (95% CI, 8.2%-26.5%), and on the hands and feet in none after at least 6 months of NBUVB phototherapy. Long-duration phototherapy should be encouraged to enhance the treatment response in vitiligo. The greatest response is anticipated on the face and neck.

Vitiligo blood transcriptomics provides new insights into disease mechanisms and identifies potential novel therapeutic targets

BackgroundSignificant gaps remain regarding the pathomechanisms underlying the autoimmune response in vitiligo (VL), where the loss of self-tolerance leads to the targeted killing of melanocytes. Specifically, there is incomplete information regarding alterations in the systemic environment that are relevant to the disease state.MethodsWe undertook a genome-wide profiling approach to examine gene expression in the peripheral blood of VL patients and healthy controls in the context of our previously published VL-skin gene expression profile. We used several in silico bioinformatics-based analyses to provide new insights into disease mechanisms and suggest novel targets for future therapy.ResultsUnsupervised clustering methods of the VL-blood dataset demonstrate a “disease-state”-specific set of co-expressed genes. Ontology enrichment analysis of 99 differentially expressed genes (DEGs) uncovers a down-regulated immune/inflammatory response, B-Cell antigen receptor (BCR) pathways, apoptosis and catabolic processes in VL-blood. There is evidence for both type I and II interferon (IFN) playing a role in VL pathogenesis. We used interactome analysis to identify several key blood associated transcriptional factors (TFs) from within (STAT1, STAT6 and NF-kB), as well as “hidden” (CREB1, MYC, IRF4, IRF1, and TP53) from the dataset that potentially affect disease pathogenesis. The TFs overlap with our reported lesional-skin transcriptional circuitry, underscoring their potential importance to the disease. We also identify a shared VL-blood and -skin transcriptional “hot spot” that maps to chromosome 6, and includes three VL-blood dysregulated genes (PSMB8, PSMB9 and TAP1) described as potential VL-associated genetic susceptibility loci. Finally, we provide bioinformatics-based support for prioritizing dysregulated genes in VL-blood or skin as potential therapeutic targets.ConclusionsWe examined the VL-blood transcriptome in context with our (previously published) VL-skin transcriptional profile to address a major gap in knowledge regarding the systemic changes underlying skin-specific manifestation of vitiligo. Several transcriptional “hot spots” observed in both environments offer prioritized targets for identifying disease risk genes. Finally, within the transcriptional framework of VL, we identify five novel molecules (STAT1, PRKCD, PTPN6, MYC and FGFR2) that lend themselves to being targeted by drugs for future potential VL-therapy.

Involvement of Different Genes Expressions during Immunological and Inflammatory Responses in Vitiligo.

Vitiligo is a condition of the skin distinguished by hypo-pigmentation. Etiology of this disorder is unknown, and several theories and mechanisms have been hypothesized. The inflammatory response in vitiligo is thought to be mediated by polymorphism in genes such as FOXP3, ACE, APE, GSTP1, TLR, SOD, CTLA-4, TAP/LMP gene cluster, etc. Theories including reactive oxygen species model, Nrf2-antioxidant response element (ARE) pathway, WNT pathway, tyrosinase activity, biochemical, molecular, and cellular alterations have been hypothesized to explain vitiligo pathogenesis. Melanosomal proteins are involved in antigen processing. The antigens are expressed to the T-cells in the form of peptides with HLA class II molecules. T-cells are activated in response to the discharge of co-stimulatory molecules such as LFA-3 as well as ICAM-1. An adaptive immune response is thus elicited, and the melanocytes eventually die or start malfunctioning and the skin undergoes hypo-pigmentation. IFN-γ is known to be a melanocyte inhibitor of paracrine origin; it is clearly involved in the early onset of symptoms of vitiligo disease. The surge in the IFN-γ levels mediates augmented expression of ICAM-1 molecule on the melanocytes, thereby establishing cytokine-mediated destruction of melanocytes. Mainly, mediators released by melanocytes and the functionality of keratinocytes decrease the disease activity. Such mediators include ET-1 as well as SCF, increase the pigmentation particularly when a patient is given with the UVB treatment. By scavenging ROS and screening UV radiation, melanin limits the damage caused to the cutaneous cells by UV radiation. Various immune responses play important roles in vitiligo.

Identification of Novel HLA-A*0201-Restricted CTL Epitopes in Chinese Vitiligo Patients.

Generalized vitiligo is an autoimmune disease characterized by melanocyte loss, which results in patchy depigmentation of skin and hair. Recent studies suggested the key role of CD8+T lymphocytes for mediating immune response in vitiligo through melanocyte differentiation antigens, including tyrosinase, gp100 and MelanA/Mart-1. However, the specific epitopes of these auto-antigens are still unknown. In our study, we predicted the possible HLA-A*0201-restricted nonapeptides overlaying the full-length amino acid sequences of these three known antigens and investigated the lymphocytes reactivity to these nonapeptides by Elispot assay. In addition, we evaluated the abilities of these nonapeptides to activate CD8+T cells. We screened out 5 possible epitopes originated from tyrosinase and gp100, numbered P28, P41, P112, P118 and P119. Among these 5 epitopes, notably, P28 and P119 played the dominant role in activating CTLs, with a significant increase in proliferation rate and Interferon-γ (IFN-γ) production of CD8+T cells. Nevertheless, antigen-specific T cell reactivity was not detected in MelanA/Mart-1 peptides. Our studies identified two novel epitopes originated from proteins of gp100 and tyrosinase, which may have implications for the development of immunotherapies for vitiligo.

Fractionated CO2 laser combined with 308-nm excimer laser for the treatment of stable vitiligo: an observational clinical study

Objective To evaluate the efficacy and safety of fractionated CO2 laser combined with 308-nm excimer laser for the treatment of stable vitiligo.Methods Forty-nine patients with 109 lesions of stable vitiligo were enrolled in this clinical trial.Each of these lesions was equally divided into 2 parts along the longest diameter,which were then assigned into the treatment group and control group respectively.The treatment group were treated with fractionated CO2 laser radiation for 15-20 minutes once every two weeks combined with 308-nm excimer laser radiation twice weekly.The control group were only treated with 308-nm excimer laser radiation twice weekly.Efficacy was evaluated on day 3 after 12 consecutive weeks of treatment.Results After the treatment,the total response rate in the treatment group and control group was 92.7％ (101/109) and 77.1％ (84/109) respectively.The marked response rate in the treatment group and control group was 85.4％ (35/41) and 65.8％ (27/41) respectively for lesions on the face and neck (x2 =4.23,P ＜ 0.05),70.6％ (24/34) and 41.2％ (14/34) respectively for lesions on the trunk (x2 =7.27,P＜ 0.01),64.0％ (16/25) and 36.0％ (9/25) respectively for lesions on the extremities (x2 =3.92,P ＜ 0.05),5/9 and 1/9 respectively for lesions on the dorsal hands (X2 =4.00,P ＜ 0.05).The number of sessions of 308-nm excimer laser therapy required for the marked response of vitiligo in the treatment group and control group was 7.24 ± 1.23 and 10.81 ± 2.01 respectively for lesions on the face and neck (t =9.70,P ＜ 0.05),15.10 ± 2.47 and 18.95 ± 3.45 respectively for lesions on the trunk (t =5.29,P＜ 0.05),17.37 ± 3.84 and 21.06 ± 4.23 respectively for lesions on the extremities (t =3.23,P ＜ 0.05).No severe adverse reactions were observed in any of the patients during the treatment.Conclusion Fractionated CO2 laser combined with 308-nm excimer laser is effective and safe in treating stable vitiligo. Key words: Vitiligo; Fractional laser; Efficacy

Survey and online discussion groups to develop a patient-rated outcome measure on acceptability of treatment response in vitiligo.

BackgroundVitiligo is a chronic depigmenting skin disorder which affects around 0.5-1% of the world’s population. The outcome measures used most commonly in trials to judge treatment success focus on repigmentation. Patient-reported outcome measures of treatment success are rarely used, although recommendations have been made for their inclusion in vitiligo trials. This study aimed to evaluate the face validity of a new patient-reported outcome measure of treatment response, for use in future trials and clinical practice.MethodAn online survey to gather initial views on what constitutes treatment success for people with vitiligo or their parents/carers, followed by online discussion groups with patients to reach consensus on what constitutes treatment success for individuals with vitiligo, and how this can be assessed in the context of trials. Participants were recruited from an existing database of vitiligo patients and through posts on the social network sites Facebook and Twitter.ResultsA total of 202 survey responses were received, of which 37 were excluded and 165 analysed. Three main themes emerged as important in assessing treatment response: a) the match between vitiligo and normal skin (how well it blends in); b) how noticeable the vitiligo is and c) a reduction in the size of the white patches. The majority of respondents said they would consider 80% or more repigmentation to be a worthwhile treatment response after 9 months of treatment. Three online discussion groups involving 12 participants led to consensus that treatment success is best measured by asking patients how noticeable their vitiligo is after treatment. This was judged to be best answered using a 5-point Likert scale, on which a score of 4 or 5 represents treatment success.ConclusionsThis study represents the first step in developing a patient reported measure of treatment success in vitiligo trials. Further work is now needed to assess its construct validity and responsiveness to change.