Therapeutic Efficacy of 308-nm Excimer Laser Combined with Matrine in Vitiligo by Modulation of Serum Immunoglobulins and Inflammatory Cytokines

Summary

The combined use of a 308-nm excimer laser and oral matrine markedly enhanced repigmentation in vitiligo by promoting melanocyte regeneration and restoring immune balance. This dual-modality therapy reduced pro-inflammatory cytokines, normalized immunoglobulins, elevated IL-10, and achieved superior clinical efficacy with excellent safety and patient tolerance.

Abstract

Vitiligo is a chronic autoimmune depigmenting disorder characterized by the loss of functional melanocytes and aberrant immune activation. Despite advances in phototherapy, clinical responses remain inconsistent, largely due to persistent inflammatory activity and inadequate immune regulation. This study investigated the therapeutic efficacy and immunologic mechanisms of combining 308-nm excimer laser phototherapy with oral matrine, a natural alkaloid possessing anti-inflammatory and immunoregulatory properties. A total of 232 patients with non-segmental vitiligo were prospectively assigned to receive either excimer laser monotherapy or combination therapy for 12 weeks. Clinical improvement was evaluated using the Vitiligo Area Scoring Index (VASI), and serum immunoglobulins and cytokines were analyzed to assess systemic immune modulation. Both regimens produced significant repigmentation, yet the combination therapy achieved a more pronounced VASI reduction (from 9.72 ± 3.24 at baseline to 5.76 ± 2.18 after treatment) than the excimer laser alone (from 9.68 ± 3.37 to 6.63 ± 2.34, p < 0.001). The proportion of patients demonstrating excellent or good repigmentation was notably higher with the combined regimen (76.7%) compared with monotherapy (58.7%). In parallel, serum IgG levels declined markedly (13.72 ± 2.64 g/L to 11.85 ± 2.18 g/L, p < 0.001), whereas IgA levels rose modestly (2.07 ± 0.68 g/L to 2.23 ± 0.61 g/L, p = 0.041). Pro-inflammatory cytokines including IFN-γ and IL-17 were significantly reduced (both p < 0.001), while anti-inflammatory IL-10 increased from 8.3 ± 3.2 to 12.9 ± 3.5 pg/mL (p < 0.001). VASI improvement correlated inversely with IFN-γ (r = –0.482, p < 0.05) and IL-17 (r = –0.451, p < 0.001) changes, and positively with IL-10 elevation (r = 0.503, p < 0.001). These findings demonstrate that matrine enhances excimer laser efficacy by promoting melanocyte regeneration and restoring immune equilibrium, establishing a biomarker-based dual-modality strategy for precise and durable management of vitiligo.

Introduction

Vitiligo is a chronic, acquired depigmenting skin disorder characterized by the selective destruction or dysfunction of epidermal melanocytes, leading to the development of well-defined white macules of variable size and distribution. It affects approximately 0.5%–2% of the global population, without gender or racial predilection, and often presents before the age of 30^1,2. Although the disease is not life-threatening, it imposes a substantial psychosocial and emotional burden, significantly impairing self-esteem, social functioning, and quality of life³. The pathogenesis of vitiligo remains multifactorial and incompletely elucidated, involving genetic predisposition, oxidative stress, autoimmune reactions, and neurohumoral factors⁴. Recent evidence has particularly emphasized the pivotal role of immune dysregulation in both the initiation and persistence of melanocyte destruction^5,6. In the epidermis, autoreactive CD8⁺ cytotoxic T lymphocytes recognize melanocyte antigens such as tyrosinase and gp100, releasing perforin and granzyme B to induce apoptosis⁷. Concurrently, pro-inflammatory cytokines, including interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), IL-6, and IL-17, amplify the inflammatory cascade, impair melanocyte survival, and inhibit pigment cell migration⁸. The imbalance between regulatory T cells (Tregs) and effector T cells further contributes to persistent immune activation and melanocyte loss⁹. Thus, therapeutic strategies aimed at both promoting melanocyte regeneration and re-establishing immune homeostasis are of major clinical importance.

Beyond local immune abnormalities, increasing evidence indicates that vitiligo represents a systemic autoimmune condition. Altered serum levels of immunoglobulins (IgG, IgA, and IgM) have been documented in patients, reflecting generalized B-cell activation and abnormal humoral immunity^10,11. Dysregulated immunoglobulin production may facilitate autoantibody formation against melanocyte-specific antigens, exacerbating tissue damage. Moreover, the cytokine milieu in vitiligo patients frequently exhibits elevated IFN-γ, TNF-α, IL-6, IL-17, and IL-23, suggesting systemic immune activation beyond lesional skin^12,13. These immune mediators not only serve as pathogenic drivers but also correlate with disease activity and therapeutic response, positioning them as potential biomarkers for treatment monitoring¹⁴. Therefore, interventions capable of restoring immune balance—by modulating both cellular and humoral immune responses—may offer superior and durable clinical outcomes. Despite the availability of topical corticosteroids, calcineurin inhibitors, systemic immunosuppressants, and phototherapy, treatment efficacy remains unsatisfactory for many patients, particularly those with extensive or refractory disease¹⁵. Consequently, combination approaches that target multiple pathophysiologic mechanisms have gained traction in recent years.

Phototherapy has long been a cornerstone in vitiligo management. Among various modalities, the 308-nm excimer laser (EL) has emerged as one of the most targeted and effective options for localized vitiligo^16,17. It delivers monochromatic UVB radiation at 308 nm directly to depigmented lesions, thereby stimulating melanocyte proliferation and migration from hair follicles while minimizing exposure of surrounding healthy tissue¹⁸. Compared with conventional narrow-band UVB, the excimer laser offers advantages of rapid onset of repigmentation, shorter cumulative exposure time, and improved safety profile^19,20. Mechanistically, low-dose 308-nm irradiation induces local immunomodulation by reducing epidermal Langerhans cell activity, increasing Treg infiltration, and enhancing melanogenesis via upregulation of tyrosinase and microphthalmia-associated transcription factor (MITF)²¹. However, responses remain variable, and many patients fail to achieve complete repigmentation. Excessive or prolonged irradiation may paradoxically trigger inflammatory cytokine release—such as IL-1β, IL-6, and TNF-α—and further melanocyte injury^22,23. Thus, while excimer laser treatment effectively stimulates melanocyte regeneration, its efficacy may be limited by concurrent inflammatory activation. This duality underscores the need for adjunctive therapies capable of mitigating inflammation and enhancing immune tolerance during phototherapy.

Matrine, a natural quinolizidine alkaloid extracted from Sophora flavescens (Ku Shen), has recently attracted considerable attention as an immunomodulatory and anti-inflammatory agent with low toxicity^24,25. Experimental studies have demonstrated that matrine can suppress the NF-κB and JAK/STAT signaling pathways, downregulate the production of pro-inflammatory cytokines (including IFN-γ, TNF-α, and IL-6), and promote the expression of anti-inflammatory mediators such as IL-10²⁶. In immune-related diseases, matrine has shown efficacy in modulating Th1/Th17 differentiation, enhancing regulatory T-cell function, and normalizing immunoglobulin profiles^27,28. Moreover, matrine exhibits antioxidant and anti-apoptotic effects that may protect melanocytes from oxidative stress-induced injury²⁹. While these properties make matrine an attractive candidate for autoimmune skin diseases, few studies have explored its role in vitiligo. The combination of matrine with phototherapy presents a novel therapeutic approach: matrine could attenuate the inflammatory microenvironment, stabilize melanocyte homeostasis, and potentiate laser-induced melanogenesis. Furthermore, matrine’s systemic immunoregulatory activity may complement the local effects of the excimer laser, resulting in synergistic clinical benefit. To our knowledge, no prior clinical study has comprehensively investigated the combined use of 308-nm excimer laser and matrine in vitiligo or evaluated its immunologic correlates through serum biomarker profiling.

Based on this rationale, we hypothesized that the combination of 308-nm excimer laser and matrine would yield superior therapeutic efficacy compared with excimer laser monotherapy, by simultaneously promoting melanocyte regeneration and suppressing aberrant immune activation. Specifically, we postulated that adjunctive matrine administration would enhance clinical repigmentation rates, modulate serum immunoglobulin levels (IgG, IgA, and IgM) toward physiological balance, and reduce pro-inflammatory cytokines such as IFN-γ, TNF-α, and IL-17, while increasing anti-inflammatory cytokines. In this study, we systematically evaluated clinical outcomes, immunologic parameters, and their correlations in patients with vitiligo treated with this combination therapy. The novelty of this investigation lies in its dual mechanistic focus—local photobiological stimulation and systemic immune modulation—and its integration of quantitative biomarker analysis to elucidate therapeutic mechanisms. By clarifying the immunoregulatory impact of matrine when combined with targeted phototherapy, our work aims to provide an evidence-based foundation for a new therapeutic paradigm in vitiligo management. Ultimately, these findings may advance the field toward precision, immune-guided phototherapy strategies that achieve not only repigmentation but also long-term disease stabilization and relapse prevention.

Protocol

This study was conducted in accordance with the ethical principles of the Declaration of Helsinki and the institutional regulations governing human research. The study was conducted in accordance with the ethical principles of the Declaration of Helsinki and approved by the Ethics Committee of Xingtai People’s Hospital, Department of Dermatology (Approval ID: 2021[029]). All participants provided written informed consent before participation.

Patient selection
A total of 232 patients clinically diagnosed with vitiligo were enrolled over a 3-year period from January 2021 to December 2023. All participants were diagnosed with non-segmental vitiligo (generalized or localized type) and classified as stable or progressive based on the absence or presence of new lesions within 3 months before enrollment. Disease duration and lesion distribution were recorded at baseline. Enrollment criteria included individuals aged 18 to 65 years with stable or progressive vitiligo confirmed by dermatologists through clinical examination, Wood’s lamp illumination, and dermoscopy. Exclusion criteria were pregnancy, lactation, photoallergic disorders, systemic autoimmune disease, severe hepatic or renal dysfunction, and prior use of systemic corticosteroids, immunosuppressants, or phototherapy within 3 months. All procedures were performed under continuous ethical supervision, ensuring patient comfort and safety throughout the treatment course.

Study overview and treatment workflow
The overall workflow of the study, including patient enrollment, group allocation, follow-up assessments, and biomarker analysis, is illustrated in Figure 1. Eligible participants were assigned in a 1:1 ratio to one of two parallel study groups: the 308-nm excimer laser monotherapy group (excimer laser alone; n = 116) and the combination therapy group (308-nm excimer laser plus oral matrine; n = 116). Group allocation was performed using a computer-generated random sequence prepared by an independent research staff member who was not involved in outcome assessment; assignments were placed in sequentially numbered, sealed envelopes and opened after enrollment to determine treatment allocation. The therapeutic workflow consisted of three major phases: (1) baseline assessment and documentation, (2) 12 weeks of active treatment according to the assigned regimen, and (3) post-treatment evaluation, including laboratory testing of serum immunoglobulins and inflammatory cytokines. Each patient received a standardized care plan, identical follow-up intervals, and uniform laboratory analysis procedures. Clinical photographs and VASI scoring were performed by dermatologists blinded to treatment allocation. All procedures were performed in the dermatology phototherapy suite of Xingtai People’s Hospital under controlled ambient conditions (room temperature 22–24 °C, relative humidity 40%–60%).

Preparation of the treatment area
Prior to each laser session, the target depigmented areas were gently cleansed with sterile physiological saline and patted dry with lint-free medical gauze. Lesional skin was inspected to confirm the absence of infection, excoriation, or crusting. When more than one lesion was treated in a single visit, each lesion was prepared and treated sequentially. Lesions exceeding a single irradiation field were subdivided into adjacent irradiation fields, and surrounding normal skin was shielded with an opaque UV-blocking sheet for each field to minimize unnecessary exposure. Patients were instructed to avoid topical agents, photosensitizing cosmetics, or perfumes for 24 h before treatment. Protective goggles were worn by both the patient and the operator throughout the procedure.

308-nm excimer laser irradiation procedure
A monochromatic 308-nm xenon-chloride (XeCl) excimer laser system was used. All laser sessions were performed by two trained dermatologic physicians under a standardized protocol to ensure consistent energy output, irradiation distance, and reproducibility. The device output was verified with a calibrated UV power meter before each treatment day, and all systems underwent weekly calibration by a certified technician to maintain an error margin below ±5%. Before the first irradiation, the minimal erythema dose (MED) for each patient was determined by applying incremental doses (100–400 mJ/cm²) to small test areas on the inner forearm and evaluating the erythema response after 24 h; results were photographed and recorded in patient charts. A representative MED documentation and session-by-session dose-adjustment chart is provided in Supplementary Table 1. MED was defined as the lowest test dose producing a clearly discernible, uniform erythema at 24 h. The initial treatment dose was set at 80%–90% of the individual MED, and subsequent dose changes followed a predefined algorithm based on the prior-session 24-h erythema response (increase by 10%–20% for absent or mild erythema, maintain the same dose for moderate erythema, and reduce by 10%–20% for blistering or significant pain). The initial therapeutic dose was set at 150–250 mJ/cm² (approximately 80%–90% of the individual MED). Each session began with the patient comfortably seated on an adjustable chair. The laser handpiece was held perpendicular (90°) to the skin at a distance of 10–15 cm, and circular or rectangular irradiation fields were aligned to fully cover depigmented areas with minimal overlap. Irradiation lasted 1–3 s per exposure field, depending on fluence. Doses were subsequently increased by 10%–20% per session according to the prior erythema response; if moderate erythema occurred, the previous dose was maintained, whereas blistering or pain warranted a 10%–20% reduction. The maximum dose did not exceed 2,000 mJ/cm². Each session covered all visible lesions and lasted 10–20 min, depending on the extent. Treatments were performed 2x weekly with at least 72 h between sessions over a total period of 12 weeks (24 sessions). Following irradiation, a thin layer of sterile aloe-based gel was applied to relieve local erythema. Patients were instructed to avoid sun exposure for 48 h and to use a broad-spectrum sunscreen (SPF >30) throughout the treatment. Lesions showing >50% repigmentation continued under the same parameters until stable pigmentation was achieved.

Oral matrine administration
In the combination group, a sterile aqueous extract of Sophora flavescens roots was prepared in accordance with the Chinese Pharmacopoeia (2020 edition)³⁰ and standardized to a concentration of 5 mg/mL with ≥98% purity, verified by high-performance liquid chromatography (HPLC). The solution was stored at 4 °C in amber glass bottles to prevent photodegradation. Random batch testing confirmed alkaloid concentration (5 ± 0.3 mg/mL) and microbial sterility. Each patient received the matrine solution by oral administration at a dose of 0.3 g (60 mL) twice daily for 12 weeks, synchronized with the laser treatment schedule. The dosage was selected based on prior pharmacological data demonstrating effective immunomodulation with a favorable safety profile in chronic inflammatory dermatoses^31,32. Patients were instructed to take the solution 30 min after meals to minimize gastrointestinal discomfort and to avoid alcohol, strong tea, and spicy food during therapy to reduce hepatic burden. Mild nausea or fatigue was managed by the administration of a small amount of warm water. Treatment adherence was assessed through a medication diary and bottle-return verification at each follow-up visit. Safety was assessed at each visit by structured symptom inquiry and documentation of adverse events, including gastrointestinal discomfort, fatigue, and any signs suggestive of hepatic intolerance. No additional systemic medications, topical corticosteroids, or immunosuppressants were permitted during the observation period to prevent confounding effects.

Evaluation of clinical response
Pigmentation changes were evaluated at baseline and at weeks 4, 8, and 12 by two experienced dermatologists blinded to treatment information. Standardized digital photographs were taken under identical lighting and camera settings (distance 60 cm, exposure 1/60 s, ISO 200). The degree of repigmentation was quantified using the Vitiligo Area Scoring Index (VASI). Lesions were additionally graded into four categories: Excellent (≥75% repigmentation), Good (50%–74%), Moderate (25%–49%), Poor (<25%). Patients also completed a 10-point Visual Analogue Scale (VAS) for satisfaction and symptom relief. Adverse events such as erythema, burning, pruritus, blistering, and hyperpigmentation were documented at each visit.

Serum sample collection
For biomarker analysis, fasting peripheral blood (5 mL) was collected from each patient at baseline and at the end of week 12 using serum separation tubes. Samples were allowed to clot for 30 min at room temperature and centrifuged at 800 x g for 10 min at 4 °C. The supernatant serum was aliquoted into 0.5 mL cryovials and stored at −80 °C until analysis. All samples were processed within 2 h of collection to minimize cytokine degradation.

Quantification of serum immunoglobulins
Serum IgG, IgA, and IgM concentrations were determined using automated immunonephelometry following the manufacturer’s instructions. Calibration curves were prepared using serial dilutions of reference standards. Each assay included quality control sera at high and low concentrations. Measurements were expressed in g/L and repeated 2x to ensure intra-assay variation < 5%. The instrument’s precision and calibration were verified daily using traceable control standards. Results were recorded electronically and reviewed by two independent technicians blinded to patient information.

Measurement of inflammatory cytokines
Cytokine profiling included IFN-γ, TNF-α, IL-1β, IL-6, IL-17, and IL-10, quantified using a multiplex enzyme-linked immunosorbent assay (ELISA) platform. Reagent preparation followed the manufacturer’s standard protocol. Briefly, 100 µL of diluted serum was added to each antibody-coated well and incubated for 2 h at 37 °C. After washing with phosphate-buffered saline containing 0.05% Tween-20 (PBST), 100 µL of biotinylated detection antibody was added and incubated for 1 h. Wells were then incubated with streptavidin-horseradish peroxidase for 30 min, followed by color development using tetramethylbenzidine (TMB) substrate for 10 min in the dark. The reaction was stopped with 50 µL of 2 mol/L sulfuric acid, and absorbance was measured at 450 nm using a microplate reader. Standard curves were generated from serial dilutions of recombinant cytokines, and concentrations were expressed as pg/mL. All samples were measured in duplicate. To ensure reproducibility, the inter-assay coefficient of variation (CV) was maintained below 10%. Blank wells contained assay buffer without serum, and negative control wells contained cytokine-free matrix processed identically to the samples and equivalent to the 0 pg/mL standard to confirm assay specificity. Any hemolyzed or lipemic samples were excluded from the final analysis.

Statistical analysis
Data were entered into a dedicated electronic database and cross-checked for accuracy by two independent data managers. Sample size was estimated based on expected effect size (Cohen’s d = 0.5) with α = 0.05 and power (1–β) = 0.8, yielding a minimum of 100 participants per group. To control for multiple comparisons across cytokines, the Bonferroni correction was applied when appropriate. Multivariate linear regression was applied where necessary to adjust for potential confounders, including age, sex, disease duration, and baseline lesion area. Normal distribution of continuous variables was verified using the Shapiro–Wilk test. Descriptive statistics were presented as mean ± standard deviation (SD) for normally distributed data or as median (interquartile range, IQR) for skewed data. Changes before and after treatment were analyzed using paired t-tests, whereas between-group comparisons were analyzed with independent-sample t-tests or Mann–Whitney U tests as appropriate. Categorical data were compared with the chi-square or Fisher’s exact test. Correlations between cytokine levels, immunoglobulins, and pigmentation improvement were assessed using Pearson’s correlation coefficient. All analyses were performed with SPSS v26.0 (RRID: SCR_002865), and a two-sided p < 0.05 was considered statistically significant.

Results

Baseline clinical characteristics demonstrated comparable demographic and disease profiles between groups
A total of 232 patients with non-segmental vitiligo were enrolled and evenly allocated to the excimer group (n = 116) or the combination therapy group receiving laser plus oral matrine (n = 116). Baseline demographic and clinical parameters, including age (35.8 ± 6.0 vs. 35.4 ± 5.6 years), sex distribution (male/female: 59/57 vs. 59/57), disease duration (4.8 ± 1.0 vs. ...

Discussion

This study introduces a combined therapeutic approach integrating a 308-nm excimer laser with oral matrine for the treatment of non-segmental vitiligo. The central proposition is that dual modulation—local photobiological stimulation of melanocytes coupled with systemic immunoregulation—can achieve more robust and sustained repigmentation than the excimer group. The findings support this hypothesis: the combination therapy produced earlier perifollicular pigmentation, greater VASI reduction, and higher patien...

Materials

List of materials used in this article

Name	Company	Catalog Number	Comments
308-nm XeCl Excimer Laser System	STRATA Skin Sciences (XTRAC)	Velocity 400 (Model)	Targeted 308-nm UVB laser for vitiligo lesions; verify model at your site; or equivalent device
–80 °C Ultra-Low Freezer	Thermo Scientific	Forma 900 Series (Model 980)	Long-term serum storage
96-Well ELISA Plates (High-Bind)	Corning Costar	9018	If using in-house coating or single-plex workflows
Adjustable Medical Chair	Midmark	641 Procedure Chair	Patient positioning for consistent irradiation distance
Aloe-based Soothing Gel	3M	9236	Thin post-irradiation layer for erythema relief; or equivalent medical gel
Amber Glass Bottle (500 mL)	Fisherbrand	02-897-2J	Light-protected storage at 4 °C for matrine solution
Analytical Balance (0.1 mg)	METTLER TOLEDO	ME104E	Gravimetric prep and QC
Automated Immunonephelometer	Siemens Healthineers	BN ProSpec System	Quantifies IgG/IgA/IgM per manufacturer’s IFU
Barcode Labels (Cryo-safe)	Diversified Biotech	CRY-1000	Sample tracking and chain-of-custody
Biotinylated Detection Antibody Set	MSD	Included with panel	Matched to capture antibodies
Broad-spectrum Sunscreen SPF ≥30	Neutrogena	070501017052 (Ultra Sheer SPF 50)	Post-session photoprotection; outpatient counseling item
Calibrators for Immunoglobulins	Siemens Healthineers	N Protein Standard SL	Traceable calibration for nephelometry
Control Sera (High/Low) for Ig Assays	Siemens Healthineers	N/T Protein Controls	Daily QC of nephelometric runs
Cryogenic Vials, 0.5 mL	Thermo Scientific Nunc	375418	Serum aliquots; external thread; DNase/RNase-free
Dermatoscope	DermLite	DL4	Polarized handheld dermatoscope for lesion inspection
Dermoscopy/Photography Scale Card	3Gen	Scale/Color Reference Card	Ensures color consistency across timepoints
Digital Camera for Standardized Images	Canon	EOS 80D	Fixed distance 60 cm; exposure 1/60 s; ISO 200; tripod recommended
Fixed-Angle Refrigerated Centrifuge	Eppendorf	5810 R	800 × g, 10 min, 4 °C serum separation
HPLC Column (C18, 4.6×250 mm, 5 µm)	Agilent	ZORBAX Eclipse Plus C18, 959990-902	Routine alkaloid separation; or equivalent
HPLC System	Agilent	1260 Infinity II (G7111B)	Purity verification and batch standardization of matrine
Image Analysis / Measurement	ImageJ (NIH)	1.54 (RRID:SCR_003070)	Optional lesion area quantification from photographs
Lint-free Medical Gauze (Sterile)	Johnson & Johnson	546112	Drying treatment area post-cleansing
Matrine (≥98%, HPLC)	MedChemExpress	HY-N0156	Oral solution preparation; verify local supplier and pharmacopeia compliance
Microplate Reader (450 nm)	BioTek (Agilent)	Synergy H1	Absorbance at 450 nm; pathlength correction
Microplate Washer	BioTek (Agilent)	ELx405	Automated wash cycles; reduces variability
Multiplex Human Cytokine Panel (Custom 6-plex)	Meso Scale Discovery (MSD)	U-PLEX Platform (K15067L)	Includes IFN-γ, TNF-α, IL-1β, IL-6, IL-17A, IL-10; or equivalent
PBS Tablets	Gibco	18912-014	PBS preparation for washes/buffers
Plate Sealer Films	Bio-Rad	MSB1001	Prevents evaporation during incubations
Protective UV Goggles (operator)	Uvex (Honeywell)	S0360X Ultra-Spec 2000	Operator eye protection; use dedicated pair
Protective UV Goggles (patient)	Uvex (Honeywell)	S0360X Ultra-Spec 2000	UV-blocking eyewear for patient safety during irradiation
Serum Separation Tubes (SST II Advance)	BD Vacutainer	367955	Fasting blood collection at baseline and week 12
Statistical Software	IBM	SPSS Statistics v26.0 (RRID:SCR_002865)	Primary data analysis per protocol
Sterile Physiological Saline (0.9%)	Baxter	2B1324 (500 mL)	Lesion cleansing prior to each laser session
Stop Solution (2 M H2SO4)	Sigma-Aldrich	258105	Stops TMB reaction
Streptavidin-HRP	Thermo Scientific	N100	Detection reagent; kit-compatible
TMB Substrate (ELISA)	Thermo Scientific	34028	Chromogenic development; 10 min in dark
Tripod with Distance Marker	Manfrotto	MKCOMPACTLT-BK	Maintains constant camera-to-subject distance
Tween-20 (for PBST 0.05%)	Sigma-Aldrich	P1379	Wash buffer surfactant
UV Radiometer / Power Meter	International Light Technologies	ILT2400	For daily output verification and MED testing; with SED240/NS254 detector or equivalent
UV-Blocking Opaque Drape/Sheet	Thorlabs	BK5 Blackout Fabric	Covers surrounding normal skin to avoid unintended exposure; or equivalent
VASI Scoring Sheets (Printed)	In-house	NA-VASI-2025	Standardized clinical scoring forms; archive with subject ID
Wood’s Lamp (UV-A, 365 nm)	Spectroline	ENF-260C	Clinical diagnosis and lesion edge assessment
Wood’s Lamp Shield Hood	DermLite	DL Hood	Improves contrast under UV-A exam