1 Dnyansadhana College of Pharmacy, Parbhani
2,3,4,5 Rupesh Badhan Institute of Pharmacy, Pimpalner, Dhule
Vitiligo is an acquired pigmentary disorder marked by the progressive loss of melanocytes, resulting in well-defined depigmented macules and patches on the skin and mucous membranes. The condition affects about 0.5–2% of the world’s population and can occur at any age or in either sex. Although the exact cause remains uncertain, current evidence supports a multifactorial origin involving genetic predisposition, autoimmune responses, oxidative stress, and environmental triggers. The disease is broadly categorized into segmental and non-segmental types, each exhibiting distinct patterns of distribution and progression. Diagnosis is mainly clinical, aided by tools such as Wood’s lamp examination and dermoscopy to assess disease activity and stability. Management of vitiligo requires an individualized, multimodal approach. Topical corticosteroids, calcineurin inhibitors, and phototherapy remain standard first-line therapies, while surgical procedures are reserved for stable and localized lesions. In recent years, targeted therapies such as Janus kinase (JAK) inhibitors and antioxidant-based regimens have demonstrated promising efficacy, expanding the therapeutic landscape. Despite these advances, complete and sustained repigmentation remains a major challenge, and relapse is common. The psychosocial impact of vitiligo is considerable, underscoring the need for holistic management strategies that address both physical and emotional well-being. This review provides a comprehensive overview of the epidemiology, pathogenesis, clinical features, diagnostic techniques, and current as well as emerging treatments for vitiligo, highlighting recent scientific progress and future research directions.
Vitiligo is a chronic, acquired depigmenting disorder of the skin and mucous membranes characterized by the selective destruction or functional loss of melanocytes, the pigment-producing cells of the epidermis. The disease manifests as well-defined, milky-white macules and patches that can appear on any part of the body, including the scalp, mucosa, and hair. Although vitiligo is medically benign, its visible disfigurement leads to significant psychosocial distress, making it a condition of high cosmetic and emotional significance rather than a purely dermatologic issue (Ezzedine et al., 2021).
Globally, vitiligo affects an estimated 0.5–2% of the population, without preference for sex, race, or geographic location. However, the disease is often more visible and stigmatizing in individuals with darker skin tones, where the contrast between depigmented and normal skin is more pronounced. The prevalence tends to be slightly higher in regions such as India (up to 8.8%) and parts of Africa, where genetic and environmental factors may interact to increase susceptibility (Krüger & Schallreuter, 2012; AL-Smadi et al., 2023).
Historical Background
The term vitiligo is derived from the Latin vitium, meaning defect or blemish. The earliest descriptions date back to ancient Egyptian and Ayurvedic texts, where depigmenting diseases were often misunderstood as contagious or divine punishment. In modern times, scientific research has reframed vitiligo as a complex autoimmune condition with well-defined genetic, biochemical, and immunological underpinnings (Taïeb & Picardo, 2020).
Pathophysiological Insights
The pathogenesis of vitiligo is multifactorial and remains an active area of investigation. Several hypotheses have been proposed to explain melanocyte destruction:
Collectively, these mechanisms indicate that vitiligo is a disorder of immune dysregulation precipitated by environmental and oxidative stress in genetically predisposed individuals.
Classification and Clinical Presentation
Clinically, vitiligo is categorized into non-segmental vitiligo (NSV) — the most common form, characterized by bilateral and often symmetrical lesions — and segmental vitiligo (SV), which is unilateral and typically stabilizes within one to two years. Other forms include focal, mucosal, and universal vitiligo. Lesions often appear on sun-exposed areas, body folds, and regions prone to trauma (Koebner phenomenon), such as elbows and knees. The disease course is unpredictable: some patients experience rapid progression, while others remain stable for years or show spontaneous repigmentation (Taïeb & Picardo, 2020).
Psychosocial and Quality-of-Life Impact
Beyond its cutaneous manifestations, vitiligo carries a heavy psychological burden. Individuals often experience anxiety, depression, low self-esteem, and social withdrawal due to cultural misconceptions and stigma. Studies have shown that up to 75% of patients report a moderate to severe reduction in quality of life, comparable to that seen in chronic diseases such as psoriasis or eczema (AL-Smadi et al., 2023; Krüger & Schallreuter, 2012).
Advances in Diagnosis and Management
Diagnosis is primarily clinical, aided by Wood’s lamp examination, dermoscopy, and histopathological confirmation in atypical cases. Disease activity can be monitored using scores such as the Vitiligo Disease Activity (VIDA) scale or the Vitiligo Area Scoring Index (VASI).
Therapeutic strategies aim to halt disease progression and induce repigmentation. Traditional treatments include topical corticosteroids, calcineurin inhibitors, and narrow-band UVB (NB-UVB) phototherapy, which remain the gold standard for widespread disease. Surgical methods such as melanocyte transplantation or split-thickness grafting are reserved for stable vitiligo. Recent years have witnessed remarkable advances in targeted therapies, particularly Janus kinase (JAK) inhibitors and antioxidant-based regimens, which show significant efficacy in reversing depigmentation and sustaining repigmentation (Rosmarin et al., 2022).
Rationale for the Review
Despite growing insight into vitiligo pathophysiology and new treatment modalities, many aspects of the disease remain poorly understood, including triggers of onset, mechanisms of relapse, and predictors of therapeutic response. There is also a need for standardized outcome measures and long-term follow-up data on novel therapies. This review aims to synthesize the current understanding of vitiligo’s epidemiology, etiology, clinical features, diagnostic tools, and management options, with a focus on emerging molecular targets and future therapeutic directions.
Psychological Aspects and Associated Disorders of Vitiligo
Psychological and Emotional Impact
Although vitiligo is not life-threatening, it exerts a profound psychosocial and emotional impact on affected individuals. The visible nature of the disease—particularly on exposed areas such as the face, hands, or genital regions—often leads to social stigma, embarrassment, and self-consciousness, resulting in significant psychological distress (Krüger & Schallreuter, 2012).
Several studies demonstrate that vitiligo patients experience higher rates of anxiety, depression, and reduced self-esteem compared to healthy controls. A systematic review and meta-analysis by Lilley et al. (2022) found that the prevalence of depressive symptoms among vitiligo patients ranged between 16% and 35%, while anxiety symptoms were reported in 20%–40% of cases (Lilley et al., 2022). Women and individuals with lesions on visible areas are particularly vulnerable.
Psychological distress often stems from misconceptions and social rejection, especially in cultures where physical appearance holds social, marital, or religious significance. In certain communities, vitiligo is erroneously associated with leprosy or contagious diseases, leading to discrimination and social isolation (AL-Smadi et al., 2023). In India, studies report that up to 70% of patients experience emotional distress and social stigma due to misunderstanding and cultural prejudice (Krüger & Schallreuter, 2012).
The age of onset is another determinant of psychological burden. Early-onset vitiligo during adolescence can interfere with body image development and peer relationships, resulting in social withdrawal or academic underperformance. A cross-sectional study in pediatric patients showed that over 50% reported bullying or teasing due to visible depigmented lesions (Bilgiç et al., 2021).
Quality of Life Impairment
Quality of life in vitiligo is significantly reduced across multiple domains, including emotional well-being, social functioning, and personal relationships. Instruments such as the Dermatology Life Quality Index (DLQI), Vitiligo Impact Scale (VIS), and Vitiligo-specific Quality of Life (VitiQoL) have been validated to assess disease burden.
A multicenter study by Ezzedine et al. (2021) reported that vitiligo’s psychosocial impairment is comparable to chronic dermatoses such as psoriasis or atopic dermatitis, despite the absence of physical symptoms like itching or pain. The VitiQoL scores were significantly worse in patients with facial lesions, generalized disease, or longer disease duration. Patients with darker skin phototypes reported greater emotional distress due to the high contrast between affected and normal skin (Ezzedine et al., 2021).
Interestingly, the extent of depigmentation does not always correlate with psychological severity; rather, location and visibility of lesions have a greater influence on emotional well-being (Radtke et al., 2020). This highlights the subjective nature of cosmetic disfigurement and the importance of individualized psychosocial care.
Psychiatric Comorbidities
Vitiligo is frequently accompanied by psychiatric disorders, particularly depression, anxiety, and social phobia. A population-based cohort study from South Korea found that vitiligo patients had a 1.5-fold increased risk of depressive disorders and a 1.4-fold increased risk of anxiety disorders compared to controls (Lee et al., 2020).
Additionally, body dysmorphic disorder (BDD) is increasingly recognized among vitiligo patients, where individuals develop excessive preoccupation with minor or perceived flaws in appearance. In severe cases, this may progress to suicidal ideation or self-harm, emphasizing the importance of early psychiatric screening and intervention (Papadopoulos et al., 2015).
Psychosocial Coping and Support
Coping mechanisms among vitiligo patients vary widely. Studies indicate that social support, self-acceptance, and access to counseling are key protective factors that mitigate emotional distress. Psychological therapies such as cognitive behavioral therapy (CBT) and support groups have demonstrated significant improvement in QoL and treatment adherence (Amer et al., 2019).
The integration of psychosocial care into dermatologic management—including patient education, camouflage therapy, and counseling—has shown to enhance treatment outcomes. A holistic approach that addresses both medical and emotional aspects is now recommended by dermatological societies worldwide (Taïeb & Picardo, 2020).
Autoimmune and Medical Comorbidities
Vitiligo is also associated with a spectrum of autoimmune and endocrine disorders, supporting its autoimmune etiology. The most frequently reported comorbid conditions include:
Autoimmune thyroid disease (AITD): The most common association; up to 20–30% of vitiligo patients show thyroid antibodies or subclinical hypothyroidism (Rashighi & Harris, 2017).
Alopecia areata: Another autoimmune condition sharing similar pathogenic pathways involving T-cell–mediated destruction of target cells.
Type 1 diabetes mellitus, Addison’s disease, pernicious anemia, and systemic lupus erythematosus (SLE) have also been reported with increased prevalence in vitiligo cohorts (Spritz, 2020).
Atopic dermatitis and psoriasis: Coexistence is observed in 5–10% of cases, possibly due to shared immune dysregulation and cytokine profiles (Alikhan et al., 2011).
These associations underscore the importance of routine screening for thyroid dysfunction, autoimmune markers, and mental health conditions in patients with vitiligo.
Systemic Disorders Associated with Vitiligo
Vitiligo is increasingly recognized not just as a localized skin disorder, but as a systemic autoimmune condition that can coexist with a variety of endocrine, autoimmune, and metabolic disorders. The prevalence of systemic comorbidities is higher in patients with vitiligo than in the general population, particularly among those with early-onset or extensive disease (Spritz, 2020).
1. Autoimmune Thyroid Disorders
The most frequent systemic association in vitiligo patients is autoimmune thyroid disease (AITD), including Hashimoto’s thyroiditis and Graves’ disease. Thyroid autoantibodies—such as anti-thyroid peroxidase (TPO) and anti-thyroglobulin (TG) antibodies—are present in 20–30% of vitiligo patients, particularly in women and those with early-onset or generalized disease (Rashighi & Harris, 2017).
Clinical manifestations may include hypothyroidism or hyperthyroidism, with subtle features such as fatigue, weight changes, or palpitations. Screening for thyroid function and autoantibodies is recommended at diagnosis and periodically during follow-up, especially in patients with progressive or extensive vitiligo (Alikhan et al., 2011).
2. Type 1 Diabetes Mellitus
Vitiligo shares genetic susceptibility and autoimmune mechanisms with type 1 diabetes mellitus (T1DM). Both conditions involve T-cell mediated autoimmunity, particularly cytotoxic CD8+ lymphocyte targeting of specific cell populations (melanocytes and pancreatic beta cells). Epidemiologic studies report that 2–5% of vitiligo patients also have T1DM, and the risk is higher in individuals with family history of autoimmune disorders (Spritz, 2020).
3. Addison’s Disease
Primary adrenal insufficiency, or Addison’s disease, has been documented in patients with vitiligo as part of autoimmune polyglandular syndromes (APS). In APS type 2, vitiligo coexists with Addison’s disease and autoimmune thyroiditis, and occasionally with T1DM. Symptoms such as fatigue, hypotension, hyperpigmentation of unaffected skin, and electrolyte disturbances may precede adrenal crisis; hence, early recognition is critical (Rashighi & Harris, 2017).
4. Pernicious Anemia
Vitiligo can coexist with pernicious anemia, an autoimmune disorder resulting in vitamin B12 deficiency due to autoantibodies against intrinsic factor or gastric parietal cells. Patients may present with fatigue, pallor, glossitis, neurological symptoms, and laboratory evidence of megaloblastic anemia. B12 deficiency is more prevalent in vitiligo patients than in the general population, reinforcing the need for hematologic and serologic screening (Spritz, 2020).
5. Alopecia Areata and Other Dermatologic Autoimmune Disorders
Alopecia areata (AA) is another autoimmune disorder frequently associated with vitiligo. Both conditions share common T-cell-mediated cytotoxic mechanisms, genetic susceptibility loci (HLA-DR4, HLA-A2), and cytokine profiles, particularly elevated IFN-γ and TNF-α. Co-occurrence rates range from 4–15%, and patients with both conditions often experience more extensive or treatment-resistant disease (Alikhan et al., 2011).
Other dermatologic autoimmune associations include lichen planus, psoriasis, and atopic dermatitis, which are linked by shared immunologic pathways, including Th1/Th17 dysregulation.
6. Systemic Lupus Erythematosus and Rheumatologic Disorders
Although less frequent, vitiligo has been associated with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and Sjögren’s syndrome, reflecting its broader autoimmune diathesis. In such patients, vitiligo may precede or coexist with systemic symptoms such as arthralgia, photosensitivity, fatigue, or organ-specific manifestations (Spritz, 2020).
7. Metabolic Syndrome and Cardiovascular Risk
Emerging evidence suggests a potential association between vitiligo and metabolic syndrome (MetS) components, including insulin resistance, dyslipidemia, and hypertension. Oxidative stress and chronic low-grade inflammation, central in vitiligo pathogenesis, may contribute to endothelial dysfunction and cardiovascular risk, although more large-scale longitudinal studies are needed to establish causality (Alkhalifah et al., 2021).
8. Gastrointestinal and Other Organ-specific Autoimmune Disorders
Autoimmune gastritis, celiac disease, and inflammatory bowel disease (IBD) have been reported in a minority of vitiligo patients, suggesting multisystem immune dysregulation. Screening is particularly indicated in patients with family history of autoimmune disease or clinical symptoms of malabsorption or gastrointestinal distress (Spritz, )
Screening Recommendations for Systemic Disorders
Given the high prevalence of systemic and autoimmune comorbidities in vitiligo, several expert guidelines recommend:
Early recognition and management of systemic comorbidities can improve quality of life, reduce complications, Vitiligo is a complex, multifactorial skin disorder characterized by the progressive loss of melanocytes, leading to depigmented patches on the skin. Understanding its aetiology and pathogenesis is crucial for developing effective treatments.
Aetiology of Vitiligo
The exact cause of vitiligo remains unclear, but several factors are believed to contribute:
1. Autoimmune Mechanism
Vitiligo is often considered an autoimmune disorder where the body's immune system mistakenly targets and destroys melanocytes. This is supported by the presence of autoantibodies against melanocyte-specific antigens and the association with other autoimmune diseases such as thyroid disorders, diabetes, and alopecia areata
2. Genetic Factors
Familial clustering of vitiligo suggests a genetic predisposition. Specific genes, including those involved in immune regulation and melanocyte function, have been implicated. For instance, polymorphisms in the catalase gene, which is involved in oxidative stress response, have been associated with vitiligo .
3. Oxidative Stress
Accumulation of reactive oxygen species (ROS), such as hydrogen peroxide, can damage melanocytes. Inadequate antioxidant defenses, possibly due to genetic factors, may exacerbate this damage, leading to melanocyte apoptosis.
4. Neurogenic Factors
Neurochemical mediators released from nerve endings in the skin can influence melanocyte function. Stress-induced neurotransmitters may trigger melanocyte destruction, linking psychological stress to vitiligo onset or progression
5. Environmental Triggers
Factors such as UV radiation, chemical exposure, and skin trauma can act as triggers in genetically predisposed individuals, initiating or exacerbating vitiligo .
Pathogenesis of Vitiligo
The pathogenesis involves a combination of genetic susceptibility, immune system dysfunction, and environmental factors:
Melanocyte Destruction Autoimmune responses lead to the destruction of melanocytes, resulting in depigmented patches. Histopathological examination typically shows a complete absence of melanocytes in affected areas (journaljammr.com)
Inflammatory Mediators Cytokines and chemokines play a role in the recruitment of immune cells to the skin, contributing to inflammation and melanocyte loss
Genetic and Biochemical Factors Genetic mutations affecting melanocyte function and antioxidant defense mechanisms can predispose individuals to vitiligo. For example, defects in the catalase gene may impair the breakdown of hydrogen peroxide, leading to oxidative stress and melanocyte damage
Neuroimmune Interactions Neurotransmitters released during stress can influence immune responses in the skin, potentially triggering or worsening vitiligo in susceptible individuals
Treatment Approaches
Treatment strategies aim to restore pigmentation and manage symptoms:
Classification of Vitiligo
Vitiligo is classified based on the pattern of depigmentation, its distribution, and disease behavior. The most widely accepted classification comes from the Vitiligo Global Issues Consensus Conference (VGICC, 2012). This helps guide prognosis and treatment.
1. Non-Segmental Vitiligo (NSV)
a. Generalized Vitiligo
b. Acrofacial Vitiligo
c. Mucosal Vitiligo
d. Universal Vitiligo
e. Focal Vitiligo
Clinical Implications:
2. Segmental Vitiligo (SV)
a. Unisegmental Vitiligo
b. Bisegmental Vitiligo
c. Plurisegmental Vitiligo
d. Mucosal Segmental Vitiligo
Clinical Implications:
3. Mixed Vitiligo
4. Unclassified Vitiligo
5. Other Classification Criteria
Vitiligo can also be classified based on disease activity and progression:
Clinical and Therapeutic Significance of Classification
|
Type/ Subtype |
Onset |
Progression |
Treatment Response |
|
NSV (Generalized) |
Adult/any age |
Slow, chronic |
Good response to phototherapy, corticosteroids |
|
Acrofacial NSV |
Any age |
Slow, chronic |
Often resistant to topical therapy |
|
SV (Unisegmental) |
Childhood |
Rapid, stabilizes |
Responds better to surgical repigmentation than phototherapy |
|
Mixed |
Any age |
Variable |
Treatment must be individualized |
|
Mucosal |
Any age |
Chronic |
Resistant to therapy; may require combination approach |
Diagnosis of Vitiligo
Vitiligo diagnosis involves a multimodal approach: detailed history, physical examination, adjunctive tools, laboratory evaluation, and sometimes histopathology. Early and precise diagnosis helps in prognosis, monitoring disease activity, and treatment planning.
1. Detailed Clinical Evaluation
a. Patient History
A thorough history provides critical clues:
Onset and progression: Age of onset often 10–30 years; segmental vitiligo typically begins in childhood. Ask about the rate of spread and stability.
Family history: Positive in 20–30% of cases; may suggest a genetic predisposition.
Triggers:
Associated autoimmune disorders: Thyroid disease (most common), diabetes mellitus, pernicious anemia, alopecia areata.
Previous treatments: Topical, phototherapy, surgical interventions, or systemic immunosuppressants.
b. Physical Examination
Examine skin and appendages carefully:
Depigmented macules/patches with well-defined margins, which are asymptomatic.
Common sites:
Hair involvement:
Leukotrichia: white hair within vitiligo patches
Nails: Rarely, nail abnormalities like leukonychia or longitudinal ridging may be present.
c. Types and Patterns
2. Diagnostic Tools
a. Wood’s Lamp Examination
UV light (~365 nm) to detect subtle or early depigmentation.
Findings:
Utility:
b. Dermoscopy
Non-invasive tool for magnified visualization:
Absence of pigment network
Perifollicular pigmentation indicates regenerative melanocyte activity
Leukotrichia or poliosis
Helps differentiate from other hypopigmented conditions like pityriasis alba, nevus depigmentosus.
c. Reflectance Confocal Microscopy (RCM)
d. Histopathology (Rarely Required)
3. Laboratory Investigations
Although vitiligo is primarily clinical, laboratory work-up may assess associated autoimmune disorders:
4. Disease Activity Assessment
a. Vitiligo Disease Activity Score (VIDA)
Measures activity over time (last 6 weeks to 1 year):
Guides treatment decisions and prognosis.
b. Vitiligo Area Scoring Index (VASI)
Quantifies extent and degree of depigmentation
Formula: VASI = Σ (Area% × Depigmentation%)
Useful for monitoring treatment response.
c. Other Scoring Systems
Differential Diagnosis Condition
Post-inflammatory hypopigmentation ,
Tinea versicolor
Idiopathic guttate hypomelanosis
Leprosy (tuberculoid type)
Chemical leukoderma
Assessment of Severity in Vitiligo
Vitiligo severity is evaluated using objective and subjective parameters, including extent of depigmentation, lesion distribution, disease activity, and impact on quality of life. Assessing severity is crucial for treatment planning, monitoring response, and prognosis.
1. Parameters for Assessing Severity
Extent of Depigmentation
Estimation methods:
Lesion Distribution
Mucosal involvement
Rate of Progression
Activity of Disease
Indicators of activity:
Psychological impact can be assessed using:
2. Scoring Systems for Vitiligo Severity
Several validated scoring systems quantify vitiligo severity:
a. Vitiligo Area Scoring Index (VASI)
Calculation:
Body divided into regions (hands, arms, trunk, legs, feet, head/neck)
VASI per region = % BSA × % depigmentation
Total VASI = sum of all regions
Interpretation:
Advantages: Objective, reproducible, sensitive to change over time.
Limitations: Requires training; time-consuming in large studies.
b. Vitiligo Disease Activity Score (VIDA)
Assesses activity rather than extent, but contributes to severity assessment.
Scoring (based on past disease activity):
Clinical relevance: Higher VIDA score indicates aggressive, severe disease.
c. Vitiligo European Task Force (VETF) Scoring
Combines extent, activity, and psychosocial impact.
Three components:
Advantage: Comprehensive, integrates physical and psychological impact.
d. Patient-Reported Outcome Measures
3. Factors Indicating Severe Vitiligo
Feature, Clinical Implication, BSA involvement >20–30%, Extensive disease, often resistant to treatment, Acrofacial or mucosal involvement ,Poorer response to therapy, cosmetic concern
Leukotrichia
4. Emerging Assessment Tools
Digital Image Analysis
High-resolution photography + software to calculate precise lesion area and pigmentation loss
Objective tracking of treatment response.
Reflectance Confocal Microscopy (RCM)
Visualizes melanocyte density
Can quantify early repigmentation or melanocyte activity in “stable” lesions.
Colorimetry / Spectrophotometry
Measures skin pigmentation objectively
Useful in clinical trials to detect subtle changes.
5. Practical Approach to Assessing Severity
History Onset, progression, triggers, family history, psychosocial impact
Clinical Examination
Photography for documentation
Laboratory assessment if autoimmune associations suspected
Classification of Severity
Relationship Between Vitiligo and Skin Cancer
Vitiligo is an acquired depigmentation disorder caused by autoimmune destruction of melanocytes, leading to melanin deficiency in affected skin. Melanin plays a critical photoprotective role by absorbing ultraviolet (UV) radiation and scavenging reactive oxygen species. This has implications for skin cancer risk, but the relationship is complex.
1. Melanin and Skin Cancer Protection
2. Mechanistic Considerations
Immune-Mediated Protection
Oxidative Stress and DNA Damage
Role of Phototherapy
3. Epidemiological Evidence
a. Melanoma Risk
Multiple studies indicate vitiligo patients have equal or reduced risk of melanoma compared to the general population.
Proposed reasons:
b. Non-Melanoma Skin Cancer (NMSC) Risk
Clinical Implications
Phototherapy Monitoring
Skin Surveillance
Look for:
Development of vitiligo during melanoma immunotherapy is often a favorable prognostic marker.
Suggests shared melanocyte antigen targets.
5. Summary of the Relationship Aspect
Evidence / Effect
Generally equal or reduced due to autoimmune surveillance
Slightly increased in depigmented skin, especially with UV exposure or phototherapy
Role of phototherapy
Natural Treatment Approaches for Vitiligo
Vitiligo is a chronic depigmentation disorder caused by autoimmune destruction of melanocytes. While conventional treatments include topical corticosteroids, calcineurin inhibitors, phototherapy, and surgical options, many patients explore natural or complementary therapies to manage or support repigmentation.
Natural treatments aim to stimulate melanogenesis, reduce oxidative stress, or modulate immune responses.
1. Antioxidant Therapy
Rationale:
Oxidative stress is a key factor in melanocyte destruction in vitiligo. Antioxidants may neutralize reactive oxygen species (ROS) and protect melanocytes.
Common Antioxidants
Evidence:
Limitations:
2. Herbal and Plant-Based Remedies
Rationale:
Certain herbs contain melanocyte-stimulating compounds or immunomodulatory agents.
Key Herbal Options
Evidence:
Limitations:
3. Dietary Interventions
Rationale:
Some nutrients are important for melanocyte function and antioxidant defense.
Key Nutrients
Evidence:
Limitations:
Mind-Body and Lifestyle Approaches
Rationale:
Stress can exacerbate autoimmune diseases, including vitiligo.
Approaches
Evidence:
Phototherapy Adjuncts with Natural Products
Limitations of Natural Therapies
|
Limitation |
Details |
|
Evidence quality |
Mostly small studies, case reports, or pilot trials |
|
Standardization |
Herbal extracts vary in concentration and purity |
|
Safety |
Risk of phototoxicity, allergic reactions, or herb-drug interactions |
|
Efficacy |
Often modest; best as adjunct to conventional therapy |
Practical Recommendations
REFERENCE
Shaikh Sohel, Minakshi Khairnar, Ganesh Ahire, Yogeshwari, Kaveri, Vitiligo Management: Current Landscape and Future Directions – A Comprehensive Review, Int. J. of Pharm. Sci., 2025, Vol 3, Issue 11, 4258-4278. https://doi.org/10.5281/zenodo.17725293
10.5281/zenodo.17725293
