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Pigmentary Physician Reviewed

Vitiligo — managed by dermatologists, not stigma

A non-contagious autoimmune condition affecting 1–2% of India's population, treated with evidence-based phototherapy, medical therapy, and surgical techniques at DermaVue's 7 clinics across Kerala & Tamil Nadu.

Leucoderma White Patches Safed Daag Depigmentation Disorder Autoimmune Depigmentation
Affects Any body site; commonly face, hands, feet, genitalia
Age Group 10 – 30 years (onset)
Contagious No
Treatment 24 – 48+ phototherapy sessions
Consultation ₹300
At a Glance
0–2%
of India's population affected — among the highest globally
0%
of vitiligo cases begin before age 30 years
0%+
DermaVue patient satisfaction across 7,400+ reviews
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7 clinics · Kerala & Tamil Nadu · ₹300 consultation

What Is It

Understanding Vitiligo

Reviewed by Dr. Minu Liz Mathew, MBBS MD DVL — February 2026

Vitiligo occurs when the immune system attacks melanocytes — the cells that produce skin pigment — causing well-defined white patches on the skin. In India, where most people have Fitzpatrick IV–VI skin tones, the contrast between affected and unaffected skin is especially visible, often leading to significant social stigma and psychological distress. Vitiligo is not contagious, not caused by diet, and not a sign of any internal disease. DermaVue dermatologists combine targeted phototherapy, immunomodulatory medications, and surgical melanocyte transfer techniques to stabilise the disease and restore pigment — tailored to each patient's disease stage, body site, and skin type.

Vitiligo is an acquired, chronic depigmentation disorder characterised by selective destruction of epidermal melanocytes, resulting in well-circumscribed, chalk-white macules and patches. Pathogenesis involves a convergence of autoimmune (CD8+ T-cell–mediated cytotoxicity), oxidative stress (elevated H2O2 and reduced catalase activity), neural, and genetic mechanisms.[1] The autoimmune model is supported by association with thyroid autoimmunity, type 1 diabetes mellitus, and pernicious anaemia. Clinically subtyped as non-segmental (generalised, acrofacial, universal) and segmental (dermatomal distribution, earlier onset, rapid stabilisation). Indian Fitzpatrick IV–VI skin phenotypes exhibit higher cosmetic impact and psychosocial burden due to stark contrast between depigmented and normally pigmented skin, necessitating aggressive repigmentation strategies including NB-UVB phototherapy, topical calcineurin inhibitors, and surgical non-cultured epidermal cell suspension (NCES) grafting.[2]

M
Dr. Minu Liz Mathew, MBBS MD DVL
Consultant Dermatologist · RealSelf Recognised · DermaVue Kochi
Last reviewed: February 2026
Signs & Symptoms

What does Vitiligo look like?

Symptoms range widely in severity. Identifying which type you have determines the right treatment.

White Patches on Skin
Well-defined, chalk-white macules or patches where melanocytes have been destroyed. May start small and gradually enlarge or coalesce. Markedly visible on Fitzpatrick IV–VI skin.
Moderate
Symmetrical Distribution
Non-segmental vitiligo typically appears symmetrically — if a patch develops on one hand, a corresponding patch often appears on the other. This bilateral pattern is a hallmark feature.
Moderate
Koebner Phenomenon
New depigmented patches appearing at sites of skin trauma — cuts, burns, friction from clothing or jewellery. Common in active/progressive vitiligo.
Moderate
Leukotrichia (White Hair)
Hair within vitiligo patches may turn white (poliosis) — on the scalp, eyebrows, eyelashes, or body hair. Indicates melanocyte loss in the hair follicle reservoir and may predict slower repigmentation.
Mod. Severe
Mucosal Involvement
Depigmentation of the lips, inside the mouth, or genital mucosa. Mucosal vitiligo is more resistant to treatment and requires specialised management.
Mod. Severe
Acrofacial Predilection
Patches commonly appear on the face (around eyes, mouth), hands, and feet — areas of high social visibility, contributing disproportionately to psychosocial burden in Indian patients.
Moderate
Rapid Spread (Progressive Phase)
Active vitiligo may show rapid spread with new patches appearing weekly. Confetti-like depigmentation and trichrome lesions (three-shade gradient at patch border) indicate high disease activity.
Severe
Sunburn Sensitivity
Depigmented skin lacks melanin photoprotection and burns easily in sunlight. Patients in Kerala's tropical climate require consistent broad-spectrum sunscreen on exposed vitiligo patches.
Mild
Root Causes

What actually causes Vitiligo?

Multiple factors act together — understanding them helps prevent recurrence after treatment.

🛡️
Autoimmune Melanocyte Destruction
CD8+ cytotoxic T lymphocytes target and destroy melanocytes. This is the primary mechanism — supported by association with other autoimmune diseases (thyroid disorders, type 1 diabetes, alopecia areata).
🧬
Genetic Susceptibility
Over 50 susceptibility loci identified. First-degree relatives have a 5–8% risk compared to 1–2% in the general population. Concordance in twins is approximately 23%, confirming polygenic inheritance with environmental triggers.
Oxidative Stress
Elevated hydrogen peroxide and reduced catalase activity in the epidermis create a toxic environment for melanocytes. Oxidative damage precedes and accelerates immune-mediated destruction.
Neural Hypothesis (Segmental)
Segmental vitiligo follows a dermatomal distribution, suggesting neuropeptide-mediated melanocyte damage. This subtype stabilises faster and responds well to surgical melanocyte transfer.
☀️
Sunburn & Skin Trauma
Severe sunburn, chemical burns, or repeated friction can trigger vitiligo at injury sites (Koebner phenomenon). In Kerala, occupational sun exposure without protection is a common initiating factor.
😰
Psychological Stress
Major life stressors frequently precede vitiligo onset or exacerbation. Stress elevates cortisol and catecholamines, which increase oxidative damage to melanocytes and modulate immune activation.
🧪
Chemical Exposure
Contact with phenolic and catecholic compounds (rubber, leather, hair dyes containing para-phenylenediamine) can trigger chemical leukoderma mimicking or initiating true vitiligo — relevant to Kerala's rubber industry workers.
Who gets vitiligo in India?
  • 1–2% of the Indian population is affected — India has one of the highest reported prevalence rates globally, with some community studies showing up to 8.8% in parts of Rajasthan and Gujarat
  • 50% of cases begin before age 20, with a second peak in early adulthood — early intervention significantly improves repigmentation outcomes
  • Fitzpatrick IV–VI skin (the majority of South Indian population) shows stark contrast between depigmented and normal skin, amplifying cosmetic and psychosocial impact
  • Kerala-specific: high prevalence of autoimmune thyroid disease in the state compounds vitiligo risk; rubber plantation workers face chemical leukoderma exposure from phenolic compounds in rubber processing
  • Social stigma in India remains a major burden — vitiligo is wrongly conflated with leprosy in some communities, affecting marriage prospects, employment, and mental health despite the condition being entirely non-contagious
Diagnosis Process

What happens at your DermaVue consultation?

A structured clinical assessment — not a quick glance and a prescription pad. Here's exactly what to expect.

01
Clinical Examination & History
Dermatologist documents patch distribution (segmental vs. non-segmental), onset age, progression rate, family history of vitiligo or autoimmune disease, and Koebner phenomenon. Baseline body surface area (BSA) calculated using rule of nines. Clinical photography for objective tracking.
02
Wood's Lamp Examination
Wood's lamp (365 nm UV) enhances contrast of depigmented patches, revealing subclinical lesions invisible to the naked eye — especially important in fair-skinned patients. Fluorescence pattern distinguishes true vitiligo from pityriasis alba, tinea versicolor, and post-inflammatory hypopigmentation.
03
Dermoscopy & Trichoscopy
Dermoscopy shows characteristic features: perifollicular pigment loss, starburst/reverse pigmentation patterns, and micro-Koebner phenomenon. Trichoscopy of hair within patches assesses follicular melanocyte reservoir — presence of pigmented hair is a positive prognostic indicator for repigmentation.
04
Autoimmune & Thyroid Screening
Baseline labs: thyroid function (TSH, T3, T4), anti-thyroid antibodies (anti-TPO, anti-thyroglobulin), fasting blood glucose, CBC, and vitamin B12/D3 levels. In India, thyroid autoimmunity co-exists in 15–20% of vitiligo patients — higher in Kerala where thyroid disease prevalence is already elevated.
05
Disease Activity Assessment & Plan
VIDA (Vitiligo Disease Activity) score assigned to guide therapy intensity. Active/spreading disease requires immunomodulation first (systemic mini-pulse steroids or phototherapy). Stable disease (>12 months without new patches) may be eligible for surgical melanocyte transfer. Personalised protocol documented with treatment milestones.
Available at DermaVue

Vitiligo treatments we offer

All procedures by board-certified MD DVL dermatologists. US-FDA approved equipment. No technician-only protocols — ever.

NB-UVB Phototherapy
Narrowband UVB (311 nm) is the gold-standard first-line treatment for generalised vitiligo. Twice-weekly sessions stimulate melanocyte stem cells in hair follicles to migrate and repigment affected skin. Typically requires 24–48 sessions for visible results.
Non-segmental vitiligo (generalised, acrofacial)
Targeted Excimer Laser (308 nm)
Focused 308 nm excimer laser delivers high-dose UVB precisely to vitiligo patches without affecting surrounding normal skin. Faster repigmentation than conventional phototherapy for localised lesions. Ideal for facial and limited-area vitiligo.
Localised patches, facial vitiligo, segmental vitiligo
Topical Immunomodulators
Tacrolimus ointment and pimecrolimus cream suppress local T-cell activity without steroid side effects. First-line for facial and periorbital vitiligo where topical corticosteroids carry atrophy risk. Combined with phototherapy for enhanced repigmentation.
Facial vitiligo, children, steroid-sensitive areas
Oral Mini-Pulse Therapy
Low-dose oral corticosteroid (dexamethasone) given on two consecutive days per week to arrest disease progression in active vitiligo. Arrests spread in 80–90% of patients within 3 months with minimal systemic side effects compared to daily steroids.
Actively spreading (progressive) vitiligo
Melanocyte Transfer Surgery
Non-cultured epidermal cell suspension (NCES) or suction blister grafting transplants the patient's own melanocytes from pigmented donor skin to stable vitiligo patches. Achieves 60–80% repigmentation in selected stable cases. Performed as a day procedure.
Stable segmental or focal vitiligo (>12 months stable)
Combination Phototherapy + Topicals
NB-UVB phototherapy combined with topical tacrolimus and/or low-potency topical steroids achieves repigmentation rates superior to monotherapy. DermaVue protocols follow IADVL combination guidelines for optimised outcomes.
Moderate–extensive vitiligo requiring multi-modal approach
Camouflage & Supportive Care
Medical-grade camouflage products matched to patient skin tone for immediate cosmetic improvement. Psychological counselling referral for patients experiencing social distress. Sunscreen prescription to protect depigmented skin and prevent contrast worsening.
Immediate cosmetic cover while repigmentation therapy is ongoing
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Treatment Journey

Your Vitiligo treatment timeline

Results are gradual, progressive, and lasting with the right protocol.

Week 1
Consultation, full-body examination, Wood's lamp, dermoscopy. Disease activity scored. Baseline photography and BSA documented. Labs ordered.
Topical immunomodulator or steroid prescribed. Phototherapy schedule planned. If active spread: oral mini-pulse therapy initiated.
Month 1–3
Phototherapy sessions underway (2× per week). Disease stabilisation expected — no new patches. Earliest perifollicular repigmentation may appear on face and trunk.
Lab results reviewed. Thyroid or vitamin deficiencies addressed. Progress photography at 3-month mark.
Month 3–6
Visible perifollicular repigmentation in 40–60% of responsive areas. Face and trunk respond first; extremities and bony prominences respond slower.
Treatment intensified if response suboptimal. Excimer laser added for resistant patches. Surgical options discussed if disease is stable.
Month 6–12
Continued repigmentation. Surgical melanocyte transfer performed for stable patches that have not responded to phototherapy alone. 60–80% colour match expected in grafted areas.
Phototherapy frequency may be tapered for responsive areas. Maintenance protocol established.
Month 12+
Long-term maintenance phase. Monthly to quarterly dermatologist follow-up. Repigmented areas monitored for colour stability. Relapse prevention with low-dose topical maintenance.
Annual thyroid and autoimmune screening continued. Sun protection protocol reinforced. Psychological well-being assessed.
FAQ

Frequently asked questions about Vitiligo

No, vitiligo is absolutely not contagious. It cannot spread through touch, sharing food, swimming together, or any form of physical contact. Vitiligo is an autoimmune condition where the body's own immune system attacks pigment-producing cells. The widespread misconception that vitiligo is contagious — sometimes wrongly linked to leprosy in Indian communities — has no medical basis whatsoever.

Vitiligo spreads when the autoimmune attack on melanocytes is active. Triggers for spreading include psychological stress, skin injuries (Koebner phenomenon), severe sunburn, and exposure to phenolic chemicals. Thyroid dysfunction, if untreated, can also drive disease activity. Oral mini-pulse corticosteroid therapy can arrest spread in 80–90% of cases within 3 months. Early dermatologist intervention during active spread is critical to limiting extent.

There is currently no permanent cure that eliminates the underlying autoimmune predisposition. However, significant repigmentation — often 70–90% colour restoration — is achievable with NB-UVB phototherapy, topical immunomodulators, and surgical melanocyte transfer in stable cases. Facial vitiligo responds best; acral areas (fingertips, toes) are most resistant. Maintenance therapy reduces relapse risk. Research into JAK inhibitors and targeted biologics is advancing rapidly.

DermaVue consultation fee is ₹300 at most branches. NB-UVB phototherapy session costs range from ₹500–1,500 per session depending on body area, with a typical course of 24–48 sessions. Excimer laser sessions range from ₹1,500–3,500 per session. Surgical melanocyte transfer costs depend on the area being treated and are discussed after stability assessment. All costs are explained transparently at your first consultation — no hidden charges.

Vitiligo itself does not affect physical health or life expectancy. However, it is associated with a higher incidence of other autoimmune conditions — particularly thyroid disorders (15–20% of patients), type 1 diabetes, and pernicious anaemia. DermaVue protocols include baseline and annual autoimmune screening to detect and manage any associated conditions early. The most significant health impact of vitiligo is psychological — depression, anxiety, and social withdrawal are common and addressed as part of comprehensive care.

Kerala's environment presents specific considerations: rubber plantation workers are exposed to phenolic compounds (para-tertiary-butylphenol) used in rubber processing, which can trigger chemical leukoderma. Intense tropical sun exposure without protection can cause sunburn that triggers Koebner phenomenon in predisposed individuals. Kerala also has a higher background prevalence of autoimmune thyroid disease, which is a known vitiligo co-morbidity. DermaVue dermatologists assess occupation, sun exposure patterns, and thyroid status as standard practice.

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