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Summary Table

Category	Details
Risk Factors	Family history of vitiligo or autoimmune disease; personal history of autoimmune thyroiditis (Hashimoto), type 1 diabetes mellitus, pernicious anemia, Addison disease, alopecia areata. Peak onset in the 10 to 30 age range. No sex predilection.
Etiology	Autoimmune destruction of melanocytes. Genetic susceptibility combined with environmental triggers (sunburn, chemical exposure, emotional stress).
Patient Presentation	Painless, progressive, well-demarcated depigmented (chalk-white) macules and patches. Often symmetric. Common sites: face (perioral, periocular), dorsal hands, wrists, axillae, groin, and genitalia. Koebner phenomenon may be reported.
Classic Physical Exam	Sharply demarcated, milk-white or chalk-white macules/patches with no scale and no epidermal change. Wood lamp examination shows bright blue-white fluorescence of affected areas. Hair within lesions may turn white (leukotrichia/poliosis).
Key Diagnostic Results	Clinical diagnosis confirmed by Wood lamp. TSH and free T4 to screen for thyroid disease. CBC, fasting glucose, anti-TPO antibodies, ANA, and vitamin B12 to screen for associated autoimmune conditions. Biopsy (rarely needed) shows absence of melanocytes.
Management	Localized disease: topical corticosteroids (first-line) or topical calcineurin inhibitors (face/intertriginous areas). Widespread disease: narrowband UVB phototherapy. Surgical melanocyte transplantation for stable, refractory cases. Sun protection is essential.
Keywords	"Chalk-white patches," "well-demarcated depigmentation," "perioral/periocular," "Koebner phenomenon," "autoimmune associations," "Wood lamp bright blue-white," "symmetric depigmentation."

1. Pathophysiology

Vitiligo is an acquired, chronic autoimmune disorder characterized by the progressive destruction of melanocytes in the epidermis, resulting in well-circumscribed areas of complete depigmentation. The fundamental defect is not a failure of melanin production but rather the loss of the melanocyte itself.

The prevailing theory is the autoimmune hypothesis, supported by the strong association of vitiligo with other autoimmune diseases and the presence of circulating anti-melanocyte antibodies and autoreactive CD8+ T cells in affected individuals. These cytotoxic T lymphocytes target melanocyte antigens (such as tyrosinase, MART-1, and gp100), leading to apoptosis and elimination of melanocytes from the basal layer of the epidermis.

Several contributing mechanisms work together. The oxidative stress theory proposes that melanocytes in vitiligo patients have an inherent defect in handling reactive oxygen species (ROS), particularly hydrogen peroxide ($H_2O_2$). Elevated $H_2O_2$ levels damage melanocytes directly and also generate neoantigens that trigger immune recognition. The neural hypothesis explains the dermatomal pattern seen in segmental vitiligo, where local neuropeptide release (such as norepinephrine) causes melanocyte toxicity in a localized distribution.

The Koebner phenomenon (isomorphic response) is a hallmark feature: new depigmented lesions arise at sites of trauma, friction, or sunburn because mechanical or inflammatory injury exposes melanocyte antigens to the immune system, triggering a localized autoimmune attack on melanocytes. This explains why lesions favor areas of repetitive friction such as the hands, elbows, and waistline.

Because melanocytes share embryologic origin (neural crest) with other cell types and because the autoimmune diathesis is systemic, patients with vitiligo carry a significantly increased risk of developing thyroid autoimmunity (most commonly Hashimoto thyroiditis), type 1 diabetes, pernicious anemia, and Addison disease. This clustering is the reason screening labs for associated conditions are part of the standard workup.

2. Classification and Clinical Manifestation

Type	Distribution Pattern	Key Features
Non-segmental (Generalized)	Bilateral, symmetric	Most common form (~85%). Progressive course. Strong autoimmune association. Koebner phenomenon present.
Acrofacial	Distal extremities + face	Subset of non-segmental. Affects fingers, toes, perioral, periocular regions. Often resistant to treatment.
Mucosal	Mucous membranes	Lips, oral mucosa, genital mucosa. Can occur alone or with other subtypes.
Universal	>80% body surface area	Most extensive form. Near-total depigmentation. Remaining pigmented islands may be present.
Segmental	Unilateral, dermatomal	Rapid onset then stabilizes. Poliosis common. Less associated with autoimmune disease. Responds well to surgical grafting. Thought to involve neural mechanisms.
Mixed	Segmental + non-segmental overlap	Uncommon. Segmental lesion appears first, then generalized disease follows.

Clinical Manifestation by Site

Site	Presentation Details
Face	Perioral and periocular depigmentation. Often the first site noticed by patients. High cosmetic concern.
Hands/Feet	Dorsal surfaces affected. Acral involvement is common and often treatment-resistant.
Trunk	Symmetric patches along the axillae, umbilicus, and trunk creases.
Genitalia/Groin	Frequently involved. Patients may be reluctant to mention this.
Scalp/Hair	Poliosis (white hair tuft) or leukotrichia within lesions. Indicates melanocyte reservoir in hair follicles is also destroyed, which is a poor prognostic sign for repigmentation.
Sites of Trauma	Koebner phenomenon: new lesions at scars, friction points, or burn sites.

3. Diagnostic Workup

Test	Purpose	Expected Finding
Clinical examination	First-line, often sufficient	Well-demarcated, chalk-white, non-scaly macules/patches
Wood lamp (365 nm UV)	Best initial test to confirm and delineate extent	Affected areas fluoresce bright blue-white (enhanced contrast). Subclinical lesions become visible.
Dermoscopy	Adjunct for subtle or early lesions	Loss of normal pigment network; residual perifollicular pigmentation (suggests repigmentation potential)
Skin biopsy	Rarely needed; reserved for diagnostic uncertainty	Complete absence of melanocytes on immunohistochemistry (Melan-A, HMB-45 negative). No inflammatory infiltrate in established lesions.
TSH, free T4, anti-TPO	Screen for thyroid autoimmunity	Elevated TSH or positive anti-TPO antibodies in concurrent Hashimoto thyroiditis
Fasting glucose / HbA1c	Screen for type 1 diabetes	Elevated in concurrent autoimmune diabetes
CBC, Vitamin B12	Screen for pernicious anemia	Macrocytic anemia, low B12
Morning cortisol, ACTH	If Addison disease suspected	Low cortisol, elevated ACTH
ANA	General autoimmune screening	May be positive; guides further workup

Vitiligo is fundamentally a clinical diagnosis. The hallmark finding on examination is a well-demarcated, completely depigmented (not hypopigmented) macule or patch with no overlying scale, induration, or textural change. The surrounding skin is entirely normal.

The best initial test to confirm and delineate extent is the Wood lamp examination. Under 365 nm ultraviolet light, vitiligo lesions fluoresce a characteristic bright blue-white color due to the total absence of melanin. This is particularly useful in fair-skinned patients where depigmentation may be subtle under ambient lighting, and it reveals subclinical lesions not yet visible to the naked eye. Wood lamp also helps distinguish vitiligo from hypopigmented conditions (such as pityriasis alba or tinea versicolor), which do not enhance as brightly because they retain some melanin.

Dermoscopy can serve as an adjunct. In vitiligo, it shows a diffuse white glow with loss of the normal pigment network. The presence of perifollicular pigmentation (pigment dots around hair follicles) is a favorable prognostic sign indicating that melanocyte stem cells in the hair bulge are preserved and repigmentation is possible with treatment.

Skin biopsy is rarely required but becomes necessary when the clinical picture is ambiguous or when ruling out conditions like hypopigmented mycosis fungoides or chemical leukoderma. Histopathology of established vitiligo shows a complete absence of melanocytes in the basal layer. Fontana-Masson stain shows absent melanin, and immunohistochemical stains (Melan-A, HMB-45, S-100) confirm melanocyte loss. Early or active lesions may show a sparse lymphocytic infiltrate at the dermoepidermal junction, representing ongoing immune-mediated melanocyte destruction.

Because vitiligo is a marker of autoimmune diathesis, screening for associated conditions is standard practice. At minimum, order TSH and anti-TPO antibodies (thyroid autoimmunity is the most common association, present in 15 to 25% of vitiligo patients). Additional screening with fasting glucose, CBC, and vitamin B12 is appropriate based on clinical suspicion.

4. Management and Treatment

Clinical Scenario	First-Line Treatment	Alternatives / Second-Line
Localized, limited disease (<10% BSA), body	Potent topical corticosteroids (e.g., clobetasol propionate 0.05%)	Topical calcineurin inhibitors (tacrolimus 0.1% or pimecrolimus)
Face and intertriginous areas	Topical calcineurin inhibitors (tacrolimus 0.1%)	Low-potency topical steroids for short courses
Widespread disease (>10% BSA)	Narrowband UVB phototherapy (311 nm)	Excimer laser (308 nm) for targeted areas
Rapidly progressive disease	Oral mini-pulse corticosteroids (dexamethasone 2.5 mg on two consecutive days per week)	Systemic immunosuppression (rarely, e.g., methotrexate)
Stable, refractory, segmental	Surgical: autologous melanocyte transplant, suction blister grafting, or punch grafting	Split-thickness skin grafting
Universal vitiligo (>80% BSA)	Depigmentation of remaining pigmented skin with monobenzone 20% cream	Cosmetic camouflage
Adjunctive (all patients)	Broad-spectrum sunscreen (SPF 30+), cosmetic camouflage	Psychological support and counseling
Newer targeted therapy	Ruxolitinib 1.5% cream (topical JAK inhibitor, FDA-approved for non-segmental vitiligo)	Oral JAK inhibitors under investigation

Topical Corticosteroids remain the cornerstone of initial treatment for localized vitiligo involving the trunk and extremities. Clobetasol propionate 0.05% cream is applied once daily for a maximum of 2 to 3 months, followed by a taper or pulsed schedule (e.g., application on weekends only) to minimize steroid atrophy. Response is expected within 2 to 4 months. If no repigmentation is observed after 3 months of consistent use, the treatment should be reconsidered. Monitor for local side effects including skin atrophy, telangiectasia, and striae, which limit prolonged use.

For facial and intertriginous lesions, topical calcineurin inhibitors are preferred over potent steroids due to the thinner skin in these areas. Tacrolimus 0.1% ointment applied twice daily is the standard choice. It works by inhibiting T-cell activation and calcineurin-dependent cytokine production, reducing the local autoimmune attack on melanocytes. The advantage is the absence of steroid-related atrophy, making it safe for prolonged use on delicate skin. Pimecrolimus 1% cream is an alternative with a similar mechanism but slightly lower potency.

Ruxolitinib 1.5% cream, a topical Janus kinase (JAK) 1/2 inhibitor, was approved by the FDA in 2022 for non-segmental vitiligo in patients aged 12 and older. It is applied twice daily to affected areas not exceeding 10% BSA. The mechanism involves blocking the JAK-STAT signaling pathway that mediates interferon-gamma-driven melanocyte destruction. It represents the first FDA-approved treatment for vitiligo repigmentation.

Narrowband UVB (NB-UVB) phototherapy at 311 nm is the treatment of choice for widespread vitiligo (greater than 10% BSA) or disease refractory to topical therapy. Sessions are performed 2 to 3 times per week, with gradual dose escalation based on the minimal erythema dose. A trial of at least 6 to 12 months (approximately 48 to 72 sessions) is recommended before declaring treatment failure. NB-UVB stimulates melanocyte stem cells in the hair follicle to migrate, proliferate, and repigment the surrounding epidermis. The characteristic pattern of repigmentation is perifollicular (tiny pigmented dots appearing around hair follicles within lesions). Combination with topical tacrolimus or corticosteroids enhances response rates.

For rapidly progressive vitiligo (new lesions appearing frequently, existing lesions expanding), oral mini-pulse corticosteroid therapy can halt disease activity. The standard protocol is dexamethasone 2.5 mg on two consecutive days per week (e.g., Saturday and Sunday) for 3 to 6 months. This regimen aims to suppress the autoimmune flare while minimizing the systemic side effects of daily corticosteroid use. Patients should be monitored for weight gain, glucose intolerance, and adrenal suppression.

Surgical options are reserved for patients with stable disease (no new lesions or expansion for at least 12 months) who have failed medical therapy. Segmental vitiligo responds particularly well to surgery. Techniques include autologous non-cultured melanocyte-keratinocyte transplantation, suction blister epidermal grafting, and punch grafting. These procedures transplant functioning melanocytes from normally pigmented donor sites into depigmented recipient areas.

For patients with universal vitiligo (greater than 80% BSA) where repigmentation is impractical, depigmentation of the remaining pigmented skin using monobenzone 20% cream is an option. This permanently destroys residual melanocytes, creating a uniformly depigmented appearance. This decision is irreversible and requires thorough counseling.

All patients should be counseled on strict sun protection (SPF 30+ broad-spectrum sunscreen, protective clothing) because depigmented skin lacks melanin photoprotection and is highly susceptible to sunburn. Cosmetic camouflage products and psychological support are important adjuncts, as vitiligo carries a significant psychosocial burden.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Pityriasis alba	Hypopigmented patches on the face, common in children	Lesions are hypopigmented (not completely white), ill-defined borders, fine scale present, and do NOT enhance brightly on Wood lamp. Associated with atopic dermatitis.
Tinea versicolor (pityriasis versicolor)	Hypopigmented macules, sometimes on the trunk	Fine, powdery scale present. KOH prep shows "spaghetti and meatballs" (hyphae and yeast). Lesions are hypopigmented, not depigmented. Wood lamp shows yellow-green fluorescence (not blue-white).
Post-inflammatory hypopigmentation	Light patches after a preceding skin condition	History of prior dermatitis, trauma, or procedure at the site. Lesions are hypopigmented (some pigment retained), not chalk-white. Gradual spontaneous resolution.
Piebaldism	Congenital depigmented patches, white forelock	Present from birth (vitiligo is acquired). Stable, non-progressive. Depigmented patches have a characteristic distribution (ventral midline). White forelock (poliosis) is classic. Autosomal dominant (KIT gene mutation).
Chemical/Contact leukoderma	Acquired depigmentation mimicking vitiligo	History of exposure to phenolic/catecholic compounds (rubber, adhesives, hair dyes). Depigmentation is localized to contact areas initially, then may spread. Occupational history is the key discriminator.
Hypopigmented mycosis fungoides	Hypopigmented patches, younger patients, trunk	Patches may have subtle wrinkling or atrophy. Lesions are hypopigmented (not chalk-white). Skin biopsy shows atypical lymphocytic infiltrate (epidermotropism of CD4+ or CD8+ T cells).
Idiopathic guttate hypomelanosis	Multiple small white macules in older adults	Lesions are small (2 to 5 mm), round, porcelain-white macules on sun-exposed areas (shins, forearms). Related to chronic UV damage and aging. Does not progress or coalesce like vitiligo.
Morphea (localized scleroderma)	Can produce hypopigmented/depigmented patches	Induration and skin thickening present. "Lilac ring" at the active border. Skin texture is altered (bound-down, waxy). Vitiligo has no textural change.
Tuberous sclerosis (ash-leaf macules)	Hypopigmented macules in children	Congenital, present from birth. Ash-leaf shaped (lanceolate). Associated with seizures, angiofibromas, and other neurocutaneous findings. Wood lamp helps detect subtle lesions in infants.
Leprosy (Hansen disease)	Hypopigmented patches with sensory loss	Hypoesthetic or anesthetic patches (loss of sensation within the lesion). Nerve thickening on palpation. Vitiligo retains normal sensation.

6. Traps and High-Yield Pearls

The most common way students lose points on vitiligo questions is by confusing depigmentation with hypopigmentation. This distinction is the single most important discriminator. Vitiligo produces complete, chalk-white depigmentation with bright blue-white enhancement on Wood lamp, because melanocytes are destroyed entirely. Conditions like pityriasis alba, tinea versicolor, and post-inflammatory changes produce hypopigmentation (reduced but not absent melanin), resulting in off-white or light tan patches that do not enhance as dramatically under Wood lamp. If the vignette describes a "well-demarcated, chalk-white patch with no scale," the answer is vitiligo until proven otherwise.

A second common trap involves the autoimmune screening question. The vignette may describe a patient with vitiligo who then develops fatigue, weight gain, or constipation. Students who fail to connect vitiligo to thyroid autoimmunity will miss the diagnosis of concurrent Hashimoto thyroiditis. Whenever a board question mentions vitiligo, immediately think about associated autoimmune conditions, particularly thyroid disease.

Another frequently tested concept is the management hierarchy based on location and extent. Students often select potent topical steroids for facial vitiligo, which is incorrect. The face and intertriginous areas require topical calcineurin inhibitors (tacrolimus) to avoid steroid-induced skin atrophy. Similarly, students may choose topical therapy for a patient with widespread disease (greater than 10 to 20% BSA), when the correct answer is narrowband UVB phototherapy.

Watch for the Koebner phenomenon trap. A vignette describing a patient who develops new white patches at the site of a recent surgical scar or sunburn is testing whether you recognize this isomorphic response. It also reinforces the importance of sun protection counseling.

Finally, be alert to the leukotrichia prognostic pearl. If the vignette mentions that the hair within a vitiligo patch has turned white, this indicates destruction of the melanocyte reservoir in the hair follicle, which predicts a poor response to medical therapy and may steer the management answer toward surgical options or phototherapy combined with topical agents.

The core competency being tested in vitiligo questions is threefold: (1) pattern recognition of depigmented versus hypopigmented lesions using the Wood lamp finding as the discriminator, (2) awareness of the autoimmune disease cluster requiring appropriate screening, and (3) correct selection of therapy based on lesion location and disease extent.

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