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23 Aug, 2018

Vitiligo is a depigmentation disorder, characterized by white colored patches on the affected regions. These patches arise due to depigmentation brought about by the death of melanocytes—the pigment-producing cells in the skin, hair and mucosal surfaces. It is an autoimmune disease. Vitiligo affects approximately 1% of the population and is equally prevalent in both males and females. Affected parts of the body include skin, hair and mucous membranes.


Model of vitiligo pathogenesis:

There are three parts of the disease etiology:

  • To determine the cellular responses to stress namely, the antioxidant pathway and the unfolded protein response. These two factors are said to be the causative agents for disease onset.
  • To identify the immune system players that bring about the destruction of the melanocytes, leading to disease progression.
  • To identify the genes which makes a person pre-disposed to the development of the disease


àThe current understanding of the condition has led to the following model which postulates that oxidative stress causes cellular disruptions, leading to interrupted protein maturation in the endoplasmic reticulum (ER). This results in the activation of the unfolded protein response (UPR) and expression of UPR regulated chemokines IL-6, IL-8.

àImmune components are recruited to the skin by the aforementioned chemokines which result in the destruction of the melanocytes. The components of the autoimmune response in vitiligo are IFN-gamma/CXCL10 axis and IL-17.

àFinally, the destruction of melanocytes by the immune cells leads to depigmentation of the skin. Also, oxidative stress is shown to increase melanocyte targeting and destruction by antigen presentation.

àGenes identified are NRF2, UPR gene, XBP1 which are antioxidant genes and Class I & II MHC genes involved in antigen presentation.


Vitiligo is classified into the following types

  • Non-segmental vitiligo (NSV)
    • Generalized—begins later in life at sites sensitive to pressure, friction, trauma etc and is known to be progressive
  • Segmental vitiligo (SV)
  • Mixed NSV and SV
  • Unclassifiable types


Known triggers of vitiligo

Vitiligo is triggered by stress caused to melanocytes which are melanin-producing cells.

  • Sunburn
  • Mechanical trauma
  • Chemical Exposures



  • Loss of skin photoprotection
  • Compromised cutaneous immunity
  • Reduction in quality of life



  • BiopsyàTo check for the presence of any pigment-producing cells
  • Blood testàTo determine other associated diseases like thyroid disorders, diabetes, anemia etc



This disorder has no cure yet but there are methods available for the management of the disease involving minimizing or halting the progression of the disease, as well as repigmentation or depigmentation.


  • Traditional therapies for repigmentation:

Topical agents-corticosteroids, calcineurin inhibitors, vitamin D analogs

Prostaglandins analogues—induction of hyperpigmentation by promoting melanocyte proliferation

  • Oral and Systemic Treatments

Low dose oral dexamethasone mini-pulse therapy—was shown to be effective in halting vitiligo in doses of 2.5 mg per day on two consecutive days of the week for thirteen weeks.

  • Minocycline—is a broad spectrum antibiotic, is antioxidant, anti-inflammatory and immunomodulatory; it scavenges free radicals and thus protects melanocytes from hydrogen peroxide (H2O2) induced apoptosis.
  • Oral statins—are primarily used to lower cholesterol. It exhibits immuno-modulatory and antioxidant properties. It scavenges free radicals and causes down-regulation of inflammatory cytokines like IL-6, IL-12, IFN-gamma, TNF-alpha etc.

Agents used for the treatment of other autoimmune diseases

  • Janus kinase (JAK) inhibitors—Known to interfere with IFN-gamma signaling eg: Tofacitinib



  • Has shown therapeutic potential in early clinical studies
  • It is a longer acting synthetic analog of the alpha-melanocyte-stimulating hormone
  • It binds to a melanocortin-1 receptor and stimulates melanocyte proliferation



Narrowband ultraviolet B radiation  (NB-UVB)/psoralen—311-313 nm, is administered to the entire body using lamps or as a focused targeted treatment using a xenon-chloride monochromatic excimer light (308 nm) emitted through a laser or an incoherent lamp. Phototherapy and application of topical creams yield faster and greater repigmentation than monotherapy.


Procedural treatmentsà

Patients who have not responded to traditional repigmentation therapies and have stable vitiligo are eligible for surgical treatment.

  • Erbium laser assisted dermabrasion and fractional CO2 lasers followed by NB-UVB. Side effects include pain, scarring and long healing time.
  • Blister graft (BG) —this technique has its use in creating donor epidermal graft tissue; a sub-epidermal bulla is created at the donor site and the roof is surgically removed and is then transplanted into the recipient site. This technique is not suitable for large lesions.
  • Split-thickness skin graft (STSG)—the dermatome is used to harvest the graft thus creating a draft of uniform thickness. It is then meshed to cover a large surface area and placed over dermabraded recipient site and covered with gauze. The STSG technique is superior to BG since it can cover a greater surface area.  Phototherapy has been shown to enhance repigmentation in both techniques.
  • Punch grafting
  • AMST involves harvesting the tissue from the donor site by one of the following methods namely BG, STSG or curettage; subsequent release of the tissue into a suspension and later transplantation into de-epithelized recipient skin.
  • Side effects of all the surgical methods involve scarring, infection, and hyperpigmentation.


Herbal compoundsà

All the herbs mentioned have a therapeutic potential in the treatment of vitiligo owing to their antioxidant, photoprotective and melanogenesis inducing properties.

  • Ginkgo biloba
  • Cucumis melo (“Muskmelon”)
  • Khellin
  • Picrorhiza kurroa (“Kutki” or “Kutaki”)
  • Polypodium leucotomos (“Calaguala”)
  • Green Tea polyphenols; extracts of green tea leaves
  • Capsaicin
  • Curcumin (“Curcuma longa”)
  • Pyrostegia venusta


Depigmentation: is used as a treatment option for those vitiligo patients who have 50% of the body covered in patches.

Monobenzone (monobenzyl ether of hydroquinone/MBEH) is used to achieve permanent depigmentation and the concentrations used are 20 to 40 percent. It brings about depigmentation by inducing the necrotic death of melanocytes.

Side effects of MBEH include skin irritation, contact dermatitis, ocular side effects etc.