A Whole System Approach to the Treatment of Vitiligo

After treating hundreds of patients with vitiligo since 2004, helping most stop the spread of their vitiligo and helping to induce at least partial repigmentation in many of those patients, I think it would be appropriate to share some of my approaches to treating vitiligo.

As virtually everyone in the vitiligo research community agrees, vitiligo is caused at least in part by the immune system attacking melanocytes, the pigment forming cells in the skin (Whitton).  Thus, the first part of a successful approach to treating vitiligo is to identify what is irritating the immune system.  That is, what is causing it to become overstimulated and what is causing it to attack the body’s own melanocytes.  Research does not have many of the answers to this yet, but clinical experience and several research papers point to some foods as triggers of the immune system (Seyhan), some potential environmental factors (Nordlund), and emotional stress (Whitton).  There is also a possible hormone connection as noted in the Ginkgo biloba for vitiligo published report (Szczurko, 2011), but research evidence is just starting to come out about this (Schallreuter, Jin).  Food allergy and sensitivity testing will be elaborated on in a future posting, but the ELISA IgE Food Antibody Pannel done routinely at my office is a very useful tool for identifying food sensitivities or allergies, as is very regimented and focused food avoidance and reintroduction.

Once the immune system triggers are identified and addressed the second step to my naturopathic treatment of vitiligo is to support the body.  There is a large amount of published research reporting on effective ways of calming the immune system including fish oils, acupuncture, deep breathing exercises, acupuncture, and many others.  Certain nutrients can be low in patients with vitiligo, and at therapeuitic doses these vitamins, minerals, amino acids and herbs have been shown to help patients with vitiligo (Szczurko, 2008).  These immune calming and supporting options must be evaluated on a case by case basis and prescribed as appropriate for the individual patient.

The goal of steps one and two is to calm the autoimmune reaction that is leading to the spread of vitiligo.  Once this is achieved, and the results are confirmed by vitiligo lesions that have been stable for a few months, the third step of the treatment of vitiligo can be initiated: repigmentation.  Repigmentation of vitiligo is best achieved by phototherapy, either narrow band UVB (nbUVB) or psoralen with UVA (PUVA).  Some debate as to the best method is still ongoing (Wind, El-Mofty), but my preference at this time is nbUVB.  Several studies report effectiveness of the regulated and regimented use of sunlight to induce repigmentation, which I have also found to be effective and safe when done correctly.

It is important to point out that there are several scientific reports of vitiligo returning to the same repigmented lesions after phototherapy has been discontinued (Nicolaidou).  I am sure this happens more often than is reported, since most studies do not do a follow up after completing the trial.  This occurs because the treatment is often done backwards: repigmentation is often the first step in the treatment of vitiligo, having completely bypassed the systemic immune overreaction (topical application of cortisone or tacrolimus addresses the immune system at the skin where the lotion is applied, but not systemically – new vitiligo usually appears in new areas in those patients).  This systemic overreaction of the immune system to melanocytes is overwhelmed by the photherapy, or potentially paused for a while, but as soon as the phototherapy stops the immune system goes right back to attacking the melanocytes it was attacking.

The treatment approach outlined above: first by identifying the cause of the autoimmunity, then supporting the bodys immune system and specific vitiligo and patient related needs followed by repigmentation only after the immune system has calmed down has been safe and effective in many of my patients who present to me for treatment of their vitiligo.


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Jin SY, Park HH, Li GZ, Lee HJ, Hong MS, Park HJ, Park HK, Seo JC, Yim SV, Chung JH, Lee MH.Association of estrogen receptor 1 intron 1 C/T polymorphism in Korean vitiligo patients. J Dermatol Sci. 2004 Sep;35(3):181-6.

Nicolaidou EAntoniou CStratigos AJStefanaki CKatsambas AD. Efficacy, predictors of response, and long-term follow-up in patients with vitiligo treated with narrowband UVB phototherapy.  J Am Acad Dermatol. 2007 Feb;56(2):274-8.

Schallreuter KU, Chiuchiarelli G, Cemeli E, Elwary SM, Gillbro JM, Spencer JD, Rokos H, Panske A, Chavan B, Wood JM, Anderson D. Estrogens can contribute to hydrogen peroxide generation and quinone-mediated DNA damage in peripheral blood lymphocytes from patients with vitiligo. J Invest Dermatol. 2006 May;126(5):1036-42.

Seyhan MKandi BAkbulut HSelımoğlu MAKarincaoğlu M. Is celiac disease common in patients with vitiligo? Turk J Gastroenterol. 2011 Feb;22(1):105-6.

Szczurko O, Shear N, Taddio A, Boon H. Ginkgo biloba for the treatment of vitilgo vulgaris: an open label pilot clinical trial. BMC Complement Altern Med. 2011 Mar 15;11:21.

Szczurko O, Boon HS. A systematic review of natural health product treatment for vitiligo. BMC Dermatol. 2008 May 22;8:2. Review.

Whitton ME, Pinart M, Batchelor J, Lushey C, Leonardi-Bee J, González U. Interventions for vitiligo.Cochrane Database Syst Rev. 2010 Jan 20;(1):CD003263. Review.

Wind B, Meesters A, Kroon M, Beek J, Van Der Veen J, Nieuweboer-Krobotová L, Bos J, Wolkerstorfer A. Punchgraft testing in vitiligo; effects of UVA, NB-UVB and 632.8 nm Helium-Neon laser on the outcome.  J Eur Acad Dermatol Venereol. 2010 Oct 6. doi: 10.1111/j.1468-3083.2010.03874.x.

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