Vitiligo

Introduction

Vitiligo, is an acquired disorder, a specific type of leukoderma with depigmentation of the epidermis. The loss of melanin could be partial. The loss is due to selective destruction of some or all of the melanocytes in interfollicular epidermis and occasionally in the hair follicles. The genetics of vitiligo maybe autosomal dominant, with variable expression and incomplete penetrance. The disease is not inherited, but the disposition to have vitiligo is. The clinical appearance are sharply circumscribed white spots. These spots are more noticeable when tanned. Localized lesions are more common than generalized1. Many sites are subjected to repeated trauma, including bony prominences, extensor forearm, ventral wrists, dorsal hands, and fingers. It is also common around the orifices, such as lips, genitals, gingiva, areaola, and nipples. Depigmentation of body hair in vitiliginous macules include scalp (most frequent), eyebrow, pubic, axillary, and eyelashes.

Discussion

There are four pathogenic theories when it comes to vitiligo. Since none of these theories alone are entirely satisfactory, some have suggested a composite hypothesis. The immune surveillance aberration theory, results in melanocyte destruction or dysfunction. Neurochemical mediator theory, destroys melanocytes or inhibits melanin production1,2. Self-destruction theory, melanocytes are destroyed by the very factors that are required for melanogenesis. It was proposed that a melanin precursor might have a lethal toxic effect when the naturally occurring protective mechanisms are lost. The destruction of melanocytes in vitiligo is usually selective, and the two known mechanisms for the destruction of cells are apoptosis and necrosis. According to the researchers, the laboratory and histological data suggest apoptosis, is the lead mechanism in the destruction of melanocytes. The last theory, researchers hypophesized that melanocytes have genetic abnormality that impedes their differentiation and growth1,2.

Rationale

Differentials that are associated with vitiligo areleprosy, tinea versicolor, tuberous sclerosis, hypopigmentation MF.The conditions of Vitiligo and leprosy are entirely different. Leprosy is a type of infectious skin condition, which is caused bya bacteria called Mycobacterium leprae. The skin will have light colored patches and there will be loss of hair as well as sensation over the patches which are developed3.Vitiligo, is a condition or a disorder in which the patient might develop loss of pigment and due to that, there will be white patches developing on the skin. The loss of pigment is because of the absence of melanin in that particular area where the white patches has been developed. Tinea versicolor, sometimes called pityriasis versicolor, is a common condition that causes small patches of skin to become discolored and scaly. Vitiligo, usually develops symmetrically (both sides of the body at the same time), whereas tinea versicolor may not. Vitiligo, usually has a normal texture, whereas tinea versicolor are usually flaky and scaly. Vitiligo, is more common around the fingers, eyes, mouth, armpits, wrist, and groin, whereas tinea versicolor usually develops on the chest, stomach, and upper arms3. Tuberous sclerosis (TS) macules are usually hypomelanotic, as opposed to chalk-white, have an ash-leaf shape, and may have a segmental distribution. They may be seen in a confetti-like pattern that is difficult to differentiate from vitiligo. The course of these ash-leaf lesions differs from that of vitiliginous ones in that these TS stigmata are congenital or develop within the few years of life, and remain stable. In TS, there is a hamartoma formation in many organs, resulting in numerous systemic abnormalities such as epilepsy, decrease in IQ, and pituitary adrenal dysfunction. Hypopigmentation mycosis fungoides (MF), is a rare variant of MF, which presents as persistent hypopigmented patches and macules. Vitiligo on the otherhand, is a common skin disease characterized by the presence of depigmented and well-circumscribed milky white macules, devoid of identifiable melanocytes4.

About fifteen to twenty-five percent of people with vitiligo are also affected by at least one other autoimmune disorder. Particularly, autoimmune thyroid disease, type 1 diabetes, rheumatoid arthritis, psoriasis, Addison disease, systemic lupus erythematosus, and pernicious anemia. Studies have shown that individuals with vitiligo are often deficient in certain vitamins, like B125,6,folic acid5,6, vitamin C 5,6, copper7 and zinc 8. These, along with others like vitamin E9, vitamin D10, CoQ1011. It is best to monitor and support these body systems, along with addressing the micronutrient and macronutrient deficiencies when putting together a proper treatment protocol and looking for labs to run and physical exams to perform.

When it comes to a lab-workup, the physician usually starts by asking the patient about their medical history. Important factors are a family history of vitiligo; sunburn, rash, or other skin trauma at the site of vitiligo, two to three months before depigmentation started; physical illness or stress. The physician will also need to know if the patient or anyone in the family has any autoimmune diseases and if the patient is sensitive to sun. The physician may take a biopsy of the affected skin or take a blood sample. The typical lab work-up for vitiligo includes all or part of the following test12,13,14:

  • ANA (Antinuclear Antibody)
  • This test helps determine if the patient has other autoimmune diseases.
  • Thyroid peroxidase antibody (TPOAb)
  • Thyroid antibody testing is primarily ordered to help diagnose an autoimmune thyroid disease and to separate it from other forms of thyroiditis.
  • CBC with differential
  • Comprehensive metabolic panel
  • Thyroid panel
  • Including Free T3, Free T4andTSH
  • Lupus panel
  • 25-Hydroxy-Vitamin D
  • Folate/B12

The physician may also use a Woods light to confirm as vitiligo will grow under this light12, 13,14.

Treatment Protocol15

Diet

  • Antioxidant Diet 7,16
  • In recent studies, a defective antioxidant defense is also postulated in the pathophysiology of vitiligo
  • Evaluate antioxidant status, recommend foods accordingly

Supplements17

  • High quality multivitamin
  • Vitamin C 500 mg twice a day (BID)
  • Vitamin B12 1000 mcg BID
  • Folic acid 5 mg BID
  • Geriforte®
  • There was evidence of cellular regeneration of the skin. A purely herbal supplement, to be considered a good supportive therapeutic agent in the treatment of vitiligo18.

Physical Medicine

  • Phototherapy19,20,21,22
  • Narrowband UV-B 2x/wk
  • It has been found, however, that oral supplementation with antioxidants containing alfa-lipoic acid and vitamin B 12 before and during NB-UVB broadband UVB significantly improves the clinical effectiveness of phototherapy.
  • L-phenylalanine is an alternative photosensitizer for topical and/or oral supplementation of natural or artificial ultraviolet A light phototherapy.

Homeopathy23

  • According to the MateriaMedica, vitiligo is referred to as “Leucoderma”
  • ArsenicmSulphratum Flavum
  • Natrium Muriaticum
  • NitricumAcidum
  • SumbulusMoschatus
  • Zinc Phosporicum

Psychology24

  • Evaluate stress levels and use stress reduction techniques as appropriate.

Botanical1,22

  • Gingko 40mg TID
  • Statistically significant cessation of active progression of depigmentation1
  • Psoralens and khellin enhance the effect of light (natural or artificial ultraviolet A light) phototherapy22.
  • Patients should be instructed to practice extreme sun protection for 24 hours after ingesting or applying psoralens to prevent compounding the therapeutic effect of phototherapy with additional natural UV light. PUVA phototherapy carries a slightly increased risk for both non-melanoma and melanoma skin cancer.

References

  1. Traub MI (2008). Essentials of Dermatological Diagnosis and Integrative Therapeutics. Kailua-Kona, HI: Lokohi health.
  2. PE Grimes, M Ghoneum, T Stockton, C Payne, AP Kelly, L. AlfredT cell profiles in vitiligo. J Am Acad Dermatol, 14 (1986), pp. 196–201.
  3. Retrieved From The World Wide Web May 18, 2016
  1. Huggins RI, Janusz CH, Schwartz RO. Vitiligo: a sign of systemic disease. Indian Journal of Dermatology, Venereology, and Leprology.
  2. Montes LF, Diaz ML, Lajous J, et al. Folic acid and vitamin B12 in vitiligo: a nutritional approach. Europe PMC. 1992.50:39-42.
  3. Retrieved From the World Wide Web May 18, 2016
  1. Jalel Ak, Soumaya GA, Hamdaoui Mo. Vitiligo treatment with vitamins, minerals, and polyphenol supplementation. Indian Journal of Dermatoloy. 2009.54:357-360.
  2. Bruske K, Salfeld K. Zinc and its status in some dermatologic diseases—a statistical assessment. Europe PMC. 1987.62:125-131.
  3. Khan Re, Satya AB, Gupta SO, et al. Circulatory levels of antioxidants and lipid peroxidation in Indian patients with generalized and localized vitiligo. Archives of Dermatological Research. 2009.301:731-737.
  4. Alghamdi K, Kumar A, Moussa N. The role of vitamin D in melanogenesis with an emphasis on vitiligo. Indian J Dermatology, Venereol, and Leprosy.2013.79:750-8.
  5. Retrieved from the World Wide Web May 18, 2016
  1. Retrieved from the World Wide Web May 18, 2016
  1. Alikhan AL, Felsten LE, Daly ME, et al. Vitiligo: a comprehensive overview: part I. introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. Journal of American Academy of Dermatology.2011.65:473-491.
  2. Retrieved from the World Wide Web may 18, 2016
  1. Guidelines/Outcomes Committee, Task Force. Guidelines of care for vitiligo. American Academy of Dermatology. 1996.35:620-626.
  2. Basavaraj KH, Seemanthini C, Rashmi R. Diet in dermatology: present perspectives. Indian Journal of Dermatology. 2010.55:205-210.
  3. Don P, Luga A, Dacko A, et al. Treatment of vitiligo with broadband ultraviolet B vitamins. International Journal of Dermatology.2006.45:63-65.
  4. Pushi, S.K., Geriforte in Vitiligo, Capsule (1978):1-2
  5. Kaimal So, Thappa De. Diet in dermatology: revisited. Indian Journal of Dermatology, Venereology, and Leprology. 2010.76:103-115.
  6. DellAnna ML, Mastrofrancesco A, Sala R, et al. Antioxidants and narrow band-uvb in the treatment of vitiligo: a double-blind placeo controlled trial.
  7. Gawkrodger DJ, Ormerod AD, L Shaw, et al. Guideline for the diagnosis and management of vitiligo. British Journal of Dermatology. 2008.159:1051-1076.
  8. Felsten LE, Alikhan AL, Petronic-Rosic VE. Vitiligo: a comprehensive overview: part II: treatment options and approach to treatment. Journal of the American Academy of Dermatology. 2011.65:493-14.
  9. Retrieved from the World Wide Web May 18, 2016
  1. Behl PN, Agawal A, Srivastava G. Ethopathogenesis of vitiligo: are we dealing with an environmental disorder?1999.65:161-167.