Vitiligo history and symptoms

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: João André Alves Silva, M.D. [2]

Overview

Vitiligo constitutes one of the most frequent pigment disorders, affecting about 1% of the world's population, with no preference of race, age, gender, or country. It commonly starts to manifest around the second decade of life, with a gradual progress of depigmentation, mostly due to loss of melanocytes.[1][2]

History

Vitiligo is one of the most common diseases of depigmentation. It affects 0.5% to 1% of the world population, without preference for a particular race, gender, age or country. For patients presenting for the first time with patches of skin depigmentation, a thorough history and physical examination should be performed, including examination under the Wood's lamp in order to rule out other potentially life-threatening disorders. The initial onset of the condition may be abrupt, however, afterwards it usually progresses slowly, with expansion of skin depigmentation with no concomitant symptoms.[3][4][5][6] It is important to inquire about history of occupational exposures, since those may aggravate underlying vitiligo lesions or may lead to depigmentation areas, with no connection to the disease.[7] There may be two major subdivisions of vitiligo which may influence the presence of different characteristics and the natural history of the disease. They may be present individually or concomitantly, in which case the segmental lesions will respond poorly to the treatment:[3][8]

Generalized or Nonsegmental

  • Common later onset.
  • Continuous progression with periods of exacerbation.
  • Hair is usually affected later in life.
  • Frequently occurs in areas of the body susceptible to trauma or keen to pressure.
  • Individual or family history of other autoimmune diseases.
  • Bad response to autologous grafting, commonly recurring on the same location.
  • The most common form of the disease, present in about 85-90% of the cases.

Segmental

  • Commonly has an earlier onset in childhood.
  • Has an abrupt onset, stabilizing afterwards.
  • Rapidly moves to involve hair regions.
  • Commonly involves the face.
  • Generally no other autoimmune diseases are present.
  • Commonly responds well to autologous grafts.
  • May be confused with nevus depigmentosus.

During the history taking, the patient should be asked about:[9]

  • Existence of family members with vitiligo.
  • Personal or family history of earlier hair graying.
  • Personal or family history of autoimmune disease.

Considering that halo nevi are more common in vitiligo patients than in the population in general, it is important to discuss personal or family history of such, since multiple halo nevi are a common indicator of autoimmunity against the nevi, increasing the risk of vitiligo, if there is history of the disease in the family.[10] Since vitiligo is often concomitant with other conditions, it is important to evaluate the possible existence of other diseases, such as:

Common Symptoms

Less Common Symptoms

References

  1. Soutor, Carol (2013). Clinical dermatology. New York: McGraw-Hill Education/Lange Medical Books. ISBN 978-0-07-177296-9.
  2. Taïeb, Alain; Picardo, Mauro (2007). "The definition and assessment of vitiligo: a consensus report of the Vitiligo European Task Force". Pigment Cell Research. 20 (1): 27–35. doi:10.1111/j.1600-0749.2006.00355.x. ISSN 0893-5785.
  3. 3.0 3.1 Taïeb, Alain; Picardo, Mauro (2009). "Vitiligo". New England Journal of Medicine. 360 (2): 160–169. doi:10.1056/NEJMcp0804388. ISSN 0028-4793.
  4. Soutor, Carol (2013). Clinical dermatology. New York: McGraw-Hill Education/Lange Medical Books. ISBN 978-0-07-177296-9.
  5. Howitz J, Brodthagen H, Schwartz M, Thomsen K (1977). "Prevalence of vitiligo. Epidemiological survey on the Isle of Bornholm, Denmark". Arch Dermatol. 113 (1): 47–52. PMID 831622.
  6. Boisseau-Garsaud AM, Garsaud P, Calès-Quist D, Hélénon R, Quénéhervé C, Claire RC (2000). "Epidemiology of vitiligo in the French West Indies (Isle of Martinique)". Int J Dermatol. 39 (1): 18–20. PMID 10651958.
  7. Boissy RE, Manga P (2004). "On the etiology of contact/occupational vitiligo". Pigment Cell Res. 17 (3): 208–14. doi:10.1111/j.1600-0749.2004.00130.x. PMID 15140065.
  8. Gauthier Y, Cario Andre M, Taïeb A (2003). "A critical appraisal of vitiligo etiologic theories. Is melanocyte loss a melanocytorrhagy?". Pigment Cell Res. 16 (4): 322–32. PMID 12859615.
  9. Mason CP, Gawkrodger DJ (2005). "Vitiligo presentation in adults". Clin Exp Dermatol. 30 (4): 344–5. doi:10.1111/j.1365-2230.2005.01779.x. PMID 15953063.
  10. Barona MI, Arrunátegui A, Falabella R, Alzate A (1995). "An epidemiologic case-control study in a population with vitiligo". J Am Acad Dermatol. 33 (4): 621–5. PMID 7673496.

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