Vitiligo

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vitiligo-types pathogenesis clinical features and treatment.

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Vitiligo

  1. 1. VITILIGO Vishnu narayanan M.R.
  2. 2. EPIDERMO-MELANIN UNIT
  3. 3. MELANOGENESIS tyrosine ↓ tyrosinase DOPA ↓ tyrosinase DOPAquinone ↓ ↓ indolequinone ↓ polymerization melanin
  4. 4. CONTROL OF MELANOGENESIS • Constitutional skin colour • UV radiation • Hormones - MSH
  5. 5. HYPOPIGMENTATION HYPOPIGME NTATION MELANOPENIC ANATOMICAL DEFECTS OF MELANOCYTES FUNCTIONAL DEFECTS OF MELANOCYTES NON- MELANOPENIC ABNORMALITIES OF VASCULATURE
  6. 6. MELANOPENIC HYPOPIGMENTATION Anatomical defect • Vitiligo • Piebaldism • Chemicals- rubber • Post inflammatory Functional defect • Pityriasis versicolor • Endocrine disorders • albinism
  7. 7. …VITILIGO… • Vitiligo is an acquired , pigmentary anomaly of the skin characterised by depigmented white patches surrounded by a normal or a hyperpigmented border
  8. 8. The Roman physician Celsus first used the term vitiligo in the second century AD. It is interesting to note that the Rigveda (6000 BC or earlier) named leukoderma as kilas, meaning a white spotted deer.
  9. 9. ETIOPATHOGENESIS 1.GENETIC: 20 % PATIENTS- POSITIVE FAMILY HISTORY POLYGENIC INHERITANCE- NALP gene , HLADR4, CATALASE GENE, …..
  10. 10. 2. AUTO-IMMUNE HYPOTHESIS • Association with other autoimmune disorders- alopecia areata and thyroid disorders • Antibodies to melanocytes • Lymphocytes in early lesions
  11. 11. 3. NEUROGENIC HYPOTHESIS • Segmental vitiligo • Nerve endings toxin destruction of melanocytes
  12. 12. Epidemiology • Incidence – 1 % population • Race – affects all races • No sex predisposition • Age – peak -10-30 years
  13. 13. Clinical features MORPHOLOGY • Depigmented macules- chalky/ milky white • Pigment loss- complete/ partial • Macules- scalloped outline • Geographical ptterns on fusion of adjacent lesions • Hairs – in older lesion- leucotrichia
  14. 14. • Trichome vitiligo
  15. 15. LEUCOTRICHIA
  16. 16. SITES • Any part can be affected • Predilection to areas with repeated friction and trauma • Dorsal aspect of hands and feets , elbows , knees
  17. 17. PATTERNS • Vitiligo vulgaris • Segmental vitiligo • Generalised vitiligo
  18. 18. Vitiligo vulgaris • Commonest type • Second decade • Family history • Progression – rapid/slow
  19. 19. Segmental vitiligo • Occurs in children • Not associated with autoimmune disorders • Depigmentation- dermatomal/ quasidermatomal • Stable course • Leucotrichia • Feathery margin • Distant lesions- uncommon • Poor response to treatment
  20. 20. Generalised vitiligo • Extensive lesions Acrofacial vitiligo • Periorificially and acral parts • Resistant to therapy due to absence of hairs Lip-tip vitiligo • lips • Tip of penis,vulva, nipples Vitiligo universalis • Widespread • Multiple endocrinopathies
  21. 21. ACROFACIAL VITILIGO
  22. 22. LIP-TIP VITILIGO
  23. 23. VITILIGO UNIVERSALIS
  24. 24. Course • Onset < 20 years • Slowly progressive usually • Segmental vitiligo – stable • Spontaneous repigmentation- 10 – 20% • Acrofacial vitiligo – resistant to treatment
  25. 25.  Absence of melanocyte and melanin in the epidermis  e/m confirms the loss of melanocytes which appears to be replaced by langerhans cells.  Increased cellularity of the dermis
  26. 26. Prognostic factors • Long standing disease • Leucotrichia • Acro facial lesions • Lesions on resistant areas Poor prognosis
  27. 27. Associations Endocrine disorders • Diabetes mellitus • Pernicious anemia • Addison’s disease • Hypoparathyroidsm • Hypothyroidism • Hyperthyroidism
  28. 28. Cutaneous disorders • Alopecia areata
  29. 29. Halo nevus
  30. 30. Atopic dermatitis
  31. 31. Malignant melanoma
  32. 32. Morphea
  33. 33. DIAGNOSIS • Age of onset • Depigmented macules with scalloped borders • Leucotrichia • Koebner’s phenomenon • Predeliction to sites of trauma
  34. 34. vitiligo albinism onset Later life At birth course Depigmentation- progress/regress Freckling on photoexposed parts Eye involvement Not seen Always present Response to treatment Partial/near complete response No response Differential diagnosis
  35. 35. Nevus achromicus Vitiligo onset At birth Not present at birth Distribution Segmental/focal Segmental/focal/g eneralised Morphology Feathered margins, uniform pigment dilution Scalloped margins, islands of pigmentation Hair No leucotrichia leucotrichia
  36. 36. Piebaldism
  37. 37. LEUCODERMA • All depigmented lesions • Idiopathic- vitiligo • Chemicals • Inflammatory skin diseases
  38. 38. TREATMENT DEPENDS ON • Age of patient • Extent of disease • Pattern of disease • Cosmetic disability • Effect on quality of life
  39. 39. General measures Physical modality Medical treatment Surgical treatment
  40. 40. Physical modality 1.Photochemotherapy  Psoralens + UVA exposure – PUVA • Mainstay of vitiligo therapy • Psoralens – tricyclic furocoumarins 8- methoxypsoralen topical/systemic • UVA- in special chambers containing UVA emitting tubes  PUVA sol – psoralen + sunlight
  41. 41. REGIMEN Topical therapy Alternate days Systemic therapy Ointment/lotion psoralen (0.6mg/kg) gradually increasing exposure till mild erythema sunlight PUVA – UVA lamps Protect from sun for 8 hrs (11:00 - 13:00) Broad spectrum sunscreens- ZnO
  42. 42. RESPONSE TO PHOTOCHEMOTHERAPY • Repigmentation- slow • Begins in perifollicular area and periphery of lesion • Becomes confluent • Most readily on face, neck and hairy regions • Slow responders – acral and non hairy parts
  43. 43. • Photo-toxicity  Excessive exposure to UVA / SUN  Topical psoralens  Treatment – withdrawal of psoralen topical corticosteroids severe – systemic steroids • Nausea , vomiting, epigastric discomfort, giddiness
  44. 44. 2. Phototherapy – narrow band UVB (311nm) • INDICATIONS – in extensive disease>10% indicated in children and pregnant women in patients in whom psoralens C/I • REGIMEN – Gradually increasing doses of UVB, given from specialized chambers. • Safe
  45. 45. Medical treatment • Single lesions esp new • adjuvantTopical steroids • Patient can’t be given physical modalities • Rapidly progressive vitiligo with PUVA • Vitiligo unresponsive to psoralens Systemic steroids
  46. 46. ORAL MINI PULSE ORAL STEROIDS- SINGLE DAY OR ON 2 CONSECUTIVE DAYS PER WEEK
  47. 47. OTHERS • FOR FACIAL LESION • CALCINEURIN INHIBITOR TACROLIMUS ,PIMECROLIMUS • IMMUNOMODULATER • WEEKLY/FORTNIGHTLY LEVAMISOLE • DEPIGMENTING AGENT MONOBENZYL ETHER OF HYDROQUINE PLACENTAL EXTRACT • PHOTOCHEMOTHERAPYKHELLIN
  48. 48. SURGICAL TREATMENT • Indications- sites poorly responsive to conventional therapy Patient with stable disease MELANOCYTE TRANSFER BLISTER GRAFTING PUNCH GRAFTING SPLIT THICKNESS SKIN GRAFTING
  49. 49. Treatment guidelines LOCALISED DISEASE New lesions Topical steroids Old lesions Topical PUVA/ PUVA sol EXTENSIVE DISEASE New lesions Oral steroids + PUVA/PUVA sol NBUVB Rapid increase Oral steroids + PUVA/PUVA sol /NBUVB Old lesions Oral PUVA/PUVA sol/NBUVB Intolerence to PUVA/NBUVB Oral steroids GENERALISED LESIONS Monobenzyl ether of hydroquinone

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