Vitiligo all are true except
Ans. is 'd' i.e. Leukotrichia has good prognosis VITILIGOEtiology:The exact etiology is not known and may vary from one pattern of disease to another GeneticA genetic factor is definitely important, since about 20-30% of patients give a positive family history.Inheritance may be polygenic.Autoimmune hypothesisEvidence points to autoimmune etiology becauseVitiligo is frequently associated with autoimmune disorders like alopecia areata and thyroid disorder.Antibodies to melanocytes have also been demonstrated.Histopathology of early lesions demonstrate presence of lymphocytes in the lesions.Neurogenic hypothesisDermatomal distribution of some types of vitiligo (e.g. segmental vitiligo) suggests that a toxin, which destroys melanocyte is released at the nerve endings.Epidemiology:Affects both sexes equallyAffects all ages, peak incidence between 10-30 years.Clinical features:Morphology * Depigmented macules are the hallmark of vitiligo.* Typical macule of vitiligo has a chalky or milky white colour, but the pigment loss may be partial in some lesions.Sometimes three shades (trichrome) occur in the same lesion i.e. the depigmented centre is surrounded by hypopigmented rim which in turn has normally pigmented skin around it.The macules have a scalloped outline and on fusion with neighbouring lesions form geographical patterns.The hairs in the lesion may remain normally pigmented though in older lesions the hair pigment may be lost (leukotrichia).Koebner's phenomenon can occur in active phase.SitesThe lesion can occur in any part of the body.Areas subjected to repeated trauma and friction are frequently affected e.g. the backs of hands and feet, elbows and knees.Diagnosis:The diagnosis of vitiligo is based upon.Age of onset (usually not present at birth).Depigmented macules (milky white) with scalloped borders.LeukotrichiaKoebner's phenomenonPredilection for sites of trauma.Guidelines for the treatment of vitiligoLocalised lesions* New lesion- Topical corticosteroids* Old lesion- Topical PUVAExtensive lesion* New lesion- Oral corticosteroid + PUVA/PUVAsol or NBUVB* Rapid increase- Oral corticosteroids + PUVA/PUVAsol or NBUVB* Old lesions- Oral PUVA/PUVAsol or NBUVB* Intolerance- Oral corticosteroids + PUVAGeneralized lesions- Monobenzyl ether of hydroquinoneNBUVB - Narrow Band Ultraviolet -B PhototherapyCourse of disease:Depigmentation usually begins before the age of 20.The disease is usually progressive but sometimes can progress rapidly, segmental vitiligo has a stable course.Spontaneous repigmentation is seen in 10-20% of patients especially in sun exposed parts.Acrofacial vitiligo is more resistant to treatment.Prognostic factors:Though there are no indicators of good prognosis, the following factors indicate poor prognosis for therapyLong standing diseaseLeukotrichiaAcrofacial lesionsLesions on resistant areas, ankles, wrist elbows, periungual areas, nipples and areolae, lips and genitalia i.e., (lesions on bony prominences, non fleshy areas, non hairy areas and muosae).TreatmentNo single therapy for vitiligo produces predictably good results in all patients.The response to therapy is highly variable.Systemic phototherapySystemic phototherapy induces cosmetically satisfactory repigmentation in upto 70% of patients.Narrow band ultraviolet (UV-B) phototherapy is widely used and produces good results.The advantage of narrow band UV-B over PUVA include shorter treatment times, no drug costs, no adverse GI effects and no need for subsequent photoprotection.Steroid therapyA topical steroid preparation is often chosen first to treat localized vitiligo.Systemic steroids have also been usedIn general intralesional corticosteroids are avoided because of the pain associated with injection.
Genetic predisposition present
Narrow range UV-B is very effective
Topical steroid used for localised lesion
Leuckotrichia has good prognosis
Disorder of Pigmentation