7.vitiligo , melasma

vitiligo and melasma

1. Dr.Alaa Mohammad AbuZaineh Teaching Assistant RAKCOMS RAKMHSU

2. Vitiligo Vitiligo is an acquired pigmentary anomaly of the skin manifested by depigmented white patches surrounded by a normal or a hyperpigmented border.

3. usually begins in childhood or young adulthood, with a peak onset between ages 10 and 30. Vitiligo has developed in recipients of bone marrow transplant from patients with vitiligo.

4. Clinical Features depigmented white patches surrounded by a normal or a hyperpigmented border. There may be intermediate tan zones between the normal skin color and depigmentation, so-called trichrome vitiligo The hairs in the vitiliginous areas usually become white as well.

5. Six types of vitiligo have been described, according to the extent and distribution of the involved areas: localized or focal (single or a few macules in one anatomic area segmental , generalized (common symmetric); most common universal; entire body surface is depigmented acrofacial ; affects the distal fingers and facial orifices (lips and tips). mucosal.

6. The most commonly affected sites are the face, upper part of the chest, dorsal aspects of the hands, axillae, and groin. The skin around orifices tends to be affected: the eyes, nose, mouth, ears, nipples, umbilicus, penis, vulva, and anus. Lesions appear at areas of trauma, so vitiligo favors the elbows and knees .

7. Halo phenomenon the initial local loss of pigment may occur around melanocytic nevi and melanomas , not all patients with halo nevi or melanoma will develop vitiligo.

8. Histopathology Biopsies demonstrate an absence of melanocytes .

9. Patients should be screened with a proper history, review of systems, and physical examination to help evaluate for the associated conditions. Vitiligo is an autoimmune disease and affected patients are at risk for other autoimmune diseases. Autoimmune thyroid disease  most common should be screened in every vitiligo patient type 1 diabetes mellitus, pernicious anemia, Addison disease, and alopecia areata . Cochlear dysfunction  60% of vitiligo patients in one study. Ocular abnormalities  including iritis and retinal pigmentary abnormalities , Idiopathic uveitis Additional screening should be directed by signs and symptoms.

10. Family History is positive in 30% of Pts The psychological effect of vitiligo should not be underestimated.

11. Wood’s light is key to evaluation because the lesions of vitiligo are depigmented.

12. Treatment Spontaneous repigmentation in some patients Non treatment is an option Patients not concerned about the appearance Sun protection, Cosmetic Products Treatment of vitiligo can be approached in two steps: (1) stopping progression (2) repigmenting the depigmented areas. Response is typically slow, taking weeks to months of therapy. Many treatments may stop the progression, but fewer lead to durable repigmentation .

13. For rapidly progressive, generalized vitiligo systemic corticosteroids Systemic corticosteroids are usually used and are tapered over several months. Once the disease is arrested, the patient can be converted to phototherapy. systemic immunosuppressives These initially may control the disease, but with chronic use, unacceptable toxicity often develops limited skin areas vitiligo Topical corticosteroids Topical immunomodulatory and immunosuppressant ointments Phototherapy narrow-band (NB) UVB two to three times weekly has become the preferred form of phototherapy to treat vitiligo. Repigmentation may begin after 15–25 treatments; however, significant improvement may take as many as 100–200 treatments (6–24 months ). Surgical treatments : minigrafts

14. Melasma

15. Melasma is a common disorder, with two predisposing factors: sun exposure and sex hormones. It tends to affect darker-complexioned individuals, especially East, West, and Southeast Asians, Hispanics, and black persons who live in areas of intense sun

16. pathogenesis  not known. observations strongly suggest that sun exposure is the primary trigger . affects the face, a sun-exposed area, and worsens in the summer . the second most important trigger is female hormones . more common and severe in women than men. It occurs frequently during pregnancy , with OCP use, or ( HRT ) at menopause. Discontinuing OCP or HRT rarely clears the pigmentation melasma of pregnancy usually clears within a few months of delivery.

17. characterized by brown patches, typically on the malar prominences and forehead. The pigmented patches are usually sharply demarcated. The forearms may also be affected.

18. Treatment sunblock with broad-spectrum UVA coverage it will modestly improve the melasma It will enhance the efficacy of bleaching creams and help prevent new lesions. Bleaching creams hydroquinone is the gold standard , containing 2% (available OTC) to 4% hydroquinone. Tretinoin cream may be added to increase efficacy. hydroquinone + tretinoin+topical corticosteroid  “ Kligman’s formula” most effective topical regimen available to treat melasma . Twice-weekly  maintenance.

19. Various surgical procedures peels and light-based treatments, have been proposed as effective for melasma , but results are mixed , light-based modalities , Laser  should be approached with caution.  These therapies may be complicated by hyperpigmentation, irritation, hypopigmentation, and even scarring, if not used appropriately.

20. Thank You Reference : William James, Dirk Elston , James Treat, Misha Rosenbach , Isaac Neuhaus - Andrews’ Diseases of the Skin_ Clinical Dermatology-Elsevier (2019) 100 Cases in Dermatology - Powell, Ann-Marie, Benton, Emma, Morris-Jones, Rachael