vitiligo and melasma

1. Dr.Alaa Mohammad AbuZaineh
Teaching Assistant
RAKCOMS
RAKMHSU

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

5. • 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.

6. 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.

7. • 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.

8. • 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.

9. 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.

10. Histopathology
• Biopsies demonstrate an absence of melanocytes.

11. 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.

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

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

14. 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.

15. • 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

19. Melasma

20. • 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

21. • 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.

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

23. 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.

24. • 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.

26. 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