Vitiligo is a chronic skin condition characterized by loss of pigment cells called melanocytes, resulting in white patches of skin. It affects around 1-2% of the world's population equally across all races and genders. The exact cause is unknown but factors like genetics and autoimmunity are thought to play a role. Clinically, it presents as chalky white macules that may join together and spread over time. Treatment focuses on repigmentation through phototherapy, photochemotherapy, topical medications and occasionally surgery. Prognosis is generally good with 30% experiencing spontaneous repigmentation, though some areas like the face respond better than others.

1. VITILIGO
Facilitator-Dr S.Kiprono
Presenter-Richard Rotich

2. Background $ definition of terms
• Basis of skin colour
Pigments &
Blood flow in the skin
Pigments may be
Those normally present
Those not normally present

3. • Pigments normally present
• Depends on presence of various
chromophores-color producing molecule.
• Melanin synthesized by melanocyte is the
most important

4. • Melanocytes-present in the basal layer of
epidermis ;their dendrites interdigitate with
keratinocytes
• Melanocyte with associated keratinocytes
(abt 36) forms an epidermal melanin unit
• Melanocytes contain organelles called
melanosomes - synthesize melanin

5. Epidermal melanin unit
0

6. • There are two types of melanin;
I. Eumelanin – brown-black, present in
spherical melanosomes
II. Pheomelanin- Red –brown or yellow present
in ovoid melanosomes
• Once the pigment is formed, the
melanosomes are injected into the
keratinocytes by dendrites of melanocytes

7. • Hypermelanosis-Increase of melanin in the
epidermis Can occur in two ways;
melanocytotic hypermelanosis -An
increase in the number of melanocytes
in the epidermis producing increased
levels of melanin e.g lentigo.
melanotic hypermelanosis- No
increase of melanocytes but an
increase in the production of melanin
only e.g melasma.

8. • Hypomelanosis -decrease of melanin in the
epidermis. This reflects mainly two types of
changes:
Melanopenic hypomelanosis- No decrease
in no of melanocytes but a decrease in the
production of melanin only e.g albinism.
Melanocytopenic hypomelanosis -A
decrease in the number or absence of
melanocytes in the epidermis producing no
or decreased levels of melanin e.g vitiligo.

9. Melanogenesis

10. Control of melanogenesis
1. Constitutional skin colour- blacks have
same no of melanocytes as caucasians
but with different activity (production of
melanosomes)blacks-they’re large and
broken down less rapidly.
2. Hormones –melanosome stimulating
hormone by pit. gland (MSH)

11. 3. UV radiation(UVR)-most important stimuli (tanning)
occurs in 2 phases;
 Immediate –exposure to UVA and is due to photo-
oxidation of preformed melanin and rearrangement of
melanosomes
 Delayed –exposure to both UVA & UVB and is due to
 proliferation of melanocytes ,
 Increased tyrosinase activity,
 Increased melanosome production,
 Increased transfer of newly formed melanosomes from
melanocytes to keratinocytes.

12. Pathogenesis of Hypopigmentation
• Hypopigmentation of skin is of two types
1. Melanopenic hypopigmentation-decrease in number
of melanosomes and can be due to
 Anatomical defect of melanocytes-Absent/damaged
melanocytes e.g Vitiligo, Piebaldism, Chemicals like
rubber, Postinflammatory
 Functional defect of melanocytes- Defective
tyrosine metabolism e.g Pityriasis versicolor, Endocrine
disorders, Albinism

13. 2.Nonmelanopenic
hypopigmentation: Due to
abnormalities of vasculature, e.g.,
nevus anemicus.

14. Definition
Vitiligo -an acquired de-pigmenting
disorder of unknown etiology.
It is a chronic skin disease,
characterized by the appearance of
white depigmented macules and
patches due to loss of melanocytes.

15. Etiology
• Exact mechanism not known;
1. Genetic-Genetic factors definitely
important, since 20% of patients have
a positive family history.
• Inheritance may be polygenic

16. 2. Autoimmune hypothesis- evidence
pointing to autoimmune etiology includes;
Frequent association with other
autoimmune disorders like alopecia
areata and thyroid disorders.
Presence of antibodies to melanocytes.
Presence of lymphocytes in early lesions.

17. 3. Neurogenic hypothesis- Segmental
vitiligo is present along a dermatome in
distribution of nerves, suggesting a
neurogenic origin. It has been
hypothesized that a toxin, which
destroys melanocytes, is released at
the nerve endings.

18. • immediate mechanism for the evolving
white macules involves progressive
destruction of selected melanocytes by
cytotoxic T cells.
• Vitiligo may follow cytokine dermatitis.
• Because of differences in the extent and
course of segmental and generalized
vitiligo, the pathogenesis of these two
types is probably different

19. Epidemiology
• Incidence: affects 1-2% of the
world’s population.
• Affects all races.
• Gender: No gender predilection.
• Age: Affects all ages; peak incidence
between 10 and 30 years

20. • In a study to determine clinical and
epidemiological xtics of pts with vitiligo in
Tanzania 122 pts were identified and results
showed;
• Mean age of onset-26.2yrs
• Types observed;
Vitiligo vulgaris-50.8%
Focal and non-segmental-41.8%
Acrofacial-12.3%

21. • Positive family hx -10%
• Commonest sites of initial onset
Head and neck-41.8%
Lower limbs-18%
• Autoimmune dse were noticed in 17.8%
with atopic dermatitis commonest
(9.8%)

22. Clinical presentation
Morphology
Depigmented macules, which are chalky or
milky white.
Sometimes, pigment loss is partial and
occasionally, three shades (trichrome) are
seen in the same lesion—depigmented center,
surrounded by a hypopigmented rim, which in
turn has normal pigmented skin around it-
represents different stages in the evolution.

23. trichrome

24. • Macules have a scalloped(wavy) outline
and form geo-graphical patterns on
fusion with neighboring lesions.
• Hairs in the lesions may remain
pigmented, (leucotrichia) though in the
older lesions the hairs may lose their
pigment.

25. geo-graphical patterns

26. leucotrichia

27. Sites
• Can occur in any part of the body.
Areas subjected to repeated
friction and trauma are
frequently affected, e.g., the
dorsal aspect of hands and feet,
elbows, and knees

28. Patterns
1. Vitiligo vulgaris
Commonest type.
Occurs after second decade.
May be slowly or rapidly progressive.
Family history is frequently present.

29. 2. Segmental vitiligo
Occurs in children.
Not associated with an autoimmune disease.
Depigmentation is dermatomal or quasi-dermatomal.
Most frequently (50%) seen in distribution of
trigeminal nerve (mandibular division).
Has a stable course, i.e., lesions increase initially
(6–12 months) and then remain static.
Leucotrichia on the depigmented areas as well as
away from vitiliginous areas frequently seen.
Margins are feathery.
Distant lesions uncommon.
Poor response to rx.

31. 3. Generalized vitiligo
Extensive lesions.
Variants of generalized vitiligo are:
a) Acrofacial vitiligo
vitiligo predominantly seen periorificially
(around eyes and on lips on the face) and
acral parts (periungual area i.e fingernails
or toenails, palms, and soles). This type of
vitiligo is more resistant to therapy due to
absence of hair in the affected parts.

34. b) Lip-tip vitiligo
 When lips, tip of penis, the vulva and
nipples are involved.
c) Vitiligo universalis
 Widespread vitiligo with only few areas of
normal pigmentation; this type of vitiligo is
often associated with multiple
endocrinopathies.

36. Associations
• Cutaneous disorders: Alopecia areata,
halo nevus, atopic dermatitis, malignant
melanoma, and morphea.
• Endocrine disorders: Diabetes mellitus,
pernicious anemia, Addison’s disease,
hypoparathyroidism, hypothyroidism, and
hyperthyroidism.

37. Course and prognosis
• Onset usually before age of 20 years.
• Usually slowly progressive, but sometimes can
progress rapidly. Segmental vitiligo progresses
initially but stabilizes in about 6 months
• Spontaneous repigmentation is seen in 30% of
patients, especially in the sun-exposed parts.
• Acrofacial vitiligo is more resistant to
treatment.

38. Prognostic factors
Following factors indicate poor response to
treatment:
• Long-standing disease.
• Leucotrichia.
• Acrofacial lesions.
• Lesions on resistant areas, i.e., bony
prominences, non-fleshy areas, non-hairy
areas and mucosae, and on ankles, wrists,
elbows, periungual areas, nipples and areolae
lips, and genitalia.

39. ddx
• Albinism
• Piebaldism
• Nevus achromicus-distribution is also fairly stable
and are nonprogressive hypopigmented patches
• Leucoderma-an acquired condition with localized
loss of pigmentation of the skin that may occur
after any number of inflammatory skin
conditions, burns, intralesional steroid injections,
postdermabrasion, etc.

40. Investigations
1) Wood lamp examination
2) Dermatopathology - Skin biopsy-show normal skin except
for absent melanocytes. Special stain is used to identify
melanocyte
3) Electron microscopy-absence of melanocytes and
melanosome in keratinocytes
4) Lab studies-T4, TSH, Fasting blood glucose, CBC with
indices(pernicious anemia),ACTH stimulation
test(Addison dse suspected)

41. management
Rx depends on
• Age of patient.
• Extent of disease.
• Pattern of disease.
• Cosmetic disability.
• Effect on quality of life

42. General measures
• Reassurance and psychological
support to the patient and
family.
• Explanation about prognosis.

43. Physical modalities of treatment
1.Photochemotherapy
• Photo-chemotherapy is use of psoralens in
combination with UVA exposure (PUVA). It
forms the mainstay of therapy in vitiligo.
Repigmetation is slow.
• Most frequently used psoralens is 8-
methoxypsoralen (8-MOP). Depending on
the extent of disease, either topical (for
localized disease) or systemic (for extensive
disease) therapy is used.

44. 2.Phototherapy
a) Broadband UVB: Is no longer used.
b) Narrow band UVB (311 nm):
• Indications: in extensive disease (>10%).
• Especially indicated in children and in pregnant women and
in patients in whom psoralens are contraindicated.
• Regimen : in gradually increasing doses of UVB, given from
specialized chambers.
• Side effects: generally safe.
c) Excimer laser (308 nm) This is effective but,
as for PUVA, repigmentation is also slow. Produces best
results in the face

45. Medical treatment
1. Steroids
Topical steroids: Are used for:
• Single lesions, (sometimes a few localized lesions)
especially of recent origin.
• As adjuvant to other forms of therapy.
Systemic steroids: Are used:
• When the patient cannot be given photo-
therapy/photochemotherapy.
• In rapidly progressive vitiligo, along with PUVA/PUVA sol.
• In vitiligo, unresponsive to psoralens.
• Side effects to steroids limit their use, though the
recently devised weekly schedule (oral mini pulse6)
probably causes fewer side effects than daily doses.

46. 2. Topical calcineurin inhibitors- Tacrolimus and
pimecrolimus.
• effective in repigmenting vitiligo but only in
sun-exposed areas.
• reported to be most effective when combined
with UVB or excimer laser therapy

47. 3. Depigmenting agents:
• Like monobenzyl ether of hydroquinone.
• Used to depigment the few normally
pigmented areas in patients with
extensive vitiligo.
• Depigmented skin of photo-exposed areas
aggressively protected with sunscreens to
prevent spotty repigmentation

48. Surgical measures
• Indications: At sites poorly responsive to
conventional therapy (ankles and knuckles), in a
patient with stable disease (for at least 6months).
• Techniques:
Melanocyte transfer.
Blister grafting.
Punch grafting.
Split thickness skin grafting.