1. Pigmentation Diseases
Fahad Al Sudairy , M.D.
Consultant Dermatologist & Dermatological Surgeon
Visiting Asst. Professor , College of Medicine

2. Hypo : decrease color
Hyper : increase color
Depigmentation : totally disappearance of the color

3. The skin gets it color from the ( melanin cells ) , these cells located in the Basal layer of the
Epidermis.
So why some people have White color and others have black color ? It depend on the activity of the Melanin cells

7. VITILIGO
Acquired cuetaneous depigmentation due to loss of normal melanocytes.
Notice that it’s depigmentation (no pigmentation) not hypo pigmentation (decreased pigmentation).
Common site :
 Keobner phenomena: Specifically on the leg, elbow and
knee because mostly these are the frictions sites.
Why does it occur? Loss of normal melanocytes. (NO more melanocytes)  due to autoimmune activity
To diagnose Vitiligo:
Woods lamp
Biopsy.

8. Causes and Pathogenesis: Multifactorial.
Genetic background.
A high proportion have positive family history
Autoimmune diseases. ( the main cause )
Anti-melanocyte antibody can be detected in a proportion of
Patients .
There is association with other autoimmune diseases such as:
Pernicious anemia
Thyroid disease
Addison’s disease
DM.
Alopecia areata.
3. Neural .

9. There is no definite treatment for Vitiligo but
Natural course:
– It varies: could be localized, then becomes systemic, could be extensive or not.
There is no rule.
There is no definite treatment for Vitiligo but
it can be well controlled.

11. •Note in the Picture there are some areas with hyper pigmentation, this is called Perifollicular repigmentation, and it is the commonest in Vitiligo, because of presence of melanocytes in the hair matrix.
•This is the commonest form of repigmentation.

12. Distribution pattern (Types)
Focal: 2 or 3 patches.
Unilateral/segmented:
This is what raised the neural theory.
We say it’s segmental or unilateral if it involved a nerve area.
Vulgaris:
In the Frictions sites (as we mentioned)
Universal:
When 90% or more of the body is involved.
In this case we don’t treat, we remove the normal area.

13. Why do we divide the Disease into the previous types :
To determine the management.
Focal and unilateral/segmental → Topical treatment.
Vulgaris → Phototherapy.
Universal → De-pigment the small normal
areas (bleach)

14. Prognosis The prognosis of Vitiligo is very varied:
– In some individuals
only a small area of skin is
affected and spontaneous regimentation occurs.
– In others there is continuing and extensive loss.
There some cases have bad prognosis :
Widely separated  it is difficult to treat.
if the tips are affected ( acral )  it is difficult to treat.

15. Psychosocial effects Pt, with this Disease have many Psychosocial
problems like :
the Society think that their disease is Contagious.
the society think that their disease is due to poor
hygiene.
It can cause great distress in the community if the
patient is dark skinned.
These effects is more among the females.

16. Special studies to be done for the
patient:
Because most probably it is associated with autoimmune diseases we screen for the following:
T4, TSH, FBS → In case the patient has thyroiditis or diabetes.
ANA/Ro/La :
prior to PUVA or NB UVB
Because we need to check if he has photosensitivity or not.
If he has photosensitivity and we applied phototherapy on the patient, it will cause burn.
For e.g. If the patient had SLE and Vitiligo (Due to SLE s/he is photosensitive so, we can’t give her/him phototherapy).

17. Treatment: 1. Sunscreen: 2. Skin camouflage
because their skin is sensitive and has no melanocytes.
Therefore no protection against sun light.
To prevent sunburn, koebnerization and tanning.
It is usually seen with universal type.
2. Skin camouflage

18. 3. Topical (limited treatment)
Corticosteroids: Class 3 topical GlucoCorticoid (steroid) → The drug of choice.
Immunomodulators:
Topical Tacrolimus
not as effective as the steroid but it’s safer.
Outdoor topical psoralen (Topical PUVA).

19. 4. Phototherapy UVA+ Psoralen= PUVA (not used anymore) NBUVA
Excimer laser: narrow band, limited and on specific areas.
Phototherapy should be used for Generalized type.
5. Systemic treatment
Usually Corticosteroids used in Rapidly progressing disease. Rare ?

20. 6. Surgical
Done for resistant cases and the patient is stable for 2 years (to avoid Keobner phenomenon)
types:
Tissue graft : take a whole piece normal skin and implant it over the affected site.
cellular : implant the melanin cells to the affected
Site.

23. 7. Depigmentation (bleaching agent)
Universal type
Side effects ?

27. Notes: So regular follow up With dermatologist is
Required. ( skin cancers ).
If the country is tropical or subtropical the main problem would be skin cancer due to sunrays.
ocular ( poor vision ).

28. Albinism pt has : Squamous cell carcinoma

29. Pathology: notes Melanocytes are present in the basal layer but
the function is abnormal
The melanocytes can be:
Tyrosinase positive: enzyme is present but poorly
functioning
Tyrosinase negative: enzyme is completely missing
Tyrosinase : is the enzyme which controls the
synthesis of melanin in melanocytes

32. Hormonally-stimulated increase in melanogenesis.
The melanocytes number is the same but there is increase in the pigmentation, melanogenesis.
Mainly affect the : Face, checks, malar area
Predisposing factor:
Pregnancy: Usually it spontaneously improved after
pregnancy in most cases).
– OCP .
Darkly pigmented skin (rarely found in fair skinned)
Sun exposure.
Treatment:
sun block
bleaching
stop the Predisposing factors ( OCP for ex )

36. More Examples of Vitiligo
Demonstration of bright white (depigmented) area with Wood’s light illumination.

37. PUVA- Cabinet

38. Is this hypopigmented or depigmented? Use the Wood’s light.

39. Wood’s light lamp

40. Wood’s light exam
Lighter areas without complete loss of pigment are “hypopigmented”

41. Thank you