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What is your diagnosis?. . Picture 1. . How would you treat?. . Picture 2. . Melasma is not homogenous The site of melasma is differentMelasma may respond to treatmentWhat is the diagnosis then?. . Pigmentary Demarcation Lines (PDL). Normal Pigmentation.
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1. Title 1: Pseudomelasmatitle 2: what you didn’t know about melasma! By
Dr Abdullah Al Somari
Dr Saad Al Mohizea
Dr Ghada Bin Seef
2007
2.
What is your diagnosis?
3. Picture 1
4.
How would you treat?
5. Picture 2
6. Melasma is not homogenous
The site of melasma is different
Melasma may respond to treatment
What is the diagnosis then?
7.
Pigmentary Demarcation Lines
(PDL)
8. Normal Pigmentation Pigmentation is generally perceived as an adaptation response of humans to UV radiation
considerable variation even in a single race:
skin color of Caucasians ranges from fair to brown
The constitutive pigmentation also differs:
females having a lighter color than males
Distribution of melanin is also uneven:
in Caucasians the upper thigh is the darkest and the lumbar, the lightest area
9. PDL Pigmentary demarcation lines (PDL) were first described by Matzumoto on the upper and lower limbs of Japanese people in 1913
Also known as Futcher’s or Voight’s lines
Pigmentary demarcation lines are borders of abrupt transition between more deeply pigmented skin and that of lighter pigmentation
They do not correspond to Blaschko’s lines or dermatomal lines but to voigt’ lines
10. Pathogenesis? More common in females
More common in darker races
PDLs are dominantly inherited
Phylogenetic importance?
Cutaneous Mosaicism?
Neural influence?
Strong hormonal influence
11. Mosaicism? Two types: functional mosaics, resulting from X inactivation or lyonization,and genomic mosaics, caused by postzygotic autosomal mutations.
Could explain the familial aggregation and the female preponderance
Either the maternal or paternal X chromosome is lyonized (deactivated) randomly, but it remains the same for all the descendants of that cell
Because of this process the heterozygous state of various X-linked gene defects may lead to a cutaneous mosaic.
Streaky or patchy pigmentation may be a clue to the presence of mosaicism
12. HORMONAL INFLUENCE Hormonal influence over pigmentary characteristics has been documented
preponderance of females exhibiting these lines could be related to sex hormones
High levels of Estrogen Progesterone and MSH
Persistance of PDL after pregnancy with estrogen therapy
Hormones are probably aggravating PDL and not causing it
13. Neural theory Maleville concluded that the axial-neural theory is the most commonly accepted in opposition to that of pigmentary mosaicism as defended by Krivo
They coincide with cutaneous nerve distribution.
Compression by the enlarged uterus of peripheral nerves issuing at S1–S2 is proposed as a mechanism of these changes in type B
14. Neural theory NEURAL control of pigmentation?
Differences in melanogenesis noted across these lines my correspond to an absence or reduced expression of certain proteins between nerve endings in neural territories controlled by different homeobox gene during development
15. PDL is common! Body PDL
Pigmentary changes are seen in nearly 85% of pregnant women
About 25% of black Africans show sharply demarcated pigmentary lines either at the anterolateral upper arm or posteromedial part of the lower limbs (Type A and B)
More in females (except type c with slight male preponderance)
Can be associated with an erythematous component
PDL over the face
(6%) were found to have demarcation lines on the face (indians).
lines were far more common in women (9%) than in men (0.75%)
Positive family history in (61%)
16. History AND Examination Asymptomatic
Strong family history (sister, mother)
Homogeneous and sharply demarcated
Symmetrical
Associated with thyroid disease?
ONSET AND COURSE
All the facial PDL’S first made their appearance around puberty Whereas the classical types presentesd Earlier in childhood
Facial PDLs become more apparent with advancing age.
17. SKIN BIOPSY Unremarkable except for hyperpigmentation of the basal cell layer without inflammatory infiltrate or melanophages in the upper dermis
18. Old groups(non facial)
20. New groups (facial PDL’s)
21. Group F ‘V’ shaped or as an inverted cone on the lateral aspect of the face in the region between the malar prominence and the temple.
Bilateral and symmetrical.
In about 20% of cases these patches merged with infraorbital pigmentation
22. Group G Two inverted cones lying in close proximity, looking like the letter W
Both patterns F and G showed evenly diffuse pigmentation with a rather well defined margin
no satellite lesions, speckling, increased hair or any textural change
23. Group H Two symmetrical linear bands of hyperpigmentation
extending from just below the angle of the mouth to the lateral aspects of the chin.
There might be an additional band running just below and parallel to the lower lip, joining the two oro-mental bands
24. Differential diagnosis melasma
post-inflammatory pigmentation
nevus of Ota or Ito
melanocytic nevus
Tuberus sclerosis
25. Clinical pearls Melasma occurs as a blotchy pigmentation over the malar areas just below the PDL F, and may involve other parts like the nose, supra-orbital areas or upper lips.
Dermal nevi often have a bluish or greenish black color and a scleral component.
26. Treatment PDL is a treatment challenge
Even if they respond to peels or laser they recur promptly within months
Better left alone?
Camouflage
Effective treatment of futcher’s line with alexandrite laser?
31. White with black stripes or black with white stripes?