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Title 1: Pseudomelasma title 2: what you didn t know about melasma

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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Title 1: Pseudomelasma title 2: what you didn t know about melasma

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    1. Title 1: Pseudomelasma title 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?

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