Melasma Clinical Trial
Official title:
Inflammation in Melasma: Study of Its Infiltrate and the Expression of Acute and Chronic Mediators
Melasma is an acquired hyperpigmentary disorder that commonly affects women from Asia and
Latin-America.There is evidence of subclinical inflammation supported by diffuse
spectrometry and by prominent inflammatory cells in affected areas; however this infiltrate
and its inflammatory mediators remains unexplored. Chronic inflammation induces
melanogenesis and angiogenesis; thus, it could be linked to its recurrent nature.Therefore,
the aim of this study is to describe the inflammatory cellular infiltrate, and the
expression of main inflammatory and angiogenic mediators in this condition, as well as to
explore its relationship with severity of disease.
Using histological, histochemistry, immunohistochemistry, and quantitative real-time PCR, we
evaluated melasma lesions from 20 healthy female patients with malar melasma without
specific solar exposure or photoprotection measures within the previous 3 weeks and compared
them to non lesional skin.
Melasma is a frequent, photoinduced, pigmentary disorder among latin-american women. Its
etiology is not completely elucidated; however, there is evidence of a melanogenic paracrine
cytokine network between the melanocyte and other skin cells, including keratinocytes,
fibroblasts, vascular and inflammatory cells, which regulate melanocyte function.
Previous reports in lesional skin have described increased mast cell infiltration in
elastotic areas, presence of a moderate lymphohistiocytic infiltrate, increased vascularity,
and up-regulation of proangiogenic factors. This histological evidence of skin inflammation
is also supported clinically by colorimetry and thermography, and by the improvement of
pigmentation with topical anti-inflammatories.
Photoinduced dermal inflammation might be related to epidermal hyperpigmentation through the
production of melanogenic cytokines, and growth factors, and through the secretion of COX-2
induced prostaglandins by keratinocytes, a mechanism involved in the pathogenesis of
postinflammatory hyperpigmentation which has not been evaluated in melasma.
The aim of this study is to describe the ongoing characteristics of inflammation in this
condition by measuring the cellular infiltrate, the expression of acute and chronic immune
inflammatory mediators, and non-immune inflammation mechanism such as COX-2, as well as to
explore its relationship with severity of disease, elastosis, and melanin staining.
Twenty healthy female patients with malar melasma without specific solar exposure or
photoprotection measures within the previous 3 weeks were enrolled. Disease severity was
estimated using the Melasma Area and Severity Index (MASI). Histological, histochemical,
immunohistochemistry, and quantitative real-time PCR were used to evaluate the presence of
these markers in melasma lesions and compare them to nonlesional skin.
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Observational Model: Case-Crossover, Time Perspective: Cross-Sectional
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