Inflammation in Melasma: Study of Its Infiltrate and the Expression of Acute and Chronic Mediators
Condition: Melasma
MeSH terms: Melanosis; Inflammation
Study type: Observational

Summary: 
      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.
    

Detailed description: 
      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.
    

Observational model: Case-Crossover
Time perspective: Cross-Sectional
Sampling method: Non-Probability Sample
Study population: 
        Women affected with malar melasma.
      
Biospecimen description: 
      3 mm Skin punch biopsies
    
Keywords: Melasma; Lymphocytes; Macrophages; Mast cells; Interleukin 17; COX-2; Inflammation