Inflammation in Melasma: Study of Its Infiltrate and the Expression of Acute and Chronic Mediators

Melasma Clinical Trial

Official title:

Inflammation in Melasma: Study of Its Infiltrate and the Expression of Acute and Chronic Mediators

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT01952379
• Other study ID #: mel-Infla1
• Status: Completed
• Phase: N/A
• First received: September 24, 2013
• Last updated: November 22, 2014
• Start date: July 2013
• Est. completion date: November 2014

Study information

• Verified date: November 2014
• Source: Universidad Autonoma de San Luis Potosí
• Contact: n/a
• Is FDA regulated: No
• Health authority: Mexico: Ethics Committee
• Study type: Observational

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 20
• Est. completion date: November 2014
• Est. primary completion date: November 2014
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: Female
• Age group: 18 Years to 50 Years

Eligibility

Inclusion Criteria:

• Women older than 18 years under signed informed consent form.

• Symmetrical and bilateral lesions.

• Melasma with MASI scores greater than 12 points.

Exclusion Criteria:

• Melasma treatment or photoprotection measures within last 2 months.

• Pregnant women or nursing.

• Miscarriage or labor in the last 12 months.

• Menopause

• Coexistence of other pigmentation disorders.

• Infrared radiation exposure.

• Regular exercise or diet restriction.

• Consumption of food supplements.

• Any type of drugs consumption in the last 2 months (i.e anti-inflammatories and hormonal treatments)

• Personal history of keloid or hypertrophic scars.

• Lidocaine allergy.

Study Design

Observational Model: Case-Crossover, Time Perspective: Cross-Sectional

Related Conditions & MeSH terms

• Inflammation
• Melasma

Locations

Country	Name	City	State
Mexico	Hospital Central Dr. Ignacio Morones Prieto	San Luis Potosi

Sponsors (2)

Lead Sponsor	Collaborator
Universidad Autonoma de San Luis Potosí	Hospital Central "Dr. Ignacio Morones Prieto"

Country where clinical trial is conducted

Mexico, 

References & Publications (5)

Espinal-Perez LE, Moncada B, Castanedo-Cazares JP. A double-blind randomized trial of 5% ascorbic acid vs. 4% hydroquinone in melasma. Int J Dermatol. 2004 Aug;43(8):604-7. — View Citation

Hernández-Barrera R, Torres-Alvarez B, Castanedo-Cazares JP, Oros-Ovalle C, Moncada B. Solar elastosis and presence of mast cells as key features in the pathogenesis of melasma. Clin Exp Dermatol. 2008 May;33(3):305-8. doi: 10.1111/j.1365-2230.2008.02724.x. — View Citation

Moncada B, Sahagún-Sánchez LK, Torres-Alvarez B, Castanedo-Cázares JP, Martínez-Ramírez JD, González FJ. Molecular structure and concentration of melanin in the stratum corneum of patients with melasma. Photodermatol Photoimmunol Photomed. 2009 Jun;25(3):159-60. doi: 10.1111/j.1600-0781.2009.00425.x. — View Citation

Navarrete-Solís J, Castanedo-Cázares JP, Torres-Álvarez B, Oros-Ovalle C, Fuentes-Ahumada C, González FJ, Martínez-Ramírez JD, Moncada B. A Double-Blind, Randomized Clinical Trial of Niacinamide 4% versus Hydroquinone 4% in the Treatment of Melasma. Dermatol Res Pract. 2011;2011:379173. doi: 10.1155/2011/379173. Epub 2011 Jul 21. — View Citation

Torres-Álvarez B, Mesa-Garza IG, Castanedo-Cázares JP, Fuentes-Ahumada C, Oros-Ovalle C, Navarrete-Solis J, Moncada B. Histochemical and immunohistochemical study in melasma: evidence of damage in the basal membrane. Am J Dermatopathol. 2011 May;33(3):291-5. doi: 10.1097/DAD.0b013e3181ef2d45. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Other	Correlation between inflammation markers and pigmentation	Analyze inflammation parameters and to correlate data with melanin, elastosis, and clinical parameters of severity.	Single time measurement	No
Primary	Inflammatory cellular infiltrate	Determine by immunohistochemistry common inflammatory cellular infiltrate in melasma lesions and non affected skin (i.e CD1, CD68, CD4, CD8).	Single time measurement	No
Secondary	Acute inflammatory mediators	Determine by immunohistochemistry, and PCR techniques, the expression of IL1 alpha, IL1 beta, IL1 alpha receptor, and VEGF in melasma lesions and non affected skin.	Single time measurement	No
Secondary	Chronic inflammatory mediators	Determine by immunohistochemistry, and PCR techniques, the expression of COX-2, and IL-17 in melasma lesions and non affected skin.	Single time measurement	No