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

NCT ID: NCT01952379

Last Updated: 2014-11-25

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

COMPLETED

Total Enrollment

20 participants

Study Classification

OBSERVATIONAL

Study Start Date

2013-07-31

Study Completion Date

2014-11-30

Brief Summary

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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

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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.

Conditions

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Melasma

Study Design

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Observational Model Type

CASE_CROSSOVER

Study Time Perspective

CROSS_SECTIONAL

Study Groups

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Melasma

Women affected by symmetric facial malar melasma.

No interventions assigned to this group

Eligibility Criteria

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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.
Minimum Eligible Age

18 Years

Maximum Eligible Age

50 Years

Eligible Sex

FEMALE

Accepts Healthy Volunteers

Yes

Sponsors

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Hospital Central "Dr. Ignacio Morones Prieto"

OTHER

Sponsor Role collaborator

Universidad Autonoma de San Luis Potosí

OTHER

Sponsor Role lead

Responsible Party

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Juan Pablo Castanedo-Cazares

Dermatology department research director

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Juan P Castanedo-Cazares, MD

Role: STUDY_DIRECTOR

Hospital Central "Dr. Ignacio Morones Prieto"

Bertha Torres-Alvarez, MD

Role: STUDY_CHAIR

Hospital Central "Dr. Ignacio Morones Prieto"

Adriana Rodriguez-Arambula, MD

Role: PRINCIPAL_INVESTIGATOR

Hospital Central "Dr. Ignacio Morones Prieto"

Locations

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Hospital Central Dr. Ignacio Morones Prieto

San Luis Potosí City, San Luis Potosí, Mexico

Site Status

Countries

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Mexico

References

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Navarrete-Solis J, Castanedo-Cazares JP, Torres-Alvarez B, Oros-Ovalle C, Fuentes-Ahumada C, Gonzalez FJ, Martinez-Ramirez 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.

Reference Type BACKGROUND
PMID: 21822427 (View on PubMed)

Torres-Alvarez B, Mesa-Garza IG, Castanedo-Cazares 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.

Reference Type BACKGROUND
PMID: 21317614 (View on PubMed)

Moncada B, Sahagun-Sanchez LK, Torres-Alvarez B, Castanedo-Cazares JP, Martinez-Ramirez JD, Gonzalez 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.

Reference Type BACKGROUND
PMID: 19438997 (View on PubMed)

Hernandez-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.

Reference Type BACKGROUND
PMID: 18419607 (View on PubMed)

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. doi: 10.1111/j.1365-4632.2004.02134.x.

Reference Type BACKGROUND
PMID: 15304189 (View on PubMed)

Other Identifiers

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mel-Infla1

Identifier Type: -

Identifier Source: org_study_id