An In Vivo Model for Postinflammatory Hyperpigmentation

NCT ID: NCT02905903

Last Updated: 2022-03-02

Basic Information

• Recruitment Status: COMPLETED
• Clinical Phase: NA
• Total Enrollment: 30 participants
• Study Classification: INTERVENTIONAL
• Study Start Date: 2016-02-14
• Study Completion Date: 2019-06-21

Brief Summary

Post-inflammatory hyperpigmentation (PIH) is an acquired hypermelanosis that occurs after cutaneous inflammation or injury that frequently affects darker skinned populations. Previously, a model of 35% TCA-induced PIH was validated against acne induced PIH, which has value in product testing for the treatment of PIH. In this second phase of the study, the investigators would like to determine if a lower concentration of TCA-induced PIH is comparable to acne-induced PIH.

Detailed Description

Post-inflammatory hyperpigmentation (PIH) is an acquired hypermelanosis that occurs after cutaneous inflammation or injury. This process can occur in all skin types but more frequently affects darker skinned patients, such as African-Americans, Hispanics, Asians, Native Americans, Pacific Islanders and those of Middle Eastern descent. PIH can occur after infection, allergic reactions, contact dermatitis, some medications, burns, following procedures, or inflammatory disease such as acne. In skin of color, PIH frequently occurs in resolving acne lesions and can persist for months after the acne lesion itself has disappeared. In many cases, the resulting PIH can be more distressing than the original insult.

During the first phase of this study, the investigators investigated the clinical, spectroscopic and histologic characteristics of acne-induced PIH versus irritant induced PIH using Trichloroacetic acid (TCA), 35% solution. From this initial study, the investigators concluded that the similarity of Investigator's Global Assessment scores, and spectroscopic measurements using Diffuse Reflectance Spectroscopy and Colorimetry in both acne and TCA-induced PIH at Day 28 suggest that TCA-induced PIH could be a reproducible model for acne induced PIH.

MicroRNAs (miRNAs) are a class of small non-coding RNA molecules that regulate the expression of multiple genes at the post-transcriptional level through degradation and translation of target mRNAs. In the initial study, the investigators hypothesized that miRNAs derived from melanocytes and immune cells during PIH development could be detected in tissue and serve as novel biomarkers for PIH and making appropriate therapeutic decisions. To test this hypothesis, the investigators first examined miRNA gene expression profiles during PIH development using different models, and then evaluated miRNAs profiles in acne- induced PIH, TCA- induced PIH and normal skin. The investigators have defined some miRNAs that potentially are involved in PIH development and may be also serve as the biomarkers for PIH. The investigators found that there were 19 miRNA changes in acne-induced PIH versus normal skin, while 43 miRNA changes in TCA-inducedPIH versus normal skin. Interestingly, about 80% changed genes in acne were included in TCA-mediated miRNA changes, suggesting TCA can partially mimic acne-PIH.

Overall, this initial model for PIH, using TCA, serves as a foundation to better understand and improve our ability to manage PIH. In this next phase of the study, the investigators will refine this in vivo model for PIH by determining the optimal concentration of TCA to induce PIH.

Conditions

Post-inflammatory Hyperpigmentation

Study Design

• Allocation Method: NA
• Intervention Model: SINGLE_GROUP
• Primary Study Purpose: OTHER
• Blinding Strategy: NONE

Study Groups

Trichloroacetic Acid

Intervention-Apply 4 concentrations of TCA (20%, 25%, 30%, 35%) to the buttocks to two spots each (total of 8 lesions) and following characteristics of these lesions and comparing them to acne induced PIH during the course of the study. Comparisons will be made using Investigators Global Assessment scoring of hyperpigmentation and erythema, colorimetry, photography, and biopsies

Group Type: OTHER

Tricholoacetic Acid (TCA)

Intervention Type: DRUG

We will be applying 4 concentrations of TCA (20%, 25%, 30%, 35%) to the buttocks to two spots each (total of 8 lesions) and following characteristics of these lesions and comparing them to acne induced PIH during the course of the study.

Interventions

Tricholoacetic Acid (TCA)

We will be applying 4 concentrations of TCA (20%, 25%, 30%, 35%) to the buttocks to two spots each (total of 8 lesions) and following characteristics of these lesions and comparing them to acne induced PIH during the course of the study.

Intervention Type: DRUG

Eligibility Criteria

Inclusion Criteria

• Patients with types I-VI skin
• Minimum age of 18 years
• Able to understand requirements of the study and risks involved
• Able to sign a consent form.
• Existing truncal acne pustules (at least two on the trunk) with or without history of post-inflammatory hyperpigmentation

Exclusion Criteria

• Patients with a recent history of vitiligo, melasma, and other disorders of pigmentation with the exception of PIH judged to be clinically significant by the investigator
• Patients with a history of keloids
• Patients with a history of cystic acne or acne conglobata
• Patients on systemic antibiotics or keratolytics (isotretinoin, etc), or topical antibiotics or keratolytic use (retinoids, benzoyl peroxide) over target areas who are unwilling to stop these medications for the duration of the study.

• Minimum Eligible Age: 18 Years
• Maximum Eligible Age: 100 Years
• Eligible Sex: ALL
• Accepts Healthy Volunteers: Yes

Sponsors

Henry Ford Health System

OTHER

Sponsor Role: lead

Responsible Party

Iltefat Hamzavi

Senior Staff Physician

Responsibility Role: PRINCIPAL_INVESTIGATOR

Principal Investigators

Iltefat Hamzavi, MD

Role: PRINCIPAL_INVESTIGATOR

Henry Ford Hospital

Locations

Department of Dermatology, Henry Ford Medical Center, 3031 West Grand Boulevard,

Detroit, Michigan, United States

Countries

United States

References

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Reference Type: BACKGROUND

PMID: 19706225 (View on PubMed)

Davis EC, Callender VD. Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color. J Clin Aesthet Dermatol. 2010 Jul;3(7):20-31.

Reference Type: BACKGROUND

PMID: 20725554 (View on PubMed)

Baumann L, Rodriguez D, Taylor SC, Wu J. Natural considerations for skin of color. Cutis. 2006 Dec;78(6 Suppl):2-19.

Reference Type: BACKGROUND

PMID: 17354519 (View on PubMed)

Grimes PE, Stockton T. Pigmentary disorders in blacks. Dermatol Clin. 1988 Apr;6(2):271-81.

Reference Type: BACKGROUND

PMID: 3378372 (View on PubMed)

Motokawa T, Kato T, Hashimoto Y, Katagiri T. Effect of Val92Met and Arg163Gln variants of the MC1R gene on freckles and solar lentigines in Japanese. Pigment Cell Res. 2007 Apr;20(2):140-3. doi: 10.1111/j.1600-0749.2007.00364.x.

Reference Type: BACKGROUND

PMID: 17371441 (View on PubMed)

Szell M, Baltas E, Bodai L, Bata-Csorgo Z, Nagy N, Dallos A, Pourfarzi R, Simics E, Kondorosi I, Szalai Z, Toth GK, Hunyadi J, Dobozy A, Kemeny L. The Arg160Trp allele of melanocortin-1 receptor gene might protect against vitiligo. Photochem Photobiol. 2008 May-Jun;84(3):565-71. doi: 10.1111/j.1751-1097.2008.00296.x. Epub 2008 Feb 11.

Reference Type: BACKGROUND

PMID: 18282185 (View on PubMed)

Other Identifiers

IRB #9920 Protocol 1

Identifier Type: -

Identifier Source: org_study_id