An In Vivo Model for Postinflammatory Hyperpigmentation

Post-inflammatory Hyperpigmentation Clinical Trial

Official title:

An In Vivo Model for Postinflammatory Hyperpigmentation: Part II

Clinical Trial Details — Status: Completed

Administrative data

• NCT number: NCT02905903
• Other study ID #: IRB #9920 Protocol 1
• Status: Completed
• Phase: N/A
• Start date: February 14, 2016
• Est. completion date: June 21, 2019

Study information

• Verified date: February 2022
• Source: Henry Ford Health System
• Contact: n/a
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial 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.

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.

Recruitment information / eligibility

• Status: Completed
• Enrollment: 30
• Est. completion date: June 21, 2019
• Est. primary completion date: May 16, 2018
• Accepts healthy volunteers: Accepts Healthy Volunteers
• Gender: All
• Age group: 18 Years to 100 Years

Eligibility

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.

Related Conditions & MeSH terms

• Hyperpigmentation
• Post-inflammatory Hyperpigmentation

Intervention

Drug:
• 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.

Locations

Country	Name	City	State
United States	Department of Dermatology, Henry Ford Medical Center, 3031 West Grand Boulevard,	Detroit	Michigan

Sponsors (1)

Lead Sponsor	Collaborator
Henry Ford Health System

Country where clinical trial is conducted

United States, 

References & Publications (6)

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

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. — View Citation

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

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. — View Citation

Széll M, Baltás E, Bodai L, Bata-Csörgo Z, Nagy N, Dallos A, Pourfarzi R, Simics E, Kondorosi I, Szalai Z, Tóth GK, Hunyadi J, Dobozy A, Kemény 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. — View Citation

Taylor S, Grimes P, Lim J, Im S, Lui H. Postinflammatory hyperpigmentation. J Cutan Med Surg. 2009 Jul-Aug;13(4):183-91. Review. — View Citation

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	Optimal TCA concentration for induction of post-inflammatory hyperpigmentation	This will be determined by comparing acne induced PIH and the different concentrations of TCA induced PIH	35 days
Primary	Study genetic components of post-inflammatory hyperpigmentation by evaluating single nucleotide polymorphism and microRNA	These will be evaluated by blood draws and biopsy	35 days
Primary	Study individual risk factors for those susceptible to developing postinflammatory hyperpigmention	These will be evaluated by surveys and comparing subjects with PIH versus no PIH	35 days
Secondary	validate a quality of life questionnaire for post-inflammatory hyperpigmentation.	Administration of PIH surveys	35 days