Post Inflammatory Hyperpigmentation PIH

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Although Post-Inflammatory Hyperpigmentation occurs in whites, it is more common in darker pigmented individuals including African Americans or Asians.

Background

Post-Inflammatory Hyperpigmentation (PIH) is a frequently encountered problem and represents the sequelae of various cutaneous disorders as well as therapeutic interventions. [1This acquired excess of pigment can be attributed to various preceding disease processes that affect the skin such as infections, allergic reactions, mechanical injuries, reactions to medications, phototoxic eruptions, trauma (e.g., burns), and inflammatory diseases (e.g., lichen planuslupus erythematosusatopic dermatitis).

Post-Inflammatory Hyperpigmentation can also be seen following treatment with a number of electromagnetic devices such as ultrasound, radiofrequency, lasers, light-emitting diodes, and visible light, as well as secondary to microdermabrasion. Typically, Post-Inflammatory Hyperpigmentation is most severe in patients whose basal cell layer of the epidermis is disrupted such as lichenoid dermatoses or lupus erythematosus.

Pathophysiology

Post-Inflammatory Hyperpigmentation is caused by 1 of 2 mechanisms that result in either epidermal or dermal melanosis. The epidermal inflammatory response (i.e., dermatitis) results in the release and subsequent oxidation of arachidonic acid to prostaglandins, leukotrienes, and other products. These products of inflammation alter the activity of both immune cells and melanocytes. When 35% trichloroacetic acid (TCA) solution was applied to skin, it was found that TCA-induced Post-Inflammatory Hyperpigmentation might serve as a good in vivo model for the study of acne-induced Post-Inflammatory Hyperpigmentation.

Specifically, these inflammatory products stimulate epidermal melanocytes, causing them to increase the synthesis of melanin and subsequently to increase the transfer of pigment to surrounding keratinocytes. Such increased stimulation and transfer of melanin granules results in epidermal hypermelanosis.

On the contrary, dermal melanosis occurs when inflammation disrupts the basal cell layer, causing melanin pigment to be released and subsequently trapped by macrophages in the papillary dermis, also known as pigmentary incontinence.

Fibroblast-derived melanogenic growth factors may be salient in mesenchymal-epithelial interactions modulating melanocyte function.

Etiology

Post-Inflammatory Hyperpigmentation can occur with various disease processes that affect the skin. These processes include allergic reactions, infections, trauma, and phototoxic eruptions. Fractional laser photothermolysis occasionally induces Post-Inflammatory Hyperpigmentation.

Common inflammatory diseases that result in Post-Inflammatory Hyperpigmentation include acne excoriée, lichen planus, systemic lupus erythematosus, chronic dermatitis, and cutaneous T-cell lymphoma, especially erythrodermic variants.

Furthermore, lesions of Post-Inflammatory Hyperpigmentation can darken with exposure to UV light and various chemicals and medications, such as tetracycline, bleomycin, doxorubicin, 5-fluorouracil, busulfan, arsenicals, silver, gold, antimalarial drugs, hormones, and clofazimine.

Epidemiology

Frequency

United States

Post-Inflammatory Hyperpigmentation is a universal response of the skin, but it is more common in individuals with darker skin (Fitzpatrick skin types III to VI). Post-Inflammatory Hyperpigmentation can be caused by any inflammatory process of the skin; however, it is more apparent in photo-induced dermatoses and more severe in lichenoid dermatoses.

International

Internationally, Post-Inflammatory Hyperpigmentation is a common inflammatory response of the skin, developing more commonly in darker skin. Despite their lighter skin colour, certain Asians (from Pacific rim countries such as Japan, Taiwan, China) are more susceptible to developing PIH following one of the inciting factors listed above.

Race

Although Post-Inflammatory Hyperpigmentation occurs in whites, it is more common in darker pigmented individuals including African Americans or Asians.

Sex

Post-Inflammatory Hyperpigmentation occurs with equal incidence in males and females; it has no sexual predilection.

Age

Post-Inflammatory Hyperpigmentation can occur in persons of any age.

Prognosis

Morbidity associated with Post-Inflammatory Hyperpigmentation is related to the underlying inflammatory process that causes Post-Inflammatory Hyperpigmentation. If the hyperpigmentation is located in cosmetically sensitive regions, a significant amount of emotional distress may result.

Post-Inflammatory Hyperpigmentation tends to fade with time and therapy, as previously discussed. Remnants of epidermal hyperpigmentation may persist for indefinite periods, typically 6-12 months, after the initial inflammatory process resolves. Dermal Post-Inflammatory Hyperpigmentation may even persist for years.

Patient Education

Educate patients about the cause of Post-Inflammatory Hyperpigmentation, prolonged therapy, and persistence of hyperpigmented lesions.

Updated on May 04, 2018.

Author: Robert A Schwartz, MD, MPH
Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Coauthors(s): Basil M Hantash MD, PHD, MBA
Medical Director, Advanced Skin Institute

Specialty Editor Board:

Francisco Talavera, PharmD, PhD
Adjunct Assistant Professor, University of Nebraska Medical Centre College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Jeffrey P Callen, MD
Professor of Medicine (Dermatology), Chief Division of Dermatology, University of Louisville School of Medicine

Chief Editor: Dirk M Elston, MD
Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Additional Contributors: Andrea Leigh Zaenglein, MD
Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Centre, Pennsylvania State University College of Medicine

Acknowledgements: Nadia l Kihiczak, MD
Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey Medical School

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