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Postinflammatory Hyperpigmentation

  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
Updated: Jun 10, 2016


Postinflammatory hyperpigmentation (PIH) is a frequently encountered problem and represents the sequelae of various cutaneous disorders as well as therapeutic interventions. This 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 (eg, burns), and inflammatory diseases (eg, lichen planus, lupus erythematosus, atopic dermatitis).

PIH 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, postinflammatory hyperpigmentation is most severe in patients whose basal cell layer of the epidermis is disrupted such as lichenoid dermatoses or lupus erythematosus.



Postinflammatory hyperpigmentation is caused by 1 of 2 mechanisms that result in either epidermal or dermal melanosis. The epidermal inflammatory response (ie, 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 postinflammatory hyperpigmentation might serve as a good in vivo model for the study of acne-induced postinflammatory hyperpigmentation.[1]

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.[2]




United States

Postinflammatory hyperpigmentation is a universal response of the skin, but it is more common in individuals with darker skin (Fitzpatrick skin types III to VI). Postinflammatory 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.


Internationally, postinflammatory hyperpigmentation is a common inflammatory response of the skin, developing more commonly in darker skin. Despite their lighter skin color, 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.


Although postinflammatory hyperpigmentation occurs in whites, it is more common in darker pigmented individuals including African Americans or Asians.


Postinflammatory hyperpigmentation occurs with equal incidence in males and females; it has no sexual predilection.


Postinflammatory hyperpigmentation can occur in persons of any age.



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

Postinflammatory 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 postinflammatory hyperpigmentation may even persist for years.


Patient Education

Educate patients about the cause of postinflammatory hyperpigmentation, prolonged therapy, and persistence of hyperpigmented lesions.

Contributor Information and Disclosures

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

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.


Basil M Hantash, MD, PhD, MBA Medical Director, Advanced Skin Institute

Basil M Hantash, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, Sigma Xi, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

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

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Andrea Leigh Zaenglein, MD Professor of Dermatology and Pediatrics, Department of Dermatology, Hershey Medical Center, Pennsylvania State University College of Medicine

Andrea Leigh Zaenglein, MD is a member of the following medical societies: American Academy of Dermatology, Society for Pediatric Dermatology

Disclosure: Received consulting fee from Galderma for consulting; Received consulting fee from Valeant for consulting; Received consulting fee from Promius for consulting; Received consulting fee from Anacor for consulting; Received grant/research funds from Stiefel for investigator; Received grant/research funds from Astellas for investigator; Received grant/research funds from Ranbaxy for other; Received consulting fee from Ranbaxy for consulting.


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

Nadia I Kihiczak, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

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Photo of a 42-year-old African American woman with macules of postinflammatory hyperpigmentation on the left side of her face as a result of acne excoriée.
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