eMedicine Specialties > Dermatology > Diseases of Pigmentation

Postinflammatory Hyperpigmentation

Author: Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Coauthor(s): Nadia I Kihiczak, MD, Staff Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey Medical School
Contributor Information and Disclosures

Updated: Mar 28, 2008

Introduction

Background

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; these processes include infections, allergic reactions, mechanical injuries, reactions to medications, phototoxic eruptions, trauma (eg, burns), and inflammatory diseases (eg, lichen planus, lupus erythematosus, atopic dermatitis). Typically, PIH is most severe in patients with lichenoid dermatoses in which the basal cell layer of the epidermis is disrupted.

Medscape's Aesthetic Medicine Resource Center and eMedicine's Skin Lightening and Depigmenting Agents article may be of interest.

Pathophysiology

PIH is caused by 1 of 2 mechanisms that result in either epidermal melanosis 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. 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.

Frequency

United States

PIH is a universal response of the skin, but it is more common in pigmented, darker skin. PIH 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, PIH is a common inflammatory response of the skin, developing more commonly in darker skin.

Mortality/Morbidity

  • Morbidity associated with PIH is related to the underlying inflammatory process that causes PIH.
  • To the author's knowledge, no cases of mortality have been associated with PIH.

Race

Although PIH occurs in whites, it is more common in dark-skinned individuals (eg, African Americans).

Sex

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

Age

PIH can occur in persons of any age.

Clinical

History

A diagnosis of PIH should be considered if a history of a preceding pathologic process or injury to the affected area of hyperpigmentation is present.

Physical

  • The distribution of the hypermelanotic lesions depends on the location of the original inflammatory dermatosis.
  • The color of the lesions ranges from light brown to black, with a lighter brown appearance if the pigment is within the epidermis (ie, epidermal melanosis) and a darker gray appearance if lesions contain dermal melanin (ie, dermal melanosis).

Causes

  • PIH 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 PIH.1
  • Common inflammatory diseases that result in PIH include acne excoriée, lichen planus, systemic lupus erythematosus, chronic dermatitis, and cutaneous T-cell lymphoma, especially erythrodermic variants.
  • Furthermore, lesions of PIH 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.

More on Postinflammatory Hyperpigmentation

Overview: Postinflammatory Hyperpigmentation
Differential Diagnoses & Workup: Postinflammatory Hyperpigmentation
Treatment & Medication: Postinflammatory Hyperpigmentation
Follow-up: Postinflammatory Hyperpigmentation
Multimedia: Postinflammatory Hyperpigmentation
References
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References

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  4. Yoshimura K, Harii K, Aoyama T, Shibuya F, Iga T. A new bleaching protocol for hyperpigmented skin lesions with a high concentration of all-trans retinoic acid aqueous gel. Aesthetic Plast Surg. Jul-Aug 1999;23(4):285-91. [Medline].

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Further Reading

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Keywords

postinflammatory hypermelanosis, melanotic hyperpigmentation, PIH, dermal melanosis, epidermal melanosis, skin inflammation, hyperpigmentation

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Contributor Information and Disclosures

Author

Robert A Schwartz, MD, MPH, Professor and Head of Dermatology, Professor of Medicine, Professor of Pediatrics, Professor of Pathology, Professor of Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

Coauthor(s)

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.

Medical Editor

Günter Burg, MD, Professor and Chairman Emeritus, Department of Dermatology, University of Zürich School of Medicine; Delegate of The Foundation for Modern Teaching and Learning in Medicine Faculty of Medicine, University of Zürich, Switzerland
Günter Burg, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, and Pacific Dermatologic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

David F Butler, MD, Professor of Dermatology, Texas A&M University College of Medicine; Director, Division of Dermatology, Scott and White Clinic; Director Dermatology Residency Training Program, Scott and White Clinic
David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa
Disclosure: 3M Pharmaceutical Grant/research funds Other; Graceway Pharmaceuticals Grant/research funds Other

Managing Editor

Jeffrey P Callen, MD, Professor of Medicine, 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, and American College of Rheumatology
Disclosure: Amgen Honoraria Consulting; Abbott Honoraria Consulting; Electrical Optical Sciences Honoraria Consulting; Centocor Honoraria Consulting

CME Editor

Catherine Quirk, MD, Clinical Assistant Professor, Department of Dermatology, Brown University
Catherine Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology
Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

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