Post-inflammatory Hyperpigmentation and Hypopigmentation (post-inflammatory hypermelanosis, post-inflammatory hypomelanosis)

Are You Confident of the Diagnosis?

What you should be alert for in the history

One should suspect postinflammatory hyperpigmentation (PIH) and hypopigmentation when a patient describes antecedent injury or inflammation of the affected area.

Characteristic findings on physical examination

Characteristic findings include hyper- and hypopigmented macules corresponding to areas of prior inflammation or injury, which may have an indistinct outline, in contrast to the discrete border seen in patients with vitiligo (depigmentation) or cafe au lait macules (hyperpigmentation). Epidermal hyperpigmentation manifests as light brown to black pigmentation, whereas dermal hypermelanosis confers a darker grey appearance to lesions. Figure 1 demonstrates post-inflammatory hyperpigmentation after acne on the back of a patient. Figure 2 is an image of post-inflammatory hypopigmentation from eczema on the arm of a child.

Figure 1.

Post-inflammatory hyperpigmentation after acne.

Figure 2.

Post-inflammatory hypopigmentation from eczema.

Expected results of diagnostic studies

Pigmentary changes may be more difficult to visualize in patients with lighter skin types. Wood’s (ultraviolet or black light) lamp allows one to differentiate between epidermal versus dermal hypermelanosis – areas of epidermal involvement will become more discrete under the lamp. Hypopigmented macules will appear more discrete under the Wood’s lamp. When noninvasive measures are equivocal, a biopsy may help to clarify the underlying etiology. In addition to standard hematoxylin-eosin staining, a Fontana-Masson silver stain for melanin can delineate the location of involvement (epidermis vs demis).

Diagnosis confirmation

Several skin conditions can mimic PIH. In the absence of an antecedent insult, the following disorders should be considered:

Medications: Carefully examine the patient’s medication list. Several medications, such as minocycline, can deposit in the dermis and appear to be PIH.

Acanthosis nigricans: will manifest as hyperpigmented, velvety plaques generally distributed to intertriginous regions.

Melasma: may present with tan to brown hyperpigmented macules (blue or black if there is dermal involvement) in malar, mandibular, or on the central face. Female patients with melasma may experience this progressive hyperpigmentation if they are on oral contraceptive pills or are pregnant. The key is that these patients will deny a history of trauma or inflammation to the area prior to the onset of hyperpigmentation.

Addison disease: may present with generalized cutaneous and mucous membrane hyperpigmentation that is worsened by sun-exposure. These patients will generally complain of malaise, weakness, anorexia, and weight loss.

Tinea versicolor: Patients may complain of hyperpigmented macules with fine scale in the winter months that become hypopigmented and more noticeable with sun exposure in the summer months. Scraping the area and performing a KOH examination under the microscope will provide evidence for presence of yeast filaments and spores.

Lichen amyloidosis/Macular amyloidosis: Both present with intense pruritus; however, lichen amyloidosis generally affects the lower extremities and is papular, whereas macular amyloidosis presents above the waist on the back and arms and is more patch-like.

Lichen planus: may also present with pruritus. Patients usually have hyperpigmented violaceous papules and plaques on flexor limbs and reticulated plaques on oral mucosa.

Poikiloderma of Civatte: presents as a symmetric, red-brown discoloration of bilateral lateral neck from chronic sun exposure. Notably, the anterior neck is spared.

Erythema dyschromicum perstans: is characterized by a progressive macular hyperpigmentation (ashy-grey) and can mimic lichen planus.

The differential for post-inflammatory hypopigmentation includes:

Vitiligo: Discrete macules are depigmented with well-circumscribed borders, unlike the hazy borders that often characterize post-inflammatory pigmentary changes.

Nevus depigmentosus: This congenital condition presents as hypopigmented macules or patches that do not progress in size or distribution after early childhood.

Idiopathic guttate hypomelanosis: Hypopigmented 2-5 mm macules may first appear on anterior legs and then progress to arms of middle-aged women and elderly patients.

Progressive macular hypomelanosis: Poorly circumscribed hypopigmented macules and patches have a distribution on the trunks of patients with Fitzpatrick skin types IV-VI. Generally there is no associated pain, itch, or antecedent inflammation.

Who is at Risk for Developing this Disease?

Post-inflammatory hyperpigmentation (PIH) and post-inflammatory hypopigmentation commonly occur in patients of all ages and genders but are more clinically obvious and longer lasting in patients with skin of color (Fitzpatrick skin types IV-VI). While the exact prevalence is unknown, PIH has been shown to be the third most common complaint for which African American patients see their dermatologist, after acne and atopic dermatitis, both of which can cause PIH.

What is the Cause of the Disease?

Post-inflammatory hyperpigmentation (PIH) and hypopigmentation are responses of pigmented skin to a variety of exogenous and endogenous insults. It involves deposition of excessive pigment from activated melanocytes in the epidermis and/or dermis in response to inflammation or injury. UV exposure can cause PIH lesions to darken. Table I outlines skin disorders that can lead to post-inflammatory pigmentary changes. Table I. Causes of postinflammatory pigmentary changes

Table I.
InfectionsFungal (eg, tinea corporis, tinea versicolor, intertrigo)Herpes (zoster, simplex)Impetigo
Inflammatory dermatosesAllergic contact dermatitisLichen planusLupus erythematosusMycosis fungoidesNummular eczemaPsoriasisVasculitisVesicobullous diseases
Medications5-fluorouracilAntimalarial drugsArsenicBleomycinBusulfanClofazimineDoxorubicinGoldOral contraceptives    SilverTetracycline
TraumaBurnsIatrogenic     Chemical peels     Cryotherapy     Dermabrasion     Laser therapyMechanical injury
MiscellaneousAcnePityriasis albaSeborrheic dermatitis

Modified from Ruiz-Maldonado, 1997


The pathogenesis of PIH is based on both inflammatory mechanisms and variability in patients’ inherited tendency for hyperpigmentation. Release of inflammatory mediators (eg, histamine) and cytokines (eg, prostaglandins, leukotrienes) from inflammatory cells, keratinocytes, and melanocytes stimulates increased melanin production and consequent epidermal hypermelanosis. The dermal variant of PIH results from disruption of the basal cell layer by exuberant inflammation, which induces engulfment and trapping of pigment by macrophages in the papillary dermis (ie, pigment incontinence).

Systemic Implications and Complications

Systemic complications may be related to PIH if caused by an underlying disorder such as lupus erythematosus, vasculitis, or mycosis fungoides. Rarely, genetic or acquired syndromes may present with pigmentary anomalies that could easily be confused with PIH or hypopigmentation, examples being Addisonian-type hyperpigmentation in Graves disease or tinea versicolor-like hypopigmentation in epidermodysplasia verruciformis.

Treatment Options

Because it is hard to predict the progression of postinflammatory pigmentation changes, treatment of hyper- and hypo-pigmentation can be difficult and time-consuming. Unfortunately, the conditions may frequently be refractory to any treatment at all. Topical treatments will mainly improve hyperpigmentation localized to the epidermis. Mild areas of hypopigmentation may regain normal coloration within a few weeks, but it may take years before severely hypopigmented areas repigment. The treatment options for post-inflammatory pigmentary changes are summarized in Table II.

Table II.
Hyperpigmentation Hypopigmentation
Broad-spectrum sunscreen and sun avoidance for all patients.
TopicalFirst Line


Azaleic acid

Hydroquinone 4%

Kojic acid


Ascorbic acid

Licorice extract


N-acetyl glucosamine





Fluocinolone acetonide 0.01%, hydroquinone 4%, tretinoin 0.05% (Triluma)


Chemical peels

Glycolic acid

Lactic acid

Salicylic acid

Laser therapy

Physical8-methoxypsoralen 0.1% + Ultraviolet A (PUVA)Phototherapy (UVA, UVB)Sun-exposure

Optimal Therapeutic Approach for this Disease

Identify and treat the underlying disease. Once all inflammation has subsided, treat post-inflammatory hyperpigmentation with depigmenting agents, such as 4% hydroquinone twice daily, along with sun avoidance and sunscreens. Hypopigmentation can be treated with sun exposure. Establish reasonable treatment expectations with patients and reinforce that resolution takes time, usually weeks to months.

Patient Management

One of the greatest limitations in the management of PIH is lack of a standardized outcome measure to assess treatment response. As such, reasonable treatment expectations should be discussed with patients before the initiation of treatment. Management of pigmentary changes is a long process and patients should be made aware of the possibility of not experiencing any improvement of their condition.

Unusual Clinical Scenarios to Consider in Patient Management

This would depend on the underlying problem, an example being Addisonian-type hyperpigmentation seen in Graves disease that would abate with the resolution of the hyperthyroid state.

What is the Evidence?

Davis, EC, Callender, VD. “Postinflammatory hyperpigmentation: a review of the epidemiology, clinical features, and treatment options in skin of color”. J Clin Aesthet Dermatol. vol. 3. 2010. pp. 20-31. (This literature review outlines epidemiologic studies on PIH and offers a guide for diagnosis and treatment of PIH in patients with Fitzpatrick skin types IV-VI.)

Halder, RM. “The role of retinoids in the management of cutaneous conditions in blacks”. J Am Acad Dermatol. vol. 39. 1998. pp. S98-103. (The authors discuss the utility of topical retinoids for treatment of some of the most common dermatologic complaints of African American patients [including acne, eczema, pigmentary disorders, and keloids].)

Ruiz-Maldonado, R, Orozco-Covarrubias, ML. “Postinflammatory hypopigmentation and hyperpigmentation”. Semin Cutan Med Surg. vol. 16. 1997. pp. 36-43. (This article proposes the concept of “individual chromatic tendency” and discusses diagnosis and treatment of postinflammatory pigmentary disorders. Table I of this chapter is adapted from the table within this article.)

White, GM, Cox, NH, White, GM, Cox, NH. “Pigmentary disorders”. Diseases of the skin. 2006. (This book chapter on pigmentary disorders discusses etiologies for hyper- and hypopigmentation, thus offering a very useful differential for postinflammatory pigmentary changes.)

Grimes, P, Nordlund, JJ, Pandya, AG, Taylor, S, Rendon, M, Ortonne, J-P. “Increasing our understanding of pigmentary disorders”. J Am Acad Dermatol. vol. 54. 2006. pp. S255-S261. (This article outlines the molecular biology of dyschromias, describes etiologies of pigmentary disorders [including genetic and systemic diseases, chemical exposures, and drug-related causes], and ends with a discussion of two primary pigmentary disorders [melasma, absent lentigines].)

Pandya, AG, Guevara, IA. “Disorders of hyperpigmentation”. Dermatol Clin. vol. 18. 2000. pp. 91-8. (The authors review the diagnosis and treatment of several pigmentary disorders, including post-inflammatory hyperpigmentation [and melasma, drug-induced hyperpigmentation, and erythema dyschromicum perstans].)

Taylor, SC, Burgess, CM, Callender, VD. “Postinflammatory hyperpigmentation: evolving combination treatment strategies”. Cutis. vol. 78. 2006 August. pp. 6-19. (This article discusses combination therapy for treatment of PIH [such as HQ 4%-retinol 0.15% in a microsponge formulation; HQ 4%-retinol 0.3%; mequinol 2%-tretinoin (RA) 0.01%; and fluocinolone acetonide (FA) 0.01%, HQ 4%, and RA 0.05%].)

Stratigos, AJ, Katsambas, AD. “Optimal management of recalcitrant disorders of hyperpigmentation in dark-skinned patients”. Am J Clin Dermatol. vol. 5. 2004. pp. 161-8. (This is another article that outlines treatment modalities employed for managing pigmentary disorders (ie melasma, PIH, drug-induced hyperpigmentation, and erythema dyschromia perstans) in patients with darker Fitzpatrick skin types.)

Relyveld, GN, Menke, HE, Westerhof, W. “Progressive macular hypomelanosis: an overview”. Am J Clin Dermatol. vol. 8. 2007. pp. 13-9. (This review article discusses the presentation, natural history, etiology, and treatment of progressive macular hypopigmentation.)