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