INTRODUCTION
Post inflammatory hyperpigmentation (PIH) is an acquired hyper-melanosis typically arising following inflammatory lesions. It is one of the most common dermatologic complaints, which may develop in all skin types, however, higher prevalence is seen in patients with Fitzpatrick skin types IV-VI. The etiology underlying PIH can either be an exogenous source (allergy, irritation, contact dermatitis, dermabrasion, laser therapy or burns), an endogenous factor (primary inflammatory or bullous dermatosis) or even induced by an infectious agent such as herpes zoster virus infection. Morphologic pattern and degree of pigmentation vary depending on causative factors and melanin distribution in the epidermis, dermis or both.1,2,3
PIH typically manifests as macules or patches in the same distribution in previous areas of inflammation, which can be classified as two clinical forms: epidermal and/or dermal. In epidermal PIH, melanocytes are activated, and release melanin resulting in tan brown or dark brown appearance and may take months to years to resolve. Dermal PIH includes activation of basal keratinocytes, which also release melanin, and present as dark brown to blue-grey discoloration that may either be permanent or resolve over an extended period of time if not treated. Differentiating between the two is difficult, and PIH is probably a result of the combination of both epidermal and dermal lesions.4 The degree of PIH varies depending on the etiological factors, skin type or “chromatic tendency” as well as exposure to UV light, certain medications and cutaneous injuries (trauma or even shaving).1,2,5,6 The discoloration is determined by the distribution and depth of pigment within the skin layers.
The pathogenesis of PIH is often related to an increase in melanin synthesis and/or irregular pigment dispersion resulting from cutaneous inflammation. It is considered the end result of: melanocyte proliferation, melanin synthesis and increased activation of tyrosinase coupled with transfer of melanosomes to neighboring keratinocytes. Although the exact mechanism is not yet fully understood, the rise in melanocyte activity and proliferation has been known to be stimulated by inflammatory mediators such as reactive oxygen species, prostaglandins and leukotrienes.1,5
PIH management is commonly addressed by prevention of the inflammatory dermatosis. A variety of medication and procedures in addition to photoprotection have been shown
PIH typically manifests as macules or patches in the same distribution in previous areas of inflammation, which can be classified as two clinical forms: epidermal and/or dermal. In epidermal PIH, melanocytes are activated, and release melanin resulting in tan brown or dark brown appearance and may take months to years to resolve. Dermal PIH includes activation of basal keratinocytes, which also release melanin, and present as dark brown to blue-grey discoloration that may either be permanent or resolve over an extended period of time if not treated. Differentiating between the two is difficult, and PIH is probably a result of the combination of both epidermal and dermal lesions.4 The degree of PIH varies depending on the etiological factors, skin type or “chromatic tendency” as well as exposure to UV light, certain medications and cutaneous injuries (trauma or even shaving).1,2,5,6 The discoloration is determined by the distribution and depth of pigment within the skin layers.
The pathogenesis of PIH is often related to an increase in melanin synthesis and/or irregular pigment dispersion resulting from cutaneous inflammation. It is considered the end result of: melanocyte proliferation, melanin synthesis and increased activation of tyrosinase coupled with transfer of melanosomes to neighboring keratinocytes. Although the exact mechanism is not yet fully understood, the rise in melanocyte activity and proliferation has been known to be stimulated by inflammatory mediators such as reactive oxygen species, prostaglandins and leukotrienes.1,5
PIH management is commonly addressed by prevention of the inflammatory dermatosis. A variety of medication and procedures in addition to photoprotection have been shown
