Postinflammatory hyperpigmentation and other disorders of hyperpigmentation

Introduction

Hyperpigmentation is a common condition encountered in dermatologic practice. It is defined as darkening of natural skin color and can have a significant impact on quality of life. Hyperpigmentation results from increased melanocyte activity resulting in increased deposition of melanin in the epidermis or dermis. Alternatively, hyperpigmentation is due to deposition of endogenous or exogenous non-melanin pigments. Pigmentary disorders may be congenital or acquired. Acquired disorders can be divided into localized dermatoses such as postinflammatory hyperpigmentation, melasma, etc., or generalized dermatoses such as those resulting from autoimmune disease, metabolic disorders, or malignancy. Clinically, conditions with primarily epidermal hypermelanosis present with tan to dark brown pigmentation whereas dermal hypermelanosis presents with dark gray to blue–gray pigmentation. This chapter will focus on acquired dermatoses and give a brief summary of treatment.

Postinflammatory Hyperpigmentation

Postinflammatory hyperpigmentation (PIH) is defined as excess melanin in the epidermis or dermis that occurs as a result of cutaneous inflammation or injury. It is more common in patients with darker skin types, possibly due to increased epidermal melanin. Epidermal melanosis occurs when melanocytes are stimulated by inflammatory mediators resulting in increased melanin production. This melanin is then transferred to surrounding keratinocytes. Dermal melanosis occurs when inflammation disrupts the basal layer of the epidermis releasing melanin into the dermis. Macrophages can then phagocytize released melanin in the dermis and form melanophages. Alternatively, macrophages can migrate to the epidermis, engulf epidermal melanosomes, and return to the dermis. Melanin can remain in dermal macrophages for years.

Other Disorders of Hyperpigmentation

There are numerous other hyperpigmentary disorders that affect people of all skin phototypes. Sun or light exposure, aging, hormones, medications, cosmetics, fragrances, and genetics are often implicated in the pathogenesis of these conditions. We will briefly address a few of these disorders below.

Freckles, or ephelides, are small, hyperpigmented macules present on sun-exposed areas such as the face, hands, and upper trunk. Freckles tend to get darker with sun exposure. Lentigines are clinically similar to freckles, but in contrast to freckles, the color of lentigines are not affected by the sun. Both are more prevalent in those with lighter skin phototypes but can occur in all individuals.

Melasma is a common condition typically affecting women of reproductive age and is most prevalent in those with darker skin phototypes. The word melasma is derived from the Greek word melas , meaning ‘black’. Melasma that occurs during pregnancy is referred to as chloasma or the mask of pregnancy. The condition appears as well-defined irregular hyperpigmented macules and patches. Three types of clinical patterns have been described: centrofacial, malar, and mandibular. The pathogenesis of melasma is multifactorial and includes genetic and environmental factors.

Phototoxic dermatitis occurs when a photosensitizing substance is applied to the skin followed by exposure to ultraviolet radiation. Systemic medications, topically applied cosmetics, fragrances, and plants containing furocoumarins are all phototoxic substances that have been implicated in phototoxic dermatitis. Berloque dermatitis is a condition that results from the use of bergamot oil in fragrances and colognes. Hyperigmentation is often present after the acute inflammatory phase subsides.

Erythema dyschromicum perstans (EDP), also called ashy dermatosis or gray dermatosis, presents as hyperpigmented ovoid gray–brown macules, mainly affecting the face, trunk, and proximal extremities. Early lesions may have a more pronounced border, which can be erythematous and slightly raised. Lichen planus pigmentosus (LPP) is a variant of lichen planus. It presents similarly to EDP. In contrast to EDP, LPP lacks an inflammatory phase and thus lacks the presence of an inflammatory border.