Hyperpigmentation: An Overview of the Common Afflictions

Kimberly A. Cayce; Amy J. McMichael; Steven R. Feldman


Dermatology Nursing. 2004;16(5) 

In This Article

Postinflammatory Hyperpigmentation

Postinflammatory hyperpigmentation characteristically presents as discrete macules with hazy, feathered margins. It ensues after resolution of inflammatory skin eruptions such as acne, contact dermatitis, atopic dermatitis, or trauma and follows the configuration of the primary rash (Ortonne et al., 2003). Some believe the pigmentary response is determined by the degree of inflammation (Takiwaki, Shirai, Kohno, Soh, & Arase, 1994) and it has been noted that a greater degree of hyperpigmentation results following long-term and/or relapsing inflammation than after short-term, acute inflammation (Ruiz-Maldonado & Orozco-Covarrubias, 1997). Presumably because of an already higher baseline epidermal melanin content, persons with darkly pigmented skin have a greater risk of hyperpigmentation than those with lighter skin color. Also, the hypermelanosis tends to be more clinically noticeable and last longer in darker-pigmented individuals (Ruiz-Maldonado & Orozco-Covarrubias, 1997). Disease characteristics are summarized in Table 4 .

The pathogenesis of this skin disorder includes at least two major processes. An increase in melanocyte activity with increased melanogenesis and transfer of melanin granules to surrounding keratinocytes may occur. In addition, accumulation of melanophages in the upper dermis as a result of destruction of the basal cell layer in the inflamed skin leads to hyperpigmentation (Tomita, Maeda, & Tagami, 1989). This distinction between epidermal versus dermal involvement is important when considering therapeutic options.

Several chemical mediators appear to play a role in postinflammatory hyperpigmentation. Arachidonic acid metabolites such as prostaglandin E2, thromboxane B2, leukotriene (LT) C4, and LTD4 exist at inflammatory sites and are known to stimulate melanocytes by increasing the amount of immunoreactive tyrosinase, a melanin-forming enzyme (Tomita et al., 1989). Other biologic effects on the cells may arise as a result of arachidonic acid itself. This chemical, when applied to the skin in small or large amounts, causes marked hyperplasia of keratinocytes as well as marked proliferation of epidermal pigment cells and enhancement of melanization. Alpha-melanocyte-stimulating hormone stimulates pigment cells in vitro and was shown to darken the pelage when applied to the skin of mice. Other implicated pigment modulators include vitamin D3 and hydrocortisone (Nordland, 1988).