Background
Nevus anemicus is a congenital vascular anomaly that presents clinically as a hypopigmented macule or patch, as shown below. The lesional pallor is due to a localized hypersensitivity to catecholamines with resultant vasoconstriction. Nevus anemicus is an uncommon disorder and was first described by Vorner in 1906.
Ill-defined, asymptomatic hypopigmented patch of nevus anemicus on the lateral leg. Pathophysiology
Intralesional injection of bradykinin, acetylcholine, serotonin, nicotine, 5-hydroxytryptamine, and histamine fails to induce the anticipated vasodilatation or erythema in the affected area. However, erythema does follow an axillary sympathetic block or intradermal injection of the alpha-adrenergic blocking agent, pilocarpine. These findings suggest that nevus anemicus is best termed a pharmacologic nevus resulting from increased vascular sensitivity to catecholamines.[1] This conclusion is further supported by autograft exchange transplantation studies that show donor site dominance. It also has been proposed that an abnormality in endothelial adhesion molecule induction (E selectin expression) may be involved, suggesting several pharmacologic anomalies are involved and further supporting the idea that nevus anemicus may best be termed a pharmacologic nevus.
Epidemiology
Frequency
United States
The prevalence of nevus anemicus is not known, but it is not rare.
Mortality/Morbidity
Lesions of nevus anemicus usually persist unchanged throughout life. They are asymptomatic.
Race
No racial predilection has been noted in the literature for nevus anemicus.
Sex
Nevus anemicus appears more frequently in females.
Age
Nevus anemicus may be present at birth or first appreciated in early childhood.
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