1. Weedon D. Lentigines, nevi, and melanomas. In: Weedon’s skin pathology. 3rd ed. Philadelphia: Churchill Livingstone Elsevier; 2010. p. 709–56. Weedon describes a Meyerson’s nevus as a junctional, compound, or dermal nevus surrounded by an “eczematous halo” that can be pruritic. Meyerson’s nevus is similar to the halo nevus; however, it does not undergo regression as a result of the inflammation present. Meyerson’s nevus typically occurs in late winter or early spring. Histopathologically, Weedon describes Meyerson’s nevus as a “subacute spongiotic dermatitis” associated with the typical pathology of a nevus. Eosinophils may be present in the infiltrate as well as exocytosis into the epidermis.
2. Meyerson LB. A peculiar papulosquamous eruption involving pigmented nevi. Arch Dermatol. 1971;103(5):510–2. In his first observations, Dr. Meyerson comments on two of his patients who had pruritic papulosquamous lesions exclusively involving nevi. One of the patients was a 22-year-old white man who had a round, 2-cm pruritic lesion on the right upper part of the chest. The other patient was a 23-year-old white man who had a pruritic eruption involving nevi on the trunk and upper arms. Meyerson noted that these are similar to halo nevi, but they are different in that the nevi persist once the eruption has cleared. He noted that histologically these lesions demonstrate pigmented nevi with overlying parakeratosis, focal spongiosis, acanthosis, and a lymphocytic perivascular infiltrate in the dermis. At that time a similar disorder had not yet been reported in the literature.
3. Sardana K, Sarkar R, Sehgal VN. Pigmented purpuric dermatoses: an overview. Int J Dermatol. 2004;43(7):482–8. Pigmented purpuric dermatoses are chronic disorders that are usually found on the lower limbs. They classically have five main clinical variants: Majocchi’s disease (purpura annularis telangiectodes), Schamberg’s disease, pigmented purpuric lichenoid dermatosis of Gougerot and Blum, eczematid-like purpura of Doucas and Kapetanakis, and a localized variant called lichen aureus. Numerous factors have been suggested to cause PPD, including exercise, clothing, alcohol ingestion, and contact allergy to dyes and drugs. PPD tends to be resistant to treatment; cases have been reported of successful treatment of PPD using griseofulvin, psoralen photochemotherapy, oral rutoside, ascorbic acid, pentoxifylline, and cyclosporine.
4. James WD, Berger TG, Elston DM, editors. Andrews’ diseases of the skin: clinical dermatology. Philadelphia: Elsevier; 2006. p. 829–30.
5. Barnhill RL, Nousari CH, Xu X, Barksdale SK. Vascular diseases. In: Elder DE, Elenitsas R, Johnson Jr BL, Murphy GF, Xu G, editors. Lever’s histopathology of the skin. 10th ed. Philadelphia: Lippincott Williams & Wilkins; 2009. p. 205–34. An abnormal T-cell process may be evident in PPD. Epidermotropism and lymphoid atypia should be considered to rule out cutaneous T-cell lymphoma.