Halo nevi associated with interferon beta-1a therapy.

The interferons are a group of more than 20 glycoproteins produced by numerous body cells in response to the presence of viruses, double-stranded RNA, polypeptides, or bacterial products. All of them share the ability to inhibit viral replication and cell proliferation, and to regulate and modulate immune cells. From an immunologic point of view, interferons increase the expression of class I or II molecules of the major histocompatibility complex and stimulate natural killer (NK) lymphocytes. There are 2 types of interferon: type 1, which is divided into alpha, beta, omega, and tao, and type 2 which comprises gamma interferon. The principal interferons of medical interest are alpha interferons, produced mainly by leukocytes, beta interferons, produced by fibroblasts, and gamma interferons, produced by T lymphocytes and NK cells. Interferons are primarily used in medicine to treat malignant neoplasms, viral diseases, and autoimmune diseases. Type 1 is more effective as an antiviral agent and type 2 has a more specific effect on regulation of the immune response. We describe a 22-year-old woman with an 8-month history of multiple sclerosis. She had been receiving interferon beta-1a subcutaneously at doses of 22 mcg 3 times weekly for the previous 3 months. The patient reported depigmentation around nevi on her skin, with onset of the depigmentation only a few weeks after interferon therapy was started. She had no personal or family history of vitiligo and presented no previous halo nevi. Physical examination revealed an achromic hypopigmented halo around almost all the nevi on the patient’s skin, a total of 15, most of them on the back (Fig. 1) as well as around several intradermal nevi on the face (Fig. 2). The nevi were stable and had been present for some time; none presented clinical or dermoscopic atypia. The interferon was well tolerated, with no liver or thyroid abnormalities and with satisfactory control of multiple sclerosis, which was in remission at the time. Halo nevi express an autoimmunity phenomenon that manifests as an achromic hypopigmented halo around the nevus, which often disappears. Histology shows a lymphohistiocytic infiltrate directed against the melanocytes. Immune involvement in the genesis of this phenomenon is supported by the presence or increased numbers of T lymphocytes, mainly CD8+ cells, and antigen-presenting cells at the site of depigmentation. Additionally, the local endogenous production and activation of type 1 interferon have been seen to be involved in the regression of melanomas and other melanocytic lesions.