Current Challenges in Deciphering Sutton Nevi-Literature Review and Personal Experience.

Roxana Nedelcu,Adina Dobritoiu,Raluca Popescu,Florentina Pantelimon,Mihaela Antohe,Daniela Ion,Sabina Zurac,Alexandra Dobre,Lorena Manea,Anastasia Coman,Mihaela Balaban,Gabriela Turcu,Razvan Andrei,Alice Brinzea,Andreea Calinescu,Elena Balasescu,Ionela Hulea,Catalin Popescu

doi:10.3390/jpm11090904

Abstract

Halo nevi, known as leukoderma acquisitum centrifugum, Sutton nevus, leukopigmentary nevus, perinevoid vitiligo, or perinevoid leukoderma, together with vitiligo and melanoma-associated hypopigmentation, belong to the group of dermatoses designated as immunological leukodermas. The etiology and pathogenesis of halo nevi has not been fully elucidated. There are several mechanisms through which a lymphocytic infiltrate can induce tumoral regression. In this review, we aimed to update the knowledge about Sutton nevi starting with the clinical appearance and dermoscopic features, continuing with information regarding conventional microscopy, immunohistochemistry, and the immunological mechanisms responsible for the occurrence of halo nevi. We also included in the article original unpublished results when discussing dermoscopic, pathologic and immunohistochemical results in halo nevi. Sutton nevi are valuable models for studying antitumor reactions that the human body can generate. The slow and effective mechanism against a melanocytic skin tumor can teach us important lessons about both autoimmune diseases and anticancer defenses.

Highlights

Leukoderma acquisitum centrifugum, later known as Sutton nevus or halo nevus, appeared in 1916 in the writings of Richard Lightburn Sutton [1,2]
The presence of halo depigmentation correlates with the onset of nevus regression, evolving towards total resorption of the melanocytic lesion with the possibility of repigmentation after many years
The larger the nevus, the larger its halo. They were the ones who described the “melanocyte antigenic unit”. It consists of melanocytes with radial disposition from the central melanocytic lesion, having the same phenotype and being functionally dependent on the central nevus

Summary

Introduction

Leukoderma acquisitum centrifugum, later known as Sutton nevus or halo nevus, appeared in 1916 in the writings of Richard Lightburn Sutton [1,2]. Sutton described two cases of peculiar brown maculo-papules, but he considered the lesions to be clinical variants of vitiligo. The mean age at onset is thought to be 15 years It is unusual and a sign of suspicion if a depigmentation around a nevus is found in an older patient [4,5]. The presence of halo depigmentation correlates with the onset of nevus regression, evolving towards total resorption of the melanocytic lesion with the possibility of repigmentation after many years. The larger the nevus, the larger its halo They were the ones who described the “melanocyte antigenic unit” (melanocyte antigenic unit—MAU). It consists of melanocytes with radial disposition from the central melanocytic lesion, having the same phenotype and being functionally dependent on the central nevus. Further studies are still needed to explore in more detail the connection between the halo and the thickness of the central nevus

Dermoscopic Pattern—Same Look as in Common Nevi?

The Microscopic Features—What Matters in Atypical Tumors?

Findings

Key Antimelanocyte Immune Reaction Lesson