Ann Dermatol. 2014 Oct;26(5):649-650. English.
Published online Sep 26, 2014.
Copyright © 2014 The Korean Dermatological Association and The Korean Society for Investigative Dermatology
letter

Generalized Eruptive Lentiginosis in a Healthy Elderly Man

Min Sung Kim, Sang Ho Youn, Chan Ho Na, Jong Kyu Kim,1 and Bong Seok Shin
    • Department of Dermatology, Chosun University Medical School, Gwangju, Korea.
    • 1Department of Neurosurgery, Chosun University Medical School, Gwangju, Korea.
Received August 28, 2013; Revised September 28, 2013; Accepted October 05, 2013.

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

Dear Editor:

Lentiginosis manifests itself in the form of circumscribed or widespread macules, and both forms are possibly part of a number of well-known syndromes affecting the cardiac, musculoskeletal, neurologic, reproductive, gastrointestinal, and auditory systems. These anomalies have been categorized into separate syndromes such as LEOPARD syndrome, LAMB syndrome, and NAME syndrome1.

A 61-year-old, healthy Korean man presented with hyperpigmented macules that varied in size on his face, trunk, and extremities (Fig. 1). The cutaneous lesions appeared 5 months ago and spread rapidly over the whole body, except the palm, sole, buccal mucosa, and conjunctiva. He had no significant past medical history such as preceding febrile illness, inflammatory skin lesions, medication, and photosensitivity. There was no family history of similar cutaneous lesions. The patient's physical development, musculoskeletal system, and joints were normal.

Fig. 1
Hundreds of hyperpigmented macules on the back and extremities. Inset: close-up view of lesions.

The patient's complete blood cell count; serum chemical profile; urine analysis results; plasma levels of cortisol, adrenocorticotropic hormone, and aldosterone; thyroid function test results; and chest radiography findings were normal. His regular medical examination results had been normal for several years. Histopathological examination showed hyperpigmentation of the lower epidermis, elongation of the rete ridges, and increased numbers of melanocytes at the rete ridges, which were strongly positive for S-100 and Melan A. No nevus cells or nests of melanocytes were present (Fig. 2).

Fig. 2
(A) Pathologic features of the skin on the trunk with lentigo (H&E, ×200). (B) Proliferation of melanocytes, positive for S-100, is evident in the basal layer of the epidermis (S-100, ×200). Inset: melanocytes on Melan A staining (×200).

Our patient's symptoms confirmed the diagnosis of generalized eruptive lentiginosis, i.e. the widespread occurrence of several 100 lentigines in a short span of time in the absence of systemic abnormalities2. Cases of adult-onset generalized eruptive lentiginosis are quite rare. In 1933, Dumas et al.3 described the case of a 58-year-old woman who developed disseminated light brown spots over 8 months. In 2006, Na et al.2 reported the case of a 40-year-old woman who broke out in innumerable hyperpigmented spots over her trunk and extremities in 3 months and whose daughter developed similar skin lesions on the bilateral axillae, trunk, and extremities in 2 months. In 2010, De et al.4 reported the case of a 35-year-old woman with lentiginosis induced by cancer chemotherapy. She had multiple lentigines over the photoprotected areas of all the 4 limbs within 6 weeks after cessation of chemotherapy.

There is little information about the natural course and pathogenesis of this disease. However, considering the fact that lentigines represent the simplest form of melanocytic proliferation and there is some continuity from lentigines to melanocytic nevi, the pathophysiologies of eruptive lentiginosis and eruptive benign melanocytic nevi might be similar. Diminished immune surveillance in the skin plays a role in the pathogenesis of these lesions. Chemotherapy, medical immunosuppression, or aging may lead to this condition4. In 2005, Xing et al.5 localized the familial locus to chromosome 4q21.1-q22.3 in a Chinese family with generalized lentiginosis. Genetic predisposition may play a role in the development of this condition. Besides, exposure to infectious agents or chemical materials might also cause this disease2. In our case, we thought that the lentigines were associated with diminished immune surveillance secondary to the aging process.

ACKNOWLEDGMENT

This study was supported by research funds from Chosun University Hospital, 2013.

References

    1. Uhle P, Norvell S Jr. Generalized lentiginosis. J Am Acad Dermatol 1988;18:444–447.
    1. Na JI, Park KC, Youn SW. Familial eruptive lentiginosis. J Am Acad Dermatol 2006;55:s38–s40.
    1. Dumas A, Petouraud C, Benoit. Lentiginose profuse et diffuse d'apparition récente chez une femmeâgée. Bull Soc Fr Dermatol Syphiligr 1930;40:1049–1051.
    1. De D, Dogra DS, Kanwar AJ, Saikia UN. Generalized eruptive lentiginosis induced by chemotherapy. Clin Exp Dermatol 2010;35:e113–e115.
    1. Xing Q, Chen X, Wang M. A locus for familial generalized lentiginosis without systemic involvement maps to 3. Hum Genet 2005;117:154–159.

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