Figure 2. Nodular lesions near the ears
A 58-year-old man presented with asymptomatic erythematous nodules and plaques on the trunk of 9-months duration. Lesions were few at onset but gradually progressed to involve the entire back, upper extremities, and the ears. There was no history of photosensitivity, sensory or motor deficit, or neuritis. There was no history of spontaneous resolution of the lesions. Cutaneous examination revealed multiple erythematous deeply infiltrated nodules and plaques on the back and upper arms. Their surface was smooth and shiny with no evidence of scaling, follicular plugging or scarring. There was nodular infiltration of the ear lobes bilaterally. All routine biochemical and hematological investigations were within normal limits. Slit-skin smear for acid fast bacilli was negative. Biopsy from a plaque revealed normal epidermis with well demarcated dense perivascular infiltrate and periadnexal infiltrate in the reticular dermis composed of mature lymphocytes.
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| Figure 1 | Figure 2 |
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| Figure 1. Infiltrated nodules and plaques on the back Figure 2. Nodular lesions near the ears |
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| Low power and close view of dermal infiltrate | |
Benign lymphocytic infiltration of skin (LIS) was first described by Jessner and Kanof in 1953 [1]. Clinically it presents with asymptomatic reddish brown nodules and plaques that may show a central clearing producing a circinate arrangement. The lesions occur most commonly on the face, although the neck and back may be involved [2]. There is a marked male preponderance with the M : F ratio of 3 : 1; however, in female patients lesions tend to occur at a younger age than males. The lesions follow an indolent course lasting for weeks or months before resolving and in many cases subsequently recurring. It has been also reported in children [3]. Little is known about the pathogenesis of LIS except that it is characterized as a T-cell disorder [4]. Patients with LIS report their onset during the summer, and this, along with classic distribution over the sun-exposed areas, led to the hypothesis that LIS is a photosensitive disorder and that intense UV light can provoke LIS [5].
Histologically a moderately dense superficial and deep perivascular lymphocytic infiltrate is seen often with mucin between collagen bundles in the reticular dermis. Epidermal changes are lacking and the lymphoid cells are shown to be T lymphocytes by enzyme, histochemical, and immunohistochemical studies [6].
Discoid lupus erythematosus (DLE), polymorphous light eruption (PLE), and lymphoma have to be considered in the differential diagnosis. Of these, DLE may be particularly difficult to differentiate from LIS. In fact, some authors believe that Jessner lymphocytic infiltrate represents a non-scarring from of DLE based on a similar histological picture, occasional photosensitivity, and response to antimalarial agents. For our patient, clinically there was no scarring or atrophy, and histologically hyperkeratosis and follicular plugging were absent, for that reason DLE was excluded. Based on the differences between the numbers of OKT 6+ Langerhans cells, HLA DR T cells, Leu 8 cells, and NK cells, monoclonal antibody studies may be of additional help in making a diagnosis. Similarly, testing the basement membrane for direct immunofluorescence would be helpful. These were not done in our patient because of financial constraints.
Differentiating LIS from PLE is often a more difficult problem. Both can share the same clinical and histological features, although early lesions of PLE usually show papillary dermal edema that is not seen in LIS. The patients history is important in the differentiation, however it may be complicated further by the fact that LIS can also be exaggerated after sun exposure. In such cases, presence of active lesions on covered skin areas along with provocative phototesting are useful clues to help make a diagnosis.
Transition of LIS into malignant lymphoma has been reported. Using monoclonal antibodies to differentiate between LIS and lymphoma is possible [7].
Topical and intralesional steroids are used often as first line treatment and can be helpful. A range of systemic preparations have been tried particularly antimalarials, thalidomide [8], and etretinate [9]. Our patient was treated with dapsone (100mg daily) with complete subsidence of lesions at the end of 2 weeks.
© 2006 Dermatology Online Journal