Jessner Lymphocytic Infiltration of the Skin Workup

Updated: Dec 13, 2017
  • Author: Kara Melissa Torres Culala, MD; Chief Editor: William D James, MD  more...
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Workup

Laboratory Studies

Serologic testing for systemic lupus erythematosus (SLE) should be considered. This testing should include, but is not limited to, screening antinuclear antibodies (ANA), erythrocyte sedimentation rate (ESR), anti-Ro (Sjögren syndrome A [SSA]) and anti-La (Sjögren syndrome B [SSB]) antibodies, CBC count, and urinalysis. [19]

Immunophenotyping may be valuable in differentiation from cutaneous lymphoma (polyclonal vs monoclonal).

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Other Tests

Both UVA and/or UVB elicit abnormal papular phototest reactions resembling lesions of lymphocytic infiltration of the skin both clinically and histologically in some patients. Lesions typically develop 3-6 days after the first UV exposure. Some data suggest that a photosensitivity history in patients with Jessner lymphocytic infiltration of the skin should be sought and confirmed using provocative phototesting. This relevant event could guide the therapeutic strategy because antimalarials have been effective for Jessner lymphocytic infiltration of the skin patients with photosensitivity.

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Procedures

Skin biopsy is the primary diagnostic study. Biopsy from a relatively new lesion is recommended, and it should be sent for routine hematoxylin and eosin (H&E) staining. Select lesions that have not been treated with topical steroids or other immunosuppressive agents.

A portion of the specimen, or an additional biopsy, may be immediately frozen in liquid nitrogen and stored at –70°C for immunohistochemical studies requiring fresh frozen tissue if later indicated. A biopsy, or portion thereof, should be placed in immunofluorescent transport medium for direct immunofluorescence studies.

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Histologic Findings

Lymphocytic infiltration of the skin is one of a group of conditions characterized histologically by a lymphocytic infiltrate in the dermis. The following are included in this group:

  • Polymorphous light eruption

  • Discoid lupus erythematosus

  • Well-differentiated lymphocytic lymphoma

  • Lymphocytoma cutis

The above conditions, along with Jessner lymphocytic infiltration of the skin, are often referred to as the 5 L 's.

The following histologic findings are characteristic of lymphocytic infiltration of the skin, and helpful differentiating features from other conditions characterized by a lymphocytic infiltrate are noted.

The epidermis usually is normal with no evidence of atrophy, follicular plugging, basal vacuolar change, or basement membrane zone thickening. Those features are more consistent with a diagnosis of DLE.

In the dermis, a moderately dense superficial and deep perivascular lymphocytic infiltrate is observed at scanning magnification. The lymphocytic infiltrate may also be perifollicular or may extend into the subcutis.

Higher magnification reveals a predominance of small mature lymphocytes. Large lymphoid cells, plasma cells, or plasmacytoid monocytes may occasionally be present. Plasmacytoid dendritic cells were also observed as perivascular and periadnexal clusters in both lupus erythematosus and LIS as compared with other forms of dermatitis, which exhibited plasmacytoid dendritic cells as single cells or scattered cells throughout the infiltrate. [10]

Eosinophils and neutrophils are lacking, and their presence should cause one to suspect an infectious etiology or arthropod bite reaction, rather than lymphocytic infiltration of the skin.

Copious dermal mucin is not observed, which helps distinguish lymphocytic infiltration of the skin from tumid lupus erythematous and reticular erythematous mucinosis.

Prominent papillary dermal edema is likewise absent, and its presence would suggest polymorphous light eruption or pernio.

Germinal follicle formation, as would be observed in lymphocytoma cutis or cutaneous follicular center cell lymphoma, is absent, as is a clonal population of B or T cells on molecular analysis.

Findings on direct immunofluorescence are negative, as opposed to classic DLE, which usually has positive findings. Tumid lupus, however, is also usually negative.

One study demonstrated an increase in circulating immune complexes in both reticular erythematous mucinosis and LIS. [7] The same study demonstrated a decrease in the immune complexes with hydroxychloroquine therapy and clinical clearing, with a resurgence upon discontinuation of treatment.

Marker studies reveal that the overwhelming population of infiltrating cells is one of mature T cells. An increased number of Leu-8 (CD62 L)–positive T cells, [20] nonexpression of ICAM-1, and negative epidermal expression of 27E10 [21] compared with discoid lupus may help distinguish those conditions. In contrast to earlier studies, an absence of T cells expressing HLA-DR antigens was observed in keratinocytes in lupus erythematosus and LIS. [21] There is also absent HLA-DR expression in polymorphous light reaction. [22]

Natural killer cell function has been found to be decreased in both reticular erythematous mucinosis and LIS. [7]

More reactive B cells may be found in the infiltrate than in DLE. [23]

Lymphocytic infiltrate contains mainly of CD8+ T cells. [17]

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