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Lymphoid Lesions

T-cell Dysplasia

The patterns of T-cell neoplasia in the skin are variable. In the primary category, a large group is characterized by lichenoid and psoriasiform patterns; common patterns of inflammatory disorders are recapitulated. The lichenoid variants can be divided into cell-rich variants (primary or established lichenoid patterns), and cell poor variants (senescent lichenoid, or poikilodermatous patterns).The infiltrates of these primary neoplasms of the skin can be graded as to degree of neoplasia. The grades include mild, moderate, and severe categories. Grading is based in part on the degree of cytologic atypia and, in part, on numerical representation of the atypical cells. In this approach, the atypical cells are to be compared with the small lymphoid cells in the infiltrates that cannot, on the basis of cytologic features, be characterized as atypical. In this approach to the classification of this particular variant of T-cell neoplasia, only the tumoral patterns are characterized as lymphomatous. The macular and plaque-like examples, in which the infiltrates are confined to a widened papillary dermis, qualifiy as T-cell dysplasias. The patterns in lymph nodes, if sufficiently developed to be characterized as lymphomatous, would take precedence over the patterns in lesions of the skin. Even the latter accommodations become arbitrary; the degree of atypia may influence the observer; he may diagnosis lymphoma on the basis of cellular atypia in the absence of infiltrates that, in their patterns, provide tumoral qualities (i.e., Reed’s “malignant reticulosis in situ”).

Cutaneous T-cell Lymphoma

 

Lymphoid Papulosis

Lymphoproliferative disorders are lymphoma-like processes which are encountered spontaneously, or in the setting of immune-deficiency. In the latter category, there is a common association with Epstein-Barr virus infection. The concept, in part, gives recognition to lymphoma-like processes (i.e., lymphoproliferative processes) which are characterized by either a remittent course, or by a tendency for regression in response to an improvement in the immune status. The latter phenomenon is a possibility for those examples in which the immune deficiency is secondary to treatment, as might be encountered in patients with organ transplants. In these phenomena, we may be observing viral induced transformations that, with a change in immune status, may revert to a more stable cell cycle - in such a reversion the degree of cytologic atypia also is lessened.

A remittent clinical course is the attribute which qualifies lymphomatoid papulosis as a lymphoproliferative disorder. On the basis of histologic patterns, a type A and a type B have been described. A type C variant also has been proposed. Perhaps, the C-type lesions are basically of the same type as those lesions which have been classified as atypical regressing histiocytosis. In type B, the infiltrates are composed of small, dark lymphoid cells. Characteristically, these cells have the convoluted nuclei of transformed T lymphocytes. In type A, the lymphoid infiltrates have a high component of large, transformed lymphoid cells. The cells have pale cytoplasm,plump, round nuclei with prominent nucleoli, and dense chromatin patterns.

The infiltrates of lymphomatoid papulosis may be tumoral, but often have an angiocentric quality. In addition, it is common for some of the affected vessels to show fibrinoid necrosis and thrombosis.

Epidermotropism is a common feature in lesions of lymphomatoid papulosis. The cytologic features and some of the histologic patterns may suggest a variant of mycosis fungoides. Characteristically, large atypical lymphoid cells with dense chromatin patterns extend from the perivascular spaces into the interstitium of the reticular dermis (“lumps of coal”). They are loosely spaced among inflammatory cells. Histiocytes are common in the infiltrates. Eosinophils are variable. Mitoses are relatively common. Some examples are tumoral and composed of a uniform population of large, atypical lymphoid cells. For such examples, a clinical history documenting a remittent course is a great aid in the proper assignment of the lesion to the lymphoproliferative category. Modulations, as manifested in degree of atypia, may be apparent, if patterns in serial biopsy material, are compared. In different material, taking at different intervals, there may be morphologic modulations from small to large cell patterns. Modulations of this type would not always be manifested in progressions to a larger, more anaplastic pattern. In some examples, even pityriasic patterns may be included as a variant in the modulations.

So-called regressing atypical histiocytosis probably should be included in the category of the lymphoproliferative disorders and could be accommodated in the category of lymphomatoid papulosis (type C?). The large cells of the infiltrate are immunoreactive for CD 45 and CD30. There is the potential for lesions in this category to regress, but there is a greater tendency for the emergence of a progressive lymphoma than is the case in  more classic examples of lymphomatoid papulosis.

Karp DL, Horn TD: Lymphomatoid papulosis. J Am Acad Dermatol 1994;30: 379-95.

 

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