Differential diagnoses

In infectious mononucleosis, the tonsils may appear histologically worrisome, with necrosis, partial effacement of architecture, and striking immunoblastic proliferation, mimicking DLBCL {431}. In contrast to the latter, there is usually a spectrum of lymphoid cells in different stages of differentiation and activation

Fig. 4.50 Plasmacytoma of the tongue. The plasmacytoma is accompanied by blood lakes.

(immunoblasts, plasmablasts and plasma cells). On immunostaining, the large cells usually consist of a mixture of B- and T-cells, and there is no immunoglobulin light chain restriction. As a rule of thumb, infectious mononucleosis has to be seriously excluded before making a diagnosis of DLBCL in young patients. Some cases of DLBCL (especially those in the tonsil) can exhibit deceptively cohesive growth and a sharp interface with the uninvolved mucosa, closely mimicking poorly differentiated carcinoma or malignant melanoma. Marked irregular nuclear foldings and amphophilic cytoplasm, if present, should point more towards a diagnosis of lymphoma. Appropriate immunostains can readily solve this diagnostic problem. Anaplastic plasmacytoma can be difficult to distinguish from DLBCL, including the plasmablastic variant. An important clue to the diagnosis is the presence of coarsely clumped 'clock-face' chromatin in the few differentiated cells that are present. There are often intermingled atypical plasma cells. There is usually no association with EBV. A prior history of multiple myeloma, if present, would be a strong point to substantiate a diagnosis of plasmacytoma.

Extramedullary myeloid sarcoma (granulocytic sarcoma) is commonly misdiagnosed as large cell lymphoma. The clues to diagnosis are the fine chromatin, presence of cytoplasmic eosinophilic granules in some cells, and interspersed eosinophilic myelocytes. The diagnosis can be confirmed by immunoreactivity for myeloid or monocytic markers (e.g. myeloperoxidase, CD13, CD33, CD117, neutrophil elastase, lysozyme, CD68).

The differential diagnosis between extra-nodal marginal zone B-cell lymphoma of MALT type in the tonsil and reactive lymphoid hyperplasia can be extremely difficult, because of the presence of reactive lymphoid follicles, minimal atypia of the lymphoid cells in the former and presence of numerous plasma cells. Furthermore, lymphoepithelial lesions in the tonsil are difficult to assess since the tonsillar epithelium is normally extensively infiltrated by small lymphoid cells. The following features would favour a diagnosis of lymphoma: lymphoid cells infiltrating beyond the fibrous band at the base of the tonsil, presence of sheets of CD20+ B-cells between the lymphoid follicles, immunoglobulin light chain restriction, and molecular evidence of clonal immunoglobulin gene rearrangement. Some extranodal NK/T cell lymphomas of nasal-type comprise predominantly small lymphoid cells with minimal atypia, rendering it difficult to distinguish from a reactive lymphoid infiltrate. Histologic clues to the diagnosis are the extensive necrosis and angiocentric growth. Demonstration of sheets of CD56+ or EBER+ cells would strongly support the diagnosis.

There is some morphologic overlap of anaplastic large cell lymphoma with eosinophilic ulcer (traumatic eosinophilic granuloma; atypical histiocytic granuloma) {645,674,701}, which is characterized by a rich inflammatory infiltrate (especially eosinophils) and occasional large cells {760}. Anaplastic large cell lymphoma can be distinguished from it by the presence of at least large aggregates of large atypical cells in areas and strong CD30 expression.

Fig. 4.51 Langerhans cell histiocytosis involving gingiva. The infiltrate comprises ovoid Langerhans cells with deeply grooved nuclei, thin nuclear membranes and abundant eosinophilic cytoplasm. There are typically many admixed eosinophils.

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