Neutrophil-rich Anaplastic Large Cell Lymphoma Research Articles

Primary Cutaneous Eosinophil-Rich Anaplastic Large Cell Lymphoma: Report of an Unusual Case and Literature Review

Cutaneous, neutrophil-rich anaplastic large cell lymphoma (ALCL) is an uncommon variant of ALCL that may be confused with inflammatory dermatoses. We describe an eosinophil-rich variant of ALCL occurring on the left ear without systemic involvement. The lesion had inflammatory characteristics, which led initially to a histological diagnosis of an inflammatory process. Two months later, a second biopsy diagnosed eosinophil-rich variant of ALCL. The patient underwent radiation therapy, but due to the extensive deformation and mutilation of the ear, the patient elected to have the ear amputated. We discuss the clinicopathological findings and the differential diagnosis To the best of our knowledge, the occurrence of a cutaneous, eosinophil-rich variant of ALCL has not been previously reported. It is important to alert pathologists to this variant of ALCL so that this possibility may be considered in the early differential diagnosis of inflammatory cutaneous conditions.

CD30-positive atypical lymphoid cells in common non-neoplastic cutaneous infiltrates rich in neutrophils and eosinophils.

CD30-positive cells characterize lymphomatoid papulosis and anaplastic large cell lymphoma but can also be found in nonneoplastic skin disorders. Purportedly, CD30 is useful in the differential diagnosis between insect bites and lymphomatoid papulosis. Recently, a subtype of neutrophil-rich CD30-positive anaplastic large cell lymphoma has been described, which may enter the differential diagnosis of cutaneous neutrophil-rich inflammatory infiltrates. We studied atypical CD30-positive lymphoid cells in five eosinophil-rich and 23 neutrophil-rich common nonneoplastic skin infiltrates. The eosinophil-rich cases included five insect bites. The neutrophil-rich cases included 9 inflammatory (hidradenitis suppurativa [n = 4], stasis ulcer [n = 2], ruptured cyst, rhynophyma, and Sweet syndrome); 12 infectious (bacterial [n = 8], viral [n = 2] and fungal [n = 2] etiologies); and 2 environmental (spider bites) cases. Atypical CD30-positive cells were found in 4 of 5 eosinophil-rich, 8 of 9 neutrophil-rich inflammatory, 6 of 12 neutrophil-rich infectious, and 2 of 2 neutrophil-rich environmental cases. Polymerase chain reaction analysis for B- and T-cell clonality and cell counts of neutrophils, eosinophils, plasma cells, B cells (using CD20), and T cells (using CD3) were performed in the cases that contained atypical CD30-positive lymphoid cells. CD30-positive cells averaged 4.8% of the cells counted in the areas where they were most concentrated. Of the 18 cases that amplified with polymerase chain reaction, all were polyclonal for T-cell receptor rearrangements; 10 were polyclonal and 8 oligoclonal for B-cell immunoglobulin rearrangements. There was no correlation between B-cell oligoclonality with CD30-positive cell counts, a particular disease, or a disease category. In conclusion, the presence of CD30-positive atypical lymphoid cells in 71.4% of the common nonneoplastic cases studied, even in the presence of clonal B-cell populations, warrants caution in the interpretation of these cells as malignant, particularly when dealing with the differential diagnosis of lymphomatoid papulosis or neutrophil-rich anaplastic large cell lymphoma.