Background. CD30 (Ki‐1)‐positive anaplastic large cell lymphoma (LCL) has been described as a morphologically distinct group of LCL that generally are associated with a poor prognosis. Recent studies indicate that these lymphomas, when confined to the skin, have a favorable prognosis. However, there is no consensus regarding the definition of these primary cutaneous CD30‐positive LCL. Reported patients have been selected variously on the basis of morphologic (anaplastic cytology) or immunophenotypical (expression of CD30 antigen) criteria. Methods. At two recent workshops aimed to achieve consensus on the definition and terminology of these lymphomas, the clinical, histologic, and immunophenotypical data of 47 patients with primary cutaneous CD30‐positive LCL from five collaborating European centers were analyzed. Results. Characteristic clinical features were presentation with solitary or localized skin lesions (42 of 47 patients), frequent cutaneous relapses (15 patients), and partial or complete spontaneous remission of skin lesions (11 patients). Twelve of 47 (25%) patients developed extracutaneous disease. The favorable prognosis of these lymphomas is indicated by the follow‐up data that show that 36 of 47 patients are alive and in complete remission, only four disease‐related deaths have occurred, and the overall median survival is 42 months (range, 2–130 months). There were no differences in clinical presentation, course, or prognosis between anaplastic and nonanaplastic CD30‐positive LCL. Conclusion. The results of this study indicate that primary cutaneous CD30‐positive LCL, regardless of their morphologic classification (anaplastic or nonanaplastic) can be considered as a distinct type of cutaneous T‐cell lymphoma. Recognition of this type of cutaneous lymphoma is important because it may prevent patients from unnecessary aggressive treatment.

Trichoblastoma and nodular basal cell carcinoma are generally held to be distinctive epithelial neoplasms with some overlapping features. We investigated 30 trichoblastomas in which the basaloid cells expressed cytokeratins (CK) CK5/6, CK14, CK17, CK19, and, in a few cells, vimentin. The cells of the periphery of small and large cysts showed the same profile. Cells lining the lumen of small cysts expressed CK14, CK17, and involucrin, and those in larger cysts showed a positivity for CK1, CK4, CK10, CK14, CK17, and involucrin. The remaining tested antibodies (CK7, CK8, CK13, CK18, CK20, alpha-smooth-muscle actin) were negative in all cases. The cells of the stroma expressed vimentin and in 22 cases, the CD34 antigen. Seventeen nodular basal cell carcinomas showed exactly the same staining pattern. Furthermore, there are striking immunohistochemical similarities between the neoplastic basaloid cells of both neoplasms and the cells of the hair germ. Therefore, trichoblastoma and nodular basal cell carcinoma cannot be distinguished by their pattern of cytokeratin expression in paraffin sections. The virtually identical cytokeratin pattern seen in trichoblastoma, basal cell carcinoma, and the developing fetal hair follicle is compelling evidence for common differentiation pathway.

We suggest the term mycosis fungoides-associated follicular mucinosis should be replaced by follicular mycosis fungoides in future lymphoma classification schemes.

No abstract