Deberah Simon

Functional markers of malignant cells from 14 patients with hairy cell leukaemia were evaluated during a 10 month period to assess the possible existence of sub‐types of the disease. Surface immunoglobulin on the hairy cells from the peripheral blood was studied initially, and again either after trypsinization and culture or after culture alone. Resynthesis of surface immunoglobulin occurred in all 12 patients studied; in four it was clearly monoclonal. Hairy cells from 11 patients were evaluated for their capacity to phagocytose zymosan; in five patients, 25% or more of the hairy cells demonstrated phagocytosis; in five others, less than 10%. One patient had only 13% zymosan phagocytosis initially, but when the study was repeated at a later date, 31% of the hairy cells phagocytosed. There was no phagocytosis of zymosan by malignant cells in 12 patients with a variety of other lymphoproliferative diseases. The percentage of E‐rosettes was correlated inversely with the percentage of circulating hairy cells. EAC‐rosettes were very low in three patients tested, all of whom had a high percentage of hairy cells. The number of tartrate‐resistant acid‐phosphatase‐positive cells varied from patient to patient, and within the same patient at different times. Platelet function was abnormal in six of 11 patients tested, who had a decreased, but not absent, epinephrine response. The significance of these findings in regard to the origin of the hairy cells in hairy cell leukaemia and in regard to the variable clinical course remains to be established.

In a prospective study of malignant cells from 13 patients with the leukemic phase of lymphoproliferative diseases, we wished to determine whether any correlation between the immunologic markers and the cell surface ultrastructure. Five patients had chronic lymphocytic leukemia, four had malignant lymphomas, poorly differentiated lymphocytic type, two had the Sezary syndrome, and one each had acute prolymphocytic leukemia and acute lymphocytic leukemia. Cell separation and isolation was done at room temperature for all specimens. Immunologic markers tested for were surface immunoglobins, a B-cell property, and E-rosettes, a T-cell property. Three patients had T-cell diseases, 6 had B-cell diseases, and 4 were classified as ''null.'' All but one patient had moderate to large numbers of microvilli on their malignant cells. The single exception had a typical B-cell form of chronic lymphocytic leukemia. There appears to be no correlation between immunologic markers and cell surface ultrastructure; therefore, SEM appears not to be valuable in the diagnosis or classification of immunologic sub-types of certain lymphoproliferative diseases.

In three patients with hairy cell leukemia (HCL), the similarity of the surface ultrastructure of cells from multiple sites was studied. These sites included peripheral blood and spleen in one patient, and peripheral blood and bone marrow in two patients. The hairy cells from the peripheral blood of these patients were also compared with those of two other patients with HCL. The cells in all five cases had a surface comprised of exaggerated, broad-based ruffles with an occasional area of short microvilli. Although the shape of the ruffles and the number of microvilli varied slightly, there was a marked similarity for all organ sites sampled, and for suspensions or pieces of tissue prepared for viewing. The malignant cells in hairy cell leukemia, whether they are harvested from the peripheral blood, the bone marrow, or the spleen and whether they are viewed in a suspension or in whole tissue, have a unique cell surface ultrastructure which is easily confirmed by scanning electron microscopy.