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Thirty one peripheral blood stem cell mobilizations using cyclophosphamide, followed by leucapheresis, were performed in 25 patients with a variety of haematological malignancies. Cyclophosphamide at doses ranging from 0.25 g/M2/day x 4 days to 4 g/M2 on one day were given. Total doses of cyclophosphamide less than 4 g/M2 failed to induce a significant mobilization of stem cells into the peripheral blood. This compares to cyclophosphamide doses of 4 g/M2 given over one or two days where 70%-75% of patients yielded adequate stem cells for transplantation (greater than 20 x 10(4) CFU-GM/kg). Both the presence of tumour cells in the bone marrow and previous chemotherapy within 12 months of cyclophosphamide infusion significantly diminished the patients stem cell mobilizations. The rate of recovery of the patient's leucocyte count following cyclophosphamide was highly correlated to the peak level of PB CFU-GM and is a good indicator of the total stem cell yield. Fever in 50% of patients during the period of cytopaenia was the only complication seen in our patients and thus high dose cyclophosphamide is a suitable and safe agent for mobilizing haemopoietic stem cells.

We used single high doses of cyclophosphamide (4 g/m2) to produce rebound increases in peripheral blood (PB) stem cells (PBSC) during recovery from myelosuppression, enabling their collection by apheresis for later autotransplantation. Thirty-three courses of cyclophosphamide were given to 30 patients with malignant lymphoma, multiple myeloma, or solid tumors. The neutrophil count was less than 0.5 x 10(9)/liter for a mean of 6.9 days (median 7 days), and fever occurred in 17 of 33 courses. Positive blood cultures occurred in two patients, one of whom died. The mean peak level of PB granulocyte-macrophage colony-forming units (CFU-GM) was 1517 x 10(3)/liter (median 2447 x 10(3)/liter), a 14-fold increase above the mean in normal subjects. The peak occurred at a mean of 16.6 days (median 16 days) after cyclophosphamide, generally coinciding with the time to reach 1.0 x 10(9) neutrophils per liter. Normal or minimally involved bone marrow and a rapid rise in leukocyte count during recovery were independent variables correlated to the peak of the rebound increase in PB CFU-GM levels. Previous chemotherapy and the duration of neutropenia were additional independent variables in the group with peak PB CFU-GM levels of greater than 1000 x 10(3)/liter. The mean total CFU-GM collected after a mean of five aphereses was 43.8 x 10(4)/kg body weight (BW) (median 35.5 x 10(4)/kg BW), significantly correlated with the mononuclear cell yield. We conclude that single 4 g/m2 doses of cyclophosphamide effectively produce high levels of PBSC, particularly but not exclusively in patients with normal or minimally involved bone marrow and who have not had intensive recent chemotherapy.

The development of hypertrophic osteoarthropathy in patients with leukaemia or lymphoma presents important diagnostic and therapeutic implications. Patients with these disorders are also predisposed to the development of invasive phycomycosis and aspergillus infections. We report a case of primary bone marrow lymphoma complicated by hypertrophic osteoarthropathy. At postmortem examination there was evidence of disseminated phycomycosis and aspergillus infections. We believe this relationship has not previously been reported.

The experience with central nervous system (CNS) non-Hodgkin's lymphoma at a 700-bed teaching hospital over five years (1979-1983) is reported. During this period 222 patients with non-Hodgkin's lymphoma were seen. Ten new cases (eight patients with secondary and two patients with primary CNS lymphoma) were diagnosed during this period, representing an overall incidence of 4.5%. The clinical, pathological and neuroradiological findings of this group are described with special emphasis on the varied appearances that were found on computer-assisted tomographic scans.

Three patients with systemic T-cell leukemia-lymphoma presented with generalized pruritic skin rash which was clinically nondiagnostic. Biopsies revealed infiltration of the superficial dermis by atypical lymphoid cells with epidermal exocytosis (Pautrier abscesses) producing a pattern of histologic involvement indistinguishable from that of mycosis fungoides and Sézary syndrome. This striking similarity suggests that the phenomenon of preferential epidermotropism is not confined to mycosis fungoides and Sézary syndrome, but may be a property shared by other subpopulations of T-lymphocytes.

Four cases of node-based T cell lymphoma are presented. The tumours had 2 distinct morphologic patterns. Two cases showed a polymorphous proliferation of pleomorphic lymphoid cells, small lymphocytes, epithelioid cells and arborizing small vessels while the others displayed a monomorphous infiltrate of large atypical lymphoid cells characterized by granular nuclei with numerous tortuous folds to produce a 'squiggly' appearance. One case showed a progression from one histological pattern to the other. Confirmation of the T cell nature of these lymphomas was based on the demonstration of E-rosette formation by morphologically atypical lymphoid cells which also stained positive for acid alpha-naphthyl acetate esterase activity. The patients had an average age of 52 yr and presented with a variable distribution of lymphadenopathy and a predominance of extranodal involvement. Two cases disclosed hypergammaglobulinaemia, one of whom had a paraproteinaemia of IgM-k type. All patients responded poorly to standard combination chemotherapy, 2 expiring 48 and 53 mth after onset of symptoms.

Immunological surface marker techniques were applied in a study of 29 cases of chronic lymphocytic leumaemia and 22 of non-Hodgkin's lymphoma. Surface marker characteristics distinguished 2 subtypes of B lymphocytes. Chronic lymphocytic leukaemia was a monoclonal proliferation of B lymphocytes which produced spontaneous rosettes with mouse erythrocytes and had faintly immunofluorescent surface immunoglobulin. The majority of non-Hodgkin's lymphomas also had their origin from B lymphocytes but in contrast, this subtype did not show receptors for mouse erythrocytes and their surface immunoglobulin was brightly staining and demonstrated "capping". The clonal origin of nodular lymphomas could also be demonstrated on frozen sections stained for surface immunoglobulin. Two cases of true histiocytic lymphoma were identified. The current information available on surface marker characteristics of the leukaemias and lymphomas is reviewed.