SUMMARYThe clinical, haematological, morphological and histological features of a series of 22 patients presenting with splenic lymphoma with circulating villous lymphocytes were assessed and compared with those of patients with other forms of chronic B cell leukaemia in an attempt to differentiate this condition from hairy cell leukaemia, prolymphocytic leukaemia, and chronic lymphocytic leukaemia, with which this condition has many features in common. The disease was twice as common in men than in women, with a mean (SD) age at diagnosis of 72 (9) years, and the most consistent presenting feature was massive enlargement of the spleen, which showed white and red pulp disease with a plasmacytic component. Small monoclonal bands were found in 60% of cases.

Using a recently devised solid phase radioimmunoassay to detect anticardiolipin antibodies, we report the presence of these antibodies in 30 of 96 patients with chronic autoimmune thrombocytopenic purpura (AITP). IgG anticardiolipin antibody levels were elevated in 14 patients and IgM anticardiolipin antibody levels were elevated in 27 patients. We suggest that these antibodies may mediate peripheral platelet destruction by binding to phospholipids in the platelet membrane. It is also conceivable that the presence of anticardiolipin antibodies may select a subpopulation of patients with chronic AITP who may go on to develop other autoimmune disorders, such as systemic lupus erythematosus.

Platelet antibodies either bound to the surface of platelets or free in the serum were sought in patients who had low platelet counts for a variety of reasons. They were detected by finding excess IgG on the surface of washed platelets either directly or after incubation of the serum with normal platelets. The technique used was a modification of that described recently (Dixon et al, 1975) in which the greater the amount of anti-IgG consumed by the reaction with platelets the less the subsequent lysis of sheep red cells coated with IgG. This test could be calibrated by adding known quantities of IgG to the antisera and thus the amount of bound IgG could be measured. Platelets from normal donors and those with thrombocytopenia due to non-immunological causes such as aplastic anaemia or acute leukaemia were found to have 15-70 ng IgG/10(7) platelets (mean 53 ng). 37 out of 38 thrombocytopenic patients in whom immune destruction of platelets was suspected were found to have excess IgG on their platelets ranging from 70 to 720 ng/10(7) (mean 297 ng, P less than 0.001) and there was a significant inverse correlation between this amount and the platelet count (r = 0.85, P less than 0.001). Antibody in the serum was found in 14 of 22 patients with 'idiopathic' thrombocytopenic purpura (ITP), three of four patients with underlying lymphoma and in all five cases of systemic lupus erythematosus (SLE). Four non-thrombocytopenic patients with autoimmune haemolytic anaemia (AIHA) due to IgG on the red cells were also studied and were shown to have no increase in platelet-bound IgG. Our results confirm the work of Dixon et al (1975) that platelet antibody as excess IgG can be readily detected on the surface of platelets in patients with immune thrombocytopenia. The clinical implications of these findings are discussed.

A high proportion of peripheral-blood lymphocytes formed spontaneous rosettes with mouse red cells in 22 out of 23 cases of chronic lymphocytic leukaemia (CLL); the proportion was significantly higher than in 19 cases of other B-lymphoproliferative disorders (non-CLL group) and in 19 normal controls. Intermediate findings were obtained in 10 cases of "hairy" cell leukaemia. Blast cells from various types of acute leukaemia did not bind mouse red cells. Pre-treatment of the lymphocytes with neuraminidase led to a significant increase in the proportion of rosettes in CLL only. This test may prove useful in distinguishing CLL from other B-lymphoproliferative disorders, particularly prolymphocytic leukaemia.

Immune thrombocytopenia (ITP) is frequently encountered in patients with lymphoproliferative disorders. However this is only rarely reported in patients with multiple myeloma. We describe three cases who presented initially with the clinical manifestations of ITP but were subsequently found to have multiple myeloma. Platelet count increments to standard treatment modalities for ITP were observed in all three patients with transient or partial response. The importance of recognizing the immune mediated thrombocytopenia in patients with myeloma and the implications of this combination are discussed.