18 patients with early stage, previously untreated B-CLL were given interferon alfa (IFN alpha) 2a. 3 MU thrice weekly, subcutaneously. The peripheral lymphocyte count decreased in all patients. Response was delayed in three patients until they had received a median of 5 months therapy, one of whom had an initial transient increase in lymphocytes. Two patients normalized their blood lymphocyte counts, but neither achieved complete remission (CR). Responses were transient in eight patients lasting a median of 5 months (3-21). Binding anti-IFN alpha antibodies were present in 9/17 patients tested (53%). Low titre binding antibodies (< 533 IBU/ml) were not associated with LHR, but high titre antibodies (> 4401 IBU/ml) were. Two of 12 patients assessed had a > 3 g/l increase in baseline serum IgG levels during IFN alpha therapy, one of whom reverted to pretreatment levels in association with LHR. Haematological toxicity was moderate, other than in two patients, one of whom developed autoimmune haemolytic anaemia and the other thrombocytopenia. We conclude that IFN alpha lowers the lymphocyte count in early stage CLL, that the response may be delayed and that anti-IFN alpha antibodies may play a role in a proportion of those in whom the response is transient.

apparently in relation to the epithelial basement membrane, with thickening of this structure. The immunofluorescence in the choroid plexus was negative in all cases ofthe control group. Histopathological changes of the choroid plexus, with a pattern similar to that of the systemic hypertension group, were found in only two of the control group.Our results indicate that in about 25% of patients with systemic hypertension the choroid plexus is a site for the deposition of Ig and fractions of C. We suggest that these findings may be secondary to increased vascular permeability produced by hypertension, leading to the passage of plasma and retention of circulating immune complexes in the walls of the choroid plexus, perhaps in a manner analogous to that which occurs in the kidney.'3 A question unanswered by this work is the nature of antigens which stimulate the immune complexes formation and lead to their precipitation in the choroid plexus in some cases of systemic hypertension. Further research into the identification of these antigens as well as the demonstration of a pathogenetic association between immune complexes and histopathological changes in the choroid plexus is needed.

Eleven patients with acute myeloid leukaemia (AML) in first complete remission (CR) were treated with alfa-2a-interferon (for short ‘interferon’) maintenance therapy, at a dose of 3 MU twice to thrice weekly subcutaneously. Adjustments were made to maintain neutrophil counts > 1 × 10⁹/1 and platelet counts > 100 × 10⁹/1· A transient fall in haemoglobin, neutrophil and platelet counts was noted in all 9 evaluable patients. Median time to nadir was 7 weeks. Initial dosage reductions were necessary in 5 patients, 3 of whom were later able to tolerate the starting dose. No episodes of infection or bleeding were documented during therapy and no red cell or platelet transfusions were necessary. At the time of writing (median follow-up of 31 weeks), 7 patients continue in CR, 6 of whom remain on interferon. One patient discontinued interferon on developing sicca syndrome. Other than in this patient, side effects were minor. Mean dose administered was 6.7 MU/patient/week. We conclude that low-dose IFN maintenance therapy is well tolerated in older patients with AML in first CR.

Summary An enzyme‐like immunosorbent assay and a blood autoanalyser were used to determine macrophage‐colony stimulating factor (M‐CSF) levels and the absolute number and percentage of circulating monocytes in 80 normal women with singleton pregnancies at 12–40 weeks’ gestation, and ten healthy non‐pregnant volunteers. The mean values of M‐CSF and absolute number and percentage of circulating monocytes of the control group were 367 U/ml (SD 43) and 389 × 1071 (SD 180) and 5.3% (SD 1.7) respectively. In pregnancy, M‐CSF was significantly higher than non‐pregnant controls only after 28 weeks’ gestation. The absolute number and the percentage of circulating monocytes increased significantly with gestation after 16 weeks. There was no significant association between the concentration of M‐CSF and the number or percentage of circulating monocytes. These data suggest that during pregnancy there is an up‐regulation of M‐CSF and monocytes.