Delayed commencement of granulocyte colony-stimulating factor following autologous bone marrow transplantation accelerates neutrophil recovery and is cost-effective.

It is known that Granulocyte colony-stimulating factor (G-CSF) accelerates neutrophil recovery following bone marrow transplantation (BMT), though the optimal timing is not clear. We have undertaken a pilot study in 19 recipients of autologous BMT for non-myeloid malignancy, in which G-CSF was commenced 10 (13 cases) or 7 (6 cases) days after BM infusion. These patients were compared with 18 historical controls, who did not receive G-CSF. The median time to achieve both 0.5 and 1.0 x 10(9) neutrophils/Litre was significantly shorter in the treated group (18 and 21 days respectively) than the control group (20.5 and 29 days; p = 0.03 and 0.02 respectively). No differences between the two groups were seen for the number of febrile days, days on antibiotics or the cost of the antibiotics. G-CSF-treated patients remained in hospital for significantly less time after marrow infusion (21 days compared to 29 days; p = 0.007). The cost of the G-CSF therapy was offset by the decreased bed utilisation, so that the median combined antibiotic, G-CSF and hospitalisation cost was 754 pounds less for G-CSF treated patients. It is concluded that delaying the commencement of G-CSF after autologous BMT accelerates neutrophil recovery, and may allow earlier discharge from hospital, whilst not adversely affecting the cost of the procedure.

Familial antithrombin III deficiency and Mycoplasma pneumoniae pneumonia.

A 10 year old girl presented with a massive femoral vein thrombosis associated with Mycoplasma pneumoniae pneumonia. Subsequently type I familial antithrombin III deficiency was diagnosed. It is suggested that prophylactic measures aimed at preventing thrombosis should be considered in acutely ill subjects with infection and familial thrombophilia.

Lupus anticoagulant.

Acquired antibodies to phospholipids form a heterogeneous group, which may be detected in vitro by the inhibition of phospholipid dependent tests of coagulation (lupus anticoagulant) and also by immunological assays, such that a combined approach is required for their reliable detection. While initially described in sufferers from systemic lupus erythematosus, these antibodies are increasingly recognised in a broad spectrum of disease, most importantly in relation to thromboembolism and recurrent fetal loss; occasionally they may also be found in otherwise healthy individuals. The mechanisms underlying the prethrombotic state associated with these antibodies have not been defined, although interference with the natural anticoagulant systems seems possible. Identification of antiphospholipid in subjects with spontaneous thromboembolism may influence therapeutic decisions, while their presence in women with recurrent fetal loss has lead to attempts to alter the outcome of further pregnancies with anticoagulant and immunosuppressive regimens, however the optimum management has not yet been determined. The recognition of these antibodies and their clinical associations is therefore highly relevant to clinical and laboratory haematology.

Screening for lupus anticoagulant and anticardiolipin antibodies in women with fetal loss.

Sixty six women with first or second trimester fetal loss were investigated for the presence of lupus anticoagulant by routine coagulation tests and the dilute Russell's viper venom time with a platelet neutralisation procedure, and for raised anticardiolipin antibodies by an enzyme linked immunosorbent assay. Of 35 women with recurrent fetal loss, seven were positive for lupus anticoagulant and six had increased IgG anticardiolipin antibodies, while of 31 women with only one or two episodes of fetal loss, one had lupus anticoagulant and none increased IgG anticardiolipin antibodies. These findings were significantly different. There was no difference in the incidence of increased IgM anticardiolipin antibodies between the two groups (three and two cases, respectively). A further 11 women with intrauterine death in the third trimester were studied and lupus anticoagulant and raised IgM anticardiolipin antibodies were found in one case. No woman was known to have systemic lupus erythematosus. It is concluded that lupus anticoagulant and increased IgG anticardiolipin antibodies are independently associated with recurrent first and second trimester fetal loss and that such cases should be investigated, even in the presence of otherwise good health, by a comprehensive methodological approach.