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A 71-year-old woman with a spontaneous anti-factor VIII inhibitor fractured her right wrist and 2 months later her left femur. She received treatment with porcine factor VIII for the first fracture and developed a secondary anti-porcine antibody response (from 10 to 200 Bethesda units). Following the second fracture she received intravenous immunoglobulin (i.v. IgG) (0.4 g/kg day for 5 days) in an attempt to reduce antibody activity. Despite further treatment with porcine factor VIII, the antibody level declined instead of rising as expected and the anti-human antibody activity also declined. We were not able to demonstrate neutralizing activity to her antibody but did demonstrate a reduced helper: suppressor ratio and reduced B-cell numbers and function after treatment with i.v. IgG. These changes were transient and as B-cell function improved over the following 4 months, her anti-human activity returned toward its previous level. Anti-porcine activity remained at its previous low level. We speculate that one of the mechanisms of action of i.v. IgG may be a direct cellular effect influencing both T-suppressor and B-lymphocyte function.

Adding calcium to a mixture of thrombin and fibrinogen increased the breaking strain of the resultant coagulum by 10-fold, but did not significantly reduce the length to which it could be stretched. There was no detectable change in the time taken for the coagulum to dissolve in urine. Simulation pyelolithotomies were performed on pig kidneys containing ball-bearings which represented calculi. Coagula formed with calcium were significantly more effective at retrieving the ball-bearings than coagula without calcium. It is concluded that the ideal coagulum formula should include 1 mmol of calcium.

A patient with multiple injuries developed a severe coagulation defect due to a deficiency of vitamin K. None of the usual predisposing factors was present and the patient's diet was very poor. Dietary deficiency of vitamin K and the importance of antibiotic therapy in its production are discussed.

Three patients who have been given intermediate purity NHS heat-treated factor VIII concentrate have been followed prospectively for 7-10 months. None had previously received more than six donor units of blood products containing factor VIII. There were no clinical side effects from concentrate administration, haemostasis was satisfactory and no patient developed clinical or laboratory evidence of hepatitis or HTLV III/LAV infection. Heat treatment resulted in the loss of slightly more than 20% of factor VIII activity but in vivo recovery of factor VIII and half disappearance times were within the expected range.

Information on performance is invaluable to those who have to decide on the choice of an instrument. More interest is being shown in the use of coagulometers. Accordingly, a tentative protocol for the evaluation of coagulometers is presented for discussion. While it is based on the use of one-stage prothrombin time, principles of evaluation are laid down which should make it generally applicable. It is hoped that the tentative protocol will form the basis of a reference protocol and to this end comments are invited from users of coagulometers and suppliers. Comments for publication may be sent to the Editor of Clinical and Laboratory Haematology or to the Secretary of the Working Party.