Cryoprecipitate therapy in haemophilia.
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Biomedical subjects
Publications and source records attributed to C D Forbes.
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Adrenoceptor antagonists are being used increasingly for the treatment of pregnancy-induced hypertension (PIH). Previous studies have shown that these drugs can inhibit platelet aggregation and thromboxane production. The aims of this study were to determine (i) whether adrenoceptor antagonists had any effect on vascular prostacyclin (PGI2) production and (ii) whether these drugs acted synergistically with PGI2 and the PGI2-like activity derived from umbilical artery to inhibit platelet aggregation in vitro. The adrenoceptor antagonists labetalol, pindolol and propranolol were found to have no effect on PGI2 production from the umbilical artery at low drug concentrations. These agents were also found to act synergistically with both pure PGI2 and PGI2-like activity derived from umbilical artery to inhibit platelet aggregation. This synergistic effect may be beneficial in the treatment of disorders which are associated with reduced PGI2 production, such as PIH where such synergy may help compensate for PGI2 deficiency.
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In a randomised double-blind controlled trial we have assessed the use of ancrod ('Arvin') in the prophylaxis of deep vein thrombosis (DVT) in patients undergoing hip replacement surgery. Thirty-five patients received daily subcutaneous injections of ancrod and 38 patients received saline injections. DVT was detected by bilateral ascending venography (67 patients) 7-19 days after surgery. The frequency of major femoral DVT (greater than or equal to 5 cm long) was significantly reduced from 18 thrombi in the limbs of the placebo group to 5 in the ancrod group (p less than 0.01). The overall frequency of thrombi including calf DVT was not significantly different between the two groups. Four patients within the ancrod group had evidence of wound bleeding, compared with 2 placebo patients. One patient had a bleeding event which was considered severe enough to require cessation of ancrod injections.
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A questionnaire was sent to 508 consultants in Scotland likely to encounter deep vein thrombosis and pulmonary embolism to assess their current standard practice in diagnosis and treatment of these disorders. Replies were received from 358 (70.5%). In deep vein thrombosis 47% and in pulmonary embolism 33% of consultants usually depended on clinical observation alone for diagnosis. In deep vein thrombosis 37% used venography to supplement clinical diagnosis and in pulmonary embolism 13% used angiography and 53% used isotopic scanning. Almost all consultants treated deep vein thrombosis (95%) and pulmonary embolism (99%) with anticoagulants. Most consultants (81%) gave heparin by intravenous infusion. Although many consultants gave intravenous heparin for more than three days (49.5% in deep vein thrombosis and 61% in pulmonary embolism), 25% of these consultants did not use any laboratory monitoring of heparin's effect. Large numbers of consultants gave warfarin for more than three months (20% in deep vein thrombosis and 47% in pulmonary embolism). There was a significant tendency to give heparin (p less than 0.01) and warfarin (p less than 0.001) for longer periods in pulmonary embolism than in deep vein thrombosis. This survey shows a widely varying practice and underlines the need for further controlled studies to provide clear guidance in the management of deep vein thrombosis and pulmonary embolism.
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