SummarySome clinical advantages are claimed for low molecular weight heparin so the mobilisation of platelet factor 4 (PF 4) from the endothelial pool by the heparins may be relevant. Unfractionated (UF) heparin has been compared with Kabi heparin fragment 2165. A single intravenous (i. v.) injection of 60 iu/kg heparin was compared with 5000 anti-Xa units of Kabi-2165. Less PF 4 was mobilised by Kabi-2165 and some apparently remained in the pool and was released when the pool was subsequently challenged by giving i.v. heparin. Subcutaneous (s. c.) injections of 5000 iu heparin twice daily were compared with 5000 anti-Xa units of Kabi-2165 once daily, each given for a week. The plasma PF 4 was never raised yet when finally challenged with i.v. heparin the pool was “empty” or refractory after the s.c. heparin but some PF 4 remained after the s.c. Kabi-2165. The two glycosaminogly-cans (GAGs) had widely differing half-lives but the t/2 of the PF 4 mobilised by the two GAGs was similar even though the PF 4 is apparently bound to the GAG.
SummaryThere is considerable evidence that the quantity or quality of plasma lipids influences platelet function tests, and clofibrate reduces high plasma lipids and alters some platelet tests. Clofibrate was accordingly given to patients with vascular disease who were at risk of thrombosis. The heparin thrombin clotting time (HTCT), initially short and thus possibly reflecting increased activation, was regularly returned to normal after about a month’s delay. The fibrinogen was also normalized but the initially abnormal anti-thrombic activity became more abnormal. ICI 55,897, an analogue of clofibrate, also normalized the HTCT and the fibrinogen and had no adverse effect on the anti-thrombin levels. This compound has no effect on plasma lipids. If it can be shown that the correction of abnormal tests conveys clinical benefit these findings suggest that ICI 55,897 might clinically be more beneficial than clofibrate. However, direct comparison of clofibrate and ICI 55,897 suggests that clofibrate is more effective in normalizing the HTCT. The mechanisms underlying these drug-induced changes are unknown but they cannot be directly related to lipid changes.
The incidence of a number of cancers is affected by socio‐economic status. We hypothesized that the incidence of head and neck squamous cell carcinoma (HNSCC) would fall with increasing affluence, that this pattern would be similar for all sites, and that more second primary tumours would appear in deprived groups. Data on all HNSCC registered between 1985 and 1991 in the South West of England was collected. Tumours of the lip and skin were excluded. The measure of socio‐economic status chosen was the Carstairs Index.1 Tumours were classified as ‘first alone’, ‘first plus others’, ‘synchronous’ (within 60 days) or ‘subsequent’. Corrected χ2 testing was applied. There were 1570 cases of HNSCC, 72% in men, 28% in women. Carstairs index could be determined for 1467 cases. Overall, socio‐economic status was inversely related to the development of HNSCC. In men, the most deprived group had a significantly higher incidence of oral carcinoma than all other groups (P < 0.01), whereas the incidence of laryngeal carcinoma showed a gradual rise with increasing deprivation. In women, the trend was less clear. Seventy‐two (4.9%) went on to develop a second primary, of which 35% were lung and 12% bladder. Socio‐economic status did not affect the development of a second primary tumour in either sex. Thus, in the South West of England, socio‐economic status affects the incidence of HNSCC, but there are different patterns in different tumour sites. However, socio‐economic status does not affect the incidence of a second primary. The association of HNSCC with carcinoma of the bladder is a new finding.
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