Aspirin and bleeding-time: dependency of age.
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Biomedical subjects
Publications and source records attributed to E Stoffersen.
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Plasma and urinary antithrombin III (AT-III) was measured in 15 cases of nephrotic syndrome. Plasma AT-III correlated well with serum albumin, but poorly with proteinuria, whereas urinary AT-III correlated well to proteinuria. The plasma AT-III level had a mean similar to 25 healthy controls, but the range was significantly wider. A case with nephrotic syndrome and left renal vein thrombosis is reported. The urinary output of AT-III rose and the plasma level fell with the activity of the disease. Although AT-III and albumin have similar molecule weight, their renal clearance was found to be different. It is suggested that urinary loss of AT-III plays a role in the hypercoagulable state sometimes found in the nephrotic syndrome.
10 cases of pernicious anaemia are reported in which 6 had abnormal aggregation with epinephrine, 3 with fibrinogen, 2 with ADP, and 2 with ristocetin. 5 patients had thrombocytopenia and 3 of these had a prolongation of the bleeding time. These abnormalities were normalized after vitamin B12 treatment. After treatment, platelet size changed toward a smaller diameter, but platelet size, however, was not significantly different from the normal platelet size distribution.
Antithrombin III (AT-III) was measured immunologically in 20 uremic patients on maintenance hemodialysis and in 10 non-dialysed uremic patients. The dialysed patients had slightly elevated AT-III levels. The non-dialysed patients had significantly elevated AT-III levels. A negative correlation was found between AT-III and serum creatinine and between AT-III and serum albumin. AT-III did not correlate to the heparin amount required for hemodialysis. A negative correlation was found between the heparin requirement and serum albumin. It is suggested, that serum albumin might facilitate the action of AT-III and heparin. It is also suggested, that AT-III levels may be high in active renal disease, decreasing as uremia advances.
Unlike arachidonic acid (eicosatetraenoic acid, C20:4omega-6, A.A.), eicosapentaenoic acid (C20:5omega-3, E.P.A.) does not induce platelet aggregation in human platelet-rich plasma (P.R.P.), probably because of the formation of thromboxane A3 (T.X.A3) which does not have platelet aggregating properties. Moreover, E.P.A., like A.A., can be utilised by the vessel wall to make an anti-aggregating substance, probably a delta17-prostacyclin (P.G.I3). This finding suggests that, in vivo, high levels of E.P.A. and low levels of A.A. could lead to an antithrombotic state in which an active P.G.I3 and a non-active T.X.A3 are formed. Eskimos have high levels of E.P.A. and low levels of A.A. and they also have a low incidence of myocardial infarction and a tendency to bleed. It is possible that dietary enrichment with E.P.A. will protect against thrombosis.
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