[Drug prevention of deep venous thrombosis and pulmonary embolism].
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Biomedical subjects
Publications and source records attributed to A N Teien.
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Serological analysis by radioimunoassay of sera from 297 patients hospitalized with acute non-toxic hepatitis was used for classification according to virus etiology. Radioimmunoassays included tests for hepatitis B surface antigen (HBsAg), antibody to HBsAg (anti-HBs), antibody to hepatitis A virus (anti-HAV), anti-HAV of IgM class, and antibody against cytomegalovirus (GMV) and Epstein-Barr virus. One patient with a significant rise in anti-CMV antibodies was classified as having CMV hepatitis. Among the 296 remaining patients serological markers indicated hepatitis A in 51 cases (17.2%) and hepatitis B in 208 cases (70.3%). The remaining 37 patients (12.5%) fulfilled criteria for acute non-A, non-B hepatitis. This type of hepatitis had symptoms and signs indistinguishable from those of hepatitis A, except for a slight tendency to milder disease on admission. A considerable proportion of patients with non-A, non-B hepatitis had a history of drug abuse (43.2%) and of recently traveling to endemic hepatitis areas (29.7%). In the remaining 27.1% no particular background was revealed. No case of post-transfusion hepatitis was seen. During the last 6 months of the study a striking change in epidemiology concerning hepatitis A was seen, apparently caused by a steep increase in the incidence of this type of hepatitis among drug addicts. No significant difference in biochemical liver tests was seen in non-a, non-B hepatitis or hepatitis A. In contrast, a marked and statistically significant difference in serum concentrations of IgM was found, with higher values (mean, 7.5 g/1; range, 3.2-13.9 g/1) in hepatitis A than in non-a, non-B hepatitis (mean, 3.3 g/1; range, 0.9-9.4 g/1). This difference may have diagnostic value.
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A purified antithrombin III (AT) preparation was infused in 8 patients with hip fractures, while 8 patients were observed as controls. The infusion was well tolerated by all patients, and the AT activity in plasma was significantly raised throughout an observation period of 48 h as compared with the controls.
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Heparin (100 U/kg body-weight) was injected intravenously, and heparin concentration in plasma determined by polybrene titration. Mean heparin half-life was 117.8 min in a group of patients with liver cirrhosis and normal renal function (n = 6) as compared to 74.0 min in the normal group (n = 6). The difference between the two groups is statistically significant (p approximately 0.02). Heparin half-life was correlated to galactose half-life in the patients (r=0.83, p= 0.05). The findings suggest that heparin is metabolized in the liver. There was a significant fall in antithrombin III activities in the normals, but not in the patients. A possible explanation may be that the normal liver removes heparin bound to antithrombin III, and that this function is impaired in liver cirrhosis.
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Of 1068 blood samples referred for evaluation of the haemostatic mechanism 135 contained heparin as judged by the polybrene titration method. Of the 57 samples with a heparin concentration in the defined therapeutic range, 65 per cent had APTT values in the "therapeutic range". Of the samples from patients who had not received any anticoagulant, 213 (24 per cent) had prolonged APTT, and 48 of these samples had APTT values in the "therapeutic range" for heparin therapy. It is suggested that the APTT test is of limited value in monitoring heparin therapy.
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Heparin (100 U/kg bodyweight) was administered as single i.v. injections, and heparin concentration in plasma determined by polybrene titration. Mean concentration half-life was 74.7 min in the normal group (n = 6), 118.6 min in the nephrectomized patients (n = 5), and 97.8 min in the other uraemic patients (n = 6). The differences between the mean values for the normals and for the 2 patient groups were statistically significant (p is less than 0.001 and p approximately 0.2 respectively). Mean anticoagulant half-life (based on thrombin clotting time) was 64.3, 75.8 and 62.7 min in the 3 groups. The differences between heparin concentration half-life and anticoagulant half-life in the 3 groups were statistically significant. These differences may be partly explained by a significant fall in heparin cofactor activity after injection of heparin. There was a strong positive individual correlation between heparin concentration half-life and anticoagulant half-life in the patients (r = 0.94), but not in the normal group (r = 0.31). There was a strong negative individual correlation between heparin tolerance and heparin concentration half-life in the patients (r = -0.84), but no correlation in the normal group. It is concluded that severely impaired renal function has a significant, but moderate influence on heparin elimination.
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