PubMed Health⌕ Search

Biomedical subjects

E Genton

Publications and source records attributed to E Genton.

At least 19 recordsLinked to original sources
PubMed1992

Niacin-induced clotting factor synthesis deficiency with coagulopathy.

Although coagulopathy is a well-known complication of severe niacin-induced hepatotoxic reaction, it is not found in patients with minimal aminotransferase level elevations. Three patients with significant clotting factor synthesis deficiency and coagulopathy (prothrombin times, greater than 1.5 times control) from sustained-release niacin had only mild aminotransferase level elevations (1.5 to 2.0 times normal). In each case, protein deficiency, coagulopathy, and aminotransferase level elevation resolved promptly after withdrawal of niacin therapy. In one case, this syndrome recurred after rechallenge with sustained-release niacin, whereas the coagulopathy did not recur in a second patient rechallenged with crystalline niacin. Deficiency in protein synthesis, including coagulation factors, and coagulopathy are unrecognized complications of sustained-release niacin therapy. These cases indicate the need to measure prothrombin times routinely in patients who develop even mild aminotransferase level elevation while receiving sustained-release niacin therapy. These data are important in light of the increasing use of sustained-release niacin in the treatment of patients with lipid disorders.

Adult↗
PubMed1990

Modification of thrombogenic factors in cardiac disease.

Thrombosis plays an important role in the development and course of most disorders affecting the heart. No effective methods are available to eliminate the thrombogenic stimulus for those conditions requiring the use of antithrombotic agents for prophylaxis or to arrest a thrombotic event. Available platelet and coagulation inhibitors are effective when properly selected and administered.

Coronary Disease↗
PubMed1979

Warfarin sodium versus low-dose heparin in the long-term treatment of venous thrombosis.

Acute deep-vein thrombosis is usually treated with intravenous heparin for a number of days, then with oral anticoagulants for weeks to months. We have compared adjusted-dose warfarin sodium with fixed low-dose subcutaneous heparin in the prevention of recurrent deep-vein thrombosis. Sixty-eight patients with acute deep-vein thrombosis confirmed by venography were treated with intravenous heparin and then randomized to secondary prophylaxis. Nine of 35 patients receiving subcutaneous heparin, but none of 33 receiving warfarin sodium, had new episodes of objectively documented venous thromboembolism (P = 0.001). Seven patients on warfarin sodium experienced bleeding complications (of which four were major), as compared with no patients receiving subcutaneous heparin (P less than 0.005). Thus, adjusted-dose warfarin sodium is more effective than low-dose subcutaneous heparin in preventing recurrent venous thromboembolism, but its use is accompanied by a significant risk of bleeding.

Acute Disease↗
PubMed1979

Plasma beta-thromboglobulin: differentiation between intravascular and extravascular platelet destruction.

To elucidate the usefulness of beta-thromboglobulin (beta TG) in the differentiation of the mechanism of thrombocytopenia, plasma beta TG concentration was measured in one patient with amegakaryocytic thrombocytopenia, four patients with autoimmune thrombocytopenia (ATP), two patients with thrombotic thrombocytopenia (TTP), and one patient with thrombocytopenia secondary to disseminated intravascular coagulation (DIC). Plasma beta TG was not measurable in amegakaryocytic thrombocytopenia, was normal in ATP, and was increased in TTP and DIC. These data indicate that in thrombocytopenic patients, increased plasma beta TG concentration may result from intravascular platelet consumption with release of platelet constituents in contrast to extravascular platelet destruction by the macrophage-monocyte system.

Adult↗
PubMed1978

Platelet-suppressant therapy in patients with coronary artery disease.

Platelets may contribute to the pathogenesis of atherosclerosis and to the complications of coronary atherosclerosis, acute myocardial infarction, unstable angina, and sudden cardiac death. In addition, platelets may contribute to saphenous vein aortocoronary graft occlusion. Of 104 men with coronary artery disease, platelet survival (SURV) (chromium51 labeling) was shortened in 68% (3.1+/-0.03 days [average+/-SEM]; normal, 3.7+/-0.03 days; P greater than .001). Three platelet-suppressant drugs, sulfinpyrazone, clofibrate, and dipyridamole increased SURV. Saphenous vein graft occlusion was associated with shortened SURV. Of 36 men with occlusion of at least one graft, SURV was shortened in 35 (2.5+/-0.08 days), whereas in 19 with all grafts open, SURV was shortened in six (3.5+/-0.10 days; P less than .01). These drugs increased SURV (2.3 +/- 0.08 to 2.7 +/- 0.11 days; P less than 0.1) and were associated with improved graft patency (four of 32 grafts after initial bypass vs 30 of 34 grafts open after second operation).

Adult↗
PubMed1978

Platelet survival determination in atherosclerosis.

Platelet survival presently represents a useful method for the study of atherosclerosis and its consequences in patients and in animal models. The currently used technique, while time consuming, appears to be reliable and reproducible for the measurement of platelet survival and turnover rate. The test offers promise to detect and perhaps quantify the degree of active vessel wall damage. In addition, it might prove useful to identify drugs with potential as platelet suppressants. Finally, the test might be used to compare with new techniques developed or used to identify vessel damage or thrombosis proneness.

Animals↗
PubMed1978

Cardiac thromboembolism: evidence for role of platelets and value of platelet suppressant therapy.

Thromboembolism remains a frequent and serious problem in cardiac patients. Methods to identify the thrombosis prone patient and the identification of safe and effective forms of treatment would be of great value. The accumulating evidence which indicates that abnormalities in platelet tests are often present in cardiac patients and may help identify those at greatest risk of thrombosis is encouraging. It suggests that patients with cardiac disease are desirable groups for investigation. It also indicates that the platelet survival test may be useful as a reference against which new and more practical tests can be compared, as well as a means to identify useful platelet suppressant drugs or to monitor the effects of these drugs.

Aspirin↗
PubMed1977

Cardiac thromboembolism: evidence for role of platelets and value of platelet suppressant therapy.

Thromboembolism remains a frequent and serious problem in cardiac patients. Methods to identify the thrombosis-prone patient and the identification of safe and effective forms of treatment would be of great value. The accumulating evidence which indicates that abnormalities in platelet tests are often present in cardiac patients and may help identify those at greatest risk of thrombosis is encouraging. It suggests that patients with cardiac disease are desirable groups for investigation. It also indicates that the platelet survival test may be useful as a reference against which new and more practical tests can be compared, as well as a means to identify useful platelet suppressant drugs or to monitor the effects of these drugs.

Blood Platelets↗
PubMed1977

Platelet survival time in patients with hypoxemia and pulmonary hypertension.

Platelet survival time (autologous labeling with 51chromium) was measured in 63 patients in order to evaluate the role of platelets in the thromboembolic complications of patients with hypoxemia and pulmonary hypertension. Thirty-eight of these patients had chronic obstructive airways disease; 13, primary pulmonary hypertension; seven, recurrent pulmonary embolism; four, the Eisenmenger syndrome; and one, multiple pulmonary arteriovenous fistula. Forty-three patients were hypeakly associated with arterial oxygen tension ( r = 0.50), but not with the arterial carbon dioxide tension or the level of pulmonary artery pressure. Sulfinpyrazone lengthened platelet survival in 12 of 24 (50%) treated patients but this drug did not alter either arterial oxygen tension arterial carbon dioxide tension, or pulmonary artery pressure. Our results suggest that hypoxemia is associated with shortened platelet survival time and that platelets may, therefore, be involved in the thromboembolic complications that develop in patients with hypoxemia.

Blood Platelets↗
PubMed1976

Clinical and physiologic studies of two siblings with prekallikrein (Fletcher factor) deficiency.

Two siblings with hereditary Fletcher factor (prekallikrein) deficiency were studied for alterations of fibrinolysis, platelet function, skin inflammatory responses, permeability factor (PF/dil) formation and leukocyte chemotaxis. In vivo stimulation of fibrinolytic activity was normal; the bleeding time and platelet functions (adhesivity, aggregation, release reaction) were also normal. Both immediate (wheal-flare reaction to histamine, bradykinin, prostaglandin E1, physical agents) and delayed sensitivity skin test reactions were within normal limits. Migration of subjects' leukocytes to attractants in skin windows and in Boyden-type chambers was the same as that of control leukocytes. Serum complement components were essentially normal. One subject's leukocytes showed normal tissue factor production on stimulation by endotoxin, although prekallikrein deficiency did impair the endotoxin-stimulated generation of serum procoagulant activity. PF/dil caused increased vessel permeability in human skin; in vitro generation of PF/dil required both the Hageman factor and prekallikrein. The Fletcher factor-deficient subjects responded in a normal manner to PF/dil. Based on the Fletcher factor-coagulation assay, the biologic half-disappearance time of prekallikrein (after the transfusion of normal plasma in one of the subjects) was estimated at 35 hours. Therefore, these studies suggest that severe prekallikrein (Fletcher factor) deficiency in man is not associated with any clinically significant impairment in hemostasis, fibrinolysis, inflammatory responses or leukocyte function.

Adolescent↗