Physiologic aspects of intravascular clotting∗

Oral and Intravenous Estrogens in the Treatment and Prevention of Bleeding Associated With Long‐term Anticoagulant Therapy

“…Cortisone and corticotropin cause a decrease in capillary permeability and a reduction in prolonged bleeding time in certain hemorrhagic states, notably “pseudohemophilia” (67). Furthermore, the corticosteriods may induce hypercoagulability of the blood as a result of thromboeytosis and decreased plasma fibrinolytic activity (possibly mediated through the inhibition of the action of serotonin in promoting fibrinolysis) (13).…”

“…Drugs of the Dicumarol‐indanedione type generally are regarded as antivitamin‐K in action, their effect being mediated through the mitochondria and resulting in depression of the synthesis of a number of coagulation proteins, particularly in the liver. There is impressive evidence that multiple coagulation defects occur during long‐term therapy, including those of prothrombin, Factor VII (proconvertin, SPCA), Factor IX (plasma thromboplastic component, PTC, Christmas factor), Factor X, plasma thromboplastin antecedent, the Hageman factor, and the Stuart‐Prower factor (13, 14). The prothrombin time test may not be sensitive to depression of several important plasma procoagulants, notably Factor IX and antihemophilic globulin (Factor VIII).…”

The Control of Gastro‐intestinal Hemorrhage in Cirrhosis by Combined Adrenocortical and Estrogenic Therapy

“… ) Cortisone and corticotropin decrease capillary permeability and reduce the prolonged bleeding time in certain hemorrhagic states, most notably “pseudo‐hemophilia” (48). ) Corticosteroids induce hypercoagulability of the blood. This effect has been attributed variously to thrombocytosis and to decreased plasma fibrinolytic activity (possibly mediated through the inhibition of the action of serotonin in promoting fibrinolysis) (25, 26, 49). ) Corticosteroids favorably influence associated hypersplenism and thrombocytopenic purpura (50). ) Cortisone therapy exerts a beneficial effect upon the massive gastric bleeding stemming from increased capillary fragility associated with gastric erosions (51). ) Corticosteroids reduce the acute hepatocellular damage that is frequently superimposed upon pre‐existing cirrhosis.…”

“…) Corticosteroids induce hypercoagulability of the blood. This effect has been attributed variously to thrombocytosis and to decreased plasma fibrinolytic activity (possibly mediated through the inhibition of the action of serotonin in promoting fibrinolysis) (25, 26, 49).…”

“…Although our data are too limited to permit statistical analysis, they would seem to be worth reporting, because of the importance of any new form of treatment that can control variceal bleeding associated with cirrhosis of the liver and can tide patients over this critical period. This is emphasized by the following facts: 1) this disease is now one of the 10 leading causes of death in the United States, being exceeded in the [45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62][63][64] year age group only by heart disease, cancer, and cerebral hemorrhage; 2 ) severe and exsanguinating hemorrhage from rupture of the associated esophageal varices is one of the major causes of the fatalities (at least half the patients do not survive two months); 3) the alarmingly high early mortality rate has not been lessened by surgery; 4) there is an acceptable survival rate despite the initial heavy death toll from hemorrhage; and 5) the gastro-intestinal bleeding frequently recurs after treatment by portacaval or splenorenal shunt. The virtually unchanged prognosis following venous-shunt operations in patients who have bled from these varices, the operative mortality of 20 per cent even in experienced hands, and the fact that selected cases often do as well with purely medical therapy, has disenchanted a number of gastroenterologists with the results of such surgery ( 2 ) .…”