pituitrin and Venous-Thrombosis

High factor VIII (FVIII) is a risk factor for venous thromboembolism (VTE). The pathomechanism by which high FVIII leads to an increased risk of VTE is unknown. Physical activity and infusion of adrenalin provoke a rise in FVIII, which can be blocked by a nonselective beta-blockade. We tested the hypothesis that in patients with a VTE beta-blockade decreases FVIII and inhibits coagulation activation. 17 male patients with high FVIII (> 170 IU/dL, n = 7) or low FVIII (<150 IU/dL, n = 10) and a history of VTE received 40 mg of propranolol thrice daily for 14 days. FVIII and vasopressin levels were measured before and during propranolol intake and 28 days thereafter. At the same time points, haemostatic system activation was investigated by measuring prothrombin fragment f1.2 (f1.2) and thrombin antithrombin complexes (TAT) in venous blood and in blood emerging from a skin incision (shed blood). The mean FVIII level before propranolol was 192 IU/dL and 115 IU/dL in patients with high and low FVIII, respectively. During and 28 days after propranolol, no significant change in FVIII was seen in both groups. Changes in f1.2 and TAT were not detectable in either venous blood or in shed blood. beta-receptor blockade did not lower FVIII or inhibit haemostatic system activation in patients with VTE and persistently high FVIII. Administration of propranolol cannot be recommended as secondary thromboprophylaxis in patients with high FVIII.

Topics: Adrenergic beta-Antagonists; Adult; Aged; Bleeding Time; Blood Coagulation; Factor VIII; Humans; Male; Middle Aged; Propranolol; Thrombin; Thromboembolism; Treatment Failure; Vasopressins; Venous Thrombosis

Published guidelines suggest that vasopressin has a role in shock treatment, although its safety has not been adequately evaluated in a clinical setting. Vasopressin causes platelet aggregation and has been associated with the release of factor VIII coagulant and von Willebrand factor.. To compare the incidence of venous thromboembolism (VTE) in patients with a diagnosis of shock who received vasopressin with those who did not receive vasopressin for hemodynamic support.. A retrospective, single-center, cohort study was conducted at an academic, tertiary care center with 350 patients with a diagnosis of shock. Patients from the intensive care unit were randomly selected and separated into 2 groups for comparison of those receiving only catecholamines with those receiving vasopressin with or without catecholamines for hypotension. Patients with diabetes insipidus or variceal hemorrhage and those with any documented history of VTE were excluded. The primary outcome, VTE occurrence, was defined as a positive Doppler ultrasound, spiral computed tomography, or documented diagnosis in the discharge records. Frequency and type of risk factors for VTE were compared between the 2 study arms. A risk factor modeling approach was performed, using logistic regression to identify potential confounders and effect modifiers in the relationship between vasopressin and VTE.. There were 175 patients in each arm of the study. The crude incidence of VTE was 7.4% and 8% in the vasopressin and catecholamine groups, respectively (p = 0.84). No significant difference in the incidence of deep venous thrombosis (vasopressin 5.1%, control 7.4%; p = 0.51) or pulmonary embolism (vasopressin 2.3%, control 0.6%; p = 0.37) was found between groups. After adjusting for covariates, there was no statistically significant difference in the incidence of VTE between the 2 arms (p = 0.72).. This investigation provides initial evidence that vasopressin infusions do not increase the risk of VTE in patients with shock.

Topics: Adult; Aged; Aged, 80 and over; Catecholamines; Female; Hemostatics; Humans; Infusions, Intravenous; Intensive Care Units; Male; Middle Aged; Pulmonary Embolism; Risk Factors; Shock; Thromboembolism; Vasopressins; Venous Thrombosis