Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Factors affecting fibrin formation and dissolution were compared for 15 women taking combined oral contraceptives and 15 women using nonpharmacological methods of birth control. The two groups were matched for age, body weight, time of blood collection, and day in menstrual cycle; none of the women was receiving other drugs known to affect the blood coagulation or fibrinolytic parameters measured in this study. Fibrinogen concentrations tended to be higher in the experimental group; the degree of fibrinogen degradation, number of fibrin cross-links, and levels of factor XIII and plasminogen were the same for both group. There were significant reductions in antithrombin activity, the euglobulin lysis time, and fibrinolytic inhibitor level in women using oral contraceptives. An estrogen dose effect was suggested for fibrinogen concentration and the degree of antithrombin activity. The increased fibrinolytic activity and decreased fibrinolytic inhibitor levels are consistent with in vitro observations that antithrombin also inhibits plasmin activity. Thus while oral contraceptive-induced depression of antithrombin III could possibly predispose to thrombosis by diminishing the inhibition of the serine protease clotting factors, the concomitant decreased level of plasmin inhibition might balance the system by favoring thrombolysis as well as the digestion and inactivation of certain clotting factors by plasmin.
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PMID:Fibrin formation and dissolution in women receiving oral contraceptive drugs. 84 77

The level of antithrombins II, III and IV decreased in proportion to the extent of intervention in destruction or removal of a part of the liver in rats. Destruction of the spleen led to depression, and removal--to activation of antithrombin IV. Back of the reticuloendothelial system caused a lesser fall of the antithrombin level than partial hepatectomy. The spleen is supposed to produce antithrombin IV inhibitor.
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PMID:[Antithromin activity following blockade of the reticuloendothelial system, splenectomy and partial removal of the liver]. 91 79

Hemostasis was investigated in 2 groups of patients with systemic scleroderma (SSD) with minimal (12 patients) and moderate (9 patients) activity of the process. It has been shown that in SSD, the triggering factor of intravascular blood coagulation is the release of Willebrand's factor, an activator of platelets, from the impaired endothelium. Hyperaggregation and labilization of platelets characterizes the course of SSD irrespective of the disease activity. The main changes in coagulation hemostasis are related to the dramatically accelerated triggered thrombin formation and deficiency of the antithrombin potential. The status of fibrinolysis confirming the thrombogenic situation is marked by a number of features: depression of contact lysis is maximally pronounced in chronic SSD with minimal activity, accumulation of the soluble complexes of fibrin monomer only correlates with the disease activity, and no significant rise of the level of fibrin/fibrinogen degradation products has been discovered.
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PMID:[The mechanisms of intravascular blood coagulation in patients with systemic scleroderma]. 239 20

The rabbits with CCl4-induced hepatic failure have revealed changes in hemostasis responses to streptokinase administration. The main distinction of hepatic dystrophy was the depression of plasma fibrinolytic activity accompanying the decrease in fibrinogen and antiplasmin concentrations. Streptokinase administration to rabbits with productive inflammatory liver disorders produced changes in hemostasis identical to those observed in intact rabbits, fibrinogen levels, however, remained unchanged. The common feature of all the toxic liver disorders is the increase of antithrombin III levels after streptokinase administration, whereas the antithrombin levels in the control animals were decreased.
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PMID:[Action of streptokinase on the hemostatic indices of rabbits with a toxic lesion of the liver due to carbon tetrachloride]. 381 94

The blood clotting systems of 21 women, aged 18 to 38 years, who had begun using oral contraceptives, were studied. 2 brands of oral contraceptives were used, both containing 1 mg progestogen and .08 mg estrogen. Tests were performed before oral contraceptive usage was begun, and again after the tenth and twentieth days. The antithrombin III and thrombin generation results were compared with the records of patients with chronic thromboembolic disease. Oral contraceptives with a quick, dramatic depression of antithrombin activity and an acceleration of thrombin generation within the first cycle. The depression of antithrompin III activity occurred within 7 days, while thrombin generation occurred within 10 days, but was further accelerated by 20 days (p .001). Levels of both returned to normal after discontinuation of oral conceptive use. Results obtained from using oral contraceptives were similar to those of the patients with thromboembolic disease. It was suggested that the change in antithrombin III activity was the most clinically significant of the 2 changes involved.
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PMID:Antithrombin 3 depression and thrombin generation acceleration in women taking oral contraceptives. 555 23

Antithrombin III activity was estimated using a chromogenic substrate perioperatively in the plasma of 200 patients undergoing major elective abdominal surgery during low-dose heparin prophylaxis. With an initial value of 10.9 +/- 2 IU/ml there was a mean postoperative lowering of plasma antithrombin activity in all patients with a minimum on the second postoperative day. In patients with empirically established increased risk of thromboembolism the postoperative depression of antithrombin was significantly more pronounced (P less than 0.01) than in the control groups. An increased risk prevailed particularly in patients with malignant diseases and in major surgery, i.e. of prolonged duration. In such cases with increased risk of thromboembolism routine assessment of antithrombin III is recommended.
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PMID:[Perioperative plasma antithrombin activity with "low-dose" heparin prophylaxis. Perioperatively acquired antithrombin III deficiency as a cause for the failure of heparin prophylaxis?]. 683 15

Eleven patients with leukemia and lymphoma were treated with 14 courses of E. coli L-asparaginase. Abnormalities of the coagulation screening tests and decreased fibrinogen levels were observed in all patients during treatment. Significant depressions of functional (mean 32%) and antigenic (mean 48%) antithrombin III were observed by day 14 of therapy. There was no laboratory evidence of intravascular coagulation during 11/14 courses of L-asparaginase. Crossed immunoelectrophoresis of plasma obtained at the antithrombin nadir did not demonstrate an abnormal pattern which can be associated with an abnormal antithrombin III or an increase in antithrombin III-coagulation factor complexes. The major underlying mechanism of this depression is believed to be decreased hepatic synthesis, and the low levels of antithrombin III may be associated with an increased risk of thrombosis.
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PMID:Depression of functional and antigenic plasma antithrombin III (AT-III) due to therapy with L-asparaginase. 704 2

Data obtained in experiments in 80 rats and in clinical observations of 24 patients with burns of the II and IIIA degrees showed the activation of vasculo-thrombocytic and procoagulant links of the hemostasis system with a simultaneous depression of the anticoagulative blood system. The thermal trauma is followed by a dramatic decrease of the concentration of heparin, fibrinogen, decreased activity of antithrombin-III, fibrinolysis and plasminogen activators. There was a simultaneous growth of concentration of antiplasmins (alpha 2-macroglobulin and alpha 1-antitrypsin).
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PMID:[The blood coagulating activity in burns]. 875 66

The authors analyse the short-term and medium-term effects of iloprost prostanoid derivate on hemostatic status in a group of patients with obliterating vascular disease of the lower limbs. The study included 10 patients (6 males, 4 females; aged 52 + 5 years old) suffering from Fontaine's stage 3 obstructive arterial disease. After a 10-hour fast each patient received a 6-hour iv infusion of iloprost at a dose of 2 ng/kg/min (approx 50 gamma) a venous blood sample was collected before and after infusion. The test was repeated using the same method after 4 weeks of treatment with the same dose of the drug. The following parameters were analysed in serum: fibrinogen (F) (IL coagulometric method), Factor VII (F VII) (IL coagulometric method), antithrombin II (AT III) (IL chromogenic method), protein C (PC) II coagulometric method) and protein S (PS) (IL coagulometric method). After the first infusion a significant increase was observed in AT III (p > 0.05), whereas other indices showed no significant variations. After treatment for 4 weeks AT III was again enhanced after infusion (p > 0.05); with regard to the basal values of other parameters, a significant reduction (p > 0.05) was found in F VII, whereas no other significant changes were observed. In the light of these results the authors suggest an antithrombotic effect of the drug documented by the short-term increase in AT III probably due to lower consumption, and a medium-term reduction in F VII due to trophic effect of the drug at a vasculoparietal level resulting in the depression of FVII tissue activation factors.
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PMID:[Modification of some prothrombotic indices after treatment with iloprost in arterial disease patients]. 905 18

Activation and inhibition of coagulation and fibrinolysis was analyzed in bronchoalveolar lavage (BAL) fluids obtained from endotoxin-challenged chimpanzees. The mediatory role of tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) on endotoxin-induced changes in bronchoalveolar coagulation and fibrinolysis was investigated in experiments in which the infusion of endotoxin was combined with the administration of monoclonal anti-TNF-alpha or anti-IL-6 antibodies. Endotoxin infusion elicited a marked increase in bronchoalveolar thrombin generation as measured by levels of prothrombin activation fragment F1+2 and thrombin-antithrombin complexes. Markers for intrinsic pathway activation were not detectable, suggesting that the thrombin generation was mediated by the tissue factor-dependent route. Levels of antithrombin were low before the injection of endotoxin and not detectable hereafter. The administration of anti-IL-6 antibody completely abolished the endotoxin-induced activation of bronchoalveolar coagulation, whereas treatment with anti-TNF-alpha antibody only partly inhibited this effect. Bronchoalveolar fibrinolytic activity, due to urokinase-type plasminogen activator (u-PA), was significantly depressed after endotoxin injection, mainly due to a striking increase in plasminogen activator inhibitor-2 levels in BAL fluid. The endotoxin-induced effects on bronchoalveolar fibrinolysis could be blocked by the simultaneous administration of anti- TNF-alpha antibodies. We conclude that endotoxemia results in the activation of bronchoalveolar coagulation, which is apparently mediated by the tissue factor route of coagulation activation and which may be amplified by consumption of antithrombin III. Bronchoalveolar fibrinolytic activity is significantly abolished by increased levels of mainly PAI-2 after the injection of endotoxin. The endotoxin-induced effects on bronchoalveolar coagulation appears to be mediated by IL-6, whereas TNF-alpha seems to be the pivotal mediator of the endotoxin-induced depression of bronchoalveolar fibrinolysis.
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PMID:Differential effects of anti-cytokine treatment on bronchoalveolar hemostasis in endotoxemic chimpanzees. 965 12


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