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)

Twelve patients with acute, untreated inflammatory bowel disease (IBD) were followed prospectively for coagulation and platelet function. With no symptomatic coagulopathy, abnormalities were found in all patients. With acute diseases, elevations of fibrinogen (9/12), factor V (8/12), and factor VIII (6/12) were common. Depressions of antithrombin III levels were also observed acutely (8/12). Abnormalities of platelets were both quantitative and qualitative. Thrombocytosis was present (11/12), and abnormalities in the rate and percent platelet aggregation were seen (9/10). During therapy, factors V and VIII, antithrombin III levels, and the quantitative and qualitative platelet abnormalities returned towards normal in direct correlation with sedimentation rate and clinical disease activity.
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PMID:Hemostatic alterations in inflammatory bowel disease: response to therapy. 71 49

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

Monitoring of anticoagulant treatment is not yet satisfactory. Otherwise optimal treatment control in special situations as low dose heparin prophylaxis in hip surgery or high dose anticoagulant treatment in patients after coronary stent implantation may be desirable. Recently available thrombin markers were analyzed in 51 patients under low dose (group 1) and 30 patients under high dose therapy with unfractionated heparin (group 2a and b) as well as in controls (n = 26). Before therapy these parameters were significantly elevated in both patient groups. Elevated thrombin-antithrombin III-complexes (TAT) despite adequate prolongation of aPTT under high dose heparin in 38.2% of patients indicate that therapeutic concentrations of heparin in these cases are insufficient for depressing this parameter completely. During low dose therapy only prothrombin fragment (F1 + 2) significantly decreased. This may be explained by catalytic induction of TAT-complex formation by heparin. Decrease of D-Dimer under heparin therapy in both groups does not parallel with TAT and F1 + 2 but was more prolonged. This can be explained by dependence of the D-Dimer level on spontaneous fibrinolytic activity and by a longer plasma half-life as well as a chronic and continuous fibrinolytic process in an older thrombus. In conclusion, thrombin markers seem to be helpful in estimating anticoagulant treatment efficacy. As a consequence, anticoagulant treatment has to be intensified in high-risk patients for complete depression of these markers. Whether the benefit of higher heparin doses is worth the risk of drug-induced hemorrhage, however, remains to be clarified in clinical studies.
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PMID:Influence of heparin treatment on biochemical markers of an activation of the coagulation system. 141 88

During the acute phase of myocardial infarction, the generation of thrombin is reflected in the sudden rise of fibrinopeptide A (FPA) and the thrombin-antithrombin III (TAT) complex in blood. We have systematically determined the FPA and TAT plasma concentrations over a period of 14 days after acute myocardial infarction in 100 patients. Mean levels of both thrombin markers were the highest on admission, remained elevated over the following few days, and then gradually declined after day 5. Still, by the end of the first week two thirds of the patients had distinctly elevated TAT and FPA levels, and by the end of the second week such an abnormality was present in half of them. Continuous intravenous heparin infusion at a dose of 20,000 units/day, administered for 1 week to patients who had either received (n = 21) or not received (n = 17) streptokinase, led to a significant depression (p less than 0.05) of thrombin markers over the first 48 hours, an effect that did not persist over the subsequent days of treatment. In patients not assigned to heparin treatment, those in heart failure had significantly (p less than 0.05) higher mean TAT and FPA values on days 3, 5, and 7 compared with patients in whom heart failure was absent. Infarct extension, pulmonary embolism, and death were also associated with a rise in one or both thrombin markers, often preceding the onset of clinical symptoms. Thrombinogenesis was not accompanied by changes in mean plasma concentrations of prothrombin, antithrombin III, or alpha 2-macroglobulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Persistent generation of thrombin after acute myocardial infarction. 157 16

The recently developed ELISA for the thrombin-antithrombin III complex (TAT) is a sensitive, specific, and simplified means of detecting intravascular coagulation. For further evaluation of the thrombogenicity of a polyamide (P) and a Hemophan (H) hollow-fibre dialyzer a cross-over study was done in ten stable patients on maintenance hemodialysis. At the same doses of heparin (mean bolus of 30 U/kg bw and maintenance doses of 86 U/kg bw), thrombin time and partial thromboplastin time were significantly lower using H. At the end of dialysis TAT was significantly higher in H (mean +/- SEM before HD 3.57 +/- .56, at 240 min 14.9 +/- 6.5 ng/ml, p less than 0.05, Wilcoxon-test) than in P (before HD 4.36 +/- .98, at 240 min 8.95 +/- 3.0 ng/ml, p less than 0.05 H 240 vs. P 240, Wilcoxon-test). Visible clotting was more pronounced in the H filter. Among other favourable features of blood compatibility the polyamide/polyvinylpyrrolidone copolymer with a hydrophilic/hydrophobic microdomain structure has less thrombogenicity. The modified cellulosic membrane H has advantages in complement activation and leukocyte depression, but thrombogenicity seems less favourable since the incorporated diethyl-amino-ethyl groups with their positive charge bind and inactivate negatively charged heparin.
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PMID:Formation of thrombin-antithrombin III complex using polyamide and hemophan dialyzers. 163 30

A study was made of blood coagulation, physiological anticoagulants and fibrinolysis in 120 elderly patients with cerebrovascular diseases, including 50 subjects in the acute period of ischemic brain stroke. To estimate activation of the fibrinolytic system, the levels of plasminogen and free plasmin were measured. Phasic changes in the system of blood coagulation were detected, variants of antithrombin III depression were delineated, and a relationship was established between the activity of enzymes of the fibrinolytic system and the site of an ischemic focus in the brain. Five coagulopathic syndromes of the acute period of brain stroke were distinguished, the principles of their differentiated treatment were based.
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PMID:[Diagnosis and treatment of coagulopathic syndromes in ischemic stroke]. 166 74

The pathogenesis of disseminated intravascular coagulation (DIC) in the early stage after burn injury remains still unclear. We investigated 12 burn injured patients by serial determination of anti-thrombin III (AT-III) activities and thrombin-antithrombin III complex (TAT) levels. Of these patients 4 developed DIC (DIC group) and the others had no hematological complications (non-DIC group). The mean levels of TAT increased markedly and peaked at 6 hr; the increment being more pronounced in DIC group (p less than 0.001). A significant correlation was recognized between TAT and Burn Index (r = 0.871, p less than 0.001). We also observed low AT-III activities those inversely related to Burn Index (r = 0.875, p less than 0.001), whereas closely correlated with serum albumin levels (r = 0.864, p less than 0.001), suggesting that this depression might be caused by both massive infusion and shifts of plasma into the extravascular space rather than consumption. These findings suggest that massive thrombin generation and decrease of anticoagulant activity, correlated to the severity of burns, might concurrently develop. Non-DIC group may remain to latent activation of coagulation cascade where anticoagulants could inactivate thrombin generated. This compensatory mechanism may fail in severe burn patients who have Burn Index of more than 90, developing DIC with high levels of TAT (316.3 +/- 104.5 ng/ml) and low AT-III activities (19.5 +/- 8.7%).
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PMID:[Disseminated intravascular coagulation in the early stage after severe burn: the role of excessive thrombin generation]. 194 44

A rat platelet factor has a high antiheparin activity. It also decreases nonenzymatic fibrinolytic activity of normal rat plasma and antithrombin III-heparin complex. The platelet factor 4 formed inactive complexes with heparin in molar ratios of 1:1 and 2:1. Intravenous injection of the platelet factor 4 before injection of albino rats with tissue thromboplastin prevented the reaction of anticoagulation system inactivated the synthesis of endogenous thrombin. This effect is accompanied by high hypercoagulation and depression of nonenzymatic fibrinolysis in blood.
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PMID:[The antiheparin thrombocyte factor 4 and its interaction with heparin]. 207 38

Since reduced antithrombin III (AT III) activity are associated with increased risk of thromboembolism, we have determined it in 39 patients with prostatic carcinoma. Pre-treatment levels were determined in 24 patients, 6 additional patients with prostatic carcinoma on estrogen treatment and 9 patients on chlormadinone acetate (CMA) therapy. In 12 of 24 patients we studied AT III levels before and after estrogen therapy was initiated. A significant decrease in AT III activity of 23.5% was found after one month on estrogen treatment, the patients on low doses of estrogen. Recovery of the levels of AT III was found after 6 months treatment even in in 5 of 6 patients who had shown depression of AT III levels initially. CMA treatment did not cause its depression. AT III levels was not connected with the stage of the disease or age of the patient.
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PMID:[Effect of estrogen treatment on antithrombin III activity in patients with carcinoma of the prostate]. 247 2

Significance of fibrinolysis in pathophysiology of progressive systemic sclerosis (PSS) has been the subject of much speculation. Renal disease in PSS was associated with significant depression of an inhibitor of fibrinolysis, antithrombin III (ATIII), independent of general disease activity. Association of ATIII depression with plasminogen consumption supports an active role for plasmin or another ATIII-inhibitable enzyme in the pathophysiology of renal disease in PSS, and may explain the thrombotic tendency and propensity for fibrin deposition.
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PMID:Perturbation of fibrinolysis inhibitors in progressive systemic sclerosis. 258 28


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