Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “HEMOSTATICS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 505 records · Page 28Linked to original sources
PubMed1991

Significance of hemostatic molecular markers during disseminated intravascular coagulation in patients with liver cirrhosis treated by endoscopic embolization for esophageal varices.

We studied the quantitative changes of hemostatic molecular markers with time during the course of disseminated intravascular coagulation (DIC) induced by endoscopic embolization using thrombin for esophageal varices in nine patients with liver cirrhosis. The plasma levels of D-dimer, a product of plasmin degradation of cross-linked fibrin, and thrombin-antithrombin-III complex (TAT) were significantly higher in patients before treatment when compared with 60 healthy individuals. The plasma levels of TAT, D-dimer, and plasmin alpha 2-plasmin inhibitor complex (PIC) increased significantly 5-15 min after thrombin injection into the varices, earlier than the changes of conventional coagulofibrinolytic factors, reached a maximum level after 180 min, and started to decline after 1 day. Although the plasma PIC level returned to normal after 7 days, both TAT and D-dimer were still above the pretreatment level. Although there was no change in urokinase-type plasminogen activator (u-PA), tissue-type plasminogen activator (t-PA) increased significantly after 5 min. The plasma level of plasminogen activator inhibitor type 1 (PAI-1) showed only a slight elevation after treatment. We propose that the hemostatic molecular markers TAT, D-dimer, and PIC are suitable for the early diagnosis of DIC after endoscopic embolization using thrombin in patients with liver cirrhosis and that the increase of PAI-1 is too small for the regulation of fibrinolysis due to t-PA in DIC occurring in liver cirrhosis.

Adult↗
PubMed1995

Anabolic-androgenic steroid abuse in weight lifters: evidence for activation of the hemostatic system.

Anabolic-androgenic steroid abuse has recently been linked with acute vascular events in athletes. To date, the relationship between steroid abuse and the potential for cardiovascular disease has been considered almost exclusively in terms of lipid metabolism. However, recent reports of thrombosis in androgen abusing athletes with no evidence of atherosclerosis suggests the hypothesis that thrombosis risk in such athletes could be mediated through androgen induced abnormalities of coagulation. To determine if anabolic-androgenic steroid abuse in weight lifters is associated with an activation of the hemostatic system we studied forty-nine weight lifters recruited through advertisements. History of androgen use or abstinence was confirmed via urine assays. Plasma was assayed for clotting and fibrinolytic activity by measuring thrombin/antithrombin complexes (TAT), prothrombin fragment 1 + 1 (F1 + 2), and D-dimers (D-di); markers of the endothelial based fibrinolytic components were assayed by measuring tissue plasminogen activator antigen (t-PA Ag) and its inhibitor (PAI-1); finally, the activity of antithrombin III, protein C, and protein S were measured. Abnormally high concentrations of TAT complexes were noted in 16% of our confirmed steroid using weight lifters compared to 6% of our confirmed nonusers (P = .01). Steroid users also demonstrated abnormally high concentrations of F1 + 2 and D-dimers when compared to nonusers (44 vs. 24%, P < .001, and 9 vs. 0%, respectively). Non-steroid users were more likely to have elevated levels of t-PA Ag and PAI-1 than our steroid using weight lifters (both P < .001). The activities of antithrombin III and protein S were more likely to be higher in users compared to nonusers (22 vs. 6%, P = .005; 19 vs. 0%, respectively). Some anabolic-androgenic steroid using weight lifters have an accelerated activation of their hemostatic system as evidence by increased generation of both thrombin and plasmin. These changes could reflect a thrombotic diatheses that may contribute to vascular occlusion reported in young athletes using these drugs. The predictive value of these coagulation abnormalities in terms of risk of thrombosis to individual steroid using weight lifters or the population as a whole remains to be studied.

Adult↗
PubMed1995

Hemostatic abnormalities and increased vascular endothelial cell markers in patients with red cell fragmentation syndrome induced by mitomycin C.

We examined red cell fragmentation syndrome (RCFS) induced by mitomycin C (MMC) (13 patients), by thrombotic thrombocytopenic purpura (TTP) (17 patients), and by disseminated intravascular coagulation (DIC) (15 patients). Plasma cytokine levels were increased in the TTP and DIC patients, but not in those whose RCFS was induced by MMC, suggesting that the activation of the immune system plays an important role in the pathogenesis of RCFS due to TTP and DIC but did not in RCFS due to MMC. Plasma thrombomodulin, tissue type plasminogen activator, and plasminogen activator inhibitor-I levels were increased in all RCFS patients, suggesting that RCFS, whether MMC induced, or due to TTP or DIC, might be associated with vascular endothelial cell injury. In TTP, von Willebrand factor (vWF) antigen and high molecular weight vWF multimer levels were reduced, possibly as a result of microthrombus consumption. The hemostatic data in this study showed that the TTP patients were in a hypercoagulable state without hyperfibrinolysis, and that DIC patients were in both a hypercoagulable and a hyperfibrinolytic state, whereas hemostatic abnormalities were slight in patients with MMC induced RCFS. These findings suggest that vascular endothelial cell injuries might be associated with RCFS, and that those injuries in MMC-induced RCFS might not be related to microthrombi or an activated immune system.

Adolescent↗
PubMed1996

Stress-induced hemodynamic and hemostatic changes in patients with systemic hypertension: effect of verapamil.

Stress-induced hemodynamic and hemostatic responses may acutely trigger atherosclerotic plaque disruption and thrombosis leading to myocardial infarction. This study was designed to evaluate the responses to three stressors and to determine if once-daily sustained release verapamil (Verelan) modified these responses. We studied 13 patients with mild to moderate hypertension in a randomized, double-blind, placebo-controlled crossover trial. After 4 weeks of therapy, patients were evaluated following assumption of the upright posture, mental stress, and cold pressor test. During placebo, the stressors produced an increase in systolic pressure (144 +/- 2 to 167 +/- 3 mmHg, p < 0.001), heart rate (70 +/- 2 to 77 +/- 2 beats/ min, p < 0.001), and platelet aggregability to adenosine diphosphate (threshold concentration fell from 2.8 +/- 0.4 to 1.9 +/- 0.1 microM, p = 0.05) and epinephrine (3.4 +/- 0.9 to 1.6 +/- 0.6 microM, p < 0.001). Verapamil lowered systolic pressure at baseline (144 +/- 2 to 134 +/- 2 mmHg, p < 0.001), and after stress (167 +/- 3 to 154 +/- 3 mmHg, p < 0.001), but did not alter the absolute increase with stress. During verapamil, platelet reactivity did not increase with stress, and the post-stress response to epinephrine was reduced (higher threshold concentration) compared with placebo (3.9 +/- 1.3 vs. 1.5 +/- 0.3 microM, p = 0.05). Verapamil also reduced the response to collagen (increased lag time) at baseline and after stress (111 +/- 9 vs. 91 +/- 3 s, p < 0.01). We conclude that verapamil blunted potentially harmful stress-induced hemodynamic and hemostatic changes. Further studies are required to determine whether these effects translate into a lower incidence of acute cardiovascular events.

Adenosine Diphosphate↗
PubMed1989

The role of vitronectin as multifunctional regulator in the hemostatic and immune systems.

Vitronectin (= complement S-protein) belongs to the group of structurally and functionally homologous adhesive proteins (fibrinogen, fibronectin, von Willebrand factor) which are essential in the procoagulant phase of the hemostatic system, interacting with platelets and the vessel wall. In addition to a structural motif in vitronectin responsible for this interaction (cell attachment domain) other functional domains in the protein molecule exist that contribute to its multifunctional role as regulator in the immune system (complement) as well as in fibrinolysis. These various activities and the ubiquitous distribution of vitronectin in the organism are discussed with regard to structure-function relationships of the protein molecule. Vitronectin may thus provide a conceptual molecular link between cell adhesion, humoral immune response and the hemostatic system, particularly at the blood-vessel wall interphase.

Amino Acid Sequence↗
PubMed1994

Hemostatic changes in patients with brain tumors.

Abnormal hemostasis is a functional property of cancer. Hemostatic abnormalities are common in patients with systemic malignant disease and brain tumors. However, the incidence of thromboembolism is higher in patients with brain tumors than in those with systemic disease. This raises the question of whether or not hemostatic abnormalities found in the blood of the two groups of patients differs, suggesting different pathogeneses. The purpose of this report is to review abnormalities in blood and clinical manifestations of abnormal hemostasis found in brain tumors and cancer patients in an attempt to answer this question. Normal hemostasis, as currently understood, will be considered with an emphasis on features unique to the central nervous system.

Blood Coagulation↗
PubMed1992

Hemostatic changes in human adoptive immunotherapy with activated blood monocytes or derived macrophages.

Human blood monocytes (Mo) and monocyte-derived macrophages (M psi) possess cytotoxic effects against tumor cell lines when appropriately stimulated by various biological response modifiers, e.g., gamma interferon (gamma IFN) and muramyltripeptide (MTP). Activated Mo/M psi represent a new tool for the treatment of human malignancies, termed "adoptive cellular immunotherapy". Activated Mo/M psi express tissue factor procoagulant activity (PCA), which is a physiological trigger of blood coagulation. PCA was evaluated in vitro using a modification of the one-stage recalcification clotting time, and hemostatic changes were studied in vivo in cancer patients. Nine patients with peritoneal carcinomatosis were injected intraperitoneally with activated Mo and 11 patients with non-small cell lung carcinomas were infused intravenously with activated M psi. Hemostatic changes were followed using activated partial thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), fibrinogen level, antithrombin III (ATIII) and protein C (PC) activities. Fibrinolytic activity was estimated by euglobulin lysis time and assays for plasminogen and fibrin/fibrinogen degradation products (FDP). These assays were performed before and after each autologous infusion and on days 2 and 3. Activated Mo and M psi expressed potent PCA (85.5 +/- 7.5 U/ml for MTP activated Mo and 50 +/- 5.3 U/ml for gamma IFN activated M psi suspensions). In both groups of patients, APTT, PT, and TT underwent no significant variations. There was no significant consumption of ATIII or PC, and fibrinolysis was not activated during the study period. In the group injected intraperitoneally with MTP-activated Mo, fibrinogen showed a significant and progressive increase in relation to the development of an inflammatory reaction, reaching a maximum average value of 6.1 g/l at the end of the therapy with a concomitant increase in FDP levels. This increase was not observed after intravenous therapy with gamma IFN-activated M psi. No patient suffered from hemorrhagic or thrombotic events. In our experience, repeated injections of activated Mo or M psi expressing potent tissue factor PCA did not induce significant in vivo activation of the coagulation system in cancer patients.

Aged↗
PubMedDate not supplied

Relationships between metabolic and hemostatic variables in uncomplicated diabetes.

Several metabolic (HbA1, HDL-C, triglycerides) and hemostatic (VIIIR: Ag, VIII:C, B-TG variables were investigated in 35 non-obese, insulin-dependent diabetics without clinically evident vascular complications. B-TG was high but did not correlate with other metabolic and hemostatic parameters, suggesting that elevated B-TG in diabetes might be an expression of in vitro platelet activation. VIIIR: Ag and the ratio of VIIIR: Ag to VIII: C were markedly increased. There was a significant correlation of the HbA1 and HDL-C levels with VIIIR: Ag, indicating that VIIIR:Ag is another reflection of metabolic control in diabetes. Additional pathogenic mechanisms, however, appear to be involved in causing the changes in VIIIR: Ag in diabetes.

Adolescent↗
PubMed1985

Hemostatic defects in experimental obstructive jaundice.

To elucidate the etiology of hemostatic abnormalities in cases of obstructive jaundice, we occluded the bile duct of rats for one week and found that the moderately jaundiced rats exhibited a marked reduction in the value of Hepaplastin test and Thrombotest with minimum histological changes in liver. All other coagulation and fibrinolysis profiles were within normal limits. These findings exclude the occurrence of a hypercoagulable state or hypofibrinolytic state in the jaundiced rats due to bile duct occlusion. Similar results were obtained in rats with tube choledochostomy. The abnormalities were almost completely prevented by the daily parenteral administration of vitamin K. These observations suggest that malabsorption of vitamin K may be the sole etiologic factor producing hemostatic defects in case of uncomplicated obstructive jaundice.

Animals↗
PubMed1991

Hemostatic studies of ex situ hepatic surgery.

Ex situ hepatic surgery, in which a diseased liver is resected from outside the body, was first reported in 1988. This study investigates the hemostatic changes occurring during such surgery in two cases. During the anhepatic period of more than 5 hours, veno-venous bypass without heparin was performed. The tests included platelet count, prothrombin activity (PT), partial thromboplastin time (PTT), fibrinogen (Fbg), factor II (F.II), factor V (F.V), and thromboelastography (TEG). Three to 4 hours after entering the anhepatic phase, marked fibrinolysis and a fall in the values of PT, Fbg and F.V. were observed. Every parameter temporarily deteriorated immediately after revascularization of the graft, however, all returned to almost normal values within 1-2 hours after hepatic reperfusion except for F.V and platelets. In conclusion, the coagulopathy during ex situ hepatic surgery is caused by the marked fibrinolysis and depletion of hemostatic factors which develop 3-4 hours after the onset of the anhepatic phase.

Adult↗
PubMed1993

Age-related changes in the hemostatic system.

The increased incidence of arterial thromboembolism in the elderly has prompted investigation of age-related changes in the hemostatic system. Aging is associated with increased plasma levels of fibrinogen, factor VII and factor VIII, which have been shown to be risk factors for thrombotic disease in five large epidemiological studies. An increased responsiveness to different aggregating stimuli, elevated levels of beta-thromboglobulin and an increased production of thromboxane A2 were reported in the platelets of the elderly. These alterations are associated with modifications of platelet membrane lipid composition (namely an increase in the cholesterol/phospholipid ratio and a decrease in linoleic acid) with possible related changes in membrane fluidity. Moreover, a decrease in the number of platelet prostacyclin and thromboxane A2 receptors was observed with aging. Fibrinolytic activity is impaired in the elderly, probably due to an increase in plasminogen activator inhibitor 1. Interestingly, hypercoagulability has been demonstrated by an increase in the activation markers of the coagulation cascade (mainly fibrinopeptide A and prothrombin activation fragment F 1 + 2). Finally, clinical and experimental evidence suggests that endothelium could play a central role in hemostatic alterations which determine a thrombophilic state in the elderly.

Aged↗
PubMedDate not supplied

Hemostatic profile in neonatal septicemia.

Hemostatic profile was studied in 25 full term non-asphyxiated neonates with blood culture-proven septicemia. Observations were compared with that of 25 healthy, non-asphyxiated, full term, birth weight and age-matched controls. Detailed coagulation tests & platelet studies were done in each of the 50 neonates by standard techniques. Hemostatic defects occurred in 96% of the septicemic neonates and none in the control group irrespective of the occurrence of clinical bleeding. The coagulation tests were deranged in 805 and platelet function tests in 92% of patients. These tests were significantly deranged in septicemic neonates as compared to control group.

Anti-Bacterial Agents↗
PubMed1997

Hemostatic markers in surgery: a different fibrinolytic activity may be of pathophysiological significance in orthopedic versus abdominal surgery.

Without prophylaxis, patients subjected to major abdominal surgery have a risk of deep vein thrombosis of approximately 30%, while the rate varies between 40% and 60% in orthopedic surgery. The reasons for this discrepancy are not completely understood. The present study was designed to compare the pre- and postoperative behavior of different coagulation and fibrinolysis parameters in patients undergoing both types of surgery, receiving low molecular weight heparin prophylaxis. Samples were taken before operation and on postoperative days 1, 3, and 7. The following parameters were assessed: prothrombin fragment 1 + 2, thrombin-antithrombin III complexes, fibrinopeptide A, tissue plasminogen activator, plasminogen activator inhibitor, plasmin-alpha 2-antiplasmin complexes, and fibrin degradation products. We found a significant increase in the clotting markers postoperatively compared with preoperative values (P < 0.05), both in abdominal and orthopedic surgery, indicating a marked hemostatic activation which remained until postoperative day 7. A significant increase in plasminogen activator inhibitor (P < 0.01) and a decrease in tissue plasminogen activator and plasmin-alpha 2-antiplasmin complexes was also observed early after operation. The plasminogen activator inhibitor activity decreased, while tissue plasminogen activator and plasmin-alpha 2-antiplasmin levels increased significantly on days 3 and 7 (P < 0.05). Fibrin degradation products significantly increased throughout the postoperative period (P < 0.01). Preoperatively, we found higher plasminogen activator inhibitor activity and lower tissue plasminogen activator and plasmin-alpha 2-antiplasmin complexes (P < 0.05) in patients undergoing hip replacement compared with abdominal surgery. Fibrin degradation products were also significantly lower on postoperative day 3 in patients undergoing hip replacement (P < 0.01). We suggest that the lower preoperative fibrinolytic activation observed in patients undergoing orthopedic surgery compared with abdominal surgery might have pathophysiological consequences. Our results also indicate that the hemostatic activation persists beyond the 7th postoperative day despite prophylaxis.

Abdomen↗
PubMed1998

Historical development of surgical instruments exemplified by hemostatic forceps.

We describe the historical development of surgical instruments exemplified by hemostatic forceps, starting with antique and medieval forceps used for the arrest of bleeding to modern atraumatic hemostatic forceps used for vascular reconstruction. Their development proceeded mainly in three steps: (1) development of ligature forceps directly for hemostasis (Celsus, first century AD; Paré, 1582; L. Heister, 1743; (2) development of atraumatic forceps, which facilitate vascular reconstruction or anastomosis creation by temporarily clamping vessels (Höpfner, 1903; Stich, 1907; Jeger, 1913; (3) construction of tangential forceps, which, by partially clamping vessels with partial maintenance of blood flow, allow the reconstruction or anastomosis of large vessels in a side-to-side technique. The first tangential occlusion clamp was developed by Friedrich Trendelenburg (1844-1924) in 1908, when he established the operative treatment for embolism of the pulmonary artery. This clamp was later modified by A. W. Meyer (1927) and V.P. Satinsky (ca. 1950).

Hemostasis, Surgical↗
PubMed2004

Decreased incidence of hepatic veno-occlusive disease and fewer hemostatic derangements associated with intravenous busulfan vs oral busulfan in adults conditioned with busulfan + cyclophosphamide for allogeneic bone marrow transplantation.

We investigated the occurrence of hepatic veno-occlusive disease (VOD) after allogeneic bone marrow transplantation (BMT) in 241 adults conditioned with busulfan + cyclophosphamide at a single institute and retrospectively compared 186 patients who received oral busulfan (O-Bu group) with 55 patients who received intravenous busulfan (I-Bu group). Various hemostatic parameters were determined at baseline and on days 0, 7, 14, and 21. Hepatic VOD occurred in 41.7% of the O-Bu group and in 18.5% of the I-Bu group. Multivariate analysis revealed that the I-Bu group had significantly decreased risk of VOD compared to the O-Bu group [p=0.006, odds ratio: (OR) 0.345]. Eleven patients in the O-Bu group and none of the I-Bu group developed severe VOD. A repeated measures analysis of variance (ANOVA) with a between-subjects factor revealed significant differences in post-transplant levels of antithrombin III, tissue plasminogen activator (tPA), plasminogen activator inhibitor 1 (PAI-1), and D-dimer according to the occurrence of VOD. The level of antithrombin III was significantly lower, whereas the level of D-dimer was significantly higher, in the O-Bu group than in the I-Bu group. These findings show that, in adults conditioned with busulfan + cyclophosphamide, intravenous busulfan was associated with significantly decreased incidence of VOD and fewer hemostatic derangements after allogeneic BMT compared to oral busulfan.

Administration, Oral↗
PubMed2002

Hemostatic parameters in Behçet's disease: a reappraisal.

Behçet's disease (BD) is a relapsing vasculitis in which orogenital ulceration is a prominent feature. The disease presents a tendency to thrombosis. The prevalence of venous or arterial thrombosis in BD reaches 40% in some series. Molecular markers of imbalance have been extensively studied in BD. The aim of this paper is to review current data on essential hemostatic parameters. The precise pathogenetic mechanism(s) underlying the prothrombotic state of BD is unknown. Thrombophilic factors could contribute to thrombosis in BD. Vasculitic endothelial injury may trigger or enhance the pathological hemostatic process.

Behcet Syndrome↗
PubMed2006

Heart rate variability, hemostatic and acute inflammatory blood parameters in healthy adults after short-term exposure to welding fume.

The present study aimed to investigate, whether short-term experimental exposure to high levels of welding fumes would be capable of exerting acute effects in healthy subjects. Specifically, we assessed cardiovascular function in terms of heart rate variability (HRV) as well as the concentrations of inflammatory mediators and hemostatic proteins in blood as outcome measures. Twenty subjects without a history of airway and cardiovascular diseases were exposed to either control air or welding fume for 1 h on 2 separate days under standardized conditions. The median concentration of the alveolar particle fraction during welding was 3.5 mg/m(3 )(quartiles: 1.4-6.3 mg/m(3); range 1.0-25.3 mg/m(3)). Five hours later a panel of clinical assessments was performed, including HRV measurement and drawing of blood samples. There were no changes in symptom ratings or lung function after welding fume exposure. Exposures did also not differ regarding effects on time- and frequency-domain parameters of HRV. Similarly, blood leukocyte numbers, cell differentials and the blood levels of fibrinogen, C-reactive protein, antithrombin III, factor VIII, von Willebrand factor, ristocetin cofactor, sICAM-1, tumor necrosis factor alpha, interleukin 6, interleukin 8 and epithelial neutrophil activating peptide 78 were not altered by welding fume inhalation. However, there was a significant fall in the level of endothelin-1 (P < 0.01). In conclusion, the data did not indicate effects of clinical significance of a short-term high-level exposure to welding fumes on HRV or a set of blood hemostatic and acute inflammatory parameters in healthy subjects. The small but statistically significant effect on endothelin levels demonstrated that measurable effects could be elicited even in these individuals. Overall, welding fumes are not likely to exert acute cardiovascular effects in healthy individuals.

Adult↗
PubMed2000

Sustained hemostatic abnormality in patients with steroid-induced osteonecrosis in the early period after high-dose corticosteroid therapy.

To determine whether the development of steroid-induced osteonecrosis in collagen disease patients was related to hemostatic abnormality after corticosteroid administration, we examined levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha2-plasmin inhibitor complex (PIC) in 32 patients who were treated with high-dose corticosteroid. All were prospectively followed for osteonecrosis, with serial magnetic resonance imaging (MRI), for at least 12 months from the beginning of corticosteroid therapy. MRI was performed on bilateral hips and knees. Of the 32 patients, 17 (53.1%) had osteonecrosis in the hip or knee. Osteonecrosis was detected on MRI at an average 3.1 months after the start of high-dose corticosteroid therapy. PIC levels were significantly higher in the group of 17 patients with osteonecrosis (ON group) than in the group of 15 patients without osteonecrosis (non-ON group) (P < 0.0001). The difference in PIC levels was most prominent 20 days after the start of the high-dose corticosteroid therapy. Moreover, the number of osteonecrotic joints was significantly correlated with PIC levels (P < 0.0001). The sustained hemostatic abnormality after corticosteroid therapy in the ON group suggests that microvascular coagulation participates in the development of osteonecrosis.

Adolescent↗