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PubMed1981

Oral contraceptives and hepatic vein thrombosis.

The purpose of this paper is to report on three cases of the Budd-Chiari syndrome in young women who were taking oral contraceptives. Two patients survived, with gradual resolution of hepatomegaly and ascites following discontinuance of the birth control pills. One death occurred soon after the patient's admission to the hospital. The pathophysiology of this phenomenon involves two major aspects. Oral contraceptives are known to cause a hypercoagulation state as well as a direct effect on the blood vessels. In this series the combination of hypercoagulation and progressive occlusion of the vessels in patients on oral contraceptives appeared to lead to the development of thrombosis of the liver vessels.

Adult↗
PubMed1992

[Coagulation and fibrinolysis in pregnancy].

We studied on coagulation and fibrinolysis systems during pregnancy by measuring plasma levels of thrombin-antithrombin III complex (TAT), plasmin-alpha 2 plasmin inhibitor complex (PIC), fibrinogen/fibrin degradation products (FDP), plasminogen (PLG) and antithrombin III (AT-III). Ninety seven pregnant, 5 post-delivery and 32 nonpregnant women aged from 20 to 52 years old were included in this study. Plasma concentrations of TAT and PIC in nonpregnant women were 3.38 +/- 1.02 micrograms/l and 0.65 +/- 0.24 micrograms/ml, respectively. TAT gradually increased with the progression of pregnancy and rapidly decreased after the delivery. Whereas PIC and AT-III concentrations did not change significantly during pregnancy. Fibrinogen, PLG and FDP concentrations changed similarly as TAT. Eight pregnants whose plasma PIC concentrations elevated more than 1.0 micrograms/l were further examined. In 6 women out of them (71.5%), FDP concentrations were elevated. In this particular group of subjects, however, they delivered normally without complications such as toxemia. These observations suggest that, at least, a hypercoagulative state progresses with pregnancy, being normalized after the delivery. Although we could not find the relationship between the hypercoagulation and clinical complications such as thrombosis and toxemia of pregnancy, present findings suggest that special caution should be paid on the pregnants whose TAT and FDP levels are elevated.

Adult↗
PubMed2002

Fontan's operation: is aspirin enough? Is coumadin too much?

BACKGROUND: Thromboembolism after Fontan's operation is attributed to low flow states, stasis in venous pathways, right to left shunts, blind cul-de-sacs, prosthetic materials, atrial arrhythmias, and hypercoagulable states. We assessed the efficacy of a strategy to reduce thromboembolic events including aspirin anticoagulation. METHODS: From January 1996 through December 2000, 72 patients underwent Fontan procedures. Management included (1) avoidance of direct caval cannulation and central venous lines, (2) inotropic support for 48 to 72 hours to optimize cardiac output, (3) aortopulmonary anastomosis or suture closure of patent pulmonary valves, and (4) administration of aspirin (81 mg per day) beginning on postoperative day one. No other anticoagulation strategies were used. Surveillance included intraoperative and postoperative transesophageal echo, transthoracic echo at discharge, at first reevaluation, and at 6 month intervals, and catheterization 1 year after surgery. RESULTS: There were no early or late deaths. Follow-up was completed with 2,882 patient-months and a mean of 40 months. There were no documented thromboembolic events; however, all suspicious occurrences were investigated by echo and brain imaging. There were no hemorrhagic events or aspirin-related complications. CONCLUSIONS: Low dose aspirin can be used safely in young patients with Fontan connections. At intermediate follow-up, the strategies described appear effective in preventing thromboembolic complications. Routine use of more aggressive anticoagulation regimens seems unwarranted.

Adolescent↗
PubMed2002

Bilateral simultaneous central retinal artery occlusions in atherosclerosis.

An 82-year-old woman with atherosclerosis developed central retinal artery occlusions (CRAOs) in both eyes within an interval of 5 minutes. There was no evidence of a thromboembolic source, systemic hypotension, vasculitis, migraine, or hypercoagulable state. Virtually simultaneous binocular CRAOs have been rarely reported, and suggest the possibility of a systemic but still undefined "hypercoagulable trigger."

Aged↗
PubMed2004

Effects of depressive symptoms and anxiety on hemostatic responses to acute mental stress and recovery in the elderly.

Depression and anxiety are prospectively associated with cardiac morbidity and mortality. Increased clotting diathesis may mediate this link. We hypothesized that there would be an association between mood and hemostatic changes that occur during and following recovery from acute mental stress. Forty-eight community-dwelling elderly subjects underwent a laboratory speech stressor task. Plasma von Willebrand factor (vWF), thrombin/antithrombin III (TAT) complexes, D-dimer, tissue-type plasminogen activator (t-PA), and type I plasminogen activator inhibitor (PAI-1) were measured at rest, after conclusion of the speech, and 14 min afterwards (recovery). Mood was assessed with the Hamilton Rating Scales for Depression (Ham-D) and Anxiety (Ham-A). Mental stress elicited a hypercoagulable state as evidenced by increases in TAT and D-dimer, and by a decrease in t-PA. Overall, hypercoagulability had increased after recovery. Ham-D scores and Ham-A scores correlated with increases in D-dimer over the testing interval (i.e. area under the curve). Ham-A (but not Ham-D) uniquely explained 8% and 17% of the variance in resting D-dimer and D-dimer area under the curve, respectively. The independent association of anxiety symptoms with resting and stress-induced fibrin formation (D-dimer) may be a mechanism linking mood with cardiovascular disease risk in the elderly.

Acute Disease↗
PubMed2006

Does the oxidation of methionine in thrombomodulin contribute to the hypercoaguable state of smokers and diabetics?

The leading cause of premature death in smokers is cardiovascular disease. Diabetics also suffer from increased cardiovascular disease. This results, in part, from the hypercoagulable state associated with these conditions. However, the molecular cause(s) of the elevated risk of cardiovascular disease and the prothrombotic state of smokers and diabetics remain unknown. It is well known that oxidative stress is increased in both conditions. In smokers, it is established that oxidation of methionine residues takes place in alpha(1)-antitrypsin in lungs and that this leads to emphysema. Thrombomodulin is a key regulator of blood clotting and is found on the endothelium. Oxidation of methionine 388 in thrombomodulin is known to slow the rate at which the thrombomodulin-thrombin complex activates protein C, a protein which, in turn, degrades the factors which activate thrombin and lead to clot formation. In analogy to the cause of emphysema, it is hypothesized that oxidation of this methionine is elevated in smokers relative to non-smokers and, perhaps, in conditions such as diabetes that impose oxidative stress on the body. Evidence for the hypothesis that such an oxidation and concomitant reduction in activated protein C levels would lead to elevated cardiovascular risk is presented.

Amino Acid Sequence↗
PubMed2003

Fibrin D-dimer: a marker of psychosocial distress and its implications for research in stress-related coronary artery disease.

Psychosocial factors might mediate their adverse impact on coronary arteries by eliciting a hypercoagulable state via changes in sympathetic nervous system activity. A recent meta-analysis of prospective studies reported an association of the hypercoagulability marker D-dimer with an increased risk for coronary events. This review provides evidence that an elevated plasma D-dimer level is a suitable marker for acute and chronic psychosocial distress. Prospective studies need to show whether stress-related changes in D-dimer may help explain the increased coronary risk with psychosocial distress.

Autonomic Nervous System↗
PubMed1993

Hypercoagulation in diabetes mellitus.

The pathogenesis of diabetic vascular disease is not completely known. Many authors have suggested that hemorheological disturbance is an important factor in the development of vascular complication. The hypercoagulable state also suggested to cause this complication. In order to assess the role of blood coagulation in diabetic patients, we investigated hypercoagulation in diabetic patients and its relation with duration of the disease, smoking habits, blood pressure, blood glucose, diabetic retinopathy, diabetic ulcers and patient treatment. A case control study was done to evaluate these factors in 60 diabetic patients in out-and in-patient clinics of the Department of Internal Medicine, General Hospital Dr M Jamil Padang, during December 1990-March 1991. The average age was 51.55 years, average duration of the disease 5, 8 years. Fibrinogen levels is higher in diabetic patient (mean +/- SD = 442.42 +/- 86.79 mg/dl), compared to normal person (mean +/- SD = 349.2 +/- 35.26 mg/dl), PT is shorter (mean +/- SD = 10.1 +/- 1.31 sec), compared to normal person (mean +/- SD = 11.04 +/- 0.93 sec), APTT is also shorter (mean +/- SD = 29.2 +/- 3.69 sec), compared to normal person (mean +/- SD = 32.16 +/- 3.77 sec). There was a significantly high fibrinogen and short PT and APTT in diabetic patients, especially those who suffered from diabetes for a long time and followed by chronic complications.

Adult↗
PubMed2002

Postprandial lipemia--effect of lipid-lowering drugs.

Exaggerated postprandial hyperlipidemia has been associated with cardiovascular disease. The mechanisms underlying this association are likely to depend on a multitude of effects. Potentially atherogenic remnants of triglyceride-rich lipoproteins (TRL) accumulate in the postprandial state. In addition, TRL may promote the formation of small dense LDL. There are some indications that the postprandial period is a hypercoagulable state and endothelial function seems to be hampered after acute fat intake. Conventional lipid lowering drugs such as statins and fibrates have the potency of reducing postprandial hyperlipidemia, but the fibrates seem to be more effective in this respect. There is a complete lack of prospective studies linking inefficient postprandial lipid metabolism with clinical endpoints and there is also a need to include investigations of postprandial lipid metabolism in the evaluation of novel drugs affecting lipid metabolism and insulin resistance.

Clinical Trials as Topic↗
PubMed2003

Lipid abnormalities in insulin resistant states.

There are many metabolic consequences of insulin resistance and multiple conditions associated with insulin resistant states. The most obvious pathology associated with insulin resistance is type 2 diabetes mellitus, but other manifestations include hypertension, central obesity, a hypercoagulable state, and dyslipidemia. The atherogenic dyslipidemia associated with insulin resistant states is characterized by hypertriglyceridemia; an increase in very-low-density lipoprotein secretion from the liver; an increase in atherogenic small, dense low-density lipoprotein; and a decrease in high-density lipoprotein cholesterol. Each of these lipid abnormalities is an independent risk factor for coronary artery disease, and in concert, the cardiovascular risk is magnified. Therefore, insulin resistant states should be identified as early as possible in patients, and these lipid abnormalities should be assessed and treated.

Cholesterol, HDL↗
PubMed1996

[Evaluation of the factor XIIa assay kit].

The assay for activated coagulation factors has recently been considered to be a useful tool for detecting hypercoagulable state. Measurement of activated factor XI and alpha 1 antitrypsin complex developed by us is the only one measure for detecting contact phase hypercoagulation. The ACTIVATED FACTOR XII kit (Shield Diagnostics) has recently been commercially available, and the reference range was reported in the instruction manual. However, because the recovery rate of purified factor XIIa (XIIa) in normal pooled plasma by this assay kit was strikingly decreased, the effects of inhibitors in plasma, such as low molecular weight serine proteinase inhibitor (diisopropyl fluoro-phosphate, DFP), the specific inhibitor for XIIa (corn trypsin inhibitor, CTI), the main inhibitor for XIIa (C1 inhibitor, C1I) were examined. These three inhibitors and XIIa were incubated for 18 hours, then the XIIa levels of these complexes and the recovery rate in the normal pooled plasma were assayed by this assay kit. The recovery ratios in the normal pooled plasma were; DFP-XIIa 82%, CTI-XIIa 63%, and C1I-XIIa 0%, XIIa without inhibitor 7%. These results suggest that this XIIa kit does not reflect the levels of complexed form of XIIa and inhibitors in plasma samples.

Adult↗
PubMed1991

C4b-binding protein exacerbates the host response to Escherichia coli.

Activated protein C is a plasma anticoagulant. For activated protein C to function as an anticoagulant, it must form a complex with protein S. Protein S anticoagulant activity is neutralized by formation of a reversible complex with C4b binding protein (C4bBP). C4bBP is an acute-phase plasma protein. When C4bBP levels increase, mass action forces the level of free protein S to decrease, giving rise to an acquired functional protein S deficiency. It has been proposed that these elevated C4bBP levels and the resultant acquired deficiency of protein S that occurs in inflammation could contribute to a hypercoagulable state. An experimental model to test this hypothesis was suggested by our previous studies that demonstrated that inhibition of protein C activation rendered baboons hypercoagulable in response to sublethal Escherichia coli infusion (J Clin Invest 79:918, 1987). We have extended these studies to examine the effect of inhibition of protein S activity with C4bBP in the host (baboon) response to infusion of sublethal concentrations of E coli organisms. Five sets of animals were studied: (1) those challenged with sublethal concentrations of E coli alone (0.4 x 10(10)/kg); (2) those supplemented only with C4bBP (20 mg/kg); (3) those challenged with the same level of E coli but supplemented with C4bBP (20 mg/kg); (4) those challenged with sublethal E coli and supplemented with C4bBP (20 mg/kg) and sufficient protein S (2.3 mg/kg) to fill the protein S binding sites on C4bBP; and (5) those challenged with lethal concentrations of E coli. Sublethal E coli infusion (group 1 animals) caused only an acute-phase response with no consumption of fibrinogen, detectable organ damage, or detectable tumor necrosis factor (TNF) in the plasma. C4bBP infusion (group 2 animals) resulted in no significant physiologic changes, no detectable plasma TNF, and little change in fibrinogen level. The group 3 animals, receiving both sublethal E coli and C4bBP, exhibited rapid consumption of fibrinogen, systemic organ damage, and detectable circulating TNF ultimately leading to death. The overall response of this group was very similar to the response of the group 5 animals receiving an LD100 dose of E coli. The group 4 animals, which were treated exactly as above except that C4bBP was supplemented with a slight excess of protein S, responded essentially like those that received sublethal E coli alone. These studies suggest that the elevation of C4bBP during an inflammatory response can contribute to fibrinogen consumption and vascular damage. This vascular damage may be associated with enhanced elaboration of cytokines like TNF.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

Coagulation, fibrinolytic and kallikrein systems in neonates with uncomplicated sepsis and septic shock.

This study evaluates the contact system, coagulation inhibitors and fibrinolysis in 23 full-term newborns with sepsis (8 with septic shock). The results were compared with a group of 20 healthy newborns. Blood samples were obtained at the time of clinical diagnosis and 3 days after the antibiotic therapy was started. The results showed that: severe infection was associated with activation of the contact system, depletion of anticoagulant proteins and elevation of C4b-binding protein levels. There was a shift in protein S to the complexed inactive form, and the thrombin-antithrombin complexes increased. These changes occurred in parallel to both activation and inhibition of fibrinolysis. These changes were more pronounced in the septic shock patients than in nonshock neonates. After therapy, this procoagulant state decreased among survivor patients while in those who died, the abnormalities in coagulation did not improve. Our study suggests that neonatal sepsis induces a hypercoagulable state that persists in nonsurvivor neonates despite a correct treatment.

Anti-Bacterial Agents↗
PubMed1994

Childhood stroke at three years of age with transient protein C deficiency, familial antiphospholipid antibodies and F. XII deficiency--a family study.

The unusual case of a boy with a stroke occurring at three years of age, transient reduction in protein C activity and high concentrations of antiphospholipid antibodies (APA) is described. APA or Lupus Anticoagulant (LA) were found in 7 of 11 relatives studied out of three different generations. In addition, antigenic Factor (F) XII deficiencies or borderline values were found in the propositus and 2 relatives. Evidence for F. XII inhibitors was found in the propositus, one of his brothers and both of his parents. Whether F. XII inhibitors in patients with APA and/or LA are pathophysiologically relevant in vivo or if they are only an in vitro phenomenon remains to be elucidated. It is reasonable to believe that the main laboratory pathology (APA and/or LA activity) in antiphospholipid syndrome is related to the clinical picture of a hypercoagulable state. There is evidence from the literature that deficiency or inhibition of F. XII might contribute to a prothrombotic state through impairment of the fibrinolytic system. There is also evidence that APA are able to reduce protein C activation. From a clinical point of view, it seems that hypercoagulability in our patient was controlled by low-dose aspirin therapy (75 mg/d). In conclusion, this case seems to support the idea of a genetic predisposition for the development of APA and/or LA. The related disturbances of the coagulatory, anticoagulatory and fibrinolytic systems might contribute in different ways to the prothrombotic state seen in patients with "antiphospholipid syndrome", eventually resulting in possible venous thrombosis or arterial thrombosis with corresponding ischaemic lesions.(ABSTRACT TRUNCATED AT 250 WORDS)

Antibodies, Antiphospholipid↗
PubMed2000

Hypercoagulation and hypofibrinolysis in horses with colic and DIC.

Changes in haemostasis in horses with colic were assessed by using specific and sensitive markers of coagulation and fibrinolysis activity. Blood samples from 41 horses with severe colic and from 30 healthy control horses were tested. Diagnosis of DIC was based on the findings of at least 3 of 6 abnormalities: thrombocytopenia, prolonged clotting times (PT and APTT), increased polyclonal FDPs, decreased fibrinogen and decreased AT-III activity. Plasma thrombin-antithrombin III complexes (TAT), monoclonal fibrin degradation products fragment D (D-dimer) and monoclonal fibrinogen degradation products (FgDP) were also tested by using ELISA kits. DIC was diagnosed in 16 of 41 horses with colic. Compared to control and non-DIC colic values, TAT was significantly (P < 0.000) greater in horses with colic and DIC (Control group, mean +/- s.d. 2.6 +/- 2; non-DIC colic group, 7.5 +/- 9, and DIC colic group, 30.9 +/- 36 ng/ml). Also, D-dimer was significantly (P < 0.000) less in the DIC group when compared to control and non-DIC colic values (mean +/- s.d. 677 +/- 119, 682 +/- 220 and 399 +/- 234 ng/ml, respectively). Compared to non-DIC colic values, FgDP was significantly (P < 0.05) lower in the DIC group (363 +/- 111, 437 +/- 230 and 293 +/- 187 ng/ml respectively). Both PT and APTT showed a significant positive correlation with TAT. DIC was more common among nonsurvivors and horses with ischaemic bowel. We conclude that a hypercoagulative state was detected in horses with colic, which was stronger in horses with colic and DIC. Hypofibrinolysis was present only in horses with DIC. Therefore, marked hypercoagulation together with hypofibrinolysis are associated with DIC in horses.

Animals↗
PubMed1982

[Antithrombin III in infantile nephrotic syndrome].

In the Nephrotic Syndrome an hypercoagulable state can cause an increased incidence of thromboembolic phenomena and the course of the syndrome. The deficiency of Antithrombin III has been suggested to explain the hypercoagulability. We measured plasma antithrombin concentration (as percentage) in 24 children suffering from N.S. and the values were correlated with serum albumin, proteinuria and Partial Thromboplastin Time (PTT). The results of this study show that plasma Antithrombin III (AT-III) is significantly correlated with serum albumin, with proteinuria and PTT. Moreover plasma AT-III concentration was found to be low particularly when patients relapsed and in 2 children who developed thombophlebitis of the safena vein.

Adolescent↗
PubMed2001

Hemostatic state and atrial fibrillation (the Framingham Offspring Study).

Atrial fibrillation (AF) is strongly associated with thromboembolic complications, although the mechanism for the increased risk has not been fully explained. To determine whether AF might be associated with a hypercoagulable state, we studied hemostatic factors in subjects with or without AF in the Framingham Heart Study. In 3,577 subjects, we measured fibrinogen, von Willebrand factor antigen, tissue plasminogen activator (tPA) antigen, and plasminogen activator inhibitor-1 antigen. Forty-seven subjects had AF at the index clinic examination and 15 had AF on a prior examination, but not on the current examination. Before matching, the 47 subjects with prevalent AF had higher levels of fibrinogen, von Willebrand factor, and tPA antigen than those without AF, all p < or =0.03. Compared with 167 referent subjects matched for age, sex, and other risk factors, those with AF had higher tPA antigen levels than those without AF, 1 1.8 +/- 4.0 ng/ml versus 10.5 +/- 3.9 ng/ml (p = 0.04). However, when further stratified according to their cardiovascular disease status, the differences in hemostatic factors were no longer significant. We conclude that the prothrombotic profile associated with AF was explained by the risk factors of the subjects and the presence of cardiovascular disease. Nonetheless, the hemostatic changes may contribute toward the propensity for thromboembolic complications in AF. Further prospective studies are needed to evaluate whether measurement of these and other hemostatic factors will identify patients with AF who are at increased risk for thromboembolic complications, and who may therefore benefit from more intensive therapy.

Aged↗
PubMed2003

Thrombotic disorders: diagnosis and treatment.

Hematologists are increasingly involved in the diagnosis and management of patients with venous and arterial thromboembolic disorders. There have been major advances in recent years in our understanding of the central role of hypercoagulability in the pathogenesis of thrombosis. This has led to new approaches to the diagnosis of patients at risk for thrombosis and the development of more rational antithrombotic strategies. In Section I, Dr. Andrew Schafer reviews current concepts of acquired and inherited hypercoagulable states. It is now recognized that most, if not all, patients with venous thromboembolism have a genetic basis for the disorder ("thrombophilia"). The level of lifelong, baseline hypercoagulability in any individual may be determined by the type(s) and number of thrombophilia(s) that are inherited. Clinical episodes of thrombosis are precipitated by acquired thrombogenic triggers, which may be overt (e.g., pregnancy) or subclinical. In Section II, Dr. Mark Levine discusses the complex problem of thrombosis in patients with cancer. The goals of treating acute venous thromboembolism in cancer patients are to prevent recurrence, minimize the risk of anticoagulant-induced bleeding, and improve quality of life. New developments have improved treatment of venous thromboembolism in these patients, including outpatient therapy and secondary prevention with low-molecular-weight heparin. In Section III, Dr. Barbara Konkle reviews the diagnosis and management of thrombotic complications associated with pregnancy and hormonal therapy. Patient management is discussed based on data on thrombotic risks associated with hormonal treatment of infertility, pregnancy and the post-partum period in women with and without underlying thrombophilic risk factors. In Section IV, Dr. Clive Kearon discusses the management of anticoagulation before and after elective surgery. In the past, there has been no consensus on the perioperative management of anticoagulation for patients who require long-term warfarin therapy. This review considers the expected risks and benefits of different approaches to anticoagulation in patients who require warfarin because of atrial fibrillation, a mechanical heart valve, or a history of venous thromboembolism.

Anticoagulants↗