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PubMed1999

Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis.

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

Antithrombin III↗
PubMed2001

Diabetes mellitus with left transverse sinus thrombosis and right transverse sinus aplasia.

A 67-year-old woman with diabetes mellitus was hospitalized due to a throbbing headache. She appeared neurologically normal, except for meningeal irritation. The cerebrospinal fluid pressure was high. There was increased fluid protein without an increased cell count. Brain CT scan showed no abnormality, however, brain magnetic resonance angiography (MRA) showed complete right transverse sinus stasis and partial left transverse sinus stasis, indicating bilateral transverse sinus thrombosis. At this time thrombin anti-thrombin III complex (TAT) and prothrombin fragment F1+2 (PTF1+2) indicating hypercoagulation had increased. Urokinase, followed by aspirin and ticlopidine hydrochloride were administered. After diet therapy and transient insulin administration, her blood glucose levels improved. By the 22nd day, the headache had disappeared. Subsequently, brain MRA showed left transverse sinus blood flow recovery and complete right transverse sinus stasis, while carotid angiography showed recovered left transverse sinus but right transverse sinus defect. TAT and PTF1+2 levels improved concomitantly with better blood glucose control. We diagnosed this case as left transverse sinus thrombosis because of the hypercoagulable state resulting from diabetes mellitus accompanied by right transverse sinus aplasia.

Aged↗
PubMed1987

Plasma fibrinopeptide A levels during insulin-induced plasma glucose falls in diabetics.

Plasma fibrinopeptide A (FPA) concentration, as a measure of thrombin activity, was determined during an insulin tolerance test in 17 non-obese diabetics. FPA was measured by a modification of the Nossel method. Administration of insulin significantly lowered plasma glucose, accompanied by a significant increase in FPA from 0.9 +/- 0.1 ng/ml to 4.3 +/- 1.6 ng/ml (P less than 0.05) as well as a significant increase in circulating levels of epinephrine and growth hormone. The magnitude of the peak in epinephrine levels correlated well with both the rate of decline of plasma glucose and the magnitude of the peak of FPA. In addition, the FPA increment was suppressed by treatment with heparin. These results indicate that insulin-induced hypoglycemia or a rapid fall in plasma glucose is associated with enhanced thrombin generation and fibrin formation, which may be considered as a contributory factor to the development of diabetic microangiopathy through a hypercoagulable state.

Adult↗
PubMed1997

Activated protein C resistance and anticardiolipin antibodies in patients with venous leg ulcers.

BACKGROUND: Hypercoagulable states, which include the presence of anticardiolipin antibodies (ACAs), have been associated with skin ulceration. Resistance to activated protein C (APC), resulting from the factor V Leiden mutation, is a common risk factor for venous thrombosis. Its prevalence among patients with venous leg ulcers is not known. OBJECTIVE: Our purpose was to determine the prevalence of factor V Leiden and ACA in patients with venous leg ulceration. METHODS: Twenty-nine consecutive patients with venous leg ulcers were studied. Resistance to APC was first determined by functional assay based on the partial thromboplastin time. Patients with an abnormally low APC ratio were then subjected to molecular analysis for confirmation of factor V Leiden. Measurements of ACA were performed by enzyme-linked immunosorbent assay. RESULTS: APC resistance was detected in 11 of 26 patients. However, only 2 of these 11 patients (7.7% overall) were found to be heterozygous for the factor V Leiden mutation. ACA was present in neither patient with the Leiden mutation but was found in 6 of 21 patients tested (29% overall). CONCLUSION: The factor V Leiden mutation, unlike ACA, may not be more prevalent in patients with venous leg ulcers than in the general population. Our results emphasize the importance of molecular analysis for factor V Leiden in patients with APC resistance.

Adult↗
PubMed1988

Pathophysiology of antithrombin III deficiency.

This article focuses on the pathophysiology of thrombosis in patients with acquired antithrombin III deficiency. Antithrombin III is an important natural inhibitor of the hemostatic mechanism, and a hypercoagulable state is often induced in diseases causing antithrombin III deficiency. Laboratory determination of antithrombin III activity is particularly useful in the clinical evaluation and therapeutic management of patients with disseminated intravascular coagulation, nephrotic syndrome, and severe hepatopathy.

Animals↗
PubMed1988

Hemostatic abnormalities in nephrotic syndrome.

Nephrotic syndrome is often associated with a hypercoagulable state and thrombotic complications. Thrombosis may be due to a number of abnormalities in blood, including AT III deficiency, increased concentrations of fibrinogen, factors V and VIII, and platelet hyperaggregability. The therapeutic approach to thrombosis in nephrotic syndrome is the use of anticoagulants as a preventive measure or an attempt at thrombolysis with streptokinase, urokinase, or stanozolol.

Animals↗
PubMed2003

Interleukin-6, endothelial activation and thrombogenesis in chronic atrial fibrillation.

BACKGROUND: A prothrombotic or hypercoagulable state has been described in AF, which could increase the risk of thromboembolism. As inflammation has been related to thrombogenesis and endothelial activation, we hypothesised that the prothrombotic state in AF (as assessed by an index of thrombogenesis, prothrombin fragment 1+2 [F1+2]) and endothelial activation (soluble E-selectin (sEsel)) could be related to an index of inflammation (interleukin-6 (IL-6)). PATIENTS AND METHODS: We studied 191 consecutive patients (98 male; mean age 72.3+/-9.2 years) with chronic non-rheumatic AF who were not on anticoagulant therapy. Plasma IL-6, sEsel and F1+2 were measured by ELISA. Research indices were compared to 74 controls in sinus rhythm matched for age and sex. In 43 patients with AF, the effects of introducing anticoagulation (INR 2.0-3.0) were also studied. RESULTS: Patients with AF had elevated levels of F1+2 (p<0.001) and IL-6 (p=0.045), but not sEsel. There was no significant correlation between F1+2 and IL-6. In multivariate analysis, only F1+2 levels were independently associated with the presence of AF (p=0.001). After oral anticoagulation, plasma levels of F1+2 and sEsel were significantly decreased (both p<0.01). CONCLUSION: High levels of IL-6 in AF suggest an inflammatory state, which appears to be more related to clinical variables of the patients, rather than to the presence of AF per se. There was no association of inflammation with endothelial activation (sEsel) or the presence of abnormal thrombogenesis (high F1+2 levels) in AF. Moreover, no changes in IL-6 levels were found despite the reduction of the other markers by oral anticoagulant therapy.

Aged↗
PubMed2001

[Duration of oral anticoagulant therapy in venous thromboembolism].

PURPOSE: The optimal duration of oral anticoagulant therapy after a first episode of venous thromboembolism is still a matter of debate. It is essential to balance the desired effect of the anticoagulants in reducing recurrences against the risk of major bleeding. The aims of this paper are to describe the current concepts in this field. CURRENT KNOWLEDGE AND KEY POINTS: Recent data, based on randomised controlled trials, suggest that it is necessary to tailor the duration of anticoagulation individually according to the topography of venous thromboembolism and the presence of risk factors. A 6-week treatment for patients with isolated calf vein thrombosis is sufficient. For proximal thrombosis and/or pulmonary embolism, a short anticoagulant course seems sufficient in patients with temporary risk factors (3 months) and a longer anticoagulant course (6 months at least) is recommended for cases with permanent risk factors or idiopathic venous thromboembolism. The inherited or acquired hypercoagulable states can be divided into those that are common and associated with a modest risk of recurrence (i.e., isolated factor V Leiden or G20210A prothrombin gene) and those that are uncommon but associated with a high risk of recurrence (i.e., antithrombin, protein C or S deficiencies and anticardiolipin antibodies). Thus, the presence of one of these last abnormalities favours more prolonged anticoagulant therapy. FUTURE PROSPECTS AND PROJECTS: 1) For patients at high risk of recurrence, there is a paucity of evidence-based medicine, particularly for patients with biological thrombophilia, and randomised controlled trials in this population are required. An assessment of low- or fixed-dose oral anticoagulation is also necessary in order to reduce the bleeding risk. 2) It is not always possible to precisely determine the optimal duration with the available data. We have performed a meta-analysis on summary data which suggests that a long course of oral anticoagulant therapy is superior to a short course. An individual meta-analytic approach is needed to draw more precise conclusions on an interesting and important clinical topic and we propose to perform this analysis in a international collaborative group.

Administration, Oral↗
PubMed1994

Extrarenal complications of the nephrotic syndrome.

The systemic complications of nephrotic syndrome are responsible for much of the morbidity and mortality seen with this condition. This review discusses the causes for the hypoalbuminemia and the associated metabolic abnormalities of the nephrotic syndrome. No unifying hypothesis exists for the induction, maintenance, and resolution of nephrotic edema. In view of the wide spectrum of renal diseases leading to the nephrotic syndrome, more than a single mechanism may be responsible for the renal salt retention in these diverse conditions. Although hypoalbuminemia may be important, especially when plasma oncotic pressure is very low (serum albumin < 1.5 to 2.0 g/dL), primary impairment of salt and water excretion by the nephrotic kidney appears to be a major factor in pathogenesis of the edema. However, the decreased serum albumin and/or oncotic pressure seen with nephrotic syndrome is a major contributing factor to the development of the hyperlipidemia of nephrotic syndrome. Patients with unremitting nephrotic syndrome should be considered for combined dietary and lipid-lowering drug therapy. Urinary losses of binding proteins lead to the observed abnormalities in the endocrine system and in trace metals, and urinary losses of coagulation factors contribute to the hypercoagulable state. At present, selective renal venography is recommended when the suspicion of renal vein thrombosis is justified by clinical presentation. The impact on renal function caused by treating asymptomatic chronic renal vein thrombosis is undetermined, but anticoagulation for chronic renal vein thrombosis is associated with relatively few complications.

Acute Kidney Injury↗
PubMed1998

Budd-Chiari syndrome during nephrotic relapse in a patient with resistance to activated protein C clotting inhibitor.

It has long been known that patients with nephrotic syndrome have a hypercoagulable state, which explains the association between nephrotic syndrome, renal vein thrombosis, and thromboembolism. However, the Budd-Chiari syndrome has never been reported in nephrotic patients. This is the first report of such an association that, most likely, depended on a primary resistance to activated protein C.

Adult↗
PubMed1997

Bilateral adrenal enlargement as a first sign of systemic vasculitis.

In this case-report we describe the fatal outcome of systemic vasculitis. A 51-year-old man was hospitalised with constant abdominal pain, chest pain, anorexia, fatigue, weight loss, dyspeptic complaints, and a period of high fever at home. Bilateral adrenal enlargement was found without a plausible cause. Endoscopy revealed a reflux oesophagitis grade I, which was treated with famotidine. His complaints disappeared without further treatment. Five days after release from hospital the patient was re-admitted with subfebrile temperature followed by an Addison's crisis due to primary adrenal failure. Laboratory tests for systemic illness were all negative. He was treated with high-dose corticosteroids. Right adrenal biopsy revealed haemorrhage, possibly of older age. After 10 days he returned with severe kidney and heart failure. He was transported to another hospital for haemodialysis. Unfortunately the patient passed away because of cardiac arrhythmias. Postmortem investigation revealed inflammation of middle-sized and small arteries in the adrenal glands, heart, lung and thyroid. In the kidneys, mesangio-proliferative glomerulonephritis was found. A definite classification of the vasculitis could not be made because of the high-dose corticosteroids therapy. Possibly, the haemorrhage of both adrenal glands was caused by venous thrombosis due to the hypercoagulable state, which is often observed in vasculitis.

Adrenal Gland Diseases↗
PubMed2001

[Thrombogenic and endothelial damage markers in patients with ischemic systolic impairment].

INTRODUCTION: Anticoagulation is rarely indicated in patients with left ventricular dysfunction who show an increased risk for thromboembolism. In theory, the three arms of the Virchow' triad may be present: abnormal blood flow, endothelial damage and prothrombotic markers. The aim of this study was to identify the last two arms. PATIENTS AND METHOD: We studied 82 consecutive patients with demonstrated ischaemic heart disease and sinus rhythm, and compared them with a control group comprised of 32 healthy subjects matched for age and sex. None or the patients had had an acute coronary event or hemodynamic decompensation within the 3 months prior to inclusion in the study. The plasma concentration or von Willebrand factor and fibrin d-dimer and fibrinogen were determined as endothelial damage and prothrombotic markers, respectively. A fractional shortening less than 29% by echography was defined as ventricular systolic dysfunction. RESULTS: The patients showed significantly higher levels of von Willebrand factor with respect to the control group (109.2 31.9 vs 85.5 32.6%, p < 0.01), with no differences in fibrinogen and fibrin d-dimer values. Twenty-six patients fulfilled criteria of left ventricular systolic dysfunction. Patients with left ventricular dysfunction showed higher fibrinogen (386 118 vs 322 102 mg/dl, p = 0.03) and fibrin d-dimer (0.36 0.22 vs 0.26 0.10 g/ml; p = 0.04) levels, with no differences in von Willebrand factor levels. CONCLUSIONS: After acute coronary events, patients with ischaemic heart disease show markers of endothelial damage. However, patients with left ventricular dysfunction show a hypercoagulable state.

Biomarkers↗
PubMed2002

[Annexin V levels in survivors of early myocardial infarction].

INTRODUCTION AND OBJECTIVES: Annexin V has an anticoagulant effect in vitro that derives from its ability to displace coagulation proteins from phospholipid surfaces, prolonging phospholipid-dependent coagulation reactions. Antiphospholipid antibodies (APL) and annexin V have an affinity for anionic phospholipids, so it has been hypothesized that one of the thrombotic mechanisms of APL may be due to displacement of annexin V from phospholipid surfaces. We studied plasma annexin V levels and analyzed its relationship to risk factors and several blood markers. PATIENTS AND METHOD: We studied 62 patients < 45 years old who had suffered myocardial infarction. The control group comprised 23 healthy subjects of similar age and sex. We analyzed the presence of APL, anti-beta2 glycoprotein I (beta2-GPI), anti-beta2-GPI/phospholipid complexes and anti-annexin V antibodies. We determined plasma annexin V levels. Cholesterol, HDL-cholesterol, triglycerides, antigenic tissue plasminogen activator and its inhibitor, von Willebrand factor, and fibrinogen levels were measured. RESULTS: We detected only 2 patients with positive anti-beta2-GPI/phospholipid complexes and 2 patients with positive anti-annexin V antibodies. We did not detect any positive APL or anti-beta2-GPI antibodies. In the control group there was only 1 patient with positive APL and anti-beta2-GPI antibodies. The myocardial infarction group showed significantly lower levels of annexin V than the control group: 0.640 ng/ml (0.520-0.818 ng/ml) vs 1.570 ng/ml (1.140-2.390 ng/ml), p < 0.01. There were no statistical associations between annexin V levels and other variables. CONCLUSIONS: The low levels of annexin V in young myocardial infarction patients could indicate a procoagulant trend. This hypercoagulable state was unrelated to the presence of APL.

Adult↗
PubMed2000

Hyperhomocysteinemia and pregnancy--review of our present understanding and therapeutic implications.

Homocysteine results from the transmethylation of methionine. Its metabolism depends primarily on three enzymes and several vitamin cofactors. Genetic abnormality in these enzymes or deficiency of these vitamins lead to hyperhomocysteinemia (HHCh). HHCh is usually biologically defined by a fasting value >15 micromol/l. HHCh belongs among the congenital hypercoagulable states and is a long-known vascular disease risk factor. The discovery that HHCh may also be responsible for several pregnancy complications has only recently been made. Studies in this area are still scarce and report on limited numbers of patients. It nevertheless appears clear that HHCh is associated with the syndromes of repeated miscarriage, pre-eclampsia, placenta abruptio, thromboembolic events, neural tube defects, and perhaps with fetal death-in-utero and intra-uterine growth retardation. Supplementation with vitamin B9 can reduce plasma HC levels, and is thus recommended in patients with HHCh. The prevention of thromboembolic events during pregnancy by anticoagulant treatment is also desirable in these patients.

Abortion, Habitual↗
PubMed2002

Cancer and thromboembolic disease: pathogenic mechanisms.

Almost all types of cancer are associated with an activation of coagulation. However, elevation of haemostatic markers of coagulation does not predict venous thrombosis. Multiple and interdependent processes between the tumour and the patient induce a hypercoagulable state. Tumour procoagulant activity, host inflammatory responses and extrinsic factors are involved. Tumour cells express the procoagulants, tissue factor and cancer procoagulant. They also release inflammatory cytokines and vascular endothelial growth factor, substances that enhance procoagulant activity and angiogenesis. Tumour-induced coagulation is intrinsically involved with tumour growth, angiogenesis and metastasis.

Blood Coagulation Factors↗
PubMed2002

Is diabetic hypercoagulability an acquired annexinopathy? Glycation of annexin II as a putative mechanism for impaired fibrinolysis in diabetic patients.

Diabetics die mainly from thrombotic complications and there is clear evidence that diabetes is a hypercoagulable state. Epidemiological and prospective intervention data link hyperglycemia to vascular complications and glycation of proteins is one favored molecular basis to explain this fact. Cell surface receptors may support fibrinolytic surveillance in both intravascular and extravascular locations by stimulating plasmin generation and by protecting plasmin from its inhibitors. The existing experimental evidence suggests that annexin II in its tetrameric form is the main physiological receptor for plasminogen on the extracellular surface of endothelial cells. We have recently shown that annexin II is an extremely vulnerable target for glycation, quickly responding to restoration of normoglycemia. We hypothesize that glycation of endothelial membrane annexin II impairs the appropriate formation of the plasminogen/tissue plasminogen activator/annexin II complex, disrupting a key regulatory mechanism in fibrinolytic vigilance. This would in turn produce decreased fibrinolytic activity and indirectly promote a thrombophilic state in diabetic patients. We base our hypothesis on our observation and on evidence for the mechanism of action of two major independent risk factors for CV events: lipoprotein (a) and hyperhomocysteinemia. Binding of plasminogen to annexin II is inhibited by Lp (a) and binding of tissue plasminogen activator to annexin II is blocked by homocysteine. If our hypothesis is correct, one of the components of the increased thrombogenicity seen in diabetic patients might then be an acquired annexinopathy.

Animals↗
PubMed1993

Placental thrombi and other vascular lesions. Classification, morphology, and clinical correlations.

Vascular lesions, most often mediated by thrombi, are second only to infections as a cause of fetal injury in the later weeks of pregnancy. In our experience many pathologists who examine placentas fail to conduct a proper search for vascular lesions and some even fail to recognize those exposed by their examination. This review is intended to define the typical clinical background or circumstances that suggest the presence of significant vascular problems, to define techniques calculated to display them well, and to identify criteria for diagnosis. Further research is needed to evaluate the prevalence of maternal and fetal hypercoagulable states and thrombi as a cause of fetal injury.

Blood Vessels↗
PubMed1979

Shock in pregnancy: pathophysiology and morphologic findings.

Sepsis and non-septic shock in pregnancy show characteristic modifications which are caused a) by physiologic changes in hemostasis primarily in the third trimester of pregnancy, b) by etiologic distinctions of shock regarded as pregnancy-specific, c) by hemodynamic changes in the circulation during pregnancy, d) by the ability of the healthy, young organism to compensate adequately. In the dead fetus syndrome and in non-septic shock, i.e., in amnionic fluid embolism and in abruptio placentae, the clinical picture is often governed by marked secundary fibrinolysis. Retroplacental hematoma, the characteristic feature of premature placental separation, remains controversial as either the cause or sequela of the hemostatic disorder. Etiologic, pathogenetic, and morphologic similarities exist between septic abortion, chorioamnionitis, and puerperal sepsis, but the varying response of the maternal organism during the course of pregnancy leads to different clinical and morphologic pictures. Due to a decrease in fibrinolytic activity as a consequence of pregnancy, the hypercoagulability state in a septic endotoxic shock predisposes the kidneys to bilateral renal cortical necrosis, principally in the amnion infection syndrome.

Abortion, Septic↗