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PubMed1984

Performance characteristics of a simple radioimmunoassay for fibrinopeptide A.

FPA, although identified 15 years ago, is now becoming an increasingly important diagnostic tool in the evaluation of the hemostatic process. Since this peptide is generated in very small amounts, only very sensitive methods, such as RIA, are useful for its quantitation. Measurement of this peptide allows for a most precise and reliable monitor of any ongoing thrombotic event in which thrombin is generated. Commercial kits have become available for fast and simple clinical evaluations of FPA. The Mallinckrodt RIA Quanti FPA kit has proved its reliability in precision, accuracy, fast turnaround time, and applicability to a routine laboratory setting. This assay kit was evaluated in our laboratory in various aspects. The following points summarize our finding: FPA is a useful diagnostic parameter to evaluate the activation of coagulation pathways in various pathologic states. A study of 170 normal plasma samples resulted in 1.7 +/- 0.5 ng/ml. No significant difference between males and females was noted. FPA levels are evaluated in patients with hypercoagulable states, DIC, and related thrombotic states. Our studies have shown that FPA levels are also elevated in certain cancers, postsurgical states, and certain other conditions in which the coagulation process is activated. During therapeutic heparinization, FPA levels are reduced; thus this form of therapy can be monitored using FPA levels. High-risk population (thrombotic) can be easily screened using FPA measurement. We propose that a multicenter study on FPA levels be conducted to prove its clinical relevance to other diseases.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Tests↗
PubMed2002

[Acquired and inherited hypercoagulability among patients with cerebral venous thrombosis].

BACKGROUND: Cerebral venous thrombosis (CVT) is considered to be a relative unusual pathology, probably underdiagnosed. Many acquired and inherited hypercoagulability states (HS) have been described as cause of CVT. OBJECTIVE: [corrected] We evaluated the incidence of acquired and inherited thrombophilic risk factors in a population of CVT patients. METHODS: Hypercoagulability studies were to carried out for patients suffering from radiologically confirmed CVT during a 3 year period (1998-2000). Prothrombin time, aPTT, protein C, protein S and antithrombin III activities, screening and confirmatory tests for lupus anticoagulant (LA), and activated protein C resistance (APCR) were tested. Genetic tests for G1691A factor V (Factor V Leiden), G20210A prothrombin and C677T methylentetrahidrofolate reductase (MTHFR) were performed. Computer database was used for descriptive statistics. RESULTS: 16 patients with CVT (M/F, 6/10) were screened for inherited and acquired coagulation disorders. Mean age of 23.66 years with standard desviation of 19.74 years. Two older patients had antecedents of thrombosis (ischemic stroke and deep-vein thrombosis in leg). We found 1 heterocygosis factor V Leiden associated to LA, 2 heterocygosis G20210A prothrombin (one associated to LA), 2 homocygosis C677T MTHFR, 1 hereditary antithrombin III deficiency and 4 LA. COMMENTS: Although this is a small series, we found a high incidence of hereditary (37.5%) and acquired (37.5%) thrombophilia in patients with CVT.

Adolescent↗
PubMed2003

Primary thrombophilia in Saudi Arabia.

OBJECTIVE: Venous thromboembolism (VTE) is a common disorder associated with significant mortality and morbidity. Considerable progress has been made in the understanding of the risk factors. Significant portion of patients develop VTE without obvious risk factors. The clinical applications of molecular techniques allowed identification of many important inherited, yet not uncommon risk factors. The aim of our study was to determine whether the activated protein C resistance (APCR)/Factor V Leiden (FVL), and prothrombin mutation as being the most common inherited risk factor for venous thrombosis among Saudi patients attending an anticoagulant clinic. METHODS: One hundred and seventy-nine consecutive patients (74 males, 105 females) accrued in a prospective study with a median age of 42 years (range 17-60 years) have been screened between October 1997 and January 2002 at the King Abdul-Aziz University Hospital (KAUH) and King Fahd Armed Forces Hospital (KFAFH), Jeddah, Kingdom of Saudi Arabia. All patients were Saudis with at least one of the following features: history of recurrent VTE, first episode of unprovoked VTE, thrombosis in unusual site or thrombosis at young age with or without positive family history. Thrombotic workup included protein C, protein S, antithrombin (AT), APCR, prothrombin mutation, lupus anticoagulant (LA), and anticardiolipin (ACL). Functional assays were carried out in 179 patients. Molecular analysis of both FVL, prothrombin G29210A mutation was performed in 67 patients. All tests were carried out in reference laboratories (Mayo Clinic, United States of America and Bioscientia, Germany). RESULTS: Protein S deficiency was the most common, identified in 26/179 (14.5%) followed by protein C in 15/179 (8.4%), while AT was not deficient in all 179 tested patients. Activated protein C resistance was present in only 4 patients (2.2%). Two patients were tested positive for prothrombin mutation; one of them was heterozygous for FVL too. Eight percent of the patients had LA, while 4% had ACL antibodies. CONCLUSION: Our study shows a different distribution pattern of the underlying thrombophilic state than reported in the western literature. If this holds true in larger trials, this may result in changing our local screening and diagnostic workup in patients with suspected hypercoagulable state.

Adolescent↗
PubMed2005

Cancer related thrombophilia: clinical importance and management strategies.

Acquired thrombophilic state associated with a significant risk of thrombosis is frequently encountered in malignancy. Venous and arterial thromboembolism is a common complication and patients with cancer, also present with a hypercoagulable state, even in the absence of thrombosis. Furthermore, clotting activation may play a role in tumor progression. The pathogenesis of thrombosis in cancer is multifactorial; however, a relevant role is attributed to the tumor cell capacity to interact with and activate the host hemostatic system. Among other factors, the prothrombotic action of antitumor therapies is also important. Thrombotic events can influence the morbidity and mortality of the underlying disease. Therefore, preventing these complications in cancer patients is a clinically relevant issue. Recently, new approaches to the prevention and cure of thrombosis in cancer have been investigated, and the hypothesis that the strategies to inhibit clotting mechanism may favorably affect malignant disease is gaining increasing interest. In this article the various aspects of the complex relationship between thrombosis and cancer, from pathophysiology to therapy, are reviewed.

Anticoagulants↗
PubMed1993

[Treatment of multiple organ failure].

Since numerous pathogenic factors are known to be involved in the development of disseminated intravascular coagulation (DIC) and multiple organ failure (MOF) in sepsis, the successful management of these clinical states is difficult. To investigate the mechanisms further, we developed experimental sepsis models associated with DIC and MOF, or endotoxin induced renal insufficiency model unaffected by prerenal factors. The hypercoagulable state leading to DIC is considered to be a prerequisite for MOF and inactivation of Xa or suppression of platelet activation is an important step to prevent the occurrence of DIC and MOF.

Alprostadil↗
PubMed1996

Intraventricular haemorrhage in preterm infants: evidence of suppressed fibrinolysis.

Intraventricular hemorrhage (IVH) in premature infants may be related to the immaturity of the vascular bed in the germinal matrix. We measured six hemostatic parameters whose alterations may represent an additional risk factor for IVH in preterm infants. On postnatal day 1 there were differences between plasminogen activator inhibitor-1 (PAI-1) activity and antigen, of both full-term and preterm infants with and without IVH (P < 0.05). Preterms with IVH were different to both full-terms and preterms without IVH. No difference was observed in plasma concentrations of fibrinogen, plasminogen and von Willebrand factor. Plasma concentrations of antithrombin III were significantly higher in full-term infants than in preterm infants. The difference between the platelet counts of preterm infants with and without IVH was not significant (P > 0.05). Elevation of crosslinked fibrin degradation products (XDP), determined by the SimpliRED D-dimer test, correlated in four out of five premature infants with the diagnosis of IVH by ultrasonography. No elevation of D-dimer XDP was observed in premature infants without IVH (11/12) and full-term infants (6/6). In conclusion, a hypercoagulable state, indicated by a rise in D-dimer XDP, may be initiated by some types of trauma to fragile blood vessels of the preterm infants who develop IVH. This hypercoagulability is further exacerbated by the increased release of PAI-1 leading to suppressed fibrinolysis.

Cerebral Hemorrhage↗
PubMed1984

The effect of spicules obtained from sickle red cells on clotting activity.

Spicules from sickle red cells were examined for their effects on the clotting activity of blood. The spicules were obtained from the sickle red cells after deoxygenation and oxygenation and were tested for clotting activity with Russell's viper venom assay. A marked increase in clotting activity was observed when spicules were added to the system. The increase was distinctly greater than that observed after the addition of sickle red cells while normal red cells had little effect. Vesicles prepared from sickle or normal red cells by incubation with the ionophore A-23187+Ca2+ also markedly increased clotting activity. The effect of spicules or vesicles on the clotting system may be related to reorganization of phospholipid in the spectrin-poor membrane of the spicules or vesicles. Because of these effects, the spicules from the sickle red cells may contribute to the hypercoagulable state in these patients and possibly to their vaso-occlusive crises since free spicules are present in their plasma. Vesicles from red cells from other types of anaemia with hypercoagulability may have a similar effect on coagulation.

Anemia, Sickle Cell↗
PubMedDate not supplied

Severe perinatal liver disease associated with fetal thrombotic vasculopathy.

Three neonates with fetal thrombotic vasculopathy in the placenta and severe neonatal liver disease are described. Symptoms included a bleeding disorder on the first day of life, followed by direct hyperbilirubinemia and elevated liver transaminases. All patients also had evidence of thrombosis outside the placenta, including cerebral infarct in two infants and thrombosis of the inferior vena cava in one infant. Liver disease was demonstrated to be thrombotic in one infant who died with Budd-Chiari syndrome. Two infants survived and had liver biopsy with cholestasis, bile duct proliferation, and portal fibrosis demonstrated at 4 weeks and 11 weeks of age, respectively. The etiology of thrombosis is unknown, though in one patient an excessively long and coiled umbilical cord may be implicated. The prenatal onset of thrombosis suggests an inherited or acquired thrombophilic state. In cases of enigmatic neonatal liver disease, an association with thrombosis should be considered and thrombi sought in placenta, umbilical cord, major blood vessels, and other organs. Evaluation for a hypercoagulable state is also suggested.

Adult↗
PubMed2002

Management of thrombophilia in renal transplant patients.

Renal allograft recipients with thrombophilia (a hypercoagulable state) are at higher risk for early allograft loss. Following an episode of allograft renal vein thrombosis in a patient subsequently diagnosed with protein C deficiency, we adopted universal screening for hypercoagulable risk factors. Patients with a history of a thromboembolic event underwent laboratory screening for thrombophilia. Eight patients with a defined hypercoagulable disorder or a strong clinical history of thrombosis even in the absence of hematologic abnormalities were treated with anticoagulation following renal transplantation. We reviewed the outcomes of these eight patients and all renal transplant recipients at our center who developed thrombotic complications after renal transplantation. Since the introduction of universal screening for hypercoagulable risk factors, 235 consecutive transplants were performed without allograft thrombosis. Eight patients with evidence of thrombophilia, recognized before renal transplantation, received perioperative heparin and postoperative oral anticoagulation. Two of these eight patients developed perinephric hematomas requiring evacuation, blood transfusion, and temporary withholding of anticoagulation. Of interest, two of the remaining 227 patients, not identified with thrombophilia before surgery, developed thrombotic complications after renal transplantation. A hypercoagulable disorder was subsequently documented in each. Identifying patients with thrombophilia before transplantation and defining their management presents many challenges. The risk of allograft thrombosis must be weighed against the risk of perioperative bleeding and the need for long-term anticoagulation. Recommendations for managing thrombophilia in renal transplant recipients are suggested based on our experience and review of the literature.

Anticoagulants↗
PubMed1996

Antibodies to prothrombin imply a risk of myocardial infarction in middle-aged men.

Antiphospholipid antibodies in patients with "antiphospholipid syndrome" may be directed at least in part against plasma phospholipid-binding proteins, such as beta 2-glycoprotein I or prothrombin, which are involved in the control of thrombosis and haemostasis. IgG-class antibodies against prothrombin and beta 2-glycoprotein I were measured by enzyme-linked immunoassay in initially healthy middle-aged dyslipidaemic men (non-high-density lipoprotein > 5.2 mml/l). Serum samples had been drawn at entry to a 5-year coronary primary-prevention trial with gemfibrozil from 106 subjects who experienced either a non-fatal myocardial infarction or cardiac death during the follow-up and from 106 subjects without coronary episodes, matched for treatment group (gemfibrozil/placebo) and geographical area. The antiprothrombin antibody level, as expressed in optical density units, was significantly higher in patients than in controls (0.26 +/- 0.17 versus 0.22 +/- 0.09; p < 0.02). A high level of antiprothrombin antibodies (highest tertile of distribution) predicted a 2.5-fold increase in the risk (95% confidence interval 1.2-5.3) of myocardial infarction or cardiac death. The distribution of IgG-class antibodies against beta 2-glycoprotein I did not differ significantly between cases and controls. The joint effect of antiprothrombin antibodies and other factors associated with hypercoagulative state: triglyceride level, lipoprotein(a) and smoking, was multiplicative for the risk. Antiprothrombin antibodies are a new immunological predictor of myocardial infarction and the effect of these antibodies may be mediated by hypercoagulative mechanisms.

Apolipoproteins↗
PubMed1999

Thrombophilic state in breast cancer.

Tumor cell metastasis and thrombosis are the major causes of death in cancer patients. Thrombosis in cancer patients may occur when physiologic antithrombotic systems are defective or when prothrombotic activities defeat normal physiologic antithrombotic mechanisms. Malignancies by themselves may already predispose to a hypercoagulable state in cancer patients. Tumor cells can either directly activate the blood clotting system or indirectly stimulate mononuclear cells to synthesize and express various procoagulants, subsequently leading to prothrombin activation, fibrin formation, and generation of a thrombus. In addition, other comorbid predisposing factors effecting thrombosis in cancer patients have to be considered, including surgery, bed rest, infection, long-term indwelling central venous catheters, anticoagulation, and chemotoxic or steroidal anticancer drugs used in adjuvant or palliative cancer treatment. Reliable information on the incidence of thromboembolism in cancer patients is available for breast cancer; less data have been reported for other malignancies. Chemo- and/or hormone therapy in patients with primary or metastatic breast cancer is associated with an increased thromboembolic risk, although the benefits of treatment far outweigh the risks. The current literature discussing the effect of chemo/hormone therapy on blood clotting factors and the associated risk of thrombosis is reviewed, with emphasis on new developments in the area of tissue-specific SERMs (selective estrogen receptor modulators). SERMs are employed as adjuvant therapy in primary breast cancer and in the palliation of advanced breast cancer and may be clinically useful as potential substitutes for long-term hormone replacement therapy, in the treatment of osteoporosis, and for cancer prevention therapy.

Antineoplastic Agents↗
PubMed2000

Antiphospholipid antibody syndrome manifested as a postoperative cerebrovascular event in a child.

Perioperative cerebrovascular events are exceedingly uncommon in pediatric patients. The etiology of such problems includes emboli from intracardiac thrombi, sickle cell disease, vascular anomalies, vasculitis affecting the cerebral vasculature, and prothrombotic states. We describe a 6-year-old boy who had right-sided hemiparesis on the second postoperative day after an uneventful patch angioplasty for renal artery stenosis. Workup revealed a possible hypercoagulable state due to an anticardiolipin antibody. The pathogenesis of the anticardiolipin antibody syndrome, its clinical manifestations, diagnostic criteria, and potential treatment strategies are reviewed.

Anticoagulants↗
PubMed1987

Preeclampsia as chronic disseminated intravascular coagulation. Study of two parameters: thrombin-antithrombin III complex and D-dimers.

Determinations of coagulation/fibrinolysis parameters thrombin-antithrombin III complex (TAT) and D-dimers (cross-linked fibrin degradation product) were carried out in order to prove that preeclampsia is a chronic disseminated intravascular coagulation (DIC) state. Besides the parameters TAT and D-dimers, antithrombin III (ATIII), fibrin degradation products and platelets were measured as well. Even in normal pregnancy there is an activation of coagulation, reflected in a hypercoagulative state that is proceeding down to the formation of thrombin. This thrombin is, however, nearly completely inactivated by ATIII, so that no fibrin is formed. This inactivation is solely reflected by the increase of TAT in the blood. In preeclampsia, however, where no such rapid changes as in acute DIC occur, the increase of TAT is accompanied by a decrease of ATIII and platelet counts and an increase of D-dimers; this demonstrates much more clearly the chronic DIC nature of preeclampsia than the results from studies carried out so far.

Antithrombin III↗
PubMedDate not supplied

Hepatic vein stenosis and inferior vena cava stenosis in a patient with chronic obstructive pulmonary disease.

The case is presented of a patient with stenosis of the intrahepatic portion of the inferior vena cava and the terminal part of hepatic veins, a state manifesting itself in ascites resistant to treatment. The case was originally seen as decompensated cirrhosis of the liver. Once properly diagnosed, it was successfully treated with angioplasty and subsequent anticoagulation. After all the relevant hypercoagulation states potentially leading to IVC and hepatic vein stenosis were ruled out, the cause of the patient's stenosis could be traced to: 1. secondary polycythemia concomitant to severe pulmonary obstruction disease and 2. simultaneous corticosteroid therapy. This cause has not been described in literature before.

Adrenal Cortex Hormones↗
PubMed2003

Changes in blood coagulation markers associated with uterine artery embolization for leiomyomata.

PURPOSE: To determine whether a transient hypercoagulable state is induced by the uterine artery embolization (UAE) procedure. MATERIALS AND METHODS: Serial periprocedure blood samples were obtained from 27 patients undergoing the UAE procedure. Five blood samples were obtained from each patient at set time intervals: before the procedure (for baseline determination), immediately before and after embolization of the uterine arteries, 90 minutes after conclusion of the procedure, and between 18 and 24 hours later. Each blood sample was analyzed for the peripheral levels of the following parameters: thrombin-antithrombin complex (TAT), prothrombin fragment 1.2 (F1.2), platelet factor 4 (PF4), D-dimer, and plasmin-alpha(2)-antiplasmin complex (PAP). For each parameter, the baseline values were statistically compared with the pre- and postembolization values for each individual to detect change over time. Overall and global occasion effects for continuous variables were assessed with the Friedman statistic and individual comparisons between occasions with the Wilcoxon signed-rank test. RESULTS: No evidence was found for a difference in coagulability among the five occasions for D-dimer (P =.7645) or PF4 (P =.09). All three of the remaining measures were found to have statistically significant differences (P <.0001 for F1.2, P =.0026 for PAP, and P =.0006 for TAT). No evidence was found for a difference between preprocedure and preembolization levels for these three latter parameters (P =.595 for F1.2, P =.128 for PAP, P =.9705 for TAT). Hypercoagulability potential as measured by prothrombinase and F1.2 generation increased between preembolization samples and each of the successive postprocedure samples (P <.0001, P <.0001, P =.0082), whereas PAP increased at 90 minutes (P =.0023) and TAT increased immediately after embolization (P <.0001). No clinically apparent thrombotic complications occurred among any of the patients studied. CONCLUSIONS: Surrogate markers of hypercoagulability increase as a result of UAE, suggesting that a prothrombotic state may result after the procedure.

Adult↗
PubMed1991

Platelets, coagulation, and fibrinolysis in sickle cell disease: their possible role in vascular occlusion.

Recent evidence suggests that sickle cell disease (SCD) can be considered a hypercoagulable state, in which both platelet activation and thrombin generation are abnormally increased. Although thrombosis is now known to play an important role in at least one of the vasocclusive complications of SCD, namely stroke, the significance of hypercoagulability in the pathogenesis of vascular occlusion in SCD remains unclear. This review summarizes current evidence regarding platelet, coagulation, and fibrinolytic abnormalities in SCD and their possible role in vascular occlusion. Potential implications for therapy are also discussed.

Anemia, Sickle Cell↗
PubMed2005

The effect of multi-factorial intervention on plasma von Willebrand factor, soluble E-selectin and tissue factor in diabetes mellitus: implications for atherosclerotic vascular disease.

BACKGROUND: Endothelial abnormalities and a hypercoagulable state may contribute to increased cardiovascular risk in diabetes mellitus, particularly in patients with overt cardiovascular disease (CVD). We sought to determine the effect of intensified multi-factorial cardiovascular risk intervention on indices of endothelial abnormality and hypercoagulability in diabetes, and if patients with overt CVD would derive similar benefit as those without. PATIENTS AND METHODS: We measured plasma von Willebrand factor (vWf, an index of endothelial damage/dysfunction), soluble E-selectin (sE-sel, marking endothelial activation) and tissue factor (TF, an initiator of coagulation) by ELISA in 94 patients with diabetes mellitus (38 with CVD and 56 without overt CVD) and 34 comparable controls. Thirty-three patients with CVD and 31 without overt CVD then participated in multi-factorial cardiovascular risk intervention over 1 year. RESULTS: Plasma levels of vWf (P = 0.009), sE-sel (P < 0.001) and TF (P < 0.001) were significantly higher in diabetic patients compared with controls, with TF highest in patients with overt CVD. Intensive multi-factorial intervention resulted in reductions in glycated haemoglobin (HbA(1c)), total and LDL-cholesterol (all P < 0.05), but no significant weight change. This was associated with reductions in vWf in patients with (by 26%P = 0.003), and without (by 47%, P < 0.001), overt CVD. TF was reduced only in patients without overt CVD (by 45%, P < 0.001). There were no significant changes in sE-sel levels in either group. CONCLUSION: Endothelial abnormalities in diabetes are only partially influenced by contemporary intensified multi-factorial cardiovascular risk intervention. These data suggest the need for earlier and more aggressive risk factor intervention.

Aged↗
PubMed1999

Prospective evaluation of hemostatic system activation and thrombin potential in healthy pregnant women with and without factor V Leiden.

Normal pregnancy is associated with alterations of the hemostatic system towards a hypercoagulable state and an increased risk of venous thromboembolism. The risk of venous thrombosis is higher in pregnant women with factor V Leiden (FVL) than in those with wildtype factor V. Routine laboratory assays are not useful to detect hypercoagulable conditions. A prospective and systematic evaluation of hemostatic system activation in women with and without FVL during an uncomplicated pregnancy employing more sensitive markers of hypercoagulability, such as prothrombin fragment 1+2 (F1+2), thrombin-antithrombin complex (TAT), D-Dimer, or the endogenous thrombin potential (ETP), an indicator of the plasma's potential to generate thrombin, has not been performed. We prospectively followed 113 pregnant women with (n = 11) and without (n = 102) FVL and measured F1+2. TAT, D-Dimer and the ETP at the 12th, 22nd and 34th gestational week as well as 3 months after delivery (baseline) in each subject. None of the women developed clinical signs of venous thromboembolism during pregnancy or postpartum. Pregnant women with and without FVL exhibited substantial activation of the coagulation and fibrinolytic system as indicated by a gradual increase of F1+2, TAT and D-Dimer throughout uncomplicated pregnancy up to levels similar to those found in acute thromboembolic events (p < 0.0001 by analysis of variance for each parameters). Levels of F1+2 and TAT were comparable between women with and without FVL, but levels of D-Dimer were significantly higher in women with FVL than in those without the mutation (p = 0.0005). The ETP remained unchanged in both women with and without FVL at all timepoints. Our data demonstrate a substantial coagulation and fibrinolytic system activation in healthy women with and without FVL during uncomplicated pregnancy. An elevated F1+2, TAT or D-Dimer level during pregnancy is not necessarily indicative for an acute thromboembolic event. The normal ETP in both women with and without FVL suggests that the capacity of the plasma to generate thrombin after in vitro activation of the clotting system is not affected by pregnancy. Higher levels of D-Dimer in women with FVL than in women with wildtype factor V at baseline as well as during pregnancy indicate increased fibrinolytic system activation in carriers of the mutation.

Adult↗