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At least 991 records · Page 55Linked to original sources
PubMed1998

Internal jugular vein thrombosis in patients with ovarian hyperstimulation syndrome.

OBJECTIVE: To describe a case of bilateral internal jugular vein thrombosis complicating ovarian hyperstimulation syndrome (OHSS). DESIGN: Case report. SETTING: Internal medicine ward in a teaching hospital. PATIENT: A 28-year-old nulliparous woman undergoing IVF. INTERVENTION(S): Ultrasonographic Doppler of the neck veins was performed because of pain and swelling in the neck, and bilateral jugular vein thromboses were detected. Laboratory evaluation revealed activated protein C resistance caused by factor V Leiden mutation. Low-molecular-weight heparin (enoxaparin) was administered for the remainder of the pregnancy and for 6 weeks after delivery. MAIN OUTCOME MEASURE: Resolution of jugular venous thromboses documented by ultrasonographic Doppler and normal progression of pregnancy. RESULT(S): The patient delivered healthy twins at term. There were no complications arising from the jugular vein thromboses or the low-molecular-weight heparin treatment. CONCLUSION(S): Unusually located venous thrombosis should prompt an evaluation for a hypercoagulable state. The high prevalence (4%-7%) of factor V Leiden mutation in most Western populations and the mutation's potential contribution to thrombotic complications in OHSS suggest that screening for this abnormality in women undergoing IVF may be indicated.

Adult↗
PubMed1996

Acute Budd-Chiari syndrome with fulminant hepatic failure in a pregnant woman with factor V Leiden mutation.

Budd-Chiari syndrome during pregnancy has rarely been reported. This report presents a case of acute hepatic failure in a 20-year-old pregnant woman attributable to Budd-Chiari syndrome with underlying resistance to activated protein C caused by factor V Leiden mutation. The patient delivered a healthy girl by cesarean section in the 31st week of pregnancy. Acute hepatic failure in the 6th week postpartum was successfully treated by emergency liver transplantation, and the patient and her child were doing well at 8-month follow-up. Liver transplantation was lifesaving; normal factor V production by the transplant corrected the underlying coagulopathy. In this patient, latent thrombophilia attributable to activated protein C resistance was apparently aggravated by the hypercoagulable state of pregnancy leading to acute Budd-Chiari syndrome. Activated protein C resistance should be sought as an etiologic factor in patients with Budd-Chiari syndrome.

Adult↗
PubMed1999

Lipoprotein(a) serum levels in patients affected by chronic obstructive pulmonary disease.

A recent study has suggested that symptoms of chronic bronchitis predict the risk of coronary disease independently of the known major cardiovascular risk factors. High serum levels of lipoprotein(a) (Lp(a)) have also been considered as an independent risk factor for coronary heart disease. Therefore, the aim of the present study was to investigate the behaviour of Lp(a) in patients affected by chronic obstructive pulmonary disease (COPD). Serum levels of total-cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), triglycerides, apolipoprotein (Apo) B-100, and Lp(a) were measured in 90 COPD patients and in 90 normal subjects matched for age, sex and smoking habit. COPD patients showed lower serum levels of Apo B-100 (P<0.0001) and Lp(a) (P<0.003) compared to controls. Conversely, TC, HDL-C, LDL-C and triglycerides were similar between patients and controls. No significant differences were found in Apo B-100 and Lp(a) levels of patients either undergoing different therapeutic regimens, or with different smoking habits. A significant correlation between Apo B-100 and Lp(a) (rho=0.433, P<0. 0001) was also observed. In conclusion, COPD patients do not show an atherogenetic lipid pattern and their increased risk of coronary disease could be attributable to different factors, such as the ongoing hypercoagulability state often associated with COPD.

Adult↗
PubMed1984

Direct fibrinolytic therapy for renal vein thrombosis: radiographic followup.

Renal vein thrombosis is a rare entity whose true incidence is unknown. The disease occurs most frequently in patients with the nephrotic syndrome but it also can occur in the presence of other hypercoagulable states. Previous modes of therapy have been limited to systemic anticoagulation or surgery. We report a case of successful dissolution of acute renal vein thrombosis using direct fibrinolytic therapy, which was documented radiographically during treatment and at 3-month followup.

Female↗
PubMed1994

The antiphospholipid and thrombosis syndromes.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The commonest thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome). The relative frequency of anticardiolipin antibodies in association with arterial and venous thrombosis strongly suggests that these should be looked for in any individual with unexplained thrombosis; all three idiotypes (IgG, IgA, and IgM) should be assessed. Also, the type of syndrome (I through IV) should be defined if possible because this may dictate both type and duration of immediate and long-term anticoagulant therapy. In contrast to those with anticardiolipin antibodies, patients with primary lupus anticoagulant thrombosis syndrome usually suffer venous thrombosis. Because the aPTT is unreliable in patients with lupus anticoagulant (prolonged in only about 40% to 50% of patients) and is not usually prolonged in patients with anticardiolipin antibodies, definitive tests (ELISA for anticardiolipin antibody and the dRVVT for lupus anticoagulant) should be immediately ordered when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events.

Antibodies, Anticardiolipin↗
PubMed2004

[Pathogenic mechanisms of thrombosis in neoplasia: therapeutic implications].

Malignancy is associated with a hypercoagulable state and a high risk for thrombohemorragic complications. Activation of blood coagulation in cancer is a complex phenomenon, involving many different pathways of the hemostatic system and numerous interactions of the tumour cell with other blood cells, including platelet, monocyte and endothelial cells. In addition, the involvement of fibrin formation in the processes of tumour spread and metastasis is important in this area. Experimental evidence suggest that TF expression in tumour cells is associated with enhanced procoagulant activity as well as increased tumour cell invasion, primary tumour growth and increased tumoral metastatic potential. Moreover, a close correlation exists between TF and the synthesis of the angiogenic cytokine VEGF in tumour cells and with angiogenesis in vivo. A number of agents designed specifically for targeting TF, VEGF and/or receptors are being evaluated in various clinical trials in cancer patients. This review discuss the current status in pharmacological interventions to block thrombogenicity and angiogenesis in the treatment of cancer.

Antineoplastic Agents↗
PubMed2002

The factor V leiden mutation and the risk of venous thromboembolism in gynecologic oncology patients1.

OBJECTIVE: To measure the strength of the association between the factor V Leiden mutation and venous thromboembolism in gynecologic oncology patients. METHODS: We conducted a case-control study of gynecologic cancer patients in a referral center who were group matched for demographics, tumor type, and treatment. The prevalence of the factor V Leiden mutation was determined in both cases and controls, and an odds ratio was calculated. The factor V Leiden mutation was detected using polymerase chain reaction amplification and nucleic acid restriction digest of deoxyribonucleic acid extracted from leukocytes. RESULTS: Seventy-five patients were enrolled in the study. Seventy-four samples were available for analysis. There were no differences between the cases and controls with respect to age, race, body mass index, smoking, cancer type, high stage (III or IV) of cancer, or treatment modality. The odds ratio for having the factor V Leiden mutation in patients with venous thromboembolism was 0.3 (95% confidence interval 0.1, 1.7). CONCLUSION: This study suggests that the factor V Leiden mutation is not associated with an increased risk of venous thromboembolism in gynecologic oncology patients. This contrasts with other studies showing a strong association between the factor V Leiden mutation and venous thromboembolism in cases of previously unexplained venous thromboembolism, and venous thromboembolism associated with other hypercoagulable states, such as pregnancy and oral contraceptive use. The risk of venous thromboembolism due to cancer outweighs the contribution of the factor V Leiden mutation.

Adult↗
PubMed1997

Predictive value of clinical criteria for the diagnosis of deep vein thrombosis.

BACKGROUND: The widespread use of ultrasonography for the diagnosis of deep vein thrombosis (DVT) has led to the overuse of ultrasonography with low diagnostic yield. We conducted this study to investigate the predictive value of clinical features in the diagnosis of DVT and their potential value as clinical guidelines for the use of ultrasonographic testing in the diagnosis of DVT. METHODS: The results of lower-extremity duplex ultrasonographic studies and clinical surveys prospectively obtained in 1526 patients suspected of having DVT were analyzed. RESULTS: There were 916 inpatients and 610 outpatients. Acute DVT was found in 16% of the inpatient duplex scans, and in 12% of the outpatient studies (p < 0.05). The incidence of acute DVT was not different between men and women in inpatient or outpatient populations. Acute DVT was found in the left leg in 60% of the outpatient studies, significantly more often (p < 0.001) than in the inpatients (35%). Bilateral DVT was more common (p < 0.05) in the inpatient population (35%) compared with the outpatient population (20%). No difference in the anatomic distribution of thrombosis was found between inpatients and outpatients. The presence of leg symptoms was associated with a significantly higher rate (p < 0.05) of positive studies compared with those patients without leg symptoms in both the inpatient and the outpatient populations. Individual symptoms, risk factors, and physical findings had low positive predictive value and sensitivity for the presence of acute DVT on duplex scan. A calf circumference discrepancy of less than 2 cm predicted the absence of DVT in 93% of inpatients and 85% of outpatients. The combination of a calf circumference discrepancy of less than 2 cm with the absence of recent operation, trauma, malignancy, previous history of DVT, or hypercoagulable state predicted the absence of DVT in 92% of the inpatients and 97% of the outpatients. CONCLUSIONS: Clinical symptoms, risk factors, and physical findings are poor predictors of the presence of acute DVT on duplex scan. However, the absence of a combination of objective clinical factors has high predictive value for the absence of acute DVT on duplex scan. These criteria may be used to establish clinical guidelines to reduce the use of duplex scanning for the diagnosis of DVT.

Adult↗
PubMed1985

Current status of coronary artery bypass grafting for coronary artery atherosclerosis.

Coronary artery bypass grafting has now undergone 18 years of proven benefit in the treatment of myocardial ischemic disease. The technique of CABG has been further extended to other situations in which myocardial blood supply is threatened, such as cardiac trauma, aneurysms of coronary arteries, and congenital lesions. The emphasis in choosing CABG over medical therapy in 1985 should be preservation of myocardium at jeopardy of infarction as well as relief of angina. Proximal stenoses in vessels subserving viable muscle that is ischemic at rest or with minimal exercise should be treated with reperfusion by angioplasty or CABG to prevent further injury. After infarction occurs and ventricular function is impaired, CABG is also necessary to preserve remaining myocardium at jeopardy. Such an aggressive approach seems warranted with today's excellent surgical results. Long-term results have also improved, as more attention has been paid to saphenous vein graft preparation, use of mammary artery grafts, complete revascularization, use of antiplatelet agents, control of spasm, and identification of hypercoagulable states that may require sodium warfarin (Coumadin). Angioplasty of vein grafts and distal anastomoses also appears promising to help extend the results of initial CABG. Figure 1 is our recommended approach for the treatment of coronary atherosclerosis.

Angina Pectoris↗
PubMed2003

Hepatic artery thrombosis in pediatric liver transplantation.

PURPOSE: Children have been reported to be at greater risk for hepatic artery thrombosis when compared to adults due to small arterial size, nonuse of intraoperative microscope, and postoperative hypercoagulable state. METHODS: We evaluated arterial anastomosis type, intraoperative field magnification, and hepatic artery complications and how they were managed. All patients underwent ultrasound, anticoagulation consisted of 41 mg aspirin once a day, and 35 patients received alprostadil (PGE) for the first 7 days after transplantation. No patients were administered intravenous heparin following liver transplantation. RESULTS: Of the 74 livers transplanted, 36 grafts (48.6%) were whole organ transplants and 38 grafts (51.4%) were partial livers. We observed HAT in 1 of 74 (1.35%) transplants in our pediatric liver transplant population. The only patient with HAT was a young girl with a history of biliary atresia. The occurrence of a hepatic artery thrombosis on day 7 was caused by the migration of an intimal plaque dissection within the artery graft. She was emergently taken back into the operating room for graft revision. This individual currently has a survival time of 426 days following her last transplant. CONCLUSIONS: Hepatic artery thrombosis may be minimized in pediatric liver transplantation without the use of microsurgery. Anticoagulation utilizing ASA and alprostadil is sufficient to avoid HAT. Accurate use of ultrasound is crucial to avoid this complication. Graft and patient salvage is possible with expedient surgical treatment; microsurgery, anticoagulant therapy, site of arterial inflow, and recipient size and weight.

Anastomosis, Surgical↗
PubMed1995

Adrenal insufficiency in the antiphospholipid antibody syndrome.

OBJECTIVE: Adrenal insufficiency (AI) is a rare complication of the antiphospholipid antibody syndrome (APS). The objective of this report is to describe a case and review the published literature to enhance recognition of this potentially fatal disorder by emphasizing its course, diagnosis, and cause. DATA SOURCES: A bibliographic database with the indexing terms adrenal insufficiency, adrenal hemorrhage, adrenal thrombosis, APS, systemic lupus erythematosus, with the constraints of human subjects only, was used. STUDY SELECTION: All 27 reports meeting the indexing terms were selected for review. DATA EXTRACTION: The specific criteria used for data extraction articles included course of the disease, causation, clinical and laboratory diagnostic criteria, and therapeutic intervention. DATA SYNTHESIS: Our patient is a previously health woman who developed a respiratory tract infection, followed by a prolonged illness with fever, hypotension, nausea, depression, and venous thromboses. She was found to have AI and APS that was alleviated with hydrocortisone and anticoagulation. Initially, her adrenal glands were normal on CT scan but subsequently became enlarged and later atrophic. Of the 27 previous case reports, a majority had thromboses and typical clinical and laboratory manifestations of AI. Hemorrhagic infarction of the adrenal gland appears to be the mechanism for AI in the APS. IgG and IgM anticardiolipin antibodies are most commonly reported in association with AI in APS. CONCLUSIONS: The hypercoagulable state in the APS may lead to adrenal vein thrombosis and subsequently to hemorrhagic necrosis of the adrenal gland. This complication of APS is important to recognize because it may be fatal if untreated.

Adrenal Glands↗
PubMed1995

Clinicopathologic correlations of the antiphospholipid syndrome.

Since the original description and definition of the antiphospholipid syndrome (APS), a number of distinct clinical manifestations related to it have appeared in the literature. These include vascular obstruction of both veins and arteries, thrombus formation on the endocardium and its consequences, as well as a group of other conditions where vascular obstructive mechanisms are either incompletely understood or unproven, eg, chorea, avascular necrosis, and pulmonary hypertension. Single vessel (large/medium) involvement or multiple vascular occlusions may cause a wide variety of presentations. Any combination of vascular occlusive events may occur in the same individual, and the time interval between them also varies considerably from weeks to months or even years. Rapid chronological occlusive events occurring over days to weeks have been termed the "catastrophic" APS. Most of these complications may be ascribed to the hypercoagulable state of which antiphospholipid antibodies appear either to be "markers" or intimately connected with the highly complex coagulation mechanisms resulting in thrombotic occlusions.

Antiphospholipid Syndrome↗
PubMed2001

Molecular basis for the relationship between thrombosis and cancer.

Cancer patients are highly susceptible to thromboembolic complications, which some have estimated accounts for a significant percentage of the morbidity and mortality of the disease. Not all of the mechanisms for the production of the hypercoagulable state characteristic of cancer are entirely understood. Those that are known seem to interdigitate the biology of cancer with the major regulatory pathways that mediate blood coagulation, platelet-vessel wall interaction, fibrinolysis and inflammatory cytokine production. In other words, the events responsible for thrombosis in cancer appears to be a result of an over exuberant host response in an attempt to delimit tumor growth. In this brief review, therefore, we attempt to put into the context of tumor growth, angiogenesis and metastasis the current information about the pathogenesis of venous thromboembolism (VTE).

Cell Communication↗
PubMed2001

The thrombolytic paradox.

Thrombolytic drugs do not only stimulate the plasmin system but also induce thrombin activation additionally to the preexisting hypercoagulative state in patients with acute myocardial infarction. Testing the in vitro-derived hypothesis of a plasmin-mediated activation of the contact phase of the coagulation leading to the procoagulant effect, several thrombolytic regimen have been evaluated. Paradoxical thrombin activation (referred to as "thrombolytic paradox") was related to absence of fibrin specificity. Highly fibrin-specific drugs like tenecteplase did not cause additional thrombin activation, while non-fibrin-specific drugs like streptokinase caused a marked additional activation of the contact phase and of thrombin. It could be shown that the thrombolytic paradox was related to the extent of systemic plasmin activation confirming the hypothesis of a plasmin-mediated factor XII/kallikrein system activation as cause of the thrombolytic paradox.

Fibrinolysin↗
PubMed2002

Markers of activated coagulation in patients with factor V Leiden and/or G20210A prothrombin gene mutation.

The activated protein C (APC) resistance phenotype associated with an abnormal factor V Leiden (FVL), and the G20210A prothrombin gene mutation are the most common findings in patients with venous thromboembolism (VTE). In a group of 210 patients, we compared the levels of markers of coagulation activation in carriers of FVL (71 heterozygous, 30 homozygous), G20210A prothrombin mutation (88 heterozygous) or both mutations combined (21 heterozygous), in order to assess whether these markers allow identification of a group of patients with a higher risk of thrombosis; they were also compared to normal values. A total of 143 patients had a personal history of VTE and 67 were asymptomatic. None of them had other hereditary causes of thrombophilia or an antiphospholipid syndrome. None were currently treated with either anticoagulant or hormonal treatment. Pregnant women were excluded. No significant difference between the four groups of patients could be found in the levels of F1+2, TAT and DDI. Levels were all significantly higher than the control values (p<0.05). The levels of F1+2 and TAT were similar in patients with or without a history of VTE, regardless of the type of mutation. DDI levels were significantly higher in patients with a history of VTE than in asymptomatic subjects (443+/-248 vs. 333+/-222 ng/ml, p=0.02) but with only 57% sensitivity and specificity. In conclusion, our study confirms the hypercoagulable state found in mutation carriers and points out the inability of F1+2 and TAT assays to identify a group of subjects at higher risk of thrombosis, within carriers of genetic risk factors. Although the sensitivity and specificity of DDI assay are low, high DDI concentrations tend to be associated with the risk of VTE.

Adult↗
PubMed2002

Observation on tissue factor pathway and some other coagulation parameters during the onset of acute cerebrocardiac thrombotic diseases.

It is widely recognized that thrombosis is the major event in the evolution of acute myocardial infarction (AMI) and acute ischemic stroke (AIS). But the contribution of coagulation factors to the development of ischemic arterial diseases is still not clearly established. The goal of this study was to establish the possible relationship between coagulation factors as well as anticoagulant and the onset of AMI and AIS. The study population consisted of 69 patients with AMI and 71 with AIS as well as 50 age-matched healthy volunteers. Compared with the control group, plasma tissue factor (TF) and tissue factor pathway inhibitor (TFPI) activities and both TF and TFPI antigens were significantly higher in the AMI group; plasma TF activity and antigen in AIS group were significantly increased, but the activity and antigen of plasma TFPI were significantly decreased in the AIS group. Plasma FVII coagulation (FVII:C) activity was markedly higher in patients with AIS, but not statistically different to the control in patients with AMI. FVIII coagulation (FVIII:C) activity was remarkably higher in patients with AMI but slightly lower than the control in patients with AIS. In the AMI and AIS groups, prothrombin activity and clottable fibrinogen were significantly higher and plasma antithrombin III activity was remarkably lower than the control. The results suggested that during the onset of AMI and AIS, the initiation of TF pathway would be associated with the thrombotic events and that the blood be in hypercoagulable state. But the changes of FVII:C, TFPI and FVIII:C in AMI are different from those in AIS.

Acute Disease↗
PubMed2003

Thrombophilia: implications for pregnancy outcome.

There is growing evidence implicating congenital and acquired thrombophilias in the pathophysiological processes underlying miscarriage, intrauterine growth restriction (IUGR) and pre-eclampsia. Pregnancy itself is notably a hypercoagulable state, at least in part, due to the physiological changes in the coagulation and fibrinolytic systems; this has the potential for interaction with an acquired or heritable thrombophilia to cause adverse experiences. Recurrent fetal loss is associated with antiphospholipid antibody syndrome, procoagulant platelet microparticles and some inherited thrombophilias such as Factor V Leiden. There have been reports of both heritable and acquired thrombophilias being associated with pre-eclampsia, IUGR and abruption. However, these associations are not consistently reported with hereditary thrombophilias. The presence of thrombophilia might influence the severity of a condition such as pre-eclampsia, rather than cause it. The risk of fetal loss related to antiphospholipid syndrome can be reduced with antithrombotic therapy with heparin and low dose aspirin. Whether this extends to other thrombophilic conditions associated with adverse pregnancy outcome is not clear and further investigation is required. Screening for, and finding a, thrombophilic disease in patients with problems such as recurrent miscarriage, intrauterine death, intrauterine growth restriction and pre-eclampsia, may reflect an increased risk of venous thromboembolism (VTE).

Abortion, Spontaneous↗
PubMed2003

Homocysteine and hemostatic disorder as a risk factor for myocardial infarction at a young age.

INTRODUCTION: Hyperhomocysteinemia is a coronary risk factor, but its pathophysiologic mechanism remains unclear. MATERIALS AND METHODS: The importance of hyperhomocysteinemia in the pathogenesis of early myocardial infarction, was determined in case-control study of 127 men with a first early myocardial infarction <or=45 years and 150 age-matched male controls. We measured plasma concentrations of homocysteine, fibrinogen, antithrombin, tissue factor, tissue factor pathway inhibitor, tissue plasminogen activator, plasminogen activator inhibitor-I, plasminogen, alpha(2)-antiplasmin, lipoprotein(a), protein C, protein S, factor VII, and activated factor VII. RESULTS: Homocysteine concentrations were higher in patients with early myocardial infarction than in controls (11.2+/-5.3 and 8.3+/-5.0 micromol/l, respectively, P<0.001). Hyperhomocysteinemia was associated with early myocardial infarction (odds ratio=2.22, P<0.001) by multivariate logistic regression analysis. Tissue factor, antithrombin, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor-I, lipoprotein(a), diabetes, and smoking also had associations. In a stepwise logistic regression analysis, hyperhomocysteinemia was the strongest predictor of early myocardial infarction (R(2)=0.19, P<0.001). Hyperhomocysteinemia also had positive correlations with tissue factor (rho=0.26, P=0.009), tissue factor pathway inhibitor (rho=0.23, P=0.020), and tissue plasminogen activator (rho=0.25, P=0.011) in patients with early myocardial infarction, but not in controls. CONCLUSIONS: Hyperhomocysteinemia is an independent risk factor for early myocardial infarction, and is associated with a hypercoagulable state mediated by the extrinsic coagulation cascade.

Adult↗