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PubMedDate not supplied

[Pulmonary Artery Sarcoma - diagnostic and treatment difficulties].

Primary Pulmonary Artery Sarcoma is a rare entity, which shares some clinical features with Thromboembolic Pulmonary Disease (TEPD), complicating differential diagnosis. The authors report a Clinical Case of a Primary Pulmonary Artery Sarcoma in a 59 years old man, admitted with a history of dyspnoea on exertion, chest pain and general symptoms. Chest X-ray, Computed Tomography Scan, Angiographies and Magnetic Resonance Imaging suggested TEPD. Blood Analysis performed before anticoagulation therapy: Lupus Anticoagulant-and Ig M Anticardiolipin +. Our presumptive initial diagnosis was TEPD in a patient with a hypercoagulable state. Intravenous heparin was started, with some clinical improvement but 2 months later he was readmitted, due to clinical and radiological deterioration. Pulmonary Thromboendarterectomy was considered but a right pneumonectomy was necessary because of bleeding. He died of ARDS in a single lung in the 7th day after surgery. Pathology revealed pulmonary artery sarcoma with pulmonary and pleural metastases.

Humans↗
PubMed2002

Intracranial hemorrhage in herpes simplex encephalitis: an unusual presentation.

We describe a 14-month-old patient with atypical presentation of herpes simplex encephalitis. She initially presented with fever, lethargy, seizures, and large hemorrhages in the right parietal lobe, and clinical findings suggestive of a hypercoagulable state. The etiology of coagulation abnormality was not identified, although it was suggested as a possible causative factor in severe bleeding along with acute neuronal lysis as a result of infection. Although large intracerebral hemorrhages are occasionally described with systemic herpes infection, this presentation is unusual beyond the infant period.

Acyclovir↗
PubMed2003

Antiphospholipid thrombosis syndromes.

Antiphospholipid antibodies are associated strongly with thrombosis and are the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, numerous theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACLAs 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). Patients with type V disease are those with antiphospholipid antibodies and RMS. It is as yet unclear how many seemingly normal individuals who may never develop manifestations of antiphospholipid syndrome (type VI) harbor asymptomatic antiphospholipid antibodies. The relative frequency of ACLAs in association with arterial and venous thrombosis strongly suggests that they 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-VI) should be defined, if possible, because this identification may dictate both the type and the duration of immediate and long-term anticoagulant therapy. Unlike those patients with ACLAs, patients with primary LA-thrombosis syndrome usually have venous thrombosis. Because the aPTT is unreliable in patients with LA (prolonged in only approximately 40%-50% of patients) and usually is not prolonged in patients with ACLAs, definitive tests, including ELISA for ACLA, the dilute Russell's viper venom time for LA, hexagonal phospholipid-neutralization procedure, and B-2-GP-I (IgG, IgA, and IgM) should be ordered immediately when suspecting antiphospholipid syndrome or in individuals with otherwise unexplained thrombotic or thromboembolic events. If these test results are negative, subgroups also should be assessedin the appropriate clinical setting. Most patients with antiphospholipid thrombosis syndrome will fail to respond to warfarin therapy, and except for retinal vascular thrombosis, may fail some types of antiplatelet therapy, so it is of major importance to make this diagnosis so patients can be treated with the most effective therapy for secondary prevention-LMWH or unfractionated heparin in most instances and clopidogrel in some instances.

Antiphospholipid Syndrome↗
PubMed1998

Lupus anticoagulants and antiphospholipid antibodies.

In recent years, clinical syndromes involving lupus anticoagulants and antiphospholipid antibodies have come into increasing clinical prominence. Since the discovery that most antiphospholipid antibodies require the presence of anionic phospholipid-binding proteins such as B2-glycoprotein I and prothrombin, a large number of studies have attempted to delineate the specificity of these antibodies. Several mechanisms have been proposed to explain the hypercoagulable state associated with these antibodies. This review attempts to summarize these data and the challenges that confront efforts to delineate the pathogenesis of the prothrombotic state associated with the presence of these antibodies.

Antibodies, Antiphospholipid↗
PubMed1996

Hypercoagulability in cancer.

The association of cancer with a hypercoagulable state is documented by numerous clinical, biochemical, pathologic, and pharmacologic studies. This association is manifested clinically by an increased incidence of intravascular thrombotic events in cancer patients and by fibrin deposition in and around tumor beds. Thromboembolic disease is a major cause of morbidity and mortality in patients with malignancy. This article discusses the complex pathogenesis of this problem and the associated laboratory and clinical syndromes with recommendations on diagnosis and treatment.

Blood Coagulation Disorders↗
PubMedDate not supplied

Echocardiographic diagnosis of pulmonary embolism in childhood.

Pulmonary embolism is a rare problem in the pediatric age group. As in adults, symptoms include tachypnea, chest discomfort, and hypoxia, but the index of suspicion in making this diagnosis in children is low. This report confirms the usefulness of two-dimensional and Doppler echocardiography in the diagnosis of pulmonary embolism, regardless of patient age. Causes of hypercoagulable states in children are also briefly discussed.

Child↗
PubMedDate not supplied

Intracardiac thrombi associated with antiphospholipid antibodies.

Two cases of intracardiac thrombi associated with antiphospholipid antibodies are presented, one in the right atrium and the other in the left ventricle, the latter occurring in the presence of normal left ventricular function. In each, the diagnosis was made by transthoracic echocardiography. Both patients had contraindications to thrombolytic therapy and underwent successful surgical thrombectomy. We suggest that serial transthoracic echocardiography may be warranted in the follow-up of patients with primary hypercoagulable states.

Adolescent↗
PubMed2003

Buerger's disease in the 21st century: diagnosis, clinical features, and therapy.

Buerger's disease (thromboangiitis obliterans or TAO) is a clinical syndrome characterized by the development of segmental thrombotic occlusions of the medium and small arteries of the extremities. It is clinically and pathologically distinguishable from arteriosclerosis and necrotizing arteritis. Afflicted patients are mostly young, male, inveterate tobacco smokers who present with distal extremity ischemia, ischemic ulcers, or frank gangrene of the toes or fingers. Large arteries are typically spared, as are the coronary, cerebral, and visceral circulations. While mortality is not increased, patients with Buerger's disease often suffer from severe ischemic pain and tissue loss culminating in minor and major limb amputation. Clinical diagnostic criteria generally include the following: (1) history of smoking or tobacco abuse; (2) age of onset less than 45 to 50 years; (3) infrapopliteal, segmental arterial occlusions with sparing of the proximal vasculature; (4) frequent distal upper extremity arterial involvement (Raynaud's syndrome or digital ulceration); (5) superficial phlebitis; and (6) exclusion of arteriosclerosis, diabetes, true arteritis, proximal embolic source, and hypercoagulable states. Typical arteriographic patterns have been described that are suggestive, but not pathognomonic. While the cause of Buerger's disease remains unknown, the disease onset and clinical course are inextricably linked to tobacco abuse. Acute Buerger's disease is characterized histopathologically by intensely cellular vessel wall inflammation, giant cell foci, and hypercellular thrombi, but with preservation of the elastic lamina and the overall vascular wall architecture. Most investigators feel that Buerger's disease is an immune-mediated endarteritis; recent immunocytochemical studies have identified the linear deposition of immunoglobulins and complement factors along the elastic lamina. The inciting antigen has not been discovered. Tobacco abstinence generally results in disease quiescence and remains the mainstay of treatment.

Humans↗
PubMed2003

Clinical and pathophysiological consequences of abdominal adiposity and abdominal adipose tissue depots.

OBJECTIVES: To highlight the clinical and metabolic correlates of abdominal obesity and various abdominal adipose tissue depots. METHODS: We researched the topic using the search terms abdominal obesity, central obesity, visceral obesity, regional obesity, and subcutaneous adipose tissue from MEDLINE (National Library of Medicine, Bethesda, MD), PubMed (National Library of Medicine, Bethesda, MD), Current Contents (Institute for Scientific Information, Thomson Scientific, Philadelphia, PA), and using manual search for the cited references. RESULTS: Abdominal obesity contributes significantly to the metabolic perturbations and cardiovascular risk in human beings. Abdominal adipose tissue depots (intraabdominal and subcutaneous [deep subcutaneous, posterior subcutaneous]) are metabolically active and appear to be important for the pathogenesis of insulin resistance, dyslipidemia, glucose intolerance, hypertension, hypercoagulable state, and cardiovascular risk. Adipocyte anatomy (size), physiology (growth, catecholamine sensitivity, lipolysis, insulin action), and biochemistry (leptin, plasminogen activator inhibitor-1, cytokines, renin-angiotensin system) are reported to be relatively site-specific, highlighting unique roles of regional adipose tissue depots. CONCLUSIONS: Several physiological and metabolic parameters are site-specific in abdominal adipose tissue. The epidemiological, clinical, and prognostic significance and relative importance of the regional adipose tissue depots, however, remain to be ascertained.

Abdomen↗
PubMed1997

Increased factor VIIa levels in systemic lupus erythematosus patients with lupus anticoagulant.

Recurrent fetal loss, and/or arterio-venous thrombosis are frequent complications in patients with the antiphospholipid antibodies (aPL), anticardiolipin antibody (aCL) and/or lupus anticoagulant (LA). Furthermore, patients with LA have been found to be more susceptible to thrombosis than those with aCL, thus suggesting differences in the pathogenesis of aCL and LA. We examined the systemic lupus erythematosus (SLE) patients with aCL and/or LA for differences in the markers for hypercoagulable state, including thrombin-antithrombin complex (TAT), prothrombin fragment 1 + 2 (F1 + 2), thrombomodulin (TM) and activated factor VII (FVIIa), and lipoprotein (a) (Lp(a)), which is a well-known risk factor for thrombosis. The FVIIa concentration was significantly higher in the LA-positive patients than in the aCL-positive and aPL-negative patients. No significant differences in TAT, F1 + 2, TM, and Lp(a) values were found among the aCL-positive, LA-positive and LA-negative patients groups. These findings indicate that patients with LA were in a more prethrombotic state than those with aCL. The measurement of FVIIa may serve as a useful predictive marker for thrombosis, but further studies are needed to clarify the mechanisms of thrombosis in this clinical setting.

Adult↗
PubMed2000

[Respiratory distress and drepanocytosis].

Acute chest syndrome (ACS) is characterized by chest pain with dyspnea and recent radiologic abnormalities, and is an acute lung complication whose problem is one of etiology. Alveolar hypoventilation linked to infarcts of the thoracic ribs, thoracoabdominal trauma, subdiaphragmatic pain, the administration of analgesics causing respiratory depression, or sleep disturbance, is a frequent cause of ACS. Bronchoalveolar lavage has revealed the frequency of fat embolism following infarcts in the long bones. Pulmonary vascular occlusion, due to thrombosis or emboli, is rare, as are the infectious pneumonia and pulmonary edema. The pathogenetic mechanisms consist of an alteration of the rheological properties of the blood, the existence of an hypercoagulability state, specific interactions between the abnormal sickle cells and the vascular endothelium, and a dysregulation of the vascular reactivity. Research centered around NO biology has led to an expanded understanding of the critical interdependence of NO, hemoglobin, and the microvasculature. An anemic patient with ACS suffers from loss of pulmonary scavenging and hypoxic pulmonary vasoconstriction and loss of peripheral NO delivery. Interruption of this cycle by transfusing normal (hemoglobin A-containing) erythrocytes might improve all the abnormalities.

Acute Disease↗
PubMed1994

Activation markers of coagulation.

Advances in our understanding of the biochemistry of the haemostatic mechanism have led to the development of sensitive methods for measuring peptides, enzyme-inhibitor complexes or enzymes that are liberated with the activation of the coagulation system in vivo. Studies employing these markers indicate that a biochemical imbalance between procoagulant and anticoagulant mechanisms can be detected in the blood of humans prior to the appearance of thrombotic phenomena. Properly designed prospective studies will be required to determine whether these assay techniques will enable us to identify individuals who are entering a clinically relevant hypercoagulable state, and intervene with appropriate therapy prior to the onset of overt thrombotic disease.

Animals↗
PubMed1987

Rheology of the sickle cell disorders.

The sickling process causes secondary changes in cell shape, size, cation and water content, and membrane structure that contribute to the impairment of intrinsic cell deformability (Figure 2). This rheological defect is partially compensated by a low haematocrit, which moderates the rise in whole-blood viscosity, and by a rise in cardiac output which increases capillary flow velocity (Berger and King, 1982). A delicate balance exists between these mechanisms and any local disturbance of this balance by pathological changes in factors extrinsic to the sickle cell (Figure 2) can precipitate vaso-occlusion. There is still considerable controversy over the site (arteriolar, capillary, or venular) of vaso-occlusion, the type of sickle cell (reversibly sickled or irreversibly sickled) that is primarily involved, and the relative importance of extra-erythrocytic precipitating factors such as stasis, hypoxia, hyperosmolality, acidosis, alteration in temperature, acute-phase rise in plasma proteins and leukocytes, prothrombotic changes in coagulation factors and platelets, and adhesion of blood cells to vascular endothelium (Figure 2). A low-grade hypercoagulable state has been described in patients with SS (Leichtman and Brewer, 1978; Richardson et al, 1979) which may be related to the procoagulant effect of the shift of phosphatidyl serine to the outer lipid bilayer of the sickle cell (Chiu et al, 1981; Franck et al, 1985). Platelets appear to accumulate at sites of vaso-occlusion (Siegel et al, 1985) and their migration to the vessel wall may be enhanced by the presence of poorly deformable erythrocytes (Aarts et al, 1984). Endothelial cell damage in the arterial or venous circulation may also contribute (Klug et al, 1982). Thus vaso-occlusion appears to result from a complex interaction between blood cells, plasma proteins and endothelium and any one of several precipitating factors may disturb the fragile steady state and cause a painful crisis. The study of sickle cells by rheological methods has considerable potential for investigating the pathophysiology of vaso-occlusive episodes in the SCD and for monitoring, both in vitro and ex vivo, the efficacy of antisickling compounds. Because of the multiple intrinsic and extrinsic factors that contribute to the rheological defect, it is not yet known which of these should be the primary target for an antisickling agent. In-vitro rheological studies in which different metabolic stresses can be applied to intact sickle cells in the presence of a putative antisickling drug should help to answer this question.(ABSTRACT TRUNCATED AT 400 WORDS)

Anemia, Sickle Cell↗
PubMed1990

The influence of smoking and plasma factors on prosthetic graft patency.

The effects of smoking and plasma risk factors on the patency of prosthetic femoro-popliteal bypass grafts were investigated in 93 patients entered into a multicentre trial of prosthetic graft materials (70 patients had patent grafts and 23 patients had occluded grafts 2 years after surgery). The smoking markers thiocyanate and fibrinogen were significantly higher in patients with occluded grafts, whereas LDL-cholesterol was significantly higher in patients with patent grafts 2 years after bypass. Based on smoking markers, graft patency in smokers was 57% at 2 years by life table, compared to 78% in non-smokers. P less than 0.05. Fibrinogen was an important variable, predicting graft occlusion with graft patency in patients with below median fibrinogen levels, being 84% at 2 years by life table compared to 51% in those with above median fibrinogen levels, P less than 0.025. Although increased levels of LDL-cholesterol have been associated with accelerated atherosclerosis, patients with above median levels of LDL-cholesterol had improved graft patency (83%) at 2 years compared to patency in patients with below median LDL-cholesterol (60%), P less than 0.05. The plasma risk factors associated with the failure of prosthetic grafts are similar to those associated with the failure of saphenous vein grafts, indicating that higher fibrinogen levels and smoking may contribute to an hypercoagulable state. Greater efforts are needed to stop patients smoking after vascular reconstruction.

Aged↗
PubMed1993

Cross-linked fibrin degradation products (XL-FDP) as marker of early rethrombosis in percutaneous transluminal angioplasty.

The thrombotic response to percutaneous transluminal angioplasty (PTA) was investigated in 31 patients treated for 1-10 cm femoropopliteal (n = 28) and tibial (n = 3) artery obstructions by measurement of cross-linked fibrin degradation products (XL-FDP) in peripheral blood samples drawn before and 30 min after PTA. XL-FDP increased from 400 +/- 147 ng/ml to 700 +/- 445 ng/ml (median +/- S.E., p = 0.0005). XL-FDP rose from 320 +/- 110 ng/ml to 540 +/- 102 ng/ml in 23 patients, whose ankle/brachial systolic blood pressure index (ABI) increased > 0.15 after PTA, whereas XL-FDP increased from 850 +/- 450 ng/ml to 2620 +/- 1472 ng/ml in eight patients, who failed to increase ABI in spite of preceding recanalisation. XL-FDP increased by more than 1000 ng/ml in 1/23 (4.3%) patients with uncomplicated PTA and in 6/8 (75%) patients with haemodynamic failure (p = 0.0005). Using a XL-FDP increase of 1000 ng/ml as cut-off, estimates of positive and negative predictive values (95% confidence limits) for early failure of PTA were 85.7% (42.1-99.6%) and 91.7% (73.0-99.0%), respectively. We conclude from this pilot study that femorotibial PTA produces a hypercoagulable state which may result in failure of early patency due to rethrombosis. We suggest for the first time XL-FDP as a marker of early rethrombosis in PTA, and report a sequential XL-FDP assay which may be useful for identification of high-risk patients requiring thrombolytic therapy after PTA for maintenance of early vascular patency.

Aged↗
PubMed1997

Dietary fatty acids and blood coagulation.

Factor VII coagulant activity (VIIc) is a risk factor for coronary heart disease (CHD). Plasma VIIc is positively associated with dietary fat intake, suggesting that fat-rich diets are accompanied by a hypercoagulable state. Reduction in total fat consumption is followed by a decrease in VIIc within 24 h. In adults taking diets rich in long-chain saturated fatty acids, a postprandial increase in VIIc occurs after a fatty meal irrespective of its fat composition. This effect has dose-response characteristics, persists for several hours, and is due to activation of factor VII. There is no acute effect of dietary fat on factor VII antigen (VIIag) concentration, but VIIag is positively related to dietary fat intake. More studies are needed on the effects of dietary fat composition on fasting and postprandial factor VII. Dietary fat appears to influence both the atherosclerotic and thrombogenic components of CHD.

Blood Coagulation↗
PubMed1999

Angina and coronary ostial lesions in a young woman as a presentation of Takayasu's arteritis.

Diagnostic considerations in young patients presenting with coronary artery disease have conventionally included familial dyslipidemias, lipoprotein(a) elevation, hyperhomocysteinemia, cocaine toxicity, hypercoagulable states, connective tissue disorders, vasculitis and the presence of other established risk factors for coronary artery disease. The case of a young woman with unstable angina and a left main coronary artery ostial lesion on cardiac catheterization is discussed. She was subsequently diagnosed with Takayasu's arteritis 4 years later.

Adrenal Cortex Hormones↗
PubMed2003

Venous thromboembolism and cancer: new issues for an old topic.

Thromboembolic complications represent the second leading cause of death for cancer patients. Even though the correlation between cancer and a hypercoagulable state has been widely recognised, the pathogenesis of thromboembolism during malignancy is not yet entirely understood. The direct or indirect activation of the coagulation cascade favours neoplastic dissemination and metastasis. Disordered coagulation is encountered in up to 90% of cancer patients, although only 15% of them develop a localised acute or chronic deep venous thrombosis or a disseminated intravascular coagulation. This risk is significantly increased by chemotherapy, hormone therapy, surgery and central venous catheters. Therefore, much effort is needed to develop efficient prophylaxis and treatment, to reduce recurrence and bleeding and finally, to improve quality of life. Better knowledge about the biochemical bases of the coagulation process represents a pivotal step in cancer biology comprehension and global therapeutic management.

Antineoplastic Agents↗