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PubMed1985

Postpartum renal vein thrombosis.

Renal vein thrombosis in adults is usually a complication of the nephrotic syndrome. Rarely, it has been reported in nonnephrotic women postpartum. The thrombosis may be a complication of the hypercoagulable state associated with both the nephrotic syndrome and pregnancy. Two postpartum patients with renal vein thrombosis and no prior history of renal disease are reported here. Neither patient had heavy proteinuria. In both cases, pyelonephritis was suspected clinically and the diagnosis of renal vein thrombosis was first suggested and confirmed by radiologic examination. Renal vein thrombosis should be considered in women presenting postpartum with flank pain.

Angiography↗
PubMed1981

Computed tomographic findings in a case of renal vein thrombosis with nephrotic syndrome.

Renal vein thrombosis is a complication of the nephrotic syndrome presumably related to compression of renal veins by edematous parenchyma and a concomitant hypercoagulable state. The diagnosis has been made by demonstrating marked widening of the left renal vein as it crosses horizontally anterior to the aorta on computed tomography. Inferior venacavography confirmed the presence of thrombosis within the vessels. CT is suggested as a method for noninvasive imaging of the renal veins which might eliminate the need for venography.

Humans↗
PubMed2001

Prevalence of deep venous thrombosis in the lower limbs and the pelvis and pulmonary embolism in patients with positive antiphospholipid antibodies.

BACKGROUND: Antiphospholipid antibodies (AA) are immunoglobulins that cross-react with phospholipid on cell membrane, and are therefore associated with a hypercoagulable state manifested by arterial/venous thromboses. We aimed to determine the prevalence of deep venous thrombosis in the lower limbs and the pelvic region (DVT) and pulmonary embolism (PE) in patients with positive AA. METHODS: Sixty-six patients (48 female, 18 male) with positive lupus anticoagulant (LA) and/or positive anticardiolipin antibody (aCL) underwent radionuclide (RN) venography with 370 MBq of 99mTc-MAA. Pulmonary perfusion scintigraphy was performed in 58 patients. Fifteen patients had positive LA and positive aCL (LA+/aCL+), 33 patients had positive LA only (LA+/ aCL-) and 18 patients had positive aCL only (LA-/aCL+). 43 patients were diagnosed with primary antiphospholipid syndrome (APS) and 19 were diagnosed with APS associated with SLE. RESULTS: DVT was detected in 21 of 66 patients (32%). Patients with LA+/aCL+ showed higher prevalence of DVT (53%) as compared to LA+/aCL- (27%) and LA-/aCL+ (22%). PE was found in 13 of 58 patients (22%). The prevalence of PE was higher in patients with positive aCL (33% in LA+/aCL+; 36% in LA-/aCL+) than in patients with negative aCL (10%). CONCLUSION: Because of the high prevalence of DVT and PE in patients with AA, RN scintigraphy must be recommended in screening for these clinical troubles. These results indicate that the prevalence of DVT and PE may vary in subgroups of AA.

Adolescent↗
PubMed1981

Excessive requirement for heparin during cardiac surgery.

A case of excessive heparin requirement during cardiopulmonary bypass is reported. A patient with sepsis secondary to a myocardial abscess require 13.5 mg x kg-1 of heparin to increase his activated coagulation time to a therapeutic level. This phenomenon might be due to individual variability, lupus vasculitis, septicaemia, repeated thromboembolic phenomenon with hypercoagulable state, or chronic disseminated intravascular coagulation with partial antithrombin deficiency.

Aged↗
PubMed2002

Blood coagulation and fibrinolysis in patients with hyperthyroidism.

Several papers concerning abnormalities of blood coagulation and fibrinolysis during hyperthyroidism, have been published. Increased von Willebrand Factor (vWF) activity and high fibrinogen levels have been reported. However, there is controversy concerning the presence of a hypercoagulable state in hyperthyroidism. We investigated various hemostatic parameters in 41 hyperthyroid patients and compared them to 20 euthyroid controls. Prothrombin time (PT), activated partial thromboplastin time (aPTT), fibrinogen, factors V, VII, VIII, IX and X activities, vWF, antithrombin III (AT III), protein C, protein S, tissue plasminogen activator (t-PA) and tissue plasminogen activator inhibitor-1 (PAI-1), as well as common lipid variables, were measured. The relationships between serum thyroid hormones and these hemostatic parameters were examined. Compared with control subjects, fibrinogen, factor IX, vWF, AT III and PAI-1 were significantly increased in patients (p<0.05, p<0.0001, p<0.05, p<0.01 and p<0.0001; respectively), whereas factor X and t-PA were decreased (p<0.05). We showed that free T4 (FT3) levels were correlated with factor VIII activity (r=0.35, p<0.05). FT4, FT3 and TSH did not correlate with fibrinogen, vWF, AT III, t-PA, or PAI-1. AT III was inversely correlated with factor VII activity (r=-0.48, p<0.01). Protein C and S were correlated with vWF levels (r=0.58, p<0.0001; r=0.55, p<0.0001, respectively). Protein C was inversely correlated with t-PA (r=-0.39, p<0.01). There was a negative correlation between triglycerides, LDL-C and F X (r=-0.45, p<0.05; r=-64, p<0.01, respectively). Mean platelet volume (MPV) was correlated with anti-thyroid peroxidase (TPO) antibodies (in Graves'disease) and F IX activity (r=0.57, p<0.05 and r=0.39, p<0.05; respectively). We found important differences in the coagulatory /fibrinolytic parameters between the hyperthyroid patients and healthy controls. Hyperthyroid patients may experience vascular endothelial dysfunction and decreased fibrinolytic activity in blood. This endothelial activation may represent a situation with a higher thromboembolic potential.

Adenoma↗
PubMed1997

Recurrent thromboembolism as a hallmark of Cushing's syndrome.

The present report describes a 54-year-old woman with a history of recurrent thromboembolic events. The clinical and physical examination led to suspect Cushing's syndrome. Screening tests (urinary free cortisol excretion and 1 mg dexamethasone) were inconclusive, but a detailed endocrine work up confirmed the presence of ACTH-dependent hypercortisolism. The patient was cured by the removal of a ACTH-secreting microadenoma by transsphenoidal route. The present case provides a clinical demonstration of a previous experimental evidence that a hypercoagulable state is present in Cushing's syndrome.

Adenoma↗
PubMed2001

[Markers for the prognosis of success of coronary interventions: focus on changes in fibrinolysis and hemostasis].

BACKGROUND: The morphology of the culprit coronary lesion is a most important factor for the prognosis of a percutaneous coronary intervention in patients with acute coronary syndrome. The most widely accepted grading of the complexity of the coronary stenosis is the modified ACC/AHA grading (from A to C). DISTURBANCES OF FIBRINOLYTIC SYSTEM: Further alterations like a hypercoagulative state and a disturbed fibrinolytic system are known in patients with unstable angina pectoris. In these patients a close correlation was observed between the complexity of stenosis morphology and the disturbances in the fibrinolytic system judged as measurement of the tissue-type plasminogen activator mass concentration or as measurement of the activity of the plasminogen activator inhibitor (PAI-1). For markers of thrombin activation no close correlation to the morphological grading was found. CONCLUSION: It should be investigated in further studies whether markers of the fibrinolytic system might be useful for assessment of the prognosis of a coronary intervention in patients with acute coronary syndrome.

Acute Disease↗
PubMed2000

[The effect of aprotinin and tranexamic acid on fibrinolysis and thrombin generation during cardiopulmonary bypass].

OBJECTIVE: Antifibrinolytic drug therapy has proved to be effective in reducing blood loss associated with cardiac surgery and cardiopulmonary bypass (CPB). Concerns remain regarding the risk of enhancing thrombosis. In the present study we investigated the effect of aprotinin (AP) and tranexamic acid (TA) on fibrinolysis and thrombin generation during CPB. METHODS: 60 patients undergoing coronary artery bypass graft surgery were randomised in 3 groups. They received either aprotinin ("high-dose-scheme"), tranexamic acid (2 g/h) or no antifibrinolytic therapy (control group). Collection of blood was performed at 7 pre-, intra- and postoperatively predetermined intervals. Fibrinolytic activity was determined by measuring concentrations of D-dimer, thrombin generation by the measurement of thrombin-antithrombin III complex (TAT). RESULTS: There was no significant increase of D-dimers in the AP or TA group. D-dimer concentration in the control group increased significantly after starting CPB. Comparing with the control group, thrombin generation in the AP group was significant less, while TA group produced significantly higher values. CONCLUSION: After the administration of AP for cardiac surgery we observed reductions in both intraoperative fibrinolysis and thrombin generation. In case of TA suppression of fibrinolytic activity in the absence of concomitant reduction in thrombin generation occurred. These results suggest that TA could potentiate a hypercoagulable state with the risk of thrombosis in the perioperative setting.

Aged↗
PubMed2002

Thromboembolic events after endovascular treatment of unruptured intracranial aneurysms in two patients with antiphospholipid-antibody syndrome.

Antiphospholipid antibodies (APAs) are circulating immunoglobulins associated with a hypercoagulable state. The antiphospholipid syndrome combines APAs and clinical manifestations, including arterial or venous thromboses and/or recurrent spontaneous fetal loss. The main risk incurred by endovascular treatment of intracranial aneurysms is the occurrence of thromboembolic events. We report two cases of patients with antiphospholipid syndrome who developed thromboembolic complications after the endovascular treatment of unruptured intracranial aneurysms.

Adult↗
PubMed2006

Silent microemboli related to diagnostic cerebral angiography: a matter of operator's experience and patient's disease.

INTRODUCTION: The aim of the present investigation was to elucidate in a large consecutive patient cohort whether the level of training has an effect on the number of microemboli detected by diffusion-weighted imaging (DWI) and which additional risk factors can be identified. METHODS: A total of 107 consecutive patients in whom a diagnostic cerebral angiography had been performed were prospectively investigated with DWI; 51 angiographies were performed by experienced neuroradiologists, 56 by neuroradiologists in training. RESULTS: In 12 patients (11.1%), a total of 17 new lesions without any clinically overt neurological symptoms were identified. Of these, 12 patients, 11 (91.7%) with 16 lesions were investigated by junior neuroradiologists. In 11 of 12 patients with DWI abnormalities (91.7%), risk factors could be identified (atherosclerotic vessel wall disease, vasculitis, hypercoagulable states). Experienced neuroradiologists performed 21 of 48 angiographies (43.8%) on patients with the above-mentioned risk factors, whereas junior neuroradiologists performed 27 angiographies in this subgroup (46.2%). The rate of diffusion abnormalities in patients with risk factors was 11/48 (22.9%) - considerably higher than in patients without risk factors (1/59; 1.7%). CONCLUSION: The level of experience and the nature of the underlying disease are predictors of the occurrence of cerebral ischemic events following neuroangiography. Alternative diagnostic modalities should be employed in patients who are investigated for diseases with the highest risk of angiographic complications (i.e., vasculitis, and arteriosclerotic vessel wall disease). If diagnostic angiography remains necessary in these patients, the highest level of practitioner training is necessary to ensure good patient outcome.

Adolescent↗
PubMed1997

Pulmonary embolism developing in patients with sickle cell disease on hypertransfusion and IV deferoxamine chelation therapy.

Pulmonary disease, including thromboembolic problems, accounts for a large portion of the morbidity of sickle cell disease. Chronic transfusion therapy is now a part of long-term treatment of sickle cell patients with stroke and chest syndrome. The resultant iron overload must be treated with chelation therapy using deferoxamine. Poor compliance with subcutaneous chelation therapy has necessitated intravenous deferoxamine treatment. We describe two patients with sickle cell disease on such a regimen, who became hypoxic as a result of pulmonary thromboembolism, secondary to venous thrombophlebitis. The thrombophlebitis and subsequent pulmonary embolism probably reflect the hypercoagulable state seen in sickle cell and are not due to the deferoxamine therapy.

Adolescent↗
PubMed2004

Acute abdominal aortic thrombosis in cancer patients.

We report two cases of acute aortic thrombosis in cancer patients. Aortic thrombosis is rare in the absence of atherosclerosis, dissection, or aneurysm. On the one hand, hypercoagulable state related to cancer is a well-known risk factor for venous thrombosis. On the other hand, arterial thrombosis has been rarely reported in cancer patients. Recognition of aortic thrombosis is important because it is a dangerous condition; furthermore, it exposes at the patient to complications such as peripheral embolism. In addition, anticoagulation can result in resolution of thrombosis.

Acute Disease↗
PubMed1999

[Blood coagulation and fibrinolysis in arteriosclerosis].

Thrombus formation at the site of atherosclerotic lesions, especially on a ruptured plaque, plays a central role in the "atherothrombosis" hypothesis. An activation of the hemostasis and a disturbed fibrinolysis are known. These alterations are especially marked in patients with acute coronary syndromes. In stable coronary artery disease, fibrinogen is elevated. Furthermore, minor alterations of the contact phase factor VII and consecutively of the thrombin system are detectable depending on the study population. Thrombin generation and activation become marked in patients with unstable angina pectoris or acute myocardial infarction. Possible reasons for this activation are an activation of the contact phase factor XII system and the release of tissue factor both from the ruptured plaque and from stimulated monocytes. The fibrinolytic system is markedly altered already in patients with stable coronary heart disease. Increased levels of tissue-type plasminogen activator and of urokinase-type plasminogen activator/receptor are measurable in atheromas. Tissue-type plasminogen activator mass concentration is systemically elevated already at early stages of atherosclerosis. Especially in patients with increased risk for acute coronary syndromes, the plasminogen activator inhibitor activity is significantly increased. Furthermore, a hypercoagulative state with increased d-dimer levels and plasmin-antiplasmin complexes can be measured. The alterations of hemostasis and especially of fibrinolysis are detectable for prolonged time period and persist much longer than the clinical symptoms of the patients. The increased plasminogen activator inhibitor activity is associated with the metabolic syndrome and constitutes an (in part genetically determined) disturbance in patients with stable or unstable coronary heart disease. However, the large intra- und interobserver as well as diurnal variability of this marker limits its use as a routine measure for risk stratification in patients. Alterations of the hemostasis and disturbances of fibrinolysis are detectable during the chronic as well as the acute phase of atherosclerosis. These changes are best documented for coronary heart disease, whereas less data are available for other manifestations of atherosclerosis. The use of newly developed molecular markers for single reaction steps of pathways instead of global functional tests and of new molecular biological methods did considerably improve the detailed knowledge on the pathomechanisms of the development of atherosclerosis, making the development of targeted therapies, e.g., against receptors possible. Future studies will investigate the quantitative impact of the various activated pathways (cause or reaction) and the effects of interventions on these pathomechanisms in patients with acute coronary syndromes. Studies will have to focus especially on the meaning of polymorphisms, early changes in the development of atherosclerosis and interactions with inflammatory processes.

Blood Coagulation Factors↗
PubMed1997

Familial Mediterranean fever and multiple sclerosis.

Central nervous system (CNS) manifestations of familial Mediterranean fever (FMF) are extremely rare. These include pseudotumor cerebri, optic neuritis, CNS complications of polyarteritis nodosa type vasculitis, or hypercoagulable states secondary to renal amyloidosis, recurrent aseptic meningitis, and amyloid ophthalmoplegia. We present three patients with FMF whose neurological findings and magnetic resonance imaging (MRI) abnormalities resembled multiple sclerosis (MS). These two conditions in the same patient could arise from either coincidence or an unknown pathophysiological relationship. Both explanations are equally speculative and this matter needs further study, especially to investigate MRI features in FMF patients without CNS symptoms.

Adult↗
PubMedDate not supplied

Stroke in pregnancy and the puerperium.

Recent studies suggest that the risk of cerebral infarction is increased during the puerperium but not during pregnancy itself. Most of the known causes of ischaemic stroke in the young have been reported during pregnancy. In most of these conditions, it is uncertain whether pregnancy is coincidental or plays a role in the occurrence of stroke. Eclampsia is the main pregnancy-specific cause, which may be associated with focal neurological deficits of sudden onset, consistent with a clinical diagnosis of stroke. However, the precise pathogenesis of these stroke-like focal deficits remains poorly understood. The two other pregnancy-specific conditions (choriocarcinoma and amniotic fluid embolism) are rarely responsible for focal cerebral ischaemia. In a significant number of patients, the cause of the stroke remains undetermined, despite an extensive aetiological investigation. Whether a hypercoagulable state and vessel wall changes associated with pregnancy may play a role in the occurrence of these otherwise unexplained ischaemic strokes remains unknown. The occurrence of cerebral venous thrombosis is clearly linked to the puerperal state, suggesting a direct role of the latter. However, cerebral venous thrombosis during pregnancy or the puerperium has been related to various aetiologies, stressing the need for an aetiological study, particularly when the thrombosis occurs during pregnancy. Pregnancy may increase the risk of subarachnoid haemorrhage, The most common cause is rupture of an arterial aneurysm. Although this is a controversial issue, the increased tendency of an aneurysm to bleed with advancing gestational age suggests that haemodynamic, hormonal or other physiological changes of pregnancy may play a role in aneurysmal rupture. The classic notion that rupture of an arterial aneurysm occurs more frequently during labour has not been confirmed. Most authors agree that surgical management after subarachnoid haemorrhage in pregnancy should be the same as that in the non-pregnant state. Data specifically devoted to intraparenchymal haemorrhage in pregnancy are scarce. Pregnancy and in particular the puerperium seem to be associated with an increased risk of intracerebral haemorrhage. The most common causes are eclampsia and ruptured vascular malformations. Whether pregnancy increases the risk of rupture of an arteriovenous malformation is controversial.

Adult↗
PubMed2001

Sequential magnetic resonance imaging findings in hypereosinophilia-induced encephalopathy.

Hypereosiophilia-induced encephalopathy (HE) is a rare but well-described clinical syndrome. However, serial magnetic resonance imaging (MRI) findings of HE have rarely been reported. We describe serial MRI findings of three patients with HE. The patients presented with acute confusion, focal neurological deficits and/or seizures. Eosinophils in repeated blood tests were more than 3000/mm3 in all the patients. Echocardiography in two patients showed findings consistent with eosinophilic endomyocardial fibrosis or global hypokinesia. The initial MRI revealed multiple high-signal lesions on T2-weighted images with gadolinium-DTPA enhancement on T1-weighted images, which were predominantly distributed in the border zone of the middle-anterior cerebral arteries and the middle-posterior cerebral arteries. The second MRIs taken prior to the initiation of steroid therapy showed that the lesions increased in size and number in the same area. The third MRIs performed long after the therapy showed that the lesions were shrunken. A brain biopsy specimen in one patient showed reactive gliosis following infarction with abundant intravascular eosinophils. The MRI-identified lesions in the patients with HE thus develop mainly in the border zone. The lesions occasionally increase in size and number and shrink if the eosinophilia is adequately treated. Although the nature of the MRI-identified lesions remains unclear, their pathogenesis may be related to multiple embolisms associated with concomitant cardiac abnormality and hypercoagulable state.

Adult↗
PubMed1998

Tissue factor is associated with the nonbacterial thrombotic endocarditis induced by a hypobaric hypoxic environment in rats.

High-altitude hypoxia causes a hypercoagulable state. In our previous study on the blood coagulation system in rats, nonbacterial thrombotic endocarditis (NBTE) developed after 4-12 weeks' exposure to the equivalent of 5500 m in altitude. We hypothesized that TF (tissue factor)-producing cells in the cardiac valves might be induced by the hypobaric hypoxic environment (HHE) and then trigger NBTE. A total of 170 male Wistar rats were housed in a chamber at the equivalent of 5500 m altitude for 1-12 weeks. We measured TF activity in the plasma and studied morphological changes in the mitral valves using immunohistochemical and immunoelectrical methods for TF protein and in situ hybridization for TF mRNA. After 4 weeks or more of exposure to HHE, 28 of the 56 surviving rats had developed NBTE. After 4-8 weeks' exposure to HHE, the plasma TF activity level was significantly higher than in control rats. There was a significant correlation between plasma TF activity and the incidence of NBTE. After 1 weeks' exposure to HHE, immunoreactivity for TF protein was detected in foamy macrophages and stromal cells in the cardiac valves. In rats with NBTE, TF protein was present in foamy macrophages and spindle stromal cells and focally present in the extracellular matrix. TF mRNA was detected in some foamy macrophages within the thrombus, TF protein was localized to the rough endoplasmic reticulum and plasma membrane of many macrophages, some fibroblasts, and a few endocardial cells. TF is associated with the pathogenesis of the NBTE induced by exposure to HHE. The accumulation of TF-producing macrophages during exposure to HHE may be responsible for initiating thrombus formation.

Animals↗
PubMed2006

Cerebral sinovenous thrombosis and idiopathic nephrotic syndrome in childhood: report of four new cases and review of the literature.

INTRODUCTION: Nephrotic children are prone to develop thromboembolic complications secondary to an acquired hypercoagulable state. Cerebral sinovenous thrombosis (CSVT) is increasingly recognised in this population, but clinical characteristics and outcome are not well documented. PATIENTS AND METHODS: The database of the Canadian Pediatric Ischemic Stroke Registry (Toronto Site) containing prospectively enrolled children from 1992-2004 with CSVT identified four children with NS. A pooled literature analysis retrieved 17 additional cases reports. RESULTS: CSVT presented in the majority of cases during the first flare or within 6 months after the onset of NS and was found to occur more often in SSNS/SDNS (n=13) than in SRNS (n=4). Clinical manifestations were non-specific and consisted primarily of seizures (n=8) and signs of raised intracranial pressure (n=16). Imaging studies revealed a predilection for superior sagittal sinus involvement (n=21) and rare parenchymal lesions (n=4). The most consistent biological risk factors were a severe hypoalbuminaemia (n=14) and, to a lesser extent, decreased antithrombin (AT) levels (n=9/16). Deficiency of other coagulation inhibitors (protein S, protein C) was not identified. Inherited thrombophilia was documented in a single case, suggesting that acquired, more than genetic, coagulation factors are involved. Anticoagulation was safe, and the outcome was good in most patients, and no recurrence of thrombotic event was reported. DISCUSSION: In conclusion, CSVT is now a well-described complication of NS with potential morbidity. A high index of suspicion is required, especially in young children with NS presenting neurological symptoms. Reliable biological predictors of CSVT are lacking.

Anticoagulants↗