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PubMedDate not supplied

Factor V Leiden is not commonly associated with idiopathic portal vein thrombosis in southern India.

BACKGROUND: Factor V Leiden has been reported in 2%-30% of patients with portal vein thrombosis. This wide variation makes it difficult to assess the importance of factor V Leiden as a predisposing factor. METHODS: Factor V Leiden was determined by restriction fragment length polymorphism in 112 patients with portal vein thrombosis, 104 with deep vein thrombosis and 98 control subjects. RESULTS: Only 3/112 (3%) patients with portal vein thrombosis had factor V Leiden, compared to 1/98 (1%) controls and 16/104 (15%) with deep vein thrombosis; of these, 3, 1 and 15, respectively, were heterozygous for this mutation. CONCLUSION: Factor V Leiden contributes little, if at all, to the development of portal vein thrombosis in southern India.

Activated Protein C Resistance↗
PubMed2006

Pulmonary vein thrombosis after lower lobectomy of the left lung.

Pulmonary vein thrombosis is a known complication after lung transplantation but has rarely been reported after lobectomy or bilobectomy. We report the case of a left upper pulmonary vein thrombosis following an uneventful left lower lobectomy for bronchial carcinoma. Postoperative arterial blood gas values and chest radiographs were normal. On postoperative day 5, the patient became progressively dyspneic, developed hemoptysis and showed total opacification of the left lung without mediastinal shift on chest radiography. The patient remained dyspneic despite intravenous antibiotic therapy for suspected pneumonia and absence of obstruction at bronchoscopy. Diagnosis of left upper pulmonary vein thrombosis was finally made by contrast-enhanced multislice computed tomography followed by pulmonary angiography. Further clinical deterioration under conservative treatment forced us to remove the remnant left upper lobe that already showed gangrenous alterations. Pulmonary vein thrombosis following lobectomy or bilobectomy is very rare. Only 7 cases have been reported in the literature so far. Conservative treatment with antibiotics and anticoagulants may be successful but in case of clinical deterioration the affected lobe has to be resected. The mechanism of thrombosis remains unclear although intraoperative torsion and injury of vessels seem to be most likely since pulmonary vein thrombosis occurred in the operated hemithorax only.

Aged↗
PubMed2007

No interaction between factor V Leiden and hyperhomocysteinemia or MTHFR 677TT genotype in venous thrombosis. Results of a meta-analysis of published studies and a large case-only study.

Homocysteine may have a thrombogenic effect through inhibition of inactivation of factor Va by activated protein C. Because factor V Leiden also leads to resistance of factor V to activated protein C, it would be possible that both factors show interaction for the risk of venous thrombosis. This has been reported in some studies, but not in others. We performed a metaanalysis to investigate a possible interaction between factor V Leiden and hyperhomocysteinemia, including 825 subjects with venous thrombosis and 2,109 controls, for the risk of venous thrombosis. In addition, we assessed a possible interaction between factor V Leiden and MTHFR 677TT genotype (the most common genetic determinant of homocysteine levels), including 2,547 subjects with venous thrombosis and 4,327 controls. We also investigated the interaction effect of factor V Leiden and hyperhomocysteinemia in a large case-only study using data of the VITRO study, including 2,077 subjects with first-time venous thrombosis. The meta-analysis yielded no evidence for additive or multiplicative interaction between factor V Leiden and hyperhomocysteinemia [relative excess risk due to interaction (RERI) -1.77 (95%CI -8.61 to 5.08) and multiplicative interaction term 0.86 (95%CI 0.35 to 2.14)]. The case-only study also showed no interaction effect [0.58 (95%CI 0.29 to 1.16)]. Also the metaanalysis on factor V Leiden and MTHFR 677TT yielded no evidence of interaction; RERI 0.13 (95%CI -3.60 to 3.86) and multiplicative interaction term 1.23 (95%CI 0.72 to 2.11). Both the meta-analyses of published studies and a large case-only study did not show evidence for interaction between factor V Leiden and hyperhomocysteinemia for risk of venous thrombosis.

Factor V↗
PubMed1991

Thrombosis and hemorrhage in thrombocytosis: evaluation of a large cohort of patients (357 cases).

We report clinical and laboratory findings in a large cohort of patients with thrombocytosis (357 cases). At the time of study, the patients showed a platelet number greater than 500 x 10(9)/L. The follow-up of patients ranged between 3 and 16 years. 123 patients were affected by polycythemia vera (PV), 97 by essential thrombocythemia (ET), 13 by chronic myeloid leukemia (CML) and 31 by myelofibrosis (MF). In 93 subjects, the thrombocytosis was reactive (ST). We found the highest incidence of thrombosis in PV patients, especially concerning the cerebro-vascular system; thrombosis, but in a lower percentage, was recognized in MF patients. Also, ET patients showed a number of thrombosis in peripheral arteries. Thrombosis of the coronary arteries were quite rare while 25% of MPD subjects showed peripheral vein thrombosis. We take into account that many patients showed thrombocytosis associated to one or more atherosclerotic risk factors. Hemorrhages were present especially in CML and in ET, but were not as frequent as thrombosis. The most common bleeding manifestations affected skin and mucosa. Hemorrhages after surgical procedures were also frequent. Gastro-intestinal bleeding was not strictly related to anti-aggregating therapy and occurred not only in PV but also in ET patients.

Adult↗
PubMed1991

[Cerebral venous thrombosis. Report of 76 cases].

Progress in neuroimaging has led to a considerable change in our knowledge of cerebral venous thrombosis (CVT). Together with a series of 76 cases, a review of literature is presented. CVT is a far from negligible variety of stroke. It may occur at any age and despite numerous causes (nowadays mostly non infective), the proportion of cases of unknown aetiology remains around 25%. Superior sagittal sinus and lateral sinus are the most frequently involved, often associated with cortical vein thrombosis. Cavernous sinus thrombosis remains the most common form of septic thrombosis. Thrombosis of the galenic system and of cerebellar veins are uncommon. The clinical picture is extremely variable with a mixture of focal signs (deficits or seizures) and symptoms of raised intracranial pressure. The mode of onset is also variable, over hours, days, weeks or months. The presentation can thus be very misleading, simulating an arterial stroke or an abscess, an encephalitis, a tumor or a pseudo-tumor cerebri. CT scan is crucial to rule out other conditions and angiography to confirm the diagnosis of cerebral venous thrombosis. MRI is very performing since it visualizes the thrombus itself and allows a non invasive follow up. Most cases have a benign course but mortality is still around 30% in infective cases and 10% in non infective ones. Although it has long been debated, the benefit of anticoagulant (heparin) is now well established.

Cerebral Veins↗
PubMed1991

Role of von Willebrand factor in arterial thrombosis. Studies in normal and von Willebrand disease pigs.

With normal and von Willebrand disease (vWD) pigs, we studied the role of von Willebrand factor (vWF) in platelet-vessel wall interactions and occlusive arterial thrombosis. Two methods of arterial injury have been used to determine the thrombotic response of flowing blood in vivo. The first involves balloon catheter injury. After superficial denudation of endothelium from coronary intima, platelets adhere to the subendothelium in a monolayer. Similar numbers of adherent platelets are found in both phenotypes, but platelets in vWD pigs have impaired pseudopod formation and are less well spread morphological indexes of limited platelet activation. Deeper injury, which involves the media, produces nonocclusive platelet-fibrin microthrombi. The second injury method involves pinching the artery at a site of superimposed stenosis, a procedure that almost always exposes media. This procedure induces platelet-fibrin microthrombi in normal and vWD pigs, but only normal pigs develop occlusive thrombosis. Both methods of arterial injury have also been performed in normal and vWD pigs with diet-induced hypercholesterolemia and atherosclerosis. Atherosclerosis promotes platelet spread in vWD pigs but does not abolish the protection from stenosis and injury-induced occlusive thrombosis. In addition, neutralization of vWF activity in normal pigs by a monoclonal antibody prevents the induction of occlusive thrombosis by the stenosis and pinch-injury procedure. This monoclonal antibody also causes performed platelet aggregates to break up. These experimental models of inducing arterial thrombosis have been used in normal and vWD pigs to demonstrate interactions between normal and atherosclerotic vessel wall constituents, circulating platelets and vWF that are fundamental in the process of arterial thrombosis.

Animals↗
PubMed1990

Upper extremity venous thrombosis. Case report and literature review.

Upper extremity venous thrombosis is a clinical entity with numerous etiologic factors. Only 2% of all cases of deep venous thrombosis involve the upper extremity, and the incidence of pulmonary embolism related to thrombosis in this location is approximately 12%. Primary or "effort" thrombosis of the upper limb is related to the inherent anatomical structure of the thoracic outlet and axillary region. Secondary thrombosis may have such diverse origins as trauma, infection, congestive heart failure, central venous catheters, neoplasms, septic phlebitis, intravenous drug use, and hypercoagulable states. Patients present with peripheral edema and prominent superficial veins, and neurologic symptoms (pain and paresthesias) are usually present as well. Clinical diagnosis is confirmed by venography or sonography. Treatment regimens include conservative measures, thrombolysis with fibrinolytic agents, and surgical correction of indicated thoracic outlet and axillary structures. We present an unusual case in which upper extremity venous thrombosis in a young healthy female athlete was associated with the presence of cervical ribs. The patient was successfully treated with focal thrombolysis and surgical resection of her ipsilateral cervical rib.

Adult↗
PubMed1990

Thrombosis in human pancreatic transplantation associated with elevated cyclosporine levels and possible protection by antihypertensive agents.

Acute thrombosis in human pancreatic transplantation (HPT) remains a serious problem occurring in 10% to 30% of many reported series. Thrombosis may result from a number of causes including technical error, acute rejection, or low-flow states secondary to conditions within the host or in the transplanted organ. Evidence accumulates suggesting cyclosporine (CSA) acts as a potent vasoconstricting agent and that antihypertensive medications such as calcium channel blocking agents may offer protection from this effect. We have reviewed 68 consecutive human pancreatic transplants at the University of Iowa, specifically evaluating CSA levels, and the use or nonuse of antihypertensive medications. We found CSA levels in patients with transplant thrombosis to be elevated above the mean in 80% of patients with levels available 24 hours prior to thrombosis. Fifty percent of these (CSA) levels were well above one standard deviation. In addition, those patients receiving routine antihypertensive medication (most commonly calcium channel blocking agents) were statistically less likely to have thrombosis of the pancreatic transplant. We suggest that elevated levels of CSA may play at least a partial role in thrombosis of HPT and antihypertensive agents may offer protection from this effect.

Adult↗
PubMed1990

[Formation of extrinsic blood thrombosis in 102 cases of thromboangiitis obliterans].

The formation of extrinsic blood thrombosis in 102 cases of thromboangiitis obliterans and 54 healthy persons were observed with chandler method and their clinical manifestations. All the 102 patients were male, of which 13 cases were in ischemic stage, 45 cases in dystrophic stage, and 44 cases in necrotic stage. According to the differentiation of TCM, 8 belong to Yin-cold type, 50 belong to downward flowing of damp-heat type, 42 belong to blood stasis type, and 2 others. Combining method of TCM-WM was adopted to give 45 cases systemic treatment, that is, taking the promotion of blood flow to remove its stasis as the dominant factor, accompanied by intravenous drip and operation. Results showed that the length, wet weight and dry weight of extrinsic blood thrombosis were higher apparently in the cases of thromboangiitis obliterans than those in healthy persons (P less than 0.001), and there were significant differences between the values of extrinsic blood thrombosis in different stages and different degrees. After systemic treatment with TCM-WM, the values of extrinsic blood thrombosis decreased remarkably, and their symptoms and signs improved or disappeared. The clinical total effective rate was 88.89%, and the decreasing rate of the values of extrinsic blood thrombosis was 98.9%. This suggested that the high blood coagulation and extrinsic thrombosis should draw special attention and may act as an approach reflecting the severity of the disease and evaluating the effects of treatment.

Adolescent↗
PubMedDate not supplied

[Thrombosis of the left auricle. Diagnostic usefulness of two-dimensional echocardiography].

The purpose of this study is to determine the sensitivity and specificity of two dimensional echocardiography in the diagnosis of thrombosis of the left atrial appendage. Sixty patients with mitral rheumatic heart disease were examined prospectively 24 to 72 hours prior to cardiac surgery. Two images were used to identify thrombosis in the appendage: parasternal short axis at the level of the aortic valve with a lateral and superior inclination of the transducer and a modified apical five chamber view with counter clockwise rotation of the transducer between the apical long axis and the five chamber view. Diagnosis was corroborated during surgery and by histopathological analysis. In all cases the presence and predominance of mitral lesion (stenosis or regurgitation) were established by clinical history, electrocardiogram, chest roentgenogram and two dimensional echocardiogram. In 58 patients the lesions were also confirmed by cardiac catheterization. Of the 60 patients (46 females and 14 males between 16 and 61 years of age), eleven cases (18.3%) of left atrial thrombosis were detected, of which seven had formed in the left atrial appendage. All were confirmed during surgical intervention and pathological analysis. One thrombus in the left atrial appendage not diagnosed by echocardiography was found during surgery (Sensitivity:90.9%). In this case pathology studies demonstrated recently formed thrombi. In all cases in which two dimensional echocardiography did not show signs suggesting thrombosis, surgery confirmed that atrial thrombosis did not exist (Specificity: 100%). This study demonstrates the utility of two dimensional echocardiography in the diagnosis of thrombosis of the left atrial appendage, thus making it possible to schedule corrective surgery and the use of anticoagulants.

Adolescent↗
PubMed1989

[Nuclear resonance in intracranial venous thrombosis].

We have reviewed the nuclear resonance NR images in three patients with intracranial venous thrombosis. Tomodensitometric findings are not reliable in intracranial venous thrombosis and cerebral angiography is required for the diagnosis. The usefulness of NR for the investigation of venous disease has been recently demonstrated. Ten patients in whom a diagnosis of intracranial venous thrombosis was made with NR have been reported. Initially, the vacuum signal in the T1 enhanced sequences disappears and the thrombus becomes hypointense in the T2 enhanced sequences. In the following phase, proton relaxation is impaired by methemoglobin production and thrombosis appears as hyperintense in both the T1 and T2 enhanced sequences. During the resolution phase, the vacuum signal in the vascular lumen reappears and the hyperintensity of the thrombus signal becomes attenuated. In our study we have shown the different stages of intracranial venous thrombosis with NR. In addition, we have demonstrated the close relation between these images and the clinical evolution. NR is a useful noninvasive investigation in patients with suspected intracranial venous thrombosis.

Aged↗
PubMed1988

The prognosis of renal vein thrombosis: a re-evaluation of 27 cases.

Twenty-seven patients with renal vein thrombosis were retrospectively studied to evaluate their long-term prognosis and relevant prognostic factors. Twenty-four patients presented with a nephrotic syndrome, and 15 had renal impairment (8 acute; 7 moderate). Ten patients had a previous history of proteinuria, and 14 of nephrotic syndrome. Renal biopsy performed in 20 patients, of whom 19 were nephrotic, showed membranous glomerulonephritis in 14, focal segmental glomerulosclerosis in three, minimal change glomerulonephritis in two, and periarteritis nodosa in one. Renal vein thrombosis was angiographically proven in all patients and was bilateral in 18, localised to the left renal vein in seven, and to the right in two. Thrombosis of the inferior vena cava was associated in seven patients. Ten patients were treated by anticoagulants alone, nine by surgical thrombectomy, seven by thrombolysis, and two did not receive any specific treatment. One patient underwent successively thrombectomy and then thrombolysis. Eleven patients died within the first 6 months, mainly from haemorrhagic complications (n = 5) or severe sepsis (n = 2). Survivors were followed up from 6 months to 19 years. Nephrotic syndrome improved or even disappeared in 12 patients, and renal function did not worsen throughout the follow-up in any patients. The main prognostic factors were initial renal function and type of nephropathy: patients with membranous glomerulonephritis had a significantly better renal function and a lower mortality rate than patients with other nephropathies. Initial renal insufficiency was significantly associated with a poor prognosis. There was no advantage, in terms of survival, kidney function and nephrotic syndrome, of either thrombectomy or thrombolysis over anticoagulants alone, despite two complete venous recanalisations after thrombolysis. Accordingly, patients with renal vein thrombosis from membranous glomerulonephritis should be treated by anticoagulants alone, since the long-term prognosis of this disease seems unaffected by intercurrent renal vein thrombosis. With respects to the risk-to-benefit ratio, thrombectomy should be avoided and thrombolysis considered only in patients with initial acute renal failure from acute renal vein thrombosis.

Adult↗
PubMed1988

[Treatment of renal vein thrombosis associated with nephrotic syndrome].

Renal vein thrombosis is a rare entity in which true incidence is unknown. The disease occurs most frequently in patients with nephrotic syndrome, but it also can occur in the presence of other hypercoagulable state. Two cases of renal vein thrombosis with nephrotic syndrome which were treated by thrombectomy are reported here. One patient was successfully treated by renal vein and inferior vena cava thrombectomy before developing severe pulmonary embolism. The other was treated by renal vein thrombectomy by which fatal shock was able to be prevented. In those cases, immediate operation was indicated, primarily to prevent additional, possibly fatal, pulmonary embolism and also to improve perfusion of the kidney. In the hope of salvaging the kidney, thrombectomy may be the treatment of choice for acute renal vein thrombosis, complication of pulmonary embolism and inferior vena cava thrombosis, right renal vein thrombosis without collateral flow and acute renal vein thrombosis with shock.

Adult↗
PubMed1985

Selective glomerular thrombosis in rats induced by combined injections of nephrotoxic antiserum and lipopolysaccharide.

Experimental glomerular thrombosis was induced in rats by combined injections of nephrotoxic antiserum and lipopolysaccharide. For the development of glomerular thrombosis, administration of nephrotoxic antiserum (greater than or equal to 0.1 ml pooled material) was required as a preparatory agent and greater than or equal to 100 ng lipopolysaccharide as a provoking agent. The severity of renal lesions was not parallel with the amounts of nephrotoxic antiserum and lipopolysaccharide injected. Transient clamping of a unilateral renal artery for 10 to 20 minutes at the time of the nephrotoxic antiserum injection partially prevented the development of glomerular thrombosis in the clamped side. Intervals between the preparatory and provoking injections were found to be -4 to 72 hours for the development of renal lesions. With the preparatory injection of 0.1 to 0.3 ml nephrotoxic antiserum a thrombotic lesion developed exclusively in glomerular capillary walls greater than or equal to 2 hours after the lipopolysaccharide injection. No thrombotic lesion was observed in other tissues such as lung, liver, or intestine, but a generalized Shwartz-manlike phenomenon was observed with the preparatory injection of 0.5 ml nephrotoxic antiserum. When rats were pretreated with nephrotoxic antiserum and 3 hours thereafter transfused with 1 to 3 X 10(8) polymorphonuclear leukocytes, which had been incubated with lipopolysaccharide for 30 minutes in vitro and washed three times with buffered physiologic saline solution, a marked glomerular thrombosis was also induced. The result indicates that lipopolysaccharide plays a role in the development of thrombosis by a direct effect on leukocytes. The development of glomerular thrombosis was prevented in a leukocytopenic state when leukocyte count was less than 600/microliter, but not in thrombocytopenic rats with a platelet count 8.7 to 30 X 10(3)/microliter. Leukocyte count and plasma fibrinogen level decreased, and prothrombin time and activated partial thromboplastin time were prolonged significantly during the pathologic course. Platelet count and FDP did not change significantly. This experimental model has a basic similarity to the generalized Shwartzman reaction, but the lesions develop exclusively in glomeruli.

Animals↗
PubMedDate not supplied

Arterial thrombosis and embolism in malignancy.

In most reviews of arterial embolism or thrombosis the source of emboli or the cause of thrombosis can reasonably be established in over 90% of patients. Still about 10% remain without demonstrable cardiac or intraarterial sources. Although hypercoagulability induced by malignancy has been alluded to as a cause of unexplained intravascular thrombosis reports of arterial thromboembolism with such association are rare. Seven patients with unequivocal thromboembolism are presented. Two distinct clinical patterns are observed, one with in situ thrombosis of small arteries and the other with occlusion of large arteries causing limb ischemia or fatal organ infarction. The various pathogenetic mechanisms of arterial thrombosis or embolism in malignancy include sustained spasm of arteries, precipitation of cryoglobulins or other abnormal proteins in small arteries, direct tumor invasion of arteries, fragmentation and embolization of intracardiac or intraarterial metastases and spontaneous arterial thrombosis due to hypercoagulability. The hypercoagulable state can be recognized by the observation of shortened bleeding and clotting times, partial thromboplastin and prothrombin times, elevation of coagulation factors, platelets and yield stress index and resistance to anticoagulation. Patients presenting with arterial thromboembolic events with out demonstrable source should be investigated for malignancy. Conversely patients with malignancy should be searched for evidence of hypercoagulability in an attempt to prevent arterial thromboembolic complications.

Adenocarcinoma↗
PubMed1985

Lytic therapy in the treatment of axillary and subclavian vein thrombosis.

The importance of individualized treatment of patients with primary and secondary axillary-subclavian vein thrombosis is described with special emphasis on the use of thrombolytic therapy. Nine patients were treated with streptokinase or urokinase. Balloon dilation of the axillary or subclavian vein and first rib resection were also selectively used. Of the five patients with primary axillary-subclavian thrombosis, three did not have symptoms after the thrombus was lysed. Two had successful lysis of the thrombus but later suffered a rethrombosis, one of which most likely resulted from an untreated stenosis. All four of the patients with secondary thrombosis had successful thrombolysis. Patients with primary axillary-subclavian thrombosis are usually young and as many as 40% continue to have intermittent upper extremity edema or pain. For this reason we believe aggressive attempts to reestablish normal venous return through the axillary and subclavian veins are warranted. Patients with secondary axillary-subclavian thrombosis usually require prolonged venous catheterization for chemotherapy or total parenteral nutrition. Since patency of major upper extremity veins is extremely important in these patients with secondary thrombosis, we believe that vigorous attempts to restore these venous access routes are indicated and appropriate.

Adult↗
PubMed1984

Graded pressure stockings in prevention of deep vein thrombosis following total hip replacement.

The occurrence and distribution of deep vein thrombosis after elective hip surgery were studied in 22 consecutive patients wearing graded pressure stockings as thromboprophylaxis. The frequency of thrombosis, as evidenced by leg-scan and phlebography, was 59%. Thirty-six per cent of the patients developed femoro-popliteal thrombosis. Thrombosis was unilateral and located in the operated limb, except for one patient who had concurrent leg-vein thrombosis in the non-operated limb. Two patients developed symptomatic lung embolism. Antithrombin III was determined pre- and postoperatively. There was no evidence of antithrombin III consumption due to postoperative thrombosis.

Aged↗
PubMed1981

Blood tests for the diagnosis of venous and arterial thrombosis.

There are many reports in the literature of blood test abnormalities occurring in patients with venous or arterial thrombosis. Most of these have not used acceptable criteria for establishing an association between thrombosis and blood tests and, therefore, their interpretation is questionable. Recently, sensitive and specific assays have been developed for the detection of products of intravascular thrombin formation, of plasmin digests of fibrin or fibrinogen and of platelet specific proteins that are released into the plasma when platelets react with stimuli. Blood abnormalities have been sought that can either predict or detect venous thrombosis. Many of the predictive tests evaluated are nonspecific acute phase reactant responses to inflammation; of these, only reduced fibrinolytic activity has been consistently reported to be associated with postoperative venous thrombosis. Hereditary antithrombin III deficiency has been consistently shown to predispose patients to venous thrombosis. Abnormalities of the plasminogen and fibrinogen molecule have also been described in patients with familial or recurrent venous thrombosis but these are rare and the association could be coincidental. Two blood tests, the fibrinopeptide A assay and the assay for fibrin/fibrinogen fragment E are highly sensitive to acute venous thromboembolism in symptomatic patients but both are nonspecific. Elevated levels of beta thromboglobulin and platelet factor 4 have been reported in patients with arterial thromboembolism but the sensitivity and specificity of these findings is presently unknown.

Antithrombin III↗