Circulating microemboli in patients with myeloproliferative disorders

Weber, C. A.; Matzdorff, Axel; Gerriets, Tibo; Villmow, T.; Stolz, Erwin

doi:10.1111/j.1468-1331.2006.01616.x

Cited by 6 publications

(5 citation statements)

References 24 publications

(32 reference statements)

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“…50–56 The microembolic signals obtained from patients with artificial heart valves and during examinations for PFO detection have also been used as a model, alongside other methods, in an attempt to differentiate between gaseous and solid microemboli. 57–59 The results of MES monitoring may also be found in some other clinical situations, where their presence 60–65 or absence 66–67 helps us to better understand the role of embolism in the development of the disease. Our case emphasizes that MES monitoring may be useful not only in detecting the emboliogenic nature of the disease, but also in exploring the precise timing of embolization (i.e., either permanent, as in the many clinical situations mentioned above, or sporadic, as in our case).…”

Section: Discussionmentioning

confidence: 95%

Microemboli monitoring by trans-cranial doppler in patient with acute cardioemboliogenic stroke due to atrial myxoma

Telman¹,

Kouperberg²,

Cohen³

et al. 2010

Neurol Int

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This is the first reported attempt to examine the emboliogenic potential of cardiac myxoma in patients with acute stroke through the monitoring of microembolic signals (MES) by transcranial doppler. A 43-year old woman was brought to the emergency department because of acute onset of generalized tonic-clonic seizures and left hemiplegia. A CT scan of the brain demonstrated a large acute infraction in the territory of the right middle cerebral artery (MCA) and another smaller one in the territory of the posterior cerebral artery on the same side. Trans-cranial doppler (TCD) microemboli monitoring did not reveal MES. Transesophagial echocardiography (TEE) identified a 5 cm left atrial mass, which was highly suspected to be an atrial myxoma attached to the interatrial septum and prolapsed through the mitral valve. After the TEE results were obtained, another TCD monitoring was performed. Again, there were no MES found in either of the MCAs.Our findings showed the absence of MES on two consecutive TCD examinations, suggesting a spontaneous occurrence, rather than the permanent presence, of embolization, even in the most acute phase of stroke. Thus, the tendency of myxomas to spontaneously produce multiple emboli emphasizes the need for the surgical excision of myxomas.

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Section: Discussionmentioning

confidence: 95%

Microemboli monitoring by trans-cranial doppler in patient with acute cardioemboliogenic stroke due to atrial myxoma

Telman¹,

Kouperberg²,

Cohen³

et al. 2010

Neurol Int

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“…So recently JAK2 V617F mutation has been considered among the possible diagnostic tools for the correct and early diagnosis of splanchnic vein thrombosis. 34 6). The authors also emphasized that, in all JAK2 V617F mutation negative patients, haplotype 46/1 expression is, in any case, linked to an increased erythropoiesis.…”

Section: Discussionmentioning

confidence: 95%

“…JAK2 mutation seems to be able to induce leukocyteplatelet aggregates and activate the coagulation cascade. 34 Given this, the presence of other molecular microaggregates, including CD11b/CD62P and CD11b/CD42b, and of blood hyperviscosity, due to the high number of red blood cells, seem to explain the thrombophilic tendency of JAK2 positive patients, beyond the presence or absence of a contemporary myeloproliferative disease. [34][35][36] Moreover, an increased tissue factor synthesis by JAK2 positive macrophages has been noticed in patients affected with SVT.…”

Section: Discussionmentioning

confidence: 99%

“…34 Given this, the presence of other molecular microaggregates, including CD11b/CD62P and CD11b/CD42b, and of blood hyperviscosity, due to the high number of red blood cells, seem to explain the thrombophilic tendency of JAK2 positive patients, beyond the presence or absence of a contemporary myeloproliferative disease. [34][35][36] Moreover, an increased tissue factor synthesis by JAK2 positive macrophages has been noticed in patients affected with SVT. So recently JAK2 V617F mutation has been considered among the possible diagnostic tools for the correct and early diagnosis of splanchnic vein thrombosis.…”

Section: Discussionmentioning

confidence: 99%

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Portal vein thrombosis and Budd-Chiari syndrome as onset of polycythemia vera

Seidita

Sprini

Bongiovì³

et al. 2013

Ital J Med

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Budd-Chiari syndrome may be defined as a heterogeneous group of vascular disorders characterized by obstruction of hepatic venous return to the level of hepatic venules, supra-hepatic veins, inferior vena cava or right atrium. The main cause of this syndrome is represented by myeloproliferative diseases and, in particular, by polycythemia vera. The latter may cause multiple splanchnic thrombosis, including portal vein thrombosis, particularly important for its clinical outcomes (ascites, collateral vessels genesis, etc.). We report 2 cases of a Budd-Chiari syndrome induced by polycythemia vera characterized by an abnormal clinical onset, both as regards subjects’ age (29 and 39 years old, respectively) and set of symptoms, signs and laboratory data. After a complete clinical, instrumental and genetic diagnosis, the patients were treated with combined therapy, using acetylsalicylic acid and hydroxyurea. The therapy proved successful and patients are still in follow up in our institution. Polycythemia vera should be suspected in patients affected with portal vein thrombosis and Budd-Chiari syndrome even if its clinical onset might be unusual. Every effort should be made to make a correct and early diagnosis in order to start appropriate therapy as soon as possible and to prevent patients from useless diagnostic and therapeutic treatments.

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“…Increased levels of platelet MPs appear to correlate with platelet dysfunction and increased risk of thrombosis in these patients. 40,41 Given the lack of markers (apart from full blood counts) to predict the occurrence of venous thromboembolism (VTE) in these conditions, measuring MPs may prove to be a useful tool in the follow-up of patients with myeloproliferative disorders.…”

Section: Myeloproliferative Disordersmentioning

confidence: 99%

Microparticles in Health and Disease

Enjeti

Lincz

Seldon

2008

Semin Thromb Hemost

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Microparticles (MPs) are small fragments of membrane-bound cytoplasm that are shed from the surface of an activated or apoptotic cell. Recently, their function as vectors of transcellular exchange of biologic information, in addition to better described forms of intercellular communication such as growth factors, cytokines, and chemokines, has become well recognized. Circulating levels of MPs are thought to reflect a balance between cell stimulation, proliferation, and death. The production of MPs is thought to predominately occur by vesiculation or blebbing of the cell membrane. The mechanisms governing the remodeling of the plasma membrane are complex, involving cytoskeletal changes and a shift from normal phospholipid asymmetry. Increased intracellular calcium subsequent to cell activation leads to intracellular increases in several proteins including gelsolin and calpain, as well as the activity of enzymes such as translocase, floppase, and scramblase, which play important roles in the homeostasis of the cell membrane. The membrane vesiculation and phospholipids asymmetry leading to the production of MPs occurs by the complex interplay of the proteins involved. There are several clinical conditions associated with elevated MPs, and most are also associated with an increased risk of thrombosis. Apart from cardiovascular disease and venous thromboembolism, MPs are also elevated in solid tumors with metastatic disease. The measurement of MPs is being regarded as a potential biomarker, given the range of conditions in which they are elevated and the association with prothrombotic states. The utility of measuring MPs as a diagnostic and prognostic marker is currently a subject of intense investigation. The further development of the various methods for the detection and measurement of MPs and prospective clinical trials establishing the utility of such tests will be critical prior to the routine measurement of MPs in the diagnostic laboratory.

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Circulating microemboli in patients with myeloproliferative disorders

Cited by 6 publications

References 24 publications

Microemboli monitoring by trans-cranial doppler in patient with acute cardioemboliogenic stroke due to atrial myxoma

Microemboli monitoring by trans-cranial doppler in patient with acute cardioemboliogenic stroke due to atrial myxoma

Portal vein thrombosis and Budd-Chiari syndrome as onset of polycythemia vera

Microparticles in Health and Disease

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