Cases reported "Thrombosis"

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1/42. Glomerular thrombosis: an unusual cause of renal failure in systemic lupus erythematosus.

    The authors report an unusual case of acute renal failure occurring in a patient with systemic lupus erythematosus and antiphospholipid antibodies. kidney biopsy revealed glomerular thrombosis, in the absence of glomerulonephritis. The authors stress the clinical and biological signs that suggest the thrombotic nature of kidney failure in lupus patients.
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2/42. Clinical implications of elevated PAI-1 revisited: multiple arterial thrombosis in a patient with essential thrombocythemia and elevated plasminogen activator inhibitor-1 (PAI-1) levels: a case report and review of the literature.

    Plasminogen activator inhibitor (PAI-1), a member of the serine protein family, is the most active in vivo inhibitor of fibrinolysis induced by plasminogen, tissue plasminogen activator (tPA), and urokinase type plasminogen activator (uPA). While the association between elevated PAI-1 and thrombogenesis has been well studied for several disease processes, including coronary disease, postoperative deep vein thrombosis (DVT), myocardial infarction, malignancy, and diabetes, few studies have concentrated on the correlation between elevated PAI-1 levels and thrombogenesis in patients with myeloproliferative disorders. Essential thrombocythemia (ET), a chronic myeloproliferative disorder, characterized by the overproduction of poorly functioning platelets, is associated with both thrombotic and hemorrhagic life-threatening complications. Although the events resulting in thrombogenesis in such patients may be multifactorial in nature, an association between elevated PAI-1 levels and thrombus formation has been proposed. Herein we present a patient diagnosed with ET complicated by multiple episodes of arterial thrombosis. Elevations in PAI-1 levels were documented repeatedly. The role of elevated PAI-1 when associated with other disease processes is also discussed.
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3/42. Therapeutic plasma exchange for the acute management of the catastrophic antiphospholipid syndrome: beta(2)-glycoprotein I antibodies as a marker of response to therapy.

    We describe two patients with the catastrophic antiphospholipid syndrome associated with elevation of beta(2)-glycoprotein I antibodies and fulminant thrombotic diatheses. Both patients were treated with therapeutic plasma exchange (TPE), which resulted in a marked decrease in antibody titer accompanied by an improved clinical outcome in one patient (IgG antibody). In the second patient, the outcome was poor despite TPE (IgA antibody). There were no significant complications of TPE in either case. Because of the fulminant nature of the catastrophic antiphospholipid syndrome, we conclude that a trial of TPE is warranted for the acute management. Further studies are needed to clarify which patients may benefit from this treatment.
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4/42. cholecystitis caused by hemocholecyst from underlying malignancy.

    Massive hemobilia is a well recognized clinical entity, particularly when it presents with jaundice, GI bleeding, and biliary pain. However, occult hemobilia is more difficult to diagnose and has seldom been reported because of its clinically silent nature. In fact, this is usually overlooked until complications arise. Hemocholecyst or clot within the gallbladder may rarely occur in this setting, leading to cystic duct obstruction and cholecystitis. Most previous reports describe cholecystitis resulting from hemocholecyst after iatrogenic trauma. We describe two cases in which hemocholecyst occurred from underlying malignancies, both resulting in cholecystitis (acute or chronic).
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5/42. The value of repeat transesophageal echocardiography in the evaluation of embolism from the aorta.

    Transesophageal echocardiography (TEE) is now widely used in the evaluation of patients with unexplained stroke or transient ischemic attack, in part to exclude the presence of protruding aortic arch atheromas. We report two cases in which repeated TEE revealed an aortic clot not seen on the earlier transesophageal echocardiogram performed immediately after embolization. These cases illustrate the dynamic nature of aortic thrombus and the role of TEE in its diagnosis.
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6/42. Acute lower limb thrombosis caused by a congenital fibrous ring of the superficial femoral artery.

    Segmentary isolated stenosis or obstructions of the superficial femoral artery in young people are rarely reported. In patients, most of them women, affected by chronic symptomatology of the lower limbs, the aetiology has been referred to fibromuscular dysplasia with unusual localization. We report a case of acute lower limb thrombosis in a young woman caused by a congenital fibrous ring of the superficial femoral artery and the treatment we performed in this situation including the complication that happened after the percutaneous transluminal angioplasty that we carried out in order to reduce the stenosis of the femoral superficial artery. Histological examination of the lesion demonstrated the nature of the fibrous ring caused by an embryological anomaly, followed by a secondary thrombosis in a woman not using oral contraceptives and without any alteration of the coagulation chain. fibromuscular dysplasia of the femoral artery is commonly caused by previous thigh injuries, thromboembolic events with recanalization of the artery or arteritis, but in some cases appears to be the consequence of primitive intimal dysplasia. When a fibromuscular dysplasia is suspected, all authors agree on the necessity for a screening of the two preferential localizations of the disease: common carotid artery and renal artery, in the case reported the result was negative.
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7/42. Transesophageal echocardiographic diagnosis of left atrial mass as thrombus by demonstrating its attachment to the patch closing atrial septal defect: a case report.

    A 65-year-old-man was referred for echocardiographic examination because of palpitations. He had a history of an atrial septal defect surgically treated with an artificial synthetic polyester textile fiber patch. TTE showed a large, mobile mass in a dilated left atrium. The attachment site of the mass was not clear by transthoracic approach, and it was difficult to diagnose the mass as a thrombus or a myxoma from the nature of the echocardiographic findings. Transesophageal echocardiography clearly demonstrated that the mass was attached to the patch closing the atrial septal defect and the mass was confirmed as thrombus at surgery. A patient with left atrial thrombus in whom transesophageal echocardiographic demonstration of the attachment of the left atrial mass to a patch closing an atrial septal defect served as an essential clue leading to accurate diagnosis is reported. Transesophageal echocardiography is feasible to evaluate the attachment site of a left atrial mass and to lead to an accurate diagnosis.
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8/42. Dural arteriovenous fistulae causing pseudotumour cerebri syndrome in an elderly man.

    The clinical presentation of dural arteriovenous fistulae (DAVF) is dependent on their location and the nature of their venous drainage. The latter plays a critical part in determining whether or not the fistula gives rise to intracranial hypertension, which is present in only a minority of cases. We present a case of the pseudotumour cerebri syndrome in an elderly man with bilateral intracranial DAVF supplied by the occipital arteries. cerebral angiography was required for definitive diagnosis, and to characterise the abnormal venous drainage. The pathophysiology of intracranial hypertension in DAVF is discussed.
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9/42. Intra-cardial thrombosis with systemic and pulmonary embolism as main symptoms in a patient with protein s deficiency.

    This report describes the unusual occurrence of both left and right atrial thrombosis with peripheral arterial and pulmonary embolism, respectively, as presenting symptoms of congenital protein s deficiency in a 31-year-old man. The coagulation study performed in the coumarin-treated propositus indicated a heterozygous protein S state. The finding of reduced free protein S antigen and protein S activity levels with normal total protein S and C4B-bp levels in five other family members (father, sister, and three relatives on the paternal side) confirmed the inherited nature of the defect. Since there is an increased frequency of arterial thrombosis in patients suffering from protein s deficiency, any case of idiopathic intra-cardial thrombosis requires careful haemostatic screening. In addition, the possibility of intra-cardial thrombosis should be considered in any thromboembolic event seen in inherited protein s deficiency.
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10/42. An autopsy case of Kawasaki disease with reference to occurrence of acute coronary thrombosis in the convalescent stage.

    A one-year, four month-old boy who had suffered from Kawasaki disease died suddenly during convalescence despite intensive gamma-globulin treatment. autopsy revealed a) sausage-like aneurysms of the left and right coronary arteries and fresh thrombosis in the right coronary aneurysm, b) fresh transmural myocardial necrosis in the whole wall of the left ventricle and the anterior part of the wall of the right ventricle, and c) swelling of the cervical lymph nodes and thymus (60 g). Histologically, fibrocellular thickening of the intima and destruction of the media and internal elastic lamina were conspicuous in the area of the aneurysm, but those of the intima and media in the areas adjacent to the aneurysm were mild. Abrupt narrowing of the lumen at the border between the aneurysm and periphery of the right coronary artery was detected, and this may have been responsible for formation of the thrombus in the right coronary aneurysm. In the systemic arteries, perivascular fibrosis was very noticeable despite less severe injury to the intima and media. These findings suggest that severe inflammation of the periarterial regions was present in the acute phase. The lymph system still showed inflammation, supporting the infectious or toxic nature of Kawasaki disease.
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