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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two patients developed heat stroke following jogging. Transient disturbance of cerebral function was the most dramatic clinical feature. Although haemorrhagic complications were not seen, marked changes in the haemostatic system occurred with both thrombocytopenia and a reduction of clotting factors synthesised by the liver. No evidence of disseminated intravascular coagulation was found. Heat stroke must now be added to the list of jogging hazards.
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PMID:Jogger's heat stroke. 28 29

Normal pregnancy changes include physiologic anemia, leukocytosis, and thrombocytopenia. Cardiac rate and stroke volume increase, vascular resistance falls, and creatinine clearance markedly rises. Thyroid binding globulin and cortisol binding globulin both increase, as do complement proteins and fibrinogen, the latter resulting in a normally high erythrocyte sedimentation rate. Estrogen and progesterone rise dramatically. Low back pain, hip and sacroiliac complaints are common. The cytolytic activity of natural killer (NK) cells is decreased, as are adhesion and chemotaxis of phagocytic cells. Antibody responses are normal. CD4 cells proportionately decrease. A large number of circulating proteins suppression lymphocyte proliferation, and T-cell interleukin-2 (IL-2) production may be suppressed. In studies of pregnant patients, controls must include normal pregnant women.
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PMID:Physiologic adaptations of pregnancy. 128 59

Antibodies directed against phospholipids are highly associated with episodes of venous and arterial thrombosis, which are often recurrent. There seems to be a skewed frequency of cerebral thrombosis when the arterial circulation is affected. Clinical clues that should lead to evaluation for aPL include stroke in a young adult, recurrent thrombosis or miscarriage, and thrombocytopenia. Associated laboratory abnormalities include a biologically false-positive test for syphilis, abnormal antinuclear antibody titers, and a high erythrocyte sedimentation rate. If the activated partial thromboplastin time is prolonged on routine screening and does not correct with mixing studies, a lupus anticoagulant should be suspected. However, more sensitive and specific tests are usually necessary to detect aPL. Many in vitro and more recently in vivo systems strongly suggest that aPL may be directly implicated in the pathogenesis of thrombosis. Optimal management of patients with aPL-associated thrombosis is unknown. The use of aggressive therapeutic management schemes with such agents as warfarin or corticosteroids is sometimes required.
Heart Dis Stroke
PMID:Antiphospholipid antibodies and ischemic stroke. 134 35

Stroke has been reported after high-dose intravenous immunoglobulin (IVIG) therapy, so a study was conducted to find out what effect IVIG has on factors influencing blood flow. The influence of IVIG on plasma viscosity, blood viscosity, and erythrocyte aggregation was examined in vitro and in vivo. For the in-vitro experiments different amounts of IVIG were added to whole blood or plasma from healthy subjects. The in-vivo effects were assessed during five courses of treatment with IVIG (24-54 g/day) in 4 patients with chronic immune thrombocytopenia (ITP). Concentration of IgG infused correlated strongly with viscosity of plasma and whole blood, both in vitro and in vivo, and plasma viscosity increased to beyond the normal range after IVIG treatment. The changes in viscosity that occur after IVIG therapy can impair blood flow, and in patients at risk of cardiovascular and thromboembolic events they might be sufficient to produce myocardial infarction or stroke.
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PMID:Effect of high-dose intravenous immunoglobulin therapy on blood rheology. 134 48

Thrombotic or thromboembolic occlusion of a cerebral artery is the most common pathophysiologic mechanism of acute ischemic stroke. An antithrombotic agent would therefore appear to be an ideal medication for treatment of this condition. Heparin is an effective anticoagulant, but it has poor bioavailability and effects on thrombin and platelets that predispose it to life-threatening complications such as hemorrhage and thrombocytopenia. Low-molecular-weight (LMW) heparins have better bioavailability, a higher anti-Xa:anti-IIa ratio, and less effect on platelets than heparin; yet their heterogeneity has hampered their proper investigation in clinical trials and it has not yet been proven that they exhibit less tendency toward hemorrhage and thrombocytopenia than conventional heparin. The LMW heparinoid, Org 10172, is superior to standard heparin in terms of its bioavailability, anti-Xa:anti-IIa ratio, and lack of effect on platelets. It is less likely than heparin and many LMW heparins to induce thrombocytopenia. Like the various heparins, Org 10172 exhibits dose-dependent hemorrhagic tendencies, yet preliminary studies have found doses that are safe for use in patients with acute ischemic stroke. These studies also suggest that Org 10172 may improve outcome and lessen mortality in this population. A prospective, randomized, double-blind, controlled trial is needed to establish the potential efficacy of Org 10172 in patients who suffer acute or progressing ischemic stroke.
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PMID:Low-molecular-weight heparins and heparinoids and their use in acute or progressing ischemic stroke. 170 55

The antiphospholipid syndrome was diagnosed in 19 of 1078 patients treated between 1987 and 1991. All patients with antiphospholipid syndrome had either anticardiolipin antibody (16/19) or lupus anticoagulant (10/19); three patients had thrombocytopenia, eight patients had a prolonged partial thromboplastin time, and 10 patients had an elevated erythrocyte sedimentation rate. The most common site of involvement was the cerebral circulation (nine patients), manifested by transient ischemic attacks or stroke. Eight patients had upper extremity disease, characterized by symptoms of Raynaud's phenomenon, with angiographic lesions involving the brachial, radial, ulnar, and/or digital arteries. Lower extremity disease occurred in seven patients, with clinical presentations similar to those of atherosclerosis and varying angiographic patterns. In comparison with the population having atherosclerosis, patients with arterial manifestations of antiphospholipid syndrome were more likely to be women (13 of 19 versus 411 of 1078, p less than 0.02), were significantly younger (46.2 years versus 63.6 years, p less than 0.0001), did not smoke (1 of 19 patients versus 700 of 1078, p less than 0.0001), had a higher percentage of upper extremity involvement (8 of 18 versus 13 of 1078, p less than 0.0001), and had a higher incidence of early graft failure (9 of 12 grafts versus 13 of 371 grafts, p less than 0.0001). The syndrome is associated with the repetitive failure of vascular reconstructions and occlusion of native vessels. Antiphospholipid syndrome should therefore be suspected in young, female, nonsmokers with vascular disease, especially those with involvement of the upper extremity, cerebrovascular disease with normal findings on extracranial carotid angiography, and premature graft failure.
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PMID:Vascular disease in the antiphospholipid syndrome: a comparison with the patient population with atherosclerosis. 172 74

We studied two children with recurrent schistocytic hemolytic anemia and thrombocytopenia beginning in the neonatal period. One patient had a stroke during one of the episodes of thrombotic thrombocytopenic purpura. The presence of unusually large von Willebrand factor multimers was demonstrated in both children during clinical and hematologic remissions. Treatment with corticosteroids and intravenous injections of immune globulin was unsuccessful in the one patient who received it. Immediate improvement occurred in both patients after the infusion of fresh-frozen plasma. Symptoms of thrombocytopenia continue to recur at regular intervals in the absence of periodic fresh-frozen plasma infusions. One of these children apparently has chronic relapsing thrombotic thrombocytopenic purpura; the second has a chronic relapsing disorder similar to thrombotic thrombocytopenic purpura.
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PMID:Chronic relapsing thrombotic thrombocytopenic purpura in infants with large von Willebrand factor multimers during remission. 144 76

The functional state of the myocardium was evaluated in 45 patients with acute leucosis. The physical, electrocardiographic and echocardiographic indices were analyzed. It was found that 40% of patients with acute leucosis in the primary-active phase showed a hypokinetic type of circulation. Revealed were prognostically unfavourable factors--leucocytes with marked blastosis in the peripheral blood and myelogram as well as thrombocytopenia that are of significance in the pathogenesis of myocardial involvement. Cardiotoxic doses of rubomycin were found that lead to lesions of the myocardium and formation of chronic cardiopathy. The authors discuss the pathogenetic mechanisms leading to deterioration of the contractile function of the myocardium, reduction of the stroke volume and reorganization of the central hemodynamics according to the hypokinetic type. Echocardiography allowed to reveal early signs of involvement of the myocardium and to institute early treatment effecting different links of pathogenesis and increase the efficiency of acute leucosis therapy.
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PMID:[Changes in the functional status of the myocardium in acute leukemia patients]. 180 47

A case is reported of a 68-year-old woman admitted to the intensive care unit with an adult respiratory distress syndrome (ARDS) due to accidental poisoning with anhydrous phthalic acid. She was given prophylactic low molecular weight heparin (Fraxiparine). During the period of intensive care (mechanical ventilation with positive end-expiratory pressure), the patient experienced a stroke from which she recovered only partially. During pleurectomy for persistent pneumothorax, a lung biopsy was carried out. It confirmed the diagnosis of ARDS and recognized multiple pulmonary arterial thrombi. Because of these two thrombotic phenomena, a coagulation defect was searched for. Platelet aggregation tests were all positive with heparin and two low molecular weight fractions. The patient recovered remarkably once she was no longer given Fraxiparine, being extubated nine days afterwards. Six months after discharge, the patient's platelets still aggregated with heparin. The possible mechanism was a heparin-platelet-endothelium complex. It is noteworthy that, in this case, no thrombocytopaenia was found. It may have been countered by thrombocytosis, induced by cellular factors released during ARDS.
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PMID:[Platelet hyperaggregation induced by low molecular weight heparin in adult respiratory distress syndrome]. 184 67

Having reviewed the literature on the association of aPL antibodies with clinical manifestations, it is clear that this group of autoantibodies are of considerable importance. The presence of aPL antibodies in some but not all individuals confers a risk of a clinical syndrome characterized by recurrent arterial or venous thrombosis, thrombocytopenia, hemolytic anemia, or positive Coombs' test, and in females, recurrent idiopathic fetal loss. In SLE, the risk is approximately 40%, compared with a risk of 15% in the absence of aPL antibodies. However, only one half of persons possessing these antibodies have SLE, and overall the risk is around 30%. In some circumstances, such as in chlorpromazine or infection-associated aPL antibodies, there appears to be no increased risk. At the other end of the spectrum are seen patients whose only clinical manifestations comprise features of this clinical syndrome, and this entity has been designated the primary antiphospholipid syndrome (PAPS). aPL antibodies are also important because they are not uncommon. They have been found frequently in women with idiopathic recurrent fetal loss (30%), in non-autoimmune patients with ischemic heart disease (20%), or venous thrombosis (up to 30%), or stroke (4-47%), and in chronic immune thrombocytopenia (30%). These autoantibodies can be detected using sensitive solid-phase immunoassays employing the CL antigen, or in appropriate coagulation tests to detect LA activity. These assays are simple to perform but require care in selection of the best test and in interpretation of results. Current tests do not distinguish between those persons at risk of the clinical events and those not at risk. Detection of specific isotypes (especially IgG) and antibody level may aid in such a designation. Treatment of aPL antibody-associated syndromes remains a controversial subject. Since thromboses are associated with significant morbidity and potential mortality, there is a good argument for long-term preventive antithrombotic therapy, at least for as long as the antibodies are detectable, in those patients in whom clinical complications have previously occurred. It is not generally recommended that this treatment be offered to individuals in whom aPL antibodies are detected but who have not suffered previous thromboses, since the risk of such events does not appear to be equal within a group of aPL antibody-positive persons. This particularly applies to pregnant women, since live births and uncomplicated pregnancies are observed regularly in the presence of aPL antibodies without specific treatment. A previous history of at least one unexplained, late fetal loss is considered a prerequisite before intervention in subsequent pregnancies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunology and clinical importance of antiphospholipid antibodies. 185 85


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