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

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease in which the predominant autoantibodies are antinuclear antibodies (ANA) reactive with DNA and histones, and antibodies reactive with the non-histone extractable nuclear antigens (ENA), Sm and Ro. Racial differences demonstrable in predisposition to SLE are also evident in the prevalence of autoantibodies, the frequency of anti-Sm and anti-Ro being 2-4 times higher in Asians with SLE than in Caucasians with SLE. Autoantibodies have also played a role in the classification of lupus and the recognition of multisystem autoimmune diseases that fail to meet the classical criteria for the identification of patients with SLE but appear to be variants of lupus. Anti-Ro is a diagnostic marker for subacute cutaneous lupus, anti-(U1)RNP a marker for mixed connective tissue disease, antibodies to phospholipids a marker for the syndrome comprising stroke, fetal wastage, thromboembolism and thrombocytopenia and antibodies to histones a marker for lupus induced by the drugs hydralazine and procainamide. There is still no unaminity on whether these antibodies play an integral role in the disease process or whether they are "epiphenomena". The challenge for research in the 1980s is the understanding of the relationship of these antibodies to the pathogenesis of SLE.
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PMID:Autoantibodies in systemic lupus erythematosus. 304 59

Arterial hypertension is the most important risk factor in all types of stroke. The significance of alcohol in the pathogenesis of stroke is less well defined. Chronic alcoholism leads to an elevation of blood pressure. Thus, the association between alcohol and stroke might be the blood pressure effect of alcohol. However, some studies have shown a significant influence of alcohol on the incidence of stroke--especially of intracerebral haemorrhage and subarachnoid haemorrhage--even after adjustment for blood pressure. Many possible pathomechanisms are discussed. Alcohol inhibits aggregation of thrombocytes, and chronic alcohol abuse may induce thrombocytopenia, which could lead to a haemorrhagic stroke. Alcohol withdrawal leads to rebound thrombocytosis. Acute alcohol ingestion induces a decrease in fibrinolytic activity and an increase in factor VIII activity, which enhances the thrombotic potential. Additionally, alcohol increases plasma osmolarity, erythrocyte aggregability, haematocrit and blood viscosity, and decreases deformability of erythrocytes. The effects of alcohol on cerebral blood flow are still under debate; there is a deterioration in autoregulation of cerebral blood flow anyway. In animal studies alcohol induced dose-dependent vasospasm of the cerebral blood vessels, which could be a possible pathomechanism in ischaemic, as well as in haemorrhagic stroke. Chronic alcoholism is the most common cause of secondary non-ischaemic cardiomyopathy, which can lead to cerebral embolism via rhythm disorders or intracardiac thrombus formation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Does alcohol consumption promote the manifestation of strokes? Considerations on pathophysiology]. 328 8

Twenty-five patients with at least 3 of 1982 ARA criteria of SLE but without the ANA, were compared with 91 patients with 4 or more of the ARA criteria of lupus with positive ANA. The ANA-negative group was characterised by the low incidence of skin involvement, serous effusions and alopecia, and a relatively high incidence of thrombocytopaenia and venous and arterial thrombosis. Three types of antiphospholipid antibodies were looked for: the VDRL, antiprothrombinase and anticardiolipin antibodies by an immuno-enzymatic method. The VDRL was the only antibody which was significantly commoner in the ANA-negative group. Statistical studies showed that the three methods of demonstrating antiphospholipid antibodies detected crossed but not identical specificities. In the ANA-positive group only the antiprothrombinase was associated with a high incidence of venous thrombosis and stroke. In the ANA-negative group, only the anticardiolipin antibodies were associated with a high incidence of arterial or venous thrombosis. Two subgroups may be identified in the group of ANA-negative lupus patients: firstly, those with high anticardiolipin antibody titres with a high incidence of thrombotic and haematological complications, and, secondly, patients with low anticardiolipin antibody levels with a high incidence of cutaneous involvement, serous effusions and Raynaud's phenomenon.
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PMID:[Antiphospholipid antibodies in a series of 25 cases of lupus without antinuclear antibodies. Comparison with a series of 91 lupus patients with antinuclear antibodies]. 349 23

Hemodynamic effects of intravenous administration of amrinone include increases in dP/dt, cardiac output, and stroke work with decreases in left ventricular filling pressure and systemic vascular resistance. Unlike other injectable positive inotropic agents, it does not increase myocardial oxygen consumption, a distinct advantage in patients with coexisting ischemic disease. Amrinone does not have deleterious effects on atrioventricular conduction and appears to have little arrhythmogenic potential. Side effects of intravenous administration are generally minor but include a reversible thrombocytopenia. Additional studies conducted in short-term low-output states are needed to define more completely its role in the treatment of this condition.
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PMID:Clinical effects of intravenous amrinone in patients with congestive heart failure. 351 Jul 75

Symptoms, therapy, and outcome of 49 cases of anaphylactic reaction are presented. Epinephrine (0.5-2.0 mg) did not produce any circulatory improvement but induced severe dysrhythmias and even ventricular fibrillation. Neither epinephrine nor prednisolone (2 g) prevented shock development, neurologic sequelae, or fatal outcome. Rapid infusion of 2000 ml 50% colloid (dextran 70 or starch, m.w. 450,000) with 50% Ringer's lactate, however, reliably restored circulation within 30 min. If elevated, airway resistance dropped in conjunction with colloid administration rather than with any other drug. Impairment of the pulmonary circulation is found to be the initial feature of anaphylaxis, manifested by a rise in pulmonary vascular resistance; then stroke volume and systemic blood pressure fall as left heart filling is reduced. Many findings indicate a high blood viscosity with resulting capillary occlusion: rapid clotting; low levels of factors I, II, V, VIII, and X; low plasma protein, which may be only 50% of its normal value; thrombocytopenia; and aggregation of white blood cells with fibrin in small lung vessels. Blood and plasma vanish from the circulation and appear to be sequestered in the pulmonary capillaries as the initial response to the antigen; later, the whole body is affected. Congestion and pain in the lymph nodes indicate that the lymphatic system may also become involved. On the basis of hemoconcentration, a blood volume deficiency in the range of 30% has been calculated.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Anaphylactic shock]. 360 58

The authors have developed a sensitive immunoenzymatic method for assaying anti-cardiolipin antibodies in the serum of patients with lupus (SLE). These antibodies were present in the serum of 43/108 SLE patients, particularly in those patients with either false syphilis serology (p less than 0.02) or circulating anticoagulant (p less than 0.05). The mean titre of anti-cardiolipin antibodies was higher in the group with positive VDRL (less than 0.03). The anti-cardiolipin antibody titre was independent of the anti-native DNA antibody titre, but there was a correlation with the anti-denatured DNA antibody titre (p less than 0.02). This correlation can be partially explained by the antigenic similarity (phosphodiester bridge) between the two molecules. The preliminary clinical studies have not shown any correlation between the presence of anti-cardiolipin antibodies and the presence of signs such as thrombocytopenia, haemolysis, cerebral vascular accident, venous thrombosis, recurrent abortion. A longitudinal study of certain patients suggests that the anti-cardiolipin antibodies may disappear at the time of thrombotic accidents, which induces fixation of these antibodies to a platelet or vascular target and as a result of corticosteroid therapy.
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PMID:[Antiphospholipid antibodies, thrombosis and lupus disease. Value of the assay of anticardiolipin antibodies by the ELISA technic]. 387 16

Blood coagulation and fibrinolysis were assessed in 55 cases of heat stroke who presented with or without bleeding tendencies during the Makkah pilgrimage of 1983. 17 patients were identified to have evidence of disseminated intravascular coagulation (DIC). Bleeders with DIC had a higher incidence of shock and a higher mortality when compared to non-bleeders. Thrombocytopenia and liver cell damage were not limited to cases with DIC. Coagulation factors and serum enzyme studies suggested non-specific tissue damage as the trigger mechanism for DIC possibly proceeding through the extrinsic system of blood clotting. We conclude that the breakdown of haemostasis in heat stroke is multifactorial: thrombocytopenia, liver cell damage and DIC.
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PMID:Blood coagulation and fibrinolysis in heat stroke. 406 8

To evaluate the potential benefit of MDL 17043, a new inotrope-vasodilator agent, in the short- and long-term management of severe heart failure, its hemodynamic effects were determined after both intravenous (cumulative average dose 3.7 mg/kg) and oral (average 18.4 mg/kg) administration in 38 patients with severe intractable heart failure. After both intravenous and oral therapy, cardiac index increased from a control value of 2.1 +/- 0.4 to 3.6 +/- 0.9 liters/min per m2, p less than 0.001 (intravenous) and from 2.2 +/- 0.5 to 3.4 +/- 0.6 liters/min per m2, p less than 0.001 (oral). Pulmonary capillary wedge pressure decreased from 26 +/- 6 to 14 +/- 7 mm Hg (p less than 0.001) and from 26 +/- 7 to 18 +/- 8 mm Hg (p less than 0.001) after intravenous and oral routes, respectively. Stroke volume index and stroke work index increased, and right atrial and pulmonary arterial pressures and systemic vascular resistance decreased by similar magnitude after both intravenous and oral MDL 17043 (all p less than 0.001). The hemodynamic effects persisted during 4 hours of observation. Thirty-seven patients were discharged while receiving MDL 17043 therapy and were followed up for a mean of 5.6 months (range 0.5 to 13). Thirty-three of the 37 patients had short-term improvement clinically by at least one New York Heart Association functional class. Undesirable effects, including nausea (35%), anorexia (27%), fluid retention (24%) and thrombocytopenia (less than 1%), necessitated discontinuation of therapy in 11 patients (30%) who were receiving multiple drug therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intravenous and oral MDL 17043 (a new inotrope-vasodilator agent) in congestive heart failure: hemodynamic and clinical evaluation in 38 patients. 623 76

Heparin-associated thrombocytopenia is a relatively common complication of heparin therapy occurring in approximately 5% of the patients who receive this drug. The incidence is higher with bovine heparin then with porcine heparin. Onset of heparin-associated thrombocytopenia usually occurs 6 to 12 days after initiation of treatment and by itself has a low morbidity. Heparin-associated thrombocytopenia plus arterial thrombosis can cause major complications including stroke, heart attack, and death. The incidence of heparin-associated thrombocytopenia plus arterial thrombosis is lower than that for heparin-associated thrombocytopenia alone. The diagnosis of heparin-associated thrombocytopenia remains one of exclusion, but testing for the presence of a heparin-dependent platelet-aggregating factor may prove to be useful. Analysis of the time of onset suggests a strategy for prevention. Oral anticoagulants could be started concomitantly with the heparin so that it could be discontinued in several days. This approach may prevent most episodes of heparin-associated thrombocytopenia.
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PMID:Heparin-associated thrombocytopenia. 636 79

Thirty-five patients with the lupus anticoagulant (LA) were followed up between 1975 and 1982. The most prevalent clinical manifestation occurring in these patients was thrombosis. Nineteen patients (54.3%) had a single or recurrent thrombotic episode. Fifteen patients (42.8%) had venous thrombosis, and arterial thrombosis manifested by stroke or transient ischemic attacks occurred in six patients. Bleeding occurred in only five patients, four of whom had severe thrombocytopenia, while no excessive bleeding was noted during 18 operative procedures. Various therapeutic regimens, including corticosteriods, nonsteroidal anti-inflammatory drugs, cytotoxic or immunosuppressive agents, had no effect on the presence of the LA in these patients. Anticoagulants were successful in the treatment and prevention of thrombotic episodes.
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PMID:Thromboembolism in patients with the 'lupus'-type circulating anticoagulant. 636 79


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