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

The antiphospholipid antibodies are immunoglobulins able to join negative charge phospholipids. The have been related to a great variety of conditions, specially among connective tissue illness although the idiopathic form seems to be the most frequent. Their presence must be ruled out in cases of young patients with stroke, deep veins thrombosis, acute heart attack and woman suffer multiple abortions and foetal death. These antibodies appear to be related to different clinical entities like Sneddon syndrome. Evans syndrome, "chorea gestationis", migraine. The laboratory determinations are based in direct methods (ELISA, RIA, ...) as well as in indirect ones (activated partial thromboplastin time, reptilase time, ...). The appropriate management and treatment may be based upon clinical expression, in case of arterial thrombosis (type II APS), or deep vein thrombosis (Type II) long term anticoagulation is indicated; Association with pentoxifylline in the case of retinal thrombosis (type IIIa), Stroke (type IIIb) cases may require long term anticoagulation as well as aspirin. Type IV cases are better managed with an individualised treatment.
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PMID:[Clinical manifestations associated with antiphospholipid antibodies]. 958 47

The antiphospholipid syndrome (APS, Hughes' syndrome), first described in 1983, is a prothrombotic disease in which neurological events feature prominently. Strokes, transient ischaemic attacks, and headaches (including migraine) are important complications. However, it is clear that other neurological symptoms, including diplopia, memory loss, ataxia, and "multiple sclerosis-like" features are common. A notable feature of Hughes' syndrome is the clinical response to anticoagulants; features such as headache and memory loss often improving dramatically with appropriate warfarin dosage. APS may well become recognised as an important (and potentially treatable) cause of neurological disease.
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PMID:Migraine, memory loss, and "multiple sclerosis ". Neurological features of the antiphospholipid (Hughes') syndrome. 1367 70

Low-angle x-ray diffraction patterns from relaxed insect flight muscle recorded on the BioCAT beamline at the Argonne APS have been modeled to 6.5 nm resolution (R-factor 9.7%, 65 reflections) using the known myosin head atomic coordinates, a hinge between the motor (catalytic) domain and the light chain-binding (neck) region (lever arm), together with a simulated annealing procedure. The best head conformation angles around the hinge gave a head shape that was close to that typical of relaxed M*ADP*Pi heads, a head shape never before demonstrated in intact muscle. The best packing constrained the eight heads per crown within a compact crown shelf projecting at approximately 90 degrees to the filament axis. The two heads of each myosin molecule assume nonequivalent positions, one head projecting outward while the other curves round the thick filament surface to nose against the proximal neck of the projecting head of the neighboring molecule. The projecting heads immediately suggest a possible cross-bridge cycle. The relaxed projecting head, oriented almost as needed for actin attachment, will attach, then release Pi followed by ADP, as the lever arm with a purely axial change in tilt drives approximately 10 nm of actin filament sliding on the way to the nucleotide-free limit of its working stroke. The overall arrangement appears well designed to support precision cycling for the myogenic oscillatory mode of contraction with its enhanced stretch-activation response used in flight by insects equipped with asynchronous fibrillar flight muscles.
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PMID:Myosin head configuration in relaxed insect flight muscle: x-ray modeled resting cross-bridges in a pre-powerstroke state are poised for actin binding. 1288 53

The objective of this study was to compare the clinical findings, laboratory data, functional outcome and chronic damage in male patients with primary antiphospholipid syndrome (PAPS) and systemic lupus erythematosus (SLE). We studied 29 male patients with PAPS and 44 with SLE. Clinical findings, laboratory data, lupus damage index (SLICC/ACR DI), and functional outcome in PAPS, were analysed in each group. The mean age at diagnosis was 29.8 +/- 10.4 years in patients with PAPS and 26 +/- 10.1 years in SLE patients. The duration of disease was 4.5 +/- 2.6 versus 5.2 +/- 3.8 years in patients with PAPS and SLE, respectively (P = NS). In patients with PAPS the most frequent clinical manifestations were venous thrombosis, thrombocytopenia, and pulmonary thromboembolism. Patients with SLE had joint, skin and renal involvement more frequently than those with PAPS (P = 0.0001). All PAPS patients had anticardiolipin antibodies (aCL), and 14 patients (48%) had lupus anticoagulant (LA). All SLE patients had antinuclear antibodies (ANAs). Anti-dsDNA antibodies were positive in 39% of SLE patients. Five patients died: one with 'catastrophic' APS and four with SLE. SLICC/ACR-DI score in SLE patients was 1.9 (SD = 1). In PAPS patients poor functional outcome was due to myocardial infarction, pulmonary thromboembolism, stroke and mesenteric thrombosis. Lupus nephritis was the principal organ damage in SLE. In conclusion, in male patients with PAPS and SLE, the clinical manifestations were significantly different. Arterial thrombosis was the major cause of functional impairment and permanent organ damage in PAPS. Renal involvement was the major cause of chronic damage in SLE.
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PMID:Clinical spectrum of males with primary antiphospholipid syndrome and systemic lupus erythematosus: a comparative study of 73 patients. 1487 Sep 12

Large increases in mortality related to premature atherosclerosis with coronary artery disease and stroke have been reported during the last few years in patients with systemic lupus erythematosus (SLE). Studies found relative risks of 5 to 7 for myocardial infarction in SLE patients. The traditional risk factors fail to fully account for accelerated atherosclerosis in SLE and APS, in addition prolonged glucocorticoid therapy and long duration of SLE seem to be of importance. The disease SLE per se is an independent risk factor. The current pathogenic hypothesis for atherosclerosis involves an inflammatory response, autoantibodies, immune complexes (containing antibodies to phospholipids, to oxidized LDLs, and to endothelial cells), CD40/CD40 ligand interactions, and bacterial or viral infections responsible for an immune response. The determination of classic and new risk factors, together with specific autoantibody titers and the use of Doppler carotid ultrasound, are useful methods to detect early atherosclerosis. Therapeutic strategies, including early risk factor intervention and effective control of inflammation, are essential to reduce morbidity and mortality and should be incorporated into the management of connective tissue disease with the goal of protecting patients against atherosclerosis.
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PMID:[Accelerated atherosclerosis in rheumatic systemic diseases as an example of systemic lupus erythematosus--what is the consequence?]. 1590 83

Antiphospholipid syndrome is characterized by arterial or venous thrombosis, and the presence of antiphospholipid antibodies (aPL). APL are considered to be a cause of an acquired hypercoagulable state leading to stroke and transient ischemic attack (TIA). We examined the causes in 50 young patients with ischemic stroke. The most prevalent cause was atherosclerosis and the incidence of APS was 12.5%. APL comprise a heterogeneous group of autoantibodies, such as beta2-glycoprotein I dependent anticardiolipin antibody (beta2-GPIaCL), lupus anticoagulant (LA), and other antiphospholid-protein antibodies. We examined the incidence and the pathogenic role of antiphospholipid protein antibodies. The subjects comprised 250 patients (155 male, 95 females) with ischemic stroke, aged 26 to 92 years (mean 72 years). We measured beta2-GPI aCL, IgG aCL, LA, phosphatidyserine dependent antiprothrtombin antibody (PS-PT), antiphosphatidyl-serine antibody (PS), antiphosphatidyl-inositol antibody (PI) in each patient. The incidence of beta2-GPI aCL, IgG aCL, LA, phosphatidyserine, PS-PT, PS, and PI was 2.8%, 12%, 9.2%, 7.2%, 9.6%, and 8.8%, respectively. The incidence of young stroke patients under 50 years was 5.2%. Among 13 young stroke patients, 5 had SLE. Among 23 patients with LA., 18 (78%) patients had PS-PT. Anti-PS-PT antibody is closely related to LA. Antinuclear antibody was detected in 79% of the patients with aPS and/or aPI. We compared the carotid ultrasonographic findings in positive aPI or aPS patients with those in negative ones. Increased IMT, plaque score and carotid stenosis were more common in aPI and aPS-positive patients than in negative ones Three of 5 patients who showed positive beta2-GPI, aCL and LA, simulataneously, had sysyemic lupus erythematosus as an immulological background. Two of 3 patients with PI and/or PS and beta2-GPI and/or LA were patients with SLE. Antiphospholipid antibody was considered to be a risk factor of stroke, especially in SLE and/or young female patients. The incidence of lupus anticoagulant is more common than beta2-GPI aCL in ischemic stroke. In SLE patients with stroke, multi-antiphospholipid-protein antibodies was inclined to be present. LA is closely related to ant-PS-PT and aPI and aPS are associated with anti-nuclear antibody and precipitation of atherosclerosis.
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PMID:[Antiphospholipid syndrome and stroke]. 1644 44

We have used a high-resolution small angle X-ray scattering system, together with a high-performance CCD camera, on the BioCAT beamline at the APS synchrotron radiation facility at the Argonne National Laboratory, to study X-ray interference effects in the meridional reflections generated by the arrays of myosin crossbridges in contracting muscle. These give information about axial movements of the myosin heads during contraction with sub-nanometer resolution. Using whole intact muscle preparations (frog sartorius) we have been able to record the detailed behavior of M3 (the first order meridional reflection from the myosin crossbridges, at 14.56 nm) at each of a number of quick releases of increasing magnitude, on the same specimen, and at the same time make similar measurements on higher order myosin meridional reflections, particularly M6. The latter provides information about the dispersion of lever arm angles of the actin-attached myosin heads. The observations show that in isometric contraction the lever arm angles are dispersed through +/- 20-25 degrees on either side of a mean orientation that is about 60 degrees away from their orientation at the end of the working stroke: and that they move towards that orientation in synchronized fashion, with constant dispersion, during quick releases. The relationship between the shift in the interference fringes (which measures the shift of the myosin heads scattering mass towards the center of the sarcomere, and the changes in the total intensity of the reflections, which measures the changes in the axial profile of the heads, is consistent with the tilting lever arm mechanism of muscle contraction. Significant fixed contributions to the meridional reflections come from unattached myosin heads and from backbone components of the myosin filaments, and the interaction of these with the contributions from actin-attached myosin heads determines the behavior of these reflections.
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PMID:X-ray interference studies of crossbridge action in muscle contraction: evidence from quick releases. 1700 71

In patients with premature atherothrombotic disease, the antiphospholipid syndrome (APS, defined as any thrombosis plus the repeated presence ofantiphospholipid antibodies) is sometimes looked for, as observational studies have suggested a link between APS and premature atherothrombosis. However, recent reviews that evaluated the prognostic value of antiphospholipid antibodies have concluded that the prognostic significance ofAPS for recurrent thrombotic disease is, at best, unclear and that its presence has no therapeutic consequences. A study that compared high- versus standard-dosage warfarin in patients with APS found no additional benefit from high-dosage warfarin. A study in patients with a recent ischaemic stroke found no additional benefit from warfarin (standard dosage) versus aspirin in patients with or without antiphospholipid antibodies. Therefore, on the basis of the evidence at hand, screening for APS in patients with premature atherosclerosis is not considered to be useful.
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PMID:[Premature cardiovascular disease: no indication for the determination of antiphospholipid antibodies or lupus anticoagulant as a possible risk factor]. 1747 73

The objective of this study was to analyse whether primary antiphospholipid syndrome (PAPS) may precede and modify the characteristics of systemic lupus erythematosus (SLE). Out of the total 362 SLE patients in our service, 223 patients had antiphospholipid antibodies (aPL), of whom 110 met the criteria of antiphospholipid syndrome. In 26 cases (7.2%) PAPS appeared 5.5 years before the onset of lupus (PAPS+SLE Group). Their clinical findings were compared to lupus patients without (SLE only Group, n = 26) and with secondary APS (SLE+SAPS Group, n = 26). The prevalence of deep venous thrombosis, stroke/TIA, recurrent fetal loss, coronary heart disease and myocardial infarction was significantly higher in PAPS+SLE Group as compared to SLE only Group. The difference in prevalence of fetal loss (P = 0.014) between PAPS+SLE and SLE+SAPS Groups was also recorded. On comparison to PAPS+SLE Group, patients without APS (SLE only Group) were younger at onset of lupus, with more frequent flares and a higher prevalence of WHO type III/IV nephritis (P = 0.007), requiring higher doses of cyclophosphamide and corticosteroids. Lupus started in the form of PAPS in 7.2% of our SLE patients, who presented with more thrombotic and less inflammatory complications than in SLE patients without a prior or with a following secondary APS. Considering the long latency between the two diseases, PAPS may be a forerunner of lupus, but it may also coexist with SLE as an independent autoimmune disorder.
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PMID:Primary antiphospholipid syndrome as the forerunner of systemic lupus erythematosus. 1757 33

Perinatal thrombosis in infants born to mothers with antiphospholipid antibodies (aPL) is a rare event, but with risk of death or severe sequelae. We analysed 16 infants with such perinatal thrombosis reported in the literature in the last 20 years. Thromboses were arterial (13/16), mostly strokes (8/16). Hydrops fetalis with left renal vein thrombosis was associated to a lupus anticoagulant (LA) present only in the child. Risk factors additional to aPL: either prenatal (preeclampsia and/or intra-uterine growth retardation) or perinatal (asphyxia, sepsis, arterial or venous catheter and congenital thrombophilia) were present (one to four of them) in nine out of the 14 evaluable babies. aPL were the only risk factor found in five full term babies who suffered from stroke in four cases and from renal thrombosis in another. Eleven of these infants with aPL in their serum presented a neonatal APS with the same antibody (LA or aCL IgG) found in neonates and their mothers, while the other infants had thrombosis with aPL only in their mother's blood. aCL IgM was only found in one neonate who suffered from sepsis. Thrombosis treatments were diverse. This analysis suggests that women with aPL should be investigated for other thrombophilic risk factors and that aPL should be detected systematically at birth in the offspring of mothers with APS.
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PMID:Infant perinatal thrombosis and antiphospholipid antibodies: a review. 1771


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