Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The antiphospholipid syndrome (APS) is defined by the presence of antiphospholipid antibodies (aPL), demonstrated by ELISAs for antibodies against phospholipids and associated phospholipid-binding cofactor proteins and/or a circulating lupus anticoagulant (LA) together with diverse systemic clinical manifestations such as thrombosis, and recurrent spontaneous abortions. According to the criteria set out in Sydney the only neurological manifestations that can be suitable as APS classification criteria are ischemic events (stroke and transient ischemic attacks). However, other neurological manifestations, including seizures in particular, have been repeatedly reported in APS patients. The present review will summarize recent research on the association of aPL, as well as other autoantibodies, with seizure disorders, with or without concomitant SLE.
Lupus 2006
PMID:Epilepsy as part of systemic lupus erythematosus and systemic antiphospholipid syndrome (Hughes syndrome). 1668 57

Autologous hematopoietic stem cell transplantation (ASCT) has the potential to eliminate autoreactive lymphocytes and may represent a therapeutic option for patients with refractory autoimmune diseases. We describe a 19-year old woman with neuropsychiatric systemic lupus erythematodes (NPSLE) presenting with acute longitudinal myelitis and aseptic meningitis. Despite therapy with methylprednisolone and cyclophosphamide (CYC), recurrence of longitudinal myelitis and a disabling stroke-like relapse occurred. Hematopoietic stem cells were mobilized by CYC at 2 g/m2 and G-CSF. The patient was conditioned by CYC at 200 mg/kg and anti-thymocyte globulin and 3.6 x 10(6) CD34+ cells/kg were infused. Hematopoietic regeneration was observed on day 12 after ASCT. Currently, 18 months after ASCT, the patient is in clinical remission with no evidence for residual serological or neuroradiological activity of SLE. Although a longer follow-up will be needed to reliably assess the efficacy of ASCT in this patient, the present case demonstrates that ASCT may represent a therapeutic option for patients with severe NPSLE.
Lupus 2006
PMID:Autologous blood stem cell transplantation in refractory systemic lupus erythematodes with recurrent longitudinal myelitis and cerebral infarction. 1668 65

We conducted the current study to determine the prevalence and predictors of neuropsychiatric damage in a cohort of Chinese patients with systemic lupus erythematosus (SLE). Patients were those newly diagnosed as having SLE between 1990 and 2004 in our unit. Demographic data, presenting and cumulative clinical features, disease activity score at diagnosis, and serial damage scores were obtained. Neuropsychiatric (NP) manifestations were classified according to the American College of Rheumatology (ACR) nomenclature. NP damage was evaluated by the NP domain of the Systemic Lupus International Collaborating Clinics/American College of Rheumatology (SLICC/ACR) Damage Index. Factors predictive of NP damage were studied by regression models. We studied 282 patients who fulfilled > or =4 of the ACR criteria for SLE. The mean age of SLE onset was 31.8 +/- 14 years. After a mean follow-up of 6.7 years, 65 patients (23%) had at least 1 NP manifestation and 50 (18%) developed NP damage (SLICC/ACR Damage Index > or = 1). Cerebrovascular accident was the most common cause of NP damage (35%), followed by seizure (20%), psychosis (12%), cranial/peripheral neuropathy (12%), cognitive dysfunction (12%), and myelopathy (9%). In a multiple regression model, disease activity at diagnosis, cumulative non-NP damage, presence of antiphospholipid antibodies, and ever use of pulse methylprednisolone were independent factors associated with NP damage. New NP damage after the first year of diagnosis was predicted by longer disease duration and the use of pulse methylprednisolone in another multivariate model. Neither early nor cumulative NP damage predicted mortality. NP damage is prevalent in Chinese patients with SLE and is independently associated with more active disease at diagnosis, antiphospholipid antibodies and the use of pulse methylprednisolone therapy. Primary prevention for cerebrovascular disease in high-risk patients may reduce NP damage.
 ...
PMID:Neuropsychiatric damage in Southern Chinese patients with systemic lupus erythematosus. 1686 47

The objective of this study was to investigate the manifestations, treatment and outcome of neuropsychiatric (NP) involvement in pediatric systemic lupus erythematosus (SLE) patients. The charts of 185 pediatric patients with SLE diagnosed between 1985 and 2005 in a tertiary referral hospital were retrospectively reviewed. NPSLE were defined using the American College of Rheumatology NPSLE case definitions. NPSLE developed in 34.6% (64/185) of the patients. The mean onset age was 15.2 years. Fourteen patients (21.9%) had NP manifestations on initial diagnosis of SLE. The median duration from the onset of SLE to NP manifestation was 11 months. The most frequent NP manifestations were seizure disorder (84.4%), ischemic stroke (28.1%) and psychosis (21.9%). However, the prevalence of manifestations of NPSLE might be underestimated by the retrospective design of our study. Higher mean C3/C4 levels, less percentage of anti-dsDNA antibodies elevation and higher percentage of elevated anticardiolipin antibodies were observed in NPSLE events than in non-NPSLE events (P < 0.05). The mortality rate of NPSLE patients decreased from 52.2% in 1985-1994 cohort to 27.8% in 1995-2005 cohort. In the past 10 years, the leading cause of death in NPSLE patients was NPSLE itself. NPSLE is common in pediatric SLE patients. It has diverse manifestations and a high mortality.
Lupus 2006
PMID:Neuropsychiatric manifestations in pediatric systemic lupus erythematosus: a 20-year study. 1712 May 91

The antiphospholipid syndrome (APS) is now recognized as a multi-system disease, the clinical expression of which may include various target-organs involvements. Despite the reported heterogeneity in clinical presentation of APS, the interrelations between various manifestations of the disease has not yet been studied. We evaluated the principle associations between a variety of clinical manifestations in APS patients, applying factor analysis. Two-hundred and forty-six APS patients were studied. The following disease manifestations were used for the factor analysis: recurrent fetal loss, intrauterine growth restriction (IUGR), venous and arterial thrombosis, cardiac valves thickening/dysfunction, valvular vegetations, stroke, epilepsy, migraine, arthritis, livedo reticularis, thrombocytopenia, leukopenia and autoimmune hemolytic anemia (AIHA). The results were further analysed in relation to sex and to primary APS versus APS associated with SLE. Five factors were derived, which accounted for 59.7% of the variance of the matrix. Factor 1 (which explained 18.5% of variance of the original matrix) represented the association between cardiac valves abnormalities, livedo reticularis and AIHA. Factor 2 (13.8% of variance) represented association between arthritis, thrombocytopenia and leukopenia. Factor 3 (10.3% of variance) represented an association between recurrent fetal loss and IUGR. Factor 4 (9.3% of variance) represented inverse correlation between arterial and venous thrombosis. Factor 5 (7.8% of variance) represented an association between epilepsy and migraine. Application of factor analysis revealed specific clusters of cardiac, cutaneous, hematological and neurological manifestations. Our result also point to a possible divergence of arterial and venous thrombotic tendency. Awareness of these patterns might give us a better understanding of the disease.
Lupus 2007
PMID:Clusters of disease manifestations in patients with antiphospholipid syndrome demonstrated by factor analysis. 1743 2

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.
Lupus 2007
PMID:Primary antiphospholipid syndrome as the forerunner of systemic lupus erythematosus. 1757 33

A variety of neuropsychiatric findings may complicate systemic lupus erythematosus (SLE) and pose diagnostic and therapeutic dilemmas. We describe the clinical and radiographic features of posterior reversible encephalopathy syndrome (PRES) and distinguish PRES from other conditions seen in SLE. Patient charts and magnetic resonance imaging (MRI) findings of four patients with SLE on immunosuppressive therapy with acute or subacute neurologic changes initially suggesting cerebritis or stroke were reviewed. The English language literature was reviewed using the Medline databases from 1996-2006 for other reports of PRES with SLE. Literature review yielded 26 other SLE cases reported with PRES. SLE patients with PRES were more commonly on immunosuppressive drugs, had episodes of relative hypertension, and had renal involvement. Characteristic findings are seen on MRI, which differentiate PRES from other CNS complications of SLE. Clinical and radiographic resolution of abnormalities within 1-4 weeks is typically seen. PRES has been increasingly recognized. Reversible changes are found on brain MRI accompanied by sometimes dramatic signs and symptoms. The therapeutic implications for separating PRES from stroke or cerebritis are important. We propose that PRES should be considered in the differential diagnosis in SLE patients with new-onset neurologic signs and symptoms.
Lupus 2007
PMID:Posterior reversible encephalopathy syndrome: another manifestation of CNS SLE? 1766 35

Longitudinal myelitis is an uncommon complication of systemic lupus erythematosus (SLE). We describe an unusual case of longitudinal myelitis and ischemic stroke in the presence of homozygous prothrombin G20210A, heterozygous MTHFR 677T mutations and the absence of antiphospholipid antibodies in a young woman with SLE.
Lupus 2007
PMID:Longitudinal myelitis in patient with systemic lupus erythematosus, homozygous prothrombin G20210A and heterozygous MTHFR 677T. 1767 Aug 51

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.
Lupus 2007
PMID:Infant perinatal thrombosis and antiphospholipid antibodies: a review. 1771

The objective of this study was to determine risk factors predicting seizures and damage caused by seizures in a multi-ethnic systemic lupus erythematosus cohort (PROFILE) that includes systemic lupus erythematosus patients (n = 1295) from five different US institutions. Only patients with seizures after systemic lupus erythematosus diagnosis (incident) were included in the analyses of clinical seizures (80/1295, 6.2%), but all patients (prevalent and incident) were included in the analyses of damage caused by seizures (51/1295, 3.9%). We examined socioeconomic-demographic, clinical, and genetic variables predictive of clinical seizures and damage from seizures by Cox proportional hazard ratios (HR) and 95% confidence intervals (CI). Independent predictors of a shorter time to the occurrence of clinical seizures were younger age (HR = 1.0; 95% CI 0.9-1.0), having Hispanic-Texan ethnicity (HR = 2.7; 95% CI 1.3-5.7) or African-American ethnicity (HR = 1.8; 95% CI 1.0-3.1), and the previous occurrence of a cerebrovascular accident (HR = 3.3; 95% CI 1.6-7.1) or an episode of psychosis (HR = 2.4; 95% CI 1.1-5.0), whereas the previous occurrence of photosensitivity (HR = 0.5; 95% CI 0.3-0.9) was the only independent predictor of a longer time to the occurrence of clinical seizures. Independent predictors of a shorter time to the occurrence of damage caused by seizures were younger age (HR = 1.0; 95% CI 0.9-1.0), male gender (HR = 2.4; 95% CI 1.1-5.4), and the occurrence of a previous cerebrovascular accident (HR = 2.7; 95% CI 1.0-7.0) or an episode of psychosis (HR = 4.7; 95% CI 2.3-9.9). No allele from the candidate genes examined (HLA-DRB1, HLA-DQB1, FCGR2A, FCGR3A, or FCG3B) predicted clinical seizures or damage caused by seizures.
Lupus 2008 Mar
PMID:Time to seizure occurrence and damage in PROFILE, a multi-ethnic systemic lupus erythematosus cohort. 1837 57


<< Previous 1 2 3 4 5 6 7 8 9 Next >>