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Query: UMLS:C0409974 (lupus)
 22,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Involvement of the central nervous system (CNS) is one of the most important complications of systemic lupus erythematosus (SLE), occurring in 14-75% of SLE patients. Neurological and psychiatric involvement is mainly manifested as cerebrovascular disease, seizures, cognitive impairment, headaches and psychosis. However, diagnosis of brain involvement in SLE (i.e., neuropsychiatric lupus: NPSLE) as well as understanding of pathogenetic mechanisms still remains a difficult challenge. Although a wide range of neurodiagnostic tools have been used in the last decade to assess CNS involvement, no single technique has proven to be definitive or reliable. Since neurometabolic impairment, neurochemistry and perfusion abnormalities in NPSLE may precede anatomic lesions, new functional techniques such as magnetic resonance spectroscopy, diffusion and perfusion weighted imaging, and magnetization transfer imaging may be useful in order to indentify pathologic changes unrevealed by conventional imaging. So these new diagnostic tools could modify diagnostic and therapeutic approaches to this major unsolved problem, also shedding some light on the physiopathology of CNS disease in SLE.
Lupus 2004
PMID:Recent advances and future perspective in neuroimaging in neuropsychiatric systemic lupus erythematosus. 1511 42

Patients with lupus (SLE) experience progressive cognitive loss without evidence of CNS vascular disease or inflammation. SLE patients produce anti-DNA antibodies that crossreact with NMDA receptors and are capable of mediating excitotoxic death. We now show that mice induced by antigen to express these antibodies have no neuronal damage until breakdown of the blood-brain barrier occurs. Following administration of lipopolysaccharide (LPS) to immunized mice, antibodies gain access to the brain. They bind preferentially to hippocampal neurons and cause neuronal death with resulting cognitive dysfunction and altered hippocampal metabolism on magnetic resonance spectroscopy. Memantine, an NMDA receptor antagonist, given prior to LPS administration, prevents neuronal damage. Thus, systemic immune responses can cause cognitive impairment in the absence of an inflammatory cascade, implicating the immune system in yet another arena of human pathobiology. Furthermore, NMDA receptor antagonists prevent antibody-mediated damage and may constitute a new approach to therapy in SLE.
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PMID:Cognition and immunity; antibody impairs memory. 1530 99

Cognitive dysfunction represents one of several neurological and psychiatric complications of Systemic Lupus Erythematosis (SLE). Additional manifestations of nervous system involvement subsumed under the term neuropsychiatric SLE (NPSLE) include cerebrovascular disorder, seizures, psychosis, acute confusional state, anxiety and mood disorders. Neuropsychological investigations have facilitated the identification and description of cognitive impairment in SLE and NPSLE. Salient findings from studies of SLE-related cognitive dysfunction are reviewed with respect to neuroimaging procedures, indices of disease activity, and potential moderator variables. Data on cognitive functioning are also discussed in reference to other disease aspects including fatigue, sleep disturbance, and impact on health-related quality of life (HRQL). To date, neuropsychological functioning has been studied extensively, albeit separately from other commonly reported SLE-related symptoms. Future research may profit from investigating relationships between cognitive impairment, sleep disturbance and fatigue and their collective impact on functional capacity and quality of life.
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PMID:Factors influencing cognitive function, sleep, and quality of life in individuals with systemic lupus erythematosus: a review of the literature. 1559 65

The objective of this study was to examine psychological processes in systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) patients in relation to measures of life stress, coping styles, social support and cognitive ability. Fifty-two SLE patients without overt neuropsychiatric symptoms, 29 RA patients and 27 healthy controls completed measures of depression, mood, disease activity, perceived health, stressful life events, coping, and social support. Variables entered into the multiple regression analysis following principal component analysis were: group, major difficult event, major life threatening event, disengaging coping, emotional coping, social support, and cognitive impairment. Depressive symptoms were associated with SLE group status (P < 0.001), major life-threatening events (P < 0.01), disengage coping (P < 0.001) and emotional coping (P < 0.05). SLE group status (P < 0.05), disengage coping (P < 0.05) and emotional coping (P < 0.05) were associated with current distressed mood. SLE patients without overt, major neuropsychiatric symptoms had greater psychological distress compared to RA and control subjects. Increased depressive symptoms and distressed mood state in SLE patients were related to use of disengaging and emotional coping styles. These findings are limited to SLE patients with no overt neuropsychiatric illness and low disease activity, suggesting the need for future studies with a greater variety of SLE patients. Interventions aimed at improving active coping and minimizing emotional response to stress may lower psychological distress in SLE patients with mild disease.
Lupus 2005
PMID:Major life stress, coping styles, and social support in relation to psychological distress in patients with systemic lupus erythematosus. 1593 36

Systemic lupus erythematosus (SLE) is an autoimmune disease that may involve the central nervous system (CNS) resulting in neuropsychiatric manifestations. The associated psychiatric disorders include depression, psychosis, mood disorders, anxiety, cognitive dysfunction, and delirium/ encephalopathy. Several autoantibodies may play a role in the pathogenesis of psychiatric complications of SLE, particularly antibodies against ribosomal P-proteins (anti-P) and possibly antibodies against endothelial cells (AECA). The reported prevalence of anti-P is highly variable in SLE patients and is dependent on different ethnic backgrounds, sensitivity and specificity of the assays employed for autoantibody detection, and the time at which sera were analysed in relation to the clinical event. Controversial data exist on the association of anti-P with psychiatric manifestations of SLE. These autoantibodies have been suggested to be specific markers of the psychiatric manifestations of SLE, particularly of the psychosis and depression, and the antibody level varied with the clinical activity of the disease. Some studies have confirmed the hypothesis of an association of anti-P antibodies with psychiatric manifestations of neuropsychiatric SLE (NPSLE) while others have disputed this relationship. This review summarizes the recent studies about relationship between anti-P antibodies and psychiatric manifestation of SLE.
Lupus 2005
PMID:Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: myth or reality? 1617 27

We report a case with epileptic seizures, cognitive dysfunction, livedo reticularis, renal microangiopathy, acute myocardial infarction and high titres of anticentromere antibodies (ACA) and IgG/IgM anticardiolipin antibodies. This is a rare association between primary antiphospholipid syndrome and ACA positivity that has not been reported so far in the literature.
Lupus 2005
PMID:A case with epilepsy, cognitive impairment, renal microangiopathy and high titres of anticentromere and anticardiolipin antibodies. 1617 35

This study was designed to determine whether there is a lateralized pattern of cognitive dysfunction in patients with systemic lupus erythematosus (SLE). Fifty right-handed patients with SLE, but no history of cerebrovascular disease participated in the study. Thirty right-handed healthy subjects matched for age and education served as controls. SLE and healthy control subjects underwent a three-hour neuropsychological evaluation designed to measure attention, memory, visual spatial skills, verbal skills reasoning, psychomotor speed, and motor function. A cognitive disability index was created to identify cognitive impairment. Percentile tables based on the performance of all subjects were constructed for 20 component scores. Any subject with five or more component scores below the 25th percentile was designated impaired. Using this criterion, cognitive impairment was identified in 50% of patients with SLE and 20% of healthy controls. Patients with SLE were impaired on measures of psychomotor speed/fluency, verbal speed/fluency and verbal memory. This pattern of performance on neuropsycholgical testing was consistent with left hemisphere brain dysfunction. The observed deficits were not clearly attributable to vascular lesions and suggest immune-mediated effects on specific brain regions in a subgroup of patients with SLE.
Lupus 2005
PMID:Lateralized cognitive dysfunction in patients with systemic lupus erythematosus. 1633 82

A 39-years-old woman was admitted to our hospital with musculoskeletal complaints (myalgias and symmetric arthralgias in proximal interphalangeal, metacarpophalangeal joints of the hands and in knees), systemic symptoms like fever, fatigue, malaise and a six months previous history of a transient ischemic attack. The presence of antibodies to double-stranded deoxyribonucleic-acid (DNA) and antiphospholipid antibodies led to the diagnosis of systemic lupus erythematosus with secondary antiphospholipid syndrome. Cerebral infarction develops significantly more often in patients with lupus and antiphospholipid antibodies, but other clinical syndromes are associated with lupus anticoagulant: cognitive dysfunction, seizures, polyneuropathy, aseptic meningitis, myelopathy.
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PMID:[Systemic lupus erythematosus with neurologic onset and secondary antiphospholipid syndrome. A Case Study]. 1660 81

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.
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PMID:Neuropsychiatric damage in Southern Chinese patients with systemic lupus erythematosus. 1686 47

Neuropsychiatric systemic lupus erythematosus, which often entails cognitive disturbances and memory loss, has become a major complication for lupus patients. Previously, we developed a murine model of neuropsychiatric lupus based on Abs that cross-react with dsDNA and the NMDA receptor (NMDAR). We showed that these murine Abs impair cognition when they access the CNS through a breach in the blood-brain barrier (BBB) triggered by lipopolysaccharide. Because studies show that lupus patients possess anti-NMDAR Abs in their serum and cerebrospinal fluid, we decided to investigate whether these human Abs contribute to cognitive dysfunction. Here, we show that serum with reactivity to DNA and NMDAR extracted from lupus patients elicited cognitive impairment in mice receiving the serum intravenously and given lipopolysaccharide to compromise the BBB integrity. Brain histopathology showed hippocampal neuron damage, and behavioral testing revealed hippocampus-dependent memory impairment. To determine whether anti-NMDAR Abs exist in the brains of systemic lupus erythematosus patients, we eluted IgG from a patient's brain. The IgG bound DNA and NMDAR and caused neuronal apoptosis when injected into mouse brains. We examined four more brains of patients with neuropsychiatric lupus and found that they displayed endogenous IgG colocalizing with anti-NMDAR Abs. Our results indicate that lupus patients have circulating anti-NMDAR Abs capable of causing neuronal damage and memory deficit, if they breach the BBB, and that the Abs exist within patients' brains. Which aspects of neuropsychiatric lupus may be mediated by anti-NMDAR Abs, how often, and in which patients are now important clinical questions.
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PMID:Human lupus autoantibodies against NMDA receptors mediate cognitive impairment. 1717 Jan 37


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