Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0024141 (systemic lupus erythematosus)
 44,322 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 18-year-old woman with systemic lupus erythematosus developed neuropsychiatric disorders, including aseptic meningoencephalitis, organic brain syndrome and seizure. A series of computed axial tomography scans revealed the progression of marked atrophy of the right cerebral hemisphere for a period of 3 years without occlusion or stenosis of large vessels on cerebral angiography. I-123 IMP single photon emission computed tomography disclosed a markedly decreased uptake of I-123 IMP in the right cerebral hemisphere, and also in the left cerebellar hemisphere (crossed cerebellar diaschisis), which disappeared within 2 years.
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PMID:Cerebral hemiatrophy in systemic lupus erythematosus: report of a case. 227 27

Quinidine, procainamide and disopyramide are antiarrhythmic drugs in the class 1A category. These drugs have a low toxic to therapeutic ratio, and their use is associated with a number of serious adverse effects during long term therapy and life-threatening sequelae following acute overdose. Class 1A agents inhibit the fast inward sodium current and decrease the maximum rate of rise and amplitude of the cardiac action potential. Prolonged Q-T interval and, to a lesser extent, QRS duration may be observed at therapeutic concentrations of quinidine. With increasing plasma concentrations, progressive depression of automaticity and conduction velocity occur. 'Quinidine syncope' (a transient loss of consciousness due to paroxysmal ventricular tachycardia, frequently of the torsade de pointes type) occurs with therapeutic dosing, often in the first few days of therapy. Extracardiac adverse effects of quinidine include potentially intolerable gastrointestinal effects and hypersensitivity reactions such as fever, rash, blood dyscrasias and hepatitis. Procainamide produces electrophysiological changes that are similar to those of quinidine, although Q-T interval prolongation with the former is less pronounced at therapeutic concentrations. Hypersensitivity reactions including fever, rash and (more seriously) agranulocytosis are associated with procainamide, and a frequent adverse effect requiring cessation of therapy is the development of systemic lupus erythematosus. Of the 3 drugs, disopyramide has the most pronounced negative inotropic effects, which are especially significant in patients with pre-existing left ventricular dysfunction. As with quinidine, unexpected 'disopyramide syncope' at therapeutic concentrations has been described. Anticholinergic side effects are common with this drug and may require cessation of therapy. Disopyramide therapy may unpredictably induce severe hypoglycaemia. Severe intoxication with the class 1A agents may result from acute accidental or intentional overdose, or from accumulation of the drugs during long term therapy. Acute overdose can result in severe disturbances of cardiac conduction and hypotension, frequently accompanied by central nervous system toxicity. Decreased renal function can cause significant accumulation of procainamide and its active metabolite acecainide (N-acetyl-procainamide), resulting in severe intoxication. Mild to moderate renal dysfunction is less likely to lead to quinidine or disopyramide intoxication, unless renal failure is severe or concurrent hepatic dysfunction is present. Management of acute intoxication with class 1A drugs includes gut decontamination with provision of respiratory support and treatment of seizures as needed. Hypertonic sodium bicarbonate, by antagonising the inhibitory effect of quinidine on sodium conductance, may reverse many or all manifestations of cardiovascular toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Poisoning due to class IA antiarrhythmic drugs. Quinidine, procainamide and disopyramide. 228 95

The marked gender influence on the occurrence of systemic lupus erythematosus (SLE) indicates that genetic and hormonal factors may be important in the etiology of this illness. However, few differences in clinical manifestations between males and females have been reported. To further investigate gender differences in SLE, the prevalence of 23 clinical manifestations of SLE were compared in a cohort of 62 men and 299 women. After adjusting for differences in age, race, and duration of followup, men were found to more commonly have seizures (odds ratio = 1.65; 95% confidence interval = 1.09, 2.49), and showed a trend to progress to renal failure more often (odds ratio = 1.40; 95% confidence interval = 0.96, 2.03) than women. Gender differences were not evident for the remaining 21 clinical features. The clinical similarity between men and women with SLE represents a circumstance in which the use of clinically defined patient subsets does not appear to facilitate the investigation of potential pathogenetic or etiologic factors.
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PMID:Systemic lupus erythematosus in men: a multivariate analysis of gender differences in clinical manifestations. 231 21

The influence of age on the prevalence of individual clinical manifestations of systemic lupus erythematosus (SLE) has not been adequately distinguished from racial or gender influences. Therefore, we examined variations in the clinical manifestations of SLE with age in a group of 361 patients. Multivariate regression techniques, including logistic regression and analysis of covariance, were used to identify clinical features associated with age, while controlling for important confounding factors, including race, gender, duration of followup, and treatment effects. Lymphopenia was found more frequently with increasing age, while malar rash, seizures, false-positive VDRL, thrombocytopenia (in whites), proteinuria (0.5-3.5 g/day), elevated antidouble stranded DNA antibodies, and hypocomplementemia were found less frequently. No age relationship was found for the prevalence of 16 of 24 clinical features examined, including the important disease manifestations of arthritis, serositis, psychosis, nephrotic-range proteinuria, renal failure, autoimmune hemolytic anemia, and leukopenia. The use of regression analysis allows the recognition of similarities and differences in cumulative clinical features of SLE due to age in isolation from the effects of other demographic factors.
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PMID:Age associated clinical manifestations of systemic lupus erythematosus: a multivariate regression analysis. 234 26

Systemic lupus erythematosus (SLE) can produce profound disturbances in the central nervous system, characterized by encephalopathy, focal neurologic deficits, cerebral infarction, psychosis, and seizures. We used 31P nuclear magnetic resonance (NMR) spectroscopy to determine the in vivo levels of high-energy phosphates in the central nervous system of 10 patients with SLE and 10 age-matched normal controls. 31P NMR spectroscopy was performed on a 1.5-Tesla unit equipped with a dual-tuned 1H-31P surface coil and a software-directed DRESS (depth resolved surface coil spectroscopy) pulse sequence. This procedure detected ADP, ATP, sugar phosphates, phosphocreatine (PCr), inorganic phosphate, phosphomonoesters, and phosphodiesters in the brain tissue of all study subjects. Levels of ATP in the deep white matter of 10 SLE patients were significantly decreased compared with the levels in 10 normal controls, as quantitated by the ratio of ATP:ATP + ADP (mean +/- SD 0.81 +/- 0.11 versus 0.91 +/- 0.05; P less than 0.02). In a subgroup of 4 patients, PCr levels were decreased to a greater extent than the ATP levels. NMR spectroscopic alterations were not related to obvious anatomic lesions, as determined by standard cranial proton magnetic resonance imaging. In 4 SLE patients with markedly abnormal 31P NMR spectra, treatment with prednisone (80 mg/day) normalized the levels of ATP and PCr. Restoration of a normal 31P profile was accompanied by an obvious improvement in the patients' mental status and clinical symptoms. 31P NMR spectroscopy is a powerful new technique for monitoring high-energy phosphate metabolism, and may be particularly useful for characterizing central nervous system disease in patients with neuropsychiatric SLE.
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PMID:Depletion of high-energy phosphates in the central nervous system of patients with systemic lupus erythematosus, as determined by phosphorus-31 nuclear magnetic resonance spectroscopy. 236 38

We describe six cases of cerebral venous thrombosis in patients with systemic lupus erythematosus. In one patient, cerebral venous thrombosis was the initial manifestation of lupus; in the five others, it occurred 1-33 years after the diagnosis of lupus. The main clinical features of cerebral venous thrombosis were persistent headache in all six patients, focal symptoms in four, and seizures in three; papilledema was present in only one patient. Cerebral venous thrombosis was diagnosed based on angiography or magnetic resonance imaging. Both the transverse (in five patients) and the superior sagittal (in three) sinuses were involved. Extracranial arterial and/or venous thrombosis were present in three patients, abortion in two, thrombocytopenia in four, and lupus anticoagulant in three. The neurologic symptoms resolved rapidly in five patients treated with steroids and heparin. Cerebral venous thrombosis should be suspected in patients with lupus who complain of persistent headache, especially in the presence of neurologic symptoms.
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PMID:Cerebral venous thrombosis in systemic lupus erythematosus. 200 96

A clinical history typical of multisclerosis began in a 20-year old man with transient, then permanent manifestations involving the optic tract and the pyramidal, extrapyramidal and cerebellar systems. The patient died at the age of 62, at the end-stage of a complex clinical situation which included paraplegia, bilateral cerebellar syndrome, optic nerve atrophy, epileptic seizures and dementia. When the patient was 54 years old, laboratory findings suggestive of systemic lupus erythematosus (SLE) were discovered, namely: antinuclear, native anti-DNA, anti-Sm antibodies, circulating anticoagulant, cryoglobulinaemia and low complement level. These abnormalities persisted up to the patient's death, 8 years later, without any non-neurological sign of SLE. Post-mortem examination showed lesions of focal demyelination characteristic of multiple sclerosis, but no evidence of cerebral or extracerebral SLE. This case raises the problem of borderlines or associations between systemic lupus erythematosus and multiple sclerosis. In our case, as in other cases of "lupoid sclerosis" reported in the literature, there was a frank and isolated elevation of serum IgM levels.
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PMID:[Multiple sclerosis associated with biological symptoms of systemic lupus erythematosus. A case with anatomical study]. 248 95

Lupus anticoagulant was found in the plasma of 4 patients who presented with late-onset epileptic seizures. Three of the patients had clinical or electroencephalographic evidence of focality. No significant cerebral pathological findings were detected by the computed tomogram except for an old infarction in one case. None of the patients fulfilled the diagnostic criteria for systemic lupus erythematosus. The relationship between late-onset seizures and the presence of lupus anticoagulant is discussed. The possible etiology of an ischemic episode due to hypercoagulability, expressed uniquely by seizures, is suggested.
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PMID:Lupus anticoagulant and late onset seizures. 210 23

The Authors submitted 53 randomly selected patients affected by systemic lupus erythematosus (SLE) to neurologic evaluation to investigate the prevalence of neurologic manifestations, establish relationships to clinical and epidemiological findings and antinuclear antibodies and/or lupus anticoagulant (LAC), as well as to assess the usefulness of electroencephalogram (EEG), saccadic eye movements (SEM) analysis, brain computerized tomography (CT). Twenty-two patients (41.5%) had nervous system involvement on anamnestic and/or clinical examination: there were seizures in 5 patients, headache in 3, involuntary movements in 3, psychosis in 2 and cerebrovascular disorders in 9. The patients were subdivided into 2 groups, with neuro-SLE and without neuro-SLE, according to clinical and/or anamnestic evidence of nervous system involvement. There were no differences between the two groups of patients regarding disease duration, disease activity, presence of antinuclear antibodies and/or LAC. EEG and/or SEM and/or brain CT abnormalities were found in 38 cases, 18 of which had no clinical evidence of neuro-SLE. Instrumental evaluation can thus document subtle nervous dysfunction and offers the possibility of classification into: a) non-neuro-SLE; b) subclinical neuro-SLE; c) overt neuro-SLE.
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PMID:[Neurological manifestations of systemic lupus erythematosus. Study of 53 cases]. 251 98

Magnetic resonance (MR) imaging and computed tomography (CT) are useful for the evaluation of central nervous system (CNS) lupus. This report describes the use of cranial MR and CT in 21 patients with systemic lupus erythematosus (SLE) with acute neuropsychiatric symptoms manifested by headache, seizures, focal neurological deficits, psychosis, or organic brain syndrome. Computed tomography was found to be insensitive and detected only diffuse atrophy (two cases), cerebral infarct (one case), and intracerebral haemorrhage (one case) in the 21 patients. Cranial MR images obtained with a General Electric 1.5 tesla Signa unit detected labile and fixed areas of increased proton intensity interpreted as focal oedema (eight cases), infarct (10 cases), haemorrhage (one), atrophy (seven), and acute sinusitis (two). Focal oedema was characterised by labile, high intensity lesions in the gray or white matter of the cerebellum, cerebrum, or brain stem, which completely resolved after aggressive corticosteroid treatment. Most high intensity reversible or fixed lesions evident on MR were not apparent on cranial CT images. In several patients sequential MR images were valuable in monitoring the efforts of treatment. Although histological confirmation of the high intensity brain lesions apparent on MR is desirable, prior necropsy studies suggest that pathological confirmation may be difficult owing to the paucity of recognisable brain lesions in patients with CNS lupus. It is concluded that for the evaluation of acute neuropsychiatric SLE MR is useful and provides more information than cranial CT.
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PMID:Magnetic resonance and computed tomographic imaging in the evaluation of acute neuropsychiatric disease in systemic lupus erythematosus. 261 53


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