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)

Various forms of cellular injury, whether induced by immune effector cells, aberrant metabolic processes, chemotherapeutic drugs or temperature shifts, result in common morphological changes consisting of the formation and shedding of membrane vesicles from the injured cell surfaces, i.e., apoptosis. This dynamic cell surface membrane behavior appears to be dependent on the disruption of cytoplasmic microtubules. Concomitant with the altered cell surface morphology, certain physiological and biochemical events have been found to be associated with cell injury. These include changes in membrane permeability, elevated oxygen consumption rates and nuclear DNA fragmentation. However, it remains to be experimentally established which of these biological changes defines a state of irreparable cell injury and/or programmed cell death (PCD). Selective cell injury and death is the goal of many therapeutic modalities aimed at the destruction of malignant cells. On the other hand, prevention of cell injury is desirable in autoimmune diseases such as systemic lupus erythematosus, thyroiditis, insulin dependent diabetes and many others. Injury to the vascular endothelium may play a role not only in thrombosis, atherosclerosis and hypertension, but may also provide the avenues for the metastasis of malignant cells. The objective of the present review is to compare and evaluate the cell injury process induced by effector lymphocytes with that caused by low temperature. The latter mimics most, if not all, the currently known criteria of immune effector cell mediated PCD of target tumor cells.
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PMID:Cell injury and apoptosis. 774 62

Since their introduction for the treatment of rheumatoid arthritis, corticosteroids have become widely used as effective agents in the control of inflammatory diseases. Although there have been undoubted benefits upon mortality in diseases such as systemic lupus erythematosus, many patients survive only to suffer a high incidence of premature atherosclerosis. There is also evidence of increased rates of vascular mortality in other corticosteroid-treated diseases, such as rheumatoid arthritis, reversible airways obstruction and transplant recipients. Possible mechanisms of damage include elevated blood pressure, impaired glucose tolerance, dyslipidaemia, and imbalances in thrombosis and fibrinolysis. This paper reviews the clinical evidence supporting the contention that there is an excess cardiovascular mortality in steroid-treated patients and the underlying mechanisms, and points to further areas of research.
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PMID:Corticosteroids: do they damage the cardiovascular system? 787 Jun 31

The occurrence of cardiac manifestations and their relationship with the lupus anticoagulant (LA) in SLE was studied in 74 patients who were followed up for 22 years (median), of which 16 years were after the initial LA testing. Pericarditis was the most common cardiac event occurring in 16 (22%) patients but it did not correlate with LA. Valvular heart disease, coronary artery disease, left ventricular failure and/or cor pulmonale were observed in 16 (22%) patients. Taken together, their occurrence was associated with a history of leg ulcers (odds 3.8, P = 0.028) but not with LA or other common clinical manifestations of the antiphospholipid syndrome. Valvular heart disease in five patients was significantly associated with LA (P = 0.05). Cor pulmonale due to chronic pulmonary embolism was present in two patients with LA. Myocardial infarctions in five patients occurred late in the course of disease but in relatively young patients (mean 43 years). Fatal myocardial infarction in the absence of atherosclerosis in two LA-positive patients supports a pathogenetic role for LA in these cases. In conclusion, of the various cardiac complications in SLE, valvular heart disease and cor pulmonale appear to be connected with the antiphospholipid syndrome. Both conditions should be actively sought in patients with LA to decrease possible adverse events (arterial emboli and right ventricular failure) affecting the patients' prognosis.
Lupus 1994 Jun
PMID:Lupus anticoagulant and cardiac manifestations in systemic lupus erythematosus. 795 2

We present the clinical case of a 26-year-old woman, suffering systemic lupus erythematosus for 15 years, who suddenly had coronary heart disease with angina pectoris on mild effort. Thallium 201 exercise test demonstrated clearcut anteroseptal and apical perfusion defects, whereas repeated echocardiography showed a hypokinetic anteroseptal segment; ECG also reported new Q wave in lead V4. After stronger corticosteroid and immunosuppressive treatment, angina pectoris attenuated and perfusion defects disappeared within few months. We hypothesize a coronary artery vasculitis in the course of systemic lupus erythematosus, probably associated with early coronary artery atherosclerosis.
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PMID:[Critical myocardial ischemia in systemic lupus erythematosus. Case report]. 797 32

The objective of this study was to determine the prevalence and clinical significance of elevated antiphospholipid antibodies (APA) in a large series of patients admitted to a department of Internal Medicine. At the end of entry phase, 1014 patients were tested (488 males-526 females, mean age: 66.7 years, range 18-97). Seventy-two (7.1%) patients were found APA positive at least once: 44 males and 28 females, mean age 69 years, range 23 to 94. Twenty fulfilled the criteria of Primary Antiphospholipid Antibody Syndrome: 10 patients were referred for deep vein thrombosis, 3 had history of deep vein thrombosis, 1 had both arterial thrombosis and a history of venous thrombosis; 2 had thrombocytopenia; 3 had stroke, 1 had a history of a stroke. One patient had SLE according to ARA classification. The most frequent associated disease was cancer: 14 patients, 9 had evolutive malignant disease, 5 were in clinical remission of neoplasia. Other clinical conditions included chronic and/or acute alcoholic intoxication (n = 8), severe atherosclerosis (n = 4), leg ulcer (n = 4). Insufficient data are available about the evolution, but 7 patients died in the year following diagnosis. Eight patients had fluctuations in APA detection: 2 initially APA positive became negative, 5 initially negative became positive and 1 patient was alternatively positive, negative and positive without steroid treatment. Thus, as expected, APA occur in a variety of clinical disorders. The association with cancer or alcoholic intoxication deserves further investigations.
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PMID:A prospective epidemiological study on the occurrence of antiphospholipid antibody: the Montpellier Antiphospholipid (MAP) Study. 798 47

There are three types of interferons (IFN), alpha, beta and gamma. IFN-alpha is produced in the leukocytes infected with virus, while IFN-beta is from fibroblasts infected with virus. IFN-gamma is induced by the stimulation of sensitized lymphocytes with antigen or non-sensitized lymphocytes with mitogens. It is believed that IFN-alpha and beta originated from the same ancestral gene, whereas IFN-gamma did not. IFN has not only an antiviral activity, but also various kinds of biological activities including cell growth inhibition, immunosuppressive effects, enhancement of macrophage, natural killer (NK) cell, killer (K) cell and neutrophil functions, and cell differentiation-inducing activity. IFN also shows the antitumor activity resulting from the integration of the above-mentioned biological activities. IFN is also deeply involved in the pathogenesis of various diseases, e.g., collagen diseases such as SLE and rheumatoid arthritis, insulin-dependent diabetes mellitus, fulminant hepatitis, severe pancreatitis, nephritis, multiple sclerosis, allergic diseases, and atherosclerosis. At present, IFN is clinically used in therapy against virus infections such as hepatitis B and C, and for malignancies such as renal cell carcinoma, multiple myeloma, malignant melanoma, glioblastoma, skin cancers, malignant lymphoma and chronic myelogenous leukemia.
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PMID:[Interferon-alpha, beta, gamma]. 799 28

In western countries, acute myocardial infarction is the commonest cause of morbidity and mortality [19]. An occlusive coronary thrombus on an ulcerated atherosclerotic plaque in the coronary arteries is the etiological event in more than 90% of patients with Q-wave myocardial infarction [38]. The underlying abnormality in non-Q-wave myocardial infarction is often a ruptured atherosclerotic plaque, which acts as a nidus for the deposition and activation of platelets. In this case, thrombosis occurs, but may not be totally occlusive, or an early spontaneous recanalization may occur. On the other hand, some clinical trials showed that a prolonged treatment with antiplatelet drugs significantly reduces the recurrence of coronary ischemia. Thus, atherosclerosis is a necessary condition for myocardial infarction, but it is not sufficient in that it usually needs the occurrence of thrombosis. However, only 25-30% of these thrombotic events are prevented by the administration of antiplatelets drugs. In recent years, epidemiological studies identified some hemostatic parameters whose abnormalities may help predict the risk of ischemic events: fibrinogen [14], plasminogen activator inhibitor-1 (PAI-1) [3], lipoprotein(a) [46], anticardiolipin antibodies (ACA) and lupus anticoagulant (LA) [10], leukocyte count [34], blood viscosity [34]. Some of these, such as fibronogen and PAI-1 are acute-phase proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma predictors of ischemic complications of atherosclerosis: open issues. 806 Dec 44

We systematically investigated clinical, laboratory, radiologic, and pathologic features, including treatment and prognosis, of stroke syndromes in 30 patients, six from our institution and 24 from the literature, with systemic lupus erythematosus (SLE) and symptomatic large cerebral vessel occlusive disease, documented by angiography or autopsy. The average age at stroke onset was 35 years, and the diagnosis of SLE was made on average 4.4 years prior to that. At least 86% had active SLE at the time of their stroke. Headache was common at onset. We found major intracranial or extracranial vessel occlusive process by (1) thrombus, (2) dissection, (3) fibromuscular dysplasia or vasculitis, and (4) atherosclerosis. The presumed mechanisms were coagulopathy, cardiogenic embolism, large cerebral vessel vasculitis or occlusive vasculopathy, cervical arterial dissection, and premature atherosclerosis. The short-term death rate was 40% and the recurrent stroke rate was 13%. We conclude that symptomatic large cerebral vessel occlusive disease in SLE generally occurs several years after the diagnosis of SLE, usually during the active phase of the disease, is related to heterogeneous mechanisms, and carries a relatively poor short-term outcome.
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PMID:Large cerebral vessel occlusive disease in systemic lupus erythematosus. 814 3

Association between systemic lupus erythematosus and coronary atherosclerosis has been reported only rarely in the medical literature. Sudden ischaemic cardiac death in such cases is an uncommon terminal event, particularly in young patients. The severity of coronary atherosclerosis in these cases may be similar to those seen in the classic coronary disease. A case of a 22-year-old female systemic lupus patient is presented in whom sudden death was found at autopsy to be due to extensive coronary atherosclerosis.
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PMID:Sudden cardiac ischaemic death associated with systemic lupus erythematosus. 815 79

Endothelium damage is associated with thrombotic risk in a variety of diseases including atherosclerosis, gram negative sepsis, viral infections and neoplastic disease. Therefore, it appears necessary to find a mean for the clinical investigation for such a damage. Among the markers of these cells, thrombomodulin which is a membrane glycoprotein, seems to be of great interest for this purpose. Actually, thrombomodulin is also found in plasma, following an endothelial lesion. Plasma levels of thrombomodulin are increased in a certain number of pathologies associated with endothelium lesion: atheromatous arterial disease, disseminated intravascular coagulation syndrome and also in systemic lupus erythematosus where the levels of plasma thrombomodulin are related to the severity of the pathology. Moreover, previous in vitro studies confirm the fact that the release of thrombomodulin from the endothelial cell membrane occurs during the course of injury by activated leukocytes or hydrogen peroxide. So, one can suppose a prospective interest in the measurement of plasma thrombomodulin as a diagnostic tool for the approach of endothelium damage.
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PMID:Plasma thrombomodulin: new approach of endothelium damage. 820 13


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