Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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

High-sensitive C-reactive protein (hs-CRP) is a marker of inflammation which has been shown in several prospective studies to independently predict myocardial infarction, stroke and peripheral artery disease. Patients with antiphospholipid antibodies (aPL) are at increased risk of recurrent thromboembolic events, but the possibility of predicting this risk seems rather limited. Similarities were recently found between aPL and CRP in the pathology of thrombosis. The current study investigated the predictive role of hs-CRP in a cohort of patients with neurological manifestations. A follow-up investigation was done in a cohort of 55 aPL-positive patients with acute manifestations of neurological disease. hs-CRP levels were measured in all patients at enrollment and were compared to the patients' condition after a median period of 32 months. Lupus anticoagulants were detected according to the Standardization of Lupus Anticoagulants (SSC) of the ISTH. Anticardiolipin tests were performed by a beta2-glycoprotein I-dependent enzyme-linked immunsorbent assay (Pharmacia ELISA). hs-CRP was measured by latex-enhanced turbidometry (dimension RXL, Dade Behring). Cerebral infarctions and transient ischemic attacks were the most frequent cerebral events. In patients with aPL, elevated levels of hs-CRP were closely associated with an increased rate of recurrent or residual symptoms (OR, 12.5; 95% CI, 3.72-41.94) and were not related to other risk factors, except smoking (p<0.05). The rate at which a given patient's condition deteriorated was also related to the level of hs-CRP. In patients with antiphospholipid syndrome (APS), elevated levels of hs-CRP may identify a group of patients which is at high risk of recurrent or residual neurological symptoms and which may benefit from more careful follow-up and from antithrombotic therapy.
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PMID:Predictive role of hs-C-reactive protein in patients with antiphospholipid syndrome. 1632 94

The complement system consists of more than 30 proteins and has 3 types of activation pathways: classical, lectin and alternative pathways. The complement system not only has a role in innate immunity but also works as an antibody-dependent effecter to eliminate pathogens. It is useful to measure serum levels of CH50, C3 and C4 in patients with immune-mediated diseases. While increased levels of CH50 are associated with non-specific inflammation, decreased levels of CH50 in combination with normal or decreased levels of C3 and C4 are associated with specific immune-mediated diseases. Recent studies have demonstrated that the defect in the clearance of immune complexes and apoptotic cells is associated with autoimmune disease. Mice deficient in Clq show a lupus-like phenotype with the appearance of antinuclear antibodies and glomerulonephritis due to a defect in the clearance of immune complexes and apoptotic cells. This at least explains the paradox that, in humans, deficiency in an early complement component is a major risk factor for SLE. It is demonstrated that mutations in factor H, membrane cofactor protein (MCP) and factor I gene are associated with atypical hemolytic uremic syndrome. Since the complement system is a central mediator of inflammation, it is recognized as a promising therapeutic target. Anti-C5 monoclonal antibody was developed to block the final stage of complement activation. Pexelizumab is a single chain, short-acting anti-C5 antibody and is used for reperfusion after myocardial infarction, or for coronary artery bypass graft surgery with cardiopulmonary bypass. Eculizumab is a long-acting anti-C5 antibody used for paroxysmal nocturnal hemoglobinuria, rheumatoid arthritis, membranous glomerulonephritis with promising results.
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PMID:[Clinical aspects of the complement system]. 1691 67

Myocardial infarction in patients with systemic lupus erythematosus (SLE) is most commonly a consequence of atherosclerosis. Coronary vasculitis with aneurysms is a rare cause of myocardial ischemia in SLE. We present a case of a 22-year-old woman with a 4-year history of SLE who was admitted with acute onset of chest pain. Although initially treated for lupus pericarditis, she was subsequently found to have an acute myocardial infarction. Cardiac catheterization revealed multiple areas of aneurysmal coronary dilatation and only moderate stenoses of the secondary branches.In view of the angiographic findings, coronary revascularization was not indicated. Anticoagulant therapy was initiated as a result of the presence of large aneurysmal coronary dilatations, which are predisposed to in situ thrombosis and distal embolization. The coronary vasculitis was treated with immunosuppressive therapy. Measures aimed at secondary prevention of coronary artery disease, including optimization of lipid profile, blood pressure control, and prevention of left ventricular postinfarct remodeling, were initiated and continued indefinitely.
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PMID:Coronary vasculitis with acute myocardial infarction in a young woman with systemic lupus erythematosus. 1704 68

The objective of this study was to quantify the incremental medical costs that are associated with untreated anemia among elderly patients with predialysis chronic kidney disease (CKD). An analysis of claims and laboratory data between January 1999 and February 2005 was conducted. Inclusion criteria were age >/=65 yr, two or more hemoglobin readings, one or more claims for CKD, and two or more GFR values of <60 ml/min per 1.73 m(2) (stages 3 to 5 CKD). Patients were excluded when they had cancer or lupus, had received organ transplantation, or were treated for anemia. An open-cohort design was used to classify patients' observation periods into anemia and nonanemia. Both univariate and multivariate analyses were conducted to compare periods of anemia and nonanemia for average monthly medical costs; the latter was adjusted for age, gender, GFR, diabetes, hypertension, liver cirrhosis, coronary artery disease, myocardial infarction, and left ventricular hypertrophy. A subset analysis of patients with moderate CKD (stage 3) was conducted. A total of 2001 patients were identified. Untreated anemia was associated with a significant increase in medical costs, with an unadjusted incremental monthly cost of $1089 (P < 0.0001) and a cost ratio of 1.8:1 relative to nonanemia. After controlling for covariates, untreated anemia remained significantly associated with a cost increase (adjusted incremental monthly cost $503; cost ratio 1.4:1; P < 0.0001). Similar significant cost burden was observed in the subset of patients with moderate CKD. The retrospective observational design may be more susceptible to bias than a randomized, controlled trial. This large study, which was based on real-life practice data, demonstrated that untreated anemia in elderly patients with predialysis CKD was associated with a significant increase in medical costs.
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PMID:Medical costs of untreated anemia in elderly patients with predialysis chronic kidney disease. 1708 45

Ischemic heart disease and myocardial infarction in patients with SLE--are usually secondary to early coronary atherosclerosis. Estimation if antiphospholipid syndrome and antiphospholipid antibodies are the risk factor for myocardial infarction and ischemic heart disease in patients with TRU. We examined 129 patients with SLE (114 women and 15 men). All the patients underwent comprehensive physical examination. ECG, ultrasound heart examinations were performed. They were followed by heart scintygraphic examination if indicated. Routine biochemical and hematological laboratory tests were performed including fasting glucose level, concentration of homocysteine, uric acid and lipids. Wide range of immunological essays were performed, testing for antinuclear antibodies (ANA), extractable nuclear antigen antibodies (ENA), antiphospholipid antibodies (anticardiolipin antibodies--aCL, lupus anticoagulant--LA, antiprothrombine antibodies aPT, anti-beta2glicoprotein-I antibodies), anti-dsDNA antibodies, anti-nucleosome antibodies, antihistone antibodies, antineutrophil cytoplasmic antibodies (ANCA) and antiendothelial antibodies (AECA). Statistical analysis was performed with chi2 Yates, chi2 Pearson and R rang Spearman tests. Multivariate regression analysis was also done. Ischemic heart disease was found in 20 (15.5%) SLE patients, myocardial infarctions were diagnosed in 9 (6.97%). Ischemic heart disease and myocardial infarction were significantly related to presence of secondary antiphospholipid syndrome (SAPS), OR: 4.21, p = 0.008 and OR: 12.8; p = 0.02 respectively). They were also related to high activity of SLE, OR: 7.18; p = 0.012 and OR: 27.3; p = 0.006 respectively. Ischemic heart disease was significantly more common in older patients (52.75 years versus 42.15 years; p = 0.0008) and in patients with hypertension (p < 0.05). Impaired glucose tolerance (OR: 8.44; p = 0.03), presence of aCL IgG (OR; 2.93; p = 0.05) and p-ANCA anti-MPO (OR: 6.08; p = 0.036) were found to be risk factors of ischemic heart disease. Myocardial infarction was significantly associated with high uric acid level (OR: 5.01; p = 0.052) and impaired glucose tolerance (OR: 7.42; p = 0.047) and with presence of the following antibodies: aCL IgG and/or aCL IgM (OR: 5.61; p = 0.039), ANCA in the indirect immunofluorescence essay (OR: 5.78; p = 0.035), anti-MPO antibodies (OR: 6.58; p = 0.051) and AECA (OR: 11.10; p = 0.026). Presence of antiphospholipid antibodies and SAPS are significant risk factors of ischemic heart disease and myocardial infarction in SLE patients. The risk factors of ischemic heart disease and myocardial infarction in SLE patients significantly differ from the ones in general population.
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PMID:[Antiphospholipid syndrome and antiphospholipid antibodies as a risk factors of ischaemic heart disease and myocardial infarction in patients with systemic lupus erythematosus]. 1719 52

Lipomembranous changes are histological findings without specific clinical correlations, and are thought to be related to vascular impairment in fatty tissue. We describe a case of systemic lupus erythematosus (SLE) in which subcutaneous induration of the lower leg showed lipomembranous changes and calcification. This patient showed thrombophilia with thrombosis of the femoral and iliac veins, and cerebellar and myocardial infarction. A biopsy specimen from the subcutaneous tissue surrounding the multiple leg ulcers revealed degeneration of fat cells, lipomembranous changes in the fatty tissues, and calcification. Another biopsy specimen from the outer edges of the ulcers showed microthrombi and fibrinoid changes in the vessel walls, and mononuclear cell infiltrates in the dermis. Lipomembranous changes have been seen in connective tissue disorders such as lupus profundus, morphoea, systemic sclerosis, and panniculitis associated with dermatomyositis, but rarely associated with SLE. We speculate that ischaemic changes due to the vascular disturbance of the lower legs may have induced lipomembranous changes and calcification in the subcutaneous tissues in the present case.
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PMID:Lipomembranous changes and calcification associated with systemic lupus erythematosus. 1726 29

A 44-year-old woman presented with an acute inferior ST elevation myocardial infarction, followed by a stroke in the right hemisphere. To search for a cardiac source of embolism, a transesophageal echocardiogram was performed, which showed a mass obstructing the origin of the right coronary artery. The mass was surgically excised and a histologic examination confirmed its thrombotic origin. The diagnosis of antiphospholipid antibody syndrome was confirmed by positive lupus anticoagulant antibodies.
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PMID:Myocardial infarction secondary to a coronary ostial thrombus in antiphospholipid syndrome. 1730 84

Deficiency of mannan-binding lectin (MBL) has been reported to impact susceptibility to severe infections and atherosclerosis in systemic lupus erythematosus (SLE). In this study, MBL gene polymorphisms were analysed in 143 SLE patients and the frequency of severe infections and organ damage according to SLICC/ACR Damage Index regarding cerebrovascular accidents, angina pectoris, coronary by-pass surgery, myocardial infarction and peripheral arterial disease leading to significant tissue loss, were recorded during a mean follow-up time of 15 years from diagnosis. In a multiple logistic regression model, smoking (P = 0.001), hypertension (P = 0.030), alcohol intake (P = 0.027) and higher triglyceride concentration (P = 0.026) were associated with cerebrovascular, cardiovascular and peripheral arterial organ damage (CPAD), while the association with MBL deficiency did not reach significance (P = 0.098). Alcohol intake (>15 g/month) was inversely correlated with CPAD (OR = 0.29, 95%CI 0.096-0.87). MBL deficiency was not significantly more common in SLE patients with severe infections in a multivariate analysis (P > 0.3). In conclusion, classical risk factors such as smoking, hypertension, low alcohol intake and elevated triglyceride concentration were relatively more important for development of CPAD than MBL deficiency in SLE. Furthermore, MBL deficiency did not contribute to development of major infections in SLE.
Lupus 2007
PMID:Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus. 1743 30

The present study aims to report a-20-year old girl with systemic lupus erythematosus (SLE) who developed myocardial infarction (MI) and also aims to review acute myocardial infarction (AMI) in young SLE cases (< or =35 years) reported in the literature. We conducted a comprehensive review of the English literature from 1975 to 2006 to analyse data on MI in SLE patients who had developed AMI either at 35 or earlier. In 32 English articles, we identified 49 SLE patients, plus our case, with AMI. They consist of 41 female and nine male patients, their mean age being 24 +/- 6.4 years (range of 5-35). Disease duration varied between 0 and 13 years. The lag time between the onset of the SLE manifestations and development of AMI was 7.7 +/- 5.4 year (range of 1 month to 20.5 years). We divided the patients into three subgroups according to their coronary involvement type (Group I: normal coronary artery or coronary thrombosis (n = 16); Group II: coronary aneurysm/arteritis (n = 12); Group III: coronary atherosclerosis (n = 22)). The lag time between the onset of the SLE manifestations and development of MI in the subgroups showed variations: Group I < Group II < Group III. Both prevalence of renal involvement and steroid therapy were higher in patients with coronary atherosclerosis than were in Group I. There were one or more risk factors for atherosclerosis in 39 SLE patients. AMI in young SLE patients may be seen, albeit rare. We suggest that clinicians should have a low threshold for cardiac evaluation in patients with SLE. Also, traditional risk factors could be managed through preventive measures.
Lupus 2007
PMID:Myocardial infarction in young patients (< or =35 years of age) with systemic lupus erythematosus: a case report and clinical analysis of the literature. 1743 37

Systemic lupus erythematosus (SLE) has numerous manifestations. Haematology is the common system influenced by the disease. The antibody antiphospholipid syndrome, secondary hematology disorder in SLE, is related to high incidence of thrombosis. The thrombosis events like myocardial infarction and stroke are high in mortality. We reported a-36-year old woman treated for lung tuberculosis (TB) with secondary infection, nephritis lupus, and pancytopenia. The general condition has improved and the patient was planned to discharge while she suddenly fell down, unconscious and had seizure. The CT-scan showed an area of hypodensity on the left thalamus. Haematology results showed high level of fibrinogen and D-dimer as the signs of thrombosis. The anticardiolipin antibody was intermediately positive for IgG and IgM, but lupus anticoagulan was weakly positive. The serial test within 2 months still showed positive IgG. The patient received supportive treatment, heparinization, neurotropic drugs and anticonvulsant. She was discharged in good condition while continuing oral anticoagulant to prevent recurrent seizure.
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PMID:Cerebral thrombosis in systemic lupus erythematosus with the antibody antiphospholipid syndrome. 1748 92


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