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

Fertility in patients with SLE and other systemic autoimmune disease is usually unaltered. However, fertility may be impaired by anovulation during episodes of active disease or chronic renal failure, administration of NSAIDs, high dose of corticosteroids and cyclophosphamide. Early pregnancy loss occurs in SLE patients with aPLs. An association of autoimmune disease with infertility has been suggested, but the studies are not conclusive. Ovulation stimulation as a fertility treatment could theoretically induce SLE. However, two recent studies did not find previous use of fertility drugs and in vitro fertilization to be more frequent in the history of SLE patients when compared with controls. Patients with SLE or primary APS, who are undergoing infertility treatment, could be at risk of flare or thrombosis. In the past 10 yrs, many reports have been published regarding the risk of lupus exacerbation associated with controlled ovarian hyperstimulation; not all found excess risk. At the moment we do not have any prospective study in this field. A trend towards a worse prognosis in cases of SLE patients undergoing assisted reproductive techniques (ARTs) for pregnancy rate, live-birth rate and maternal complications can be seen. If hormonal ovarian stimulation is useful, well-advised management would administer a low effective gonadotropin dose in a patient whose disease has been silent preferably for at least 6 months. Further data are needed to establish safety and efficacy of ART in SLE patients.
 ...
PMID:Treating infertility in autoimmune patients. 1850 85

The involvement of the central nervous system (CNS) is one of the major causes of morbidity and mortality in systemic lupus erythematosus (SLE) patients and the less understood aspect of the disease. Its recognition and treatment continue to represent a major diagnostic and therapeutic challenge. Due to the lack of controlled randomized trials, current therapeutic approach is still empirical and based on clinical experience. The therapeutic choice depends on accurate diagnosis, identification of underlying pathogenic mechanism, severity of the presenting neuropsychiatric symptoms, and on prompt identification and management of contributing causes of CNS disease. Mild neuropsychiatric manifestations may need symptomatic treatment only. In more severe CNS disease it is important to distinguish between thrombotic and non-thrombotic mechanisms. Focal CNS manifestations, particularly TIA and stroke, are associated with the presence of antiphospholipid antibodies (aPL). Anticoagulation is warranted in patients with thrombotic disease, particularly in those with the antiphospholipid (Hughes) syndrome (APS). Other CNS manifestations, such as demyelinating syndrome, transverse myelitis, chorea, seizures, migraine and/or cognitive dysfunction, when associated with persistent positivity for aPL, may also benefit from anticoagulation in selected patients. Severe diffuse CNS manifestations, such as acute confusional state, generalised seizures, mood disorders and psychosis, generally require corticosteroids in the first instance. Pulse intravenous cyclophosphamide therapy may help when more severe manifestations are refractory to corticosteroids and other immunosuppressive agents, generally when response is not seen in 3-5 days. Plasmapheresis may also be added in severe cases of symptoms refractory to conventional treatment. Intravenous immunoglobulins, mycophenolate mofetil, rituximab, intratecal methotrexate and dexametasone deserve further studies to confirm their usefulness in the treatment of neuropsychiatric SLE. This article reviews the clinical approach to therapy in patients with SLE and neuropsychiatric involvement.
 ...
PMID:Neuropsychiatric involvement in systemic lupus erythematosus: current therapeutic approach. 1853 50

SLE patients with identified and probable APS compared with those having no APS have been found to have more significant endothelial function disorders, carotid artery intima-media thickness (IMT) and intensity of atherosclerotic vascular impairment. At the same time antibody level to beta-2-glycoprotein 1 reliably correlates (r= 0.39, 0.38, 0.33) with endothelial dysfunction specificity and carotic artery atherosclerotic impairment. The development of structural and functional myocardial defect in SLE patients less depends on APS presence. Persons with high antibody level to beta-2-glycoprotein 1 were found to have oftener a left ventricular myocardial hyperthrophy and impairment of diastolic heart function than patients with no antibodies to beta-2-glycoprotein 1.
 ...
PMID:[Particularities of endothelial function disorders, atherosclerotic vascular impairment and morphofunctional myocardium condition in SLE patients with antiphospholipid syndrome]. 1866 10

Nonbacterial thrombotic (noninfectious, pseudoinfectious--PIE) endocarditis is characterized by precipitation of thrombus, not containing bacteria, on the valve cusps. Mitral and aortal valves are affected most frequently. Vegetations, as a rule, do not exceed 6-7 mm and have a high inclination to embolism. Hypercoagulation plays a leading role in PIE pathogenesis. The most frequent acquired causes of sterile vegetation forming are malignant tumors and rheumatic diseases (especially systemic lupus erythematosus--SLE and antiphospholipid syndrome--APS). Valve pathology is most frequent lesion of heart in APS patients. It is supposed, that antibodies to phospholipids (aPL) have a special importance in valve lesion pathogenesis at APS, besides, changes in valve apparatus at SLE are associated exactly with aPL. Main problems of PIE patients are recurrent thromboembolism, development of valve dysfunction with clinical signs of heart failure (4-6% cases), difficulties in differential diagnostics: PIE is hard to diagnose if basic disease is accompanied by fever (diffuse diseases of connective tissue etc.). Transesophageal echocardiography is a leading method in PIE diagnostics. The main therapeutic option in PIE treatment is anticoagulant therapy: nonfractional or subcutaneous heparin in presence of systemic or pulmonary embolism, in patients with disseminated malignant tumors--complete doses of nonfractional heparin.
 ...
PMID:[Pseudoinfectious endocarditis]. 1872 Jul 5

Autoimmune manifestations have long been perceived as paradoxical in patients with primary immune deficiencies (PID). However, a defect in the mechanisms of control of self-reactive B and T cells may favour these manifestations. Three PID are defined by the occurrence of autoimmune manifestations: APECED (Autoimmune Polyendocrinopathy-Candidiasis-Ectodermal Dystrophy), autoimmune lymphoproliferative syndrome (ALPS) and IPEX syndrome (immunodysregulation, polyendocrinopathy, enteropathy, X-linked syndrome). In these conditions, organ specific autoimmune diseases such as type 1 diabetes mellitus or Hashimoto's thyroiditis are prominently encountered. Several other PID such as common variable immunodeficiency (CVID), Good syndrome and hyper-IgM syndrome are associated with a wide variety of autoimmune manifestations, mainly autoimmune cytopenias. Thus, autoimmune manifestations have been reported in 22% of patients with CVID, increasing to 50% in the subgroup of patients with systemic granulomatosis. Complement deficiencies involving components of the classical pathway are associated with systemic lupus erythematosus (SLE). Homozygous C2 deficiency, which is the most frequent hereditary deficiency in complement classical pathway components, is associated with SLE in 10% of the cases. Complete C1q and C4 deficiencies are less frequent but associated with a higher prevalence of SLE.
 ...
PMID:Autoimmune manifestations in primary immune deficiencies. 1902 7

Primary immune thrombocytopenic purpura (ITP) remains a diagnosis of exclusion both from nonimmune causes of thrombocytopenia and immune thrombocytopenia that develops in the context of other disorders (secondary immune thrombocytopenia). The pathobiology, natural history, and response to therapy of the diverse causes of secondary ITP differ from each other and from primary ITP, so accurate diagnosis is essential. Immune thrombocytopenia can be secondary to medications or to a concurrent disease, such as an autoimmune condition (eg, systemic lupus erythematosus [SLE], antiphospholipid antibody syndrome [APS], immune thyroid disease, or Evans syndrome), a lymphoproliferative disease (eg, chronic lymphocytic leukemia or large granular T-lymphocyte lymphocytic leukemia), or chronic infection, eg, with Helicobacter pylori, human immunodeficiency virus (HIV), or hepatitis C virus (HCV). Response to infection may generate antibodies that cross-react with platelet antigens (HIV, H pylori) or immune complexes that bind to platelet Fcgamma receptors (HCV), and platelet production may be impaired by infection of megakaryocyte (MK) bone marrow-dependent progenitor cells (HCV and HIV), decreased production of thrombopoietin (TPO), and splenic sequestration of platelets secondary to portal hypertension (HCV). Sudden and severe onset of thrombocytopenia has been observed in children after vaccination for measles, mumps, and rubella or natural viral infections, including Epstein-Barr virus, cytomegalovirus, and varicella zoster virus. This thrombocytopenia may be caused by cross-reacting antibodies and closely mimics acute ITP of childhood. Proper diagnosis and treatment of the underlying disorder, where necessary, play an important role in patient management.
 ...
PMID:Pathobiology of secondary immune thrombocytopenia. 1924 30

Vascular dysfunction is key to the development of thrombosis in the antiphospholipid syndrome. This has been largely demonstrated by the upregulation of various cell surface and intracellular signalling molecules, as well as proinflammatory cytokine release from activated endothelial cells. Endothelial microparticles (EMP) are a further marker of endothelial activation but have been less extensively studied. We summarise evidence suggesting that these microparticles may be critical effectors of thrombosis in the antiphospholipid syndrome. There is evidence that levels of EMP are raised in patients with circulating antiphospholipid antibodies and that these EMP may be prothrombotic. The balance between markers of endothelial dysfunction (including EMP and circulating endothelial cells) and markers of repair such as circulating endothelial progenitor cells may be abnormal in patients with APS but this has not been proved and requires further study.
Lupus 2009 Jul
PMID:Are endothelial microparticles potential markers of vascular dysfunction in the antiphospholipid syndrome? 1950 61

The antigenic specificity of antiphospholipid antibodies (APA) is a matter of intensive investigation. Difference in the reported involvement of APA in clinical manifestation may be due, in part, to the polyclonal nature of these antibodies and the use of serum and serum fractions for analysis. To circumvent this issue, we generated mouse monoclonal APA and compared their antigen binding patterns and conditions of this reaction. Monoclonal APA 5A1 and 1B10 reacted with cardiolipin in a beta2-glycoprotein 1-dependent manner. The epitope for these antibodies consisted of beta2-glycoprotein 1 bound to cardiolipin or immobilized on plastic plates. The specificity is similar to the autoimmune anticardiolipin antibodies described in patients with SLE, APS and other autoimmune diseases. Monoclonal APA 510, 183, 238 reacted with cardiolipin in the absence of beta2-glicoprotein 1. beta2-Glicoprotein 1 , either in the fluid phase or bound to cardiolipin, inhibited the binding of these antibodies. Monoclonal APA 510 was cofactor-independent while monoclonal APA 183 and 238 reacted with cardiolipin only in the presence of human serum. The results of this study indicate that APA comprise a highly heterogeneous population of antibodies with respect to the antigens they recognize, as well as depending on presence of serum components.
 ...
PMID:[Analysis of specificity of antiphospholipid antibodies with the use of monoclonal antibodies to phospholipids]. 1961 52

We report a case of HELLP syndrome, multiple liver infarctions, and intrauterine fetal death in a woman in the 17th week of pregnancy with SLE and APS who had been in remission on a regimen of low-dose prednisolone and aspirin. An increase in the dosage of corticosteroid together with intravenous heparin infusion led to improvement of the clinical symptoms, laboratory parameters, and multifocal low-density liver lesions detected by computed tomography. Early onset and signs of severe organ involvement are the characteristic features of HELLP syndrome associated with APS, and patients that are at risk should be followed up carefully.
 ...
PMID:HELLP syndrome, multiple liver infarctions, and intrauterine fetal death in a patient with systemic lupus erythematosus and antiphospholipid syndrome. 1972 3

We investigated the genetic background regarding major histocompatibility complex (MHC) II alleles in patients with systemic lupus erythematosus (SLE) only, in patients with SLE with secondary antiphospholipid syndrome (SLE+SAPS), and in patients whose clinical course began as primary antiphospholipid syndrome (PAPS) and subsequently progressed to SLE (PAPS+SLE) in order to explain the phenotypical differences found in our previous study. Those with primary or secondary APS present more thrombotic and less inflammatory activity. Fetal wastage was the highest in the PAPS+SLE group. We performed human leukocyte antigen (HLA)-DRB1 and HLA-DQB1 genotyping in 63 patients (26, 22, and 15 in SLE only, SLE+SAPS, and PAPS+SLE groups, respectively) and in 57 healthy controls, using PCR with sequence-specific primers. We found that, as reported in the literature, the occurrence of DRB1*03 and DQB1*0201 alleles was higher in SLE patients than in controls, but these alleles were rare in the PAPS+SLE group (13% in PAPS+SLE vs. 46% in the SLE only group; P = 0.044). HLA-DRB1*04 alleles were expressed frequently in both primary and secondary APS. DRB1*13, DQB1*06, and DQB1*0302 alleles were present more frequently in the PAPS+SLE patients than in the other groups, while the DQB1*0301 allele was rare. In this study we have shown that the SLE-associated DRB1*03/DQB1*02 alleles occurred frequently in our lupus patients as well as in SLE patients with secondary APS. In patients who started as PAPS and later progressed to SLE, the allele frequency was fundamentally different. Taken together, our results confirmed that the HLA-DRB1 and HLA-DQB1 profile of PAPS and SAPS is different. Therefore it is unlikely that these alleles are responsible for the partly similar phenotype of the two groups.
 ...
PMID:Human leukocyte antigen-DRB1 and -DQB1 genotyping in lupus patients with and without antiphospholipid syndrome. 1975 97


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>