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)

Celiac disease in children has been occasionally reported to be associated with various disorders such as arthritis, cutaneous vasculitis and diabetes mellitus. We report on a 12-year-old girl with celiac disease, diagnosed at 1 year of age, who developed systemic lupus erythematosus. This association has not yet been reported in children.
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PMID:Celiac disease associated with systemic lupus erythematosus. 804 53

We reviewed 44 cases of ischemia and infarction of the spinal cord at two university hospitals. Three patients experienced transient ischemic attacks. Etiologies of completed strokes were diverse and included rupture and surgical repair of aortic aneurysms, aortic dissection, aortic rupture and thrombosis, global ischemia, anterior spinal artery embolism, repair and thrombosis of spinal arteriovenous malformations, hematomyelia, epidural hematoma, cervical osteophytosis, celiac plexus block, systemic lupus erythematosus, coagulopathy, and decompression sickness. Motor function improved in 12 patients, was substantial in only one, and occurred largely within the first 2 to 4 weeks. Favorable ambulatory outcome correlated with improving neurologic examinations and relatively preserved strength in hip abductors and knee extensors. More extensive deficits without initial improvement portended a more severe prognosis. Autonomic dysfunction, pain, paresthesia, and depression were common and impeded recovery in some patients. The mean level of deficit was at T-8 and in cases of global ischemia was at T-9, which leads us to dispute the classical view of a midthoracic watershed zone of ischemic vulnerability near T-4.
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PMID:Spinal cord infarction: etiology and outcome. 915 13

GM and KM immunoglobulin (Ig) allotypes and their interactions with HLA antigens have been analyzed in various autoimmune diseases: multiple sclerosis, rheumatoid arthritis, insulin-dependent diabetes mellitus (IDDM), systemic lupus erythematosus, coeliac disease, Crohn's disease, Graves' disease, atrophic thyroiditis, Hashimoto's thyroiditis, myasthenia gravis, chronic active hepatitis, alopecia areata, uveitis, vitiligo, Turner's syndrome, glomerular nephritis, Berger's disease and idiopathic dilated cardiomyopathy. This review reports published results about associations or linkages, as well as the origins of the populations, the numbers of patients and controls tested. The possible role of Ig polymorphisms in the physiopathology of autoimmune diseases is discussed. Ig allotypes and statistical methods used to analyse the HLA and Ig data are also described.
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PMID:Immunoglobulin allotypes (GM and KM) and their interactions with HLA antigens in autoimmune diseases: a review. 878 16

Celiac disease (CD) is an immune disease triggered by the cereal antigen gliadin, resulting in villous atrophy in the small intestine. Susceptibility to the development of CD is strongly influenced by genes in the major histocompatibility complex, in particular alleles of the DQ genes in the class II region. However recent evidence has suggested that the major histocompatibility complex (MHC) class III region may be linked to celiac disease independently of the class II region. Among the genes located in this area is TNF-alpha, which encodes the cytokine tumor necrosis factor-alpha which has a broad range of pro-inflammatory, immunomodulatory and catabolic activities. Therefore, aberrant expression of TNF-alpha could be important in the pathogenesis of MHC-associated immune disorders. A TNF-alpha variant with a polymorphism in its promoter region has been described and designated TNF2. TNF2 has been associated with a variety of MHC-linked diseases, including systemic lupus erythematosus, dermatitis herpetiformis and insulin-dependent diabetes mellitus (IDDM), as well as parasitic infections. TNF2 has previously been shown to be associated with the MHC haplotype HLA A1-B8-DR3-DQ2, which confers susceptibility to CD. We have analyzed the distribution of TNF2 alleles in a group of celiac patients (n = 52) compared to controls (n = 52) in an effort to evaluate its role, if any, in susceptibility to the condition. TNF2 has a frequency of 0.5000 (SE +/- 0.0490) in CD, compared to 0.1635 (+/- 0.0362) in a control sample (p < 10(-6)). Of 52 patients, 44 carried one or more TNF2 alleles. Analysis indicates that the distribution of TNF2 is best explained by assuming 100% allelic association between it and HLA-DQB1*0201 (frequency = 0.7791 +/- 0.0447). However, the number of TNF2 heterozygotes significantly exceeds expectations and measurements of linkage disequilibrium confirm that allelic associations spanning the DQ and TNF regions are strongly maintained in CD. Taken together, these results indicate that TNF2 may have a role in the pathogenesis of CD; however, since it is not an independent association, the possibility that TNF2 constitutes a passive component of the CD haplotype cannot be excluded.
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PMID:TNF2, a polymorphism of the tumour necrosis-alpha gene promoter, is a component of the celiac disease major histocompatibility complex haplotype. 881 55

It has previously been shown that immunization with pathogenic anti-DNA idiotypes (Ids; e.g. 16/6 Id) leads to the induction of experimental system lupus erythematosus (SLF) in naive mice. The disease is characterized by serological (e.g. anti-double-strand DNA), clinical (elevation of erythrocyte sedimentation rate, leukopenia and proteinuria) and histological (immune complex deposition in kidneys) parameters. To determine whether the 16/6 Id carrying anti-DNA antibodies has unique pathogenic ability, in the current study we have employed diverse sources of anti-DNA antibodies to induce experimental SLE. An IgM anti-DNA antibody lacking the 16/6 Id was able to induce the production of the serological markers of experimental SLE, but not the clinico-histological findings. Furthermore, an IgA anti-DNA (16/6 Id derived from the serum of a patient with celiac disease was very effective in inducing the whole presentation of experimental SLE. Other anti-DNA antibodies failed to induce the autoimmune condition. Combined with our previous experience, the current study points to the diverse potential of various anti-DNA antibodies to induce SLE. The 16/6 Id is only one of a list of the potent pathogenic anti-DNA Ids. These facts may explain in part the diversity of clinical presentations of SLE, including asymptomatic subjects who carry high serum titers of anti-DNA antibodies.
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PMID:The diverse pathogenic potential of anti-DNA antibodies from various sources to induce experimental systemic lupus erythematosus. 885 93

Systemic lupus erythematosus (SLE) patients, especially those with antiphospholipid antibodies, have a high incidence of arterial and venous thrombotic manifestations. However, renovascular hypertension (RVH) has been rarely reported in these patients. We describe here a 49-year-old female with antiphospholipid antibodies, complicated with RVH and presenting with sudden onset of severe hypertension, headache and nausea. She had experienced phlebitis and arterial thrombosis of the right leg. At the age of 38 years, she was diagnosed as SLE and steroid therapy was started, but she had poor drug compliance and irregularly visited our clinic. On admission, hypertension was recognized and abdominal bruit was audible on physical examination. Serological findings were compatible with SLE. She was also found to have IgG anti-cardiolipin antibody and lupus anticoagulant. Peripheral plasma renin activity (PRA) was elevated, and captopril test showed hyper-response of PRA with lowering of blood pressure. Renal echography and scintigram showed a small and poorly perfused right kidney. Selective angiography demonstrated a severe stenosis of the right renal artery at origin. A stenosis at the origin of both the superior mesenteric artery (SMA) and celiac trunk was also detected. Percutaneous transluminal angioplasty was performed, achieving successful dilatation of the right renal artery and SMA, whereas the attempt to insert the catheter into the celiac trunk was unsuccessful. After this procedure, abdominal bruit has not been audible. Following the initiation of steroid pulse therapy combined with heparin and dipyridamole, her blood pressure was gradually depressed and the test for lupus anticoagulant became negative. Therefore, RVH of this patient is thought to be associated with antiphospholipid antibodies.
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PMID:[Renovascular hypertension associated with antiphospholipid antibodies in a woman with systemic lupus erythematosus]. 891 95

A patient had both lupus anticoagulant hypoprothrombinemia syndrome and celiac disease. The presence of a neutralizing antiprothrombin antibody in the patient's serum was demonstrated by coagulation tests, immunoadsorption, and Western blot analysis. The probable cause for the severe hypoprothrombinemia was clearance of prothrombin-antibody complexes from the circulation. Studies showed the antiprothrombin antibody binding to human prothrombin was phospholipid- and Ca(++)-independent; the antibody did not bind to human thrombin. The target epitope of the antibody was studied by Western blot analysis of mutated recombinant human prothrombin molecules. The antibody reacted with the fragment 2-A region of prothrombin, spanning the second kringle domain and the thrombin A chain within prothrombin. Based on this new method, the proposed mechanism for the neutralizing action of the antibody is impairment of prothrombin activation by the prothrombinase complex, either by steric hindrance of the hydrolysis of prothrombin by factor Xa or by interference of the interaction of prothrombin with factor Va; both reactions are required for efficient conversion of prothrombin to thrombin.
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PMID:A new method for characterization and epitope determination of a lupus anticoagulant-associated neutralizing antiprothrombin antibody. 902 68

Anti-murine IL-1 alpha, IL-6 antibodies were intra-peritoneally injected to the lupus-like NZB/W F1 mice of 4 months with the dosage of 10 micrograms per day for three days and then per month for three months. The mice were killed at the age of 11 months. The results showed that the treatment of the dosage could not absolutely prevent lupus nephritis--it could alleviate proteinuria, obviously reduce the levels of serum IL-1 alpha and inhibit the secretion of IL-1 alpha by celiac macrophage. As to the level of IL-6 and TNF-alpha no significant change was observed.
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PMID:Immunoregulation of lupus-like NZB/W F1 mice by anti-murine IL-1 alpha, IL-6 antibodies. 938 83

Antigliadin antibodies (AGA) mark celiac disease, but AGA are also encountered in IgA-nephritis, psoriasis, sickle-cell anemia, hepatic disorders, juvenile rheumatoid arthritis, autoimmune thyroidism and in persons who occupationally contact great amounts of wheat. AGA IgA and/or IgG were registered in 19 of 60 subjects (51 adults and 9 children) with various immunomediated diseases without symptoms of celiac disease: in 4 cases of chronic active hepatitis, in 2 of 4 cases of chronic persistent hepatitis, in 4 of 16 cases of rheumatoid arthritis, in 3 of 19 cases of IgA-deficiency, in 1 of 8 cases of SLE, in 2 cases of postvaccine reaction, in all the single cases of juvenile rheumatoid arthritis, focal scleroderma, macroglobulinemia. IgA only occurred in in 6 patients, IgG- in 6 patients, both IgA and IgG in 7 patients. The most pronounced positive reaction to AGA was recorded in 8-year-old girl with juvenile rheumatoid arthritis. The emergence of AGA in immunomediated diseases may be attributed to the response to food protein in pathological conditions and is often unrelated closely with celiac disease.
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PMID:[Antigliadin antibodies in the absence of celiac disease]. 955 58

Calreticulin (CRT), a high-affintiy calcium binding protein and chaperone, was recently identified as one of the targets of autoantibodies in coeliac disease. We evaluated the level of IgA and IgG antibodies to CRT in sera from patients with coeliac disease and various autoimmune diseases. The level of antibodies to gliadin (shown previously to cross-react with CTR), isolated enterocytes and tissue transglutaminase were determined for comparison. The mean level of IgA antibodies to CRT was significantly higher (P< 0.001) in sera from coeliac patients with active disease (139.9+/-11.2 AU/+/-SE) than in healthy controls (20.9+/-1.7 AU). In sera of patients with systemic lupus erythematosus (SLE), insulin dependent diabetes mellitus (IDDM), multiple sclerosis (MS) and autoimmune thyroiditis (AT) or inflammatory bowel disease (IBD) the mean level (25.8+/-3.7 to 38.1+/-5.6 AU) did not exceed the cut-off value. A low level of these antibodies, however, was detected in some sera of patients with MS and IBD. The level of IgG anti-CRT antibodies was increased in coeliac patients (mean 125.4+/-8.0 AU, P< 0.001) when compared to that in healthy controls (33.9+/-2.3 AU). The IgG anti-CRT antibodies were also detected in about 30% of SLE patients sera (54.1+/-3.6 AU, P< 0.001), but the mean level reached only half that detected in coeliac patients.
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PMID:Occurrence of IgA and IgG autoantibodies to calreticulin in coeliac disease and various autoimmune diseases. 1109 Feb 43


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