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)

The risk factors of stroke in young adults and in the whole population are the same in general, but there are some special risk factors in young adults. They are congenital or early acquired diseases which are complicating with early stroke. We studied the risk factors of cerebrovascular insults in 150 patients, 20-49 years old (Table 1). This was 26.04 percent of all patients that were hospitally treated in the urgent neurological department over one year. However, twenty years ago, this percent was 20.20 [2]. We found that arterial hypertension was dominant both among young adults (47.99 percent) and in the whole population (Table 2) [1-3]. Essential hypertension was the most frequent, and renal and thyreotoxical hypertensions were rare. The atherogenic level of low density and high density lipoproteins (LDL/HDL) was present in 14.66 percent of young adult patients [3]. Diabetes mellitus, a known risk factor of stroke, was found in 5.33 percent of our studied patients, especially in the juvenile form [1-3]. Besides juvenile diabetes mellitus, we found other risk factors that were characteristic of young adults: systemic lupus erythematosus (3.33 percent), which began at an early vital age, and numerous cerebrovascular complications appeared during the first five years of illness [7]. In this group of young adults, we found no other type of vasculitis, which also can be a risk factor of stroke. Great risk factors of stroke in young adults were arterial-venous malformation, brain aneurysm and congenital muscular hypoplasia of the carotide and middle caliber cerebral arteries-multiple progressive intracranial arterial occlusion or Nishimoto Takeuchi disease or Moya Moya disease, which were found in 3.99 percent of our patients. These diseases were complicated by cerebrovascular haemorrhagic or ischaemic insults over the young vital period [9]. The similar was with congenital or early acquired (rheumatic fever) heart valve defects (3.99 percent in our group), with early cerebrovascular complications due to cardiogenic thromboembolism mechanisms [10]. In 2 percent of patients the stroke was the consequence of anticoagulant therapy. These were the patients with operated heart valve defects (haemodynamic risk factor was eliminated, but haemorrheological risk factor was evident) [2, 3]. Also, disturbances of cardiac rhythm were risk factors of stroke in 2 percent of our patients. The mechanism of stroke originated is cardiogenic thromboembolism or global hypotension and the following ischaemia in the border brain zone [11]. All these risk factors were present in a relatively small number of patients, but they were "strong" risk factors of stroke, especially in young adults. On the other hand, there were nicotinism, alcoholism and obesity. They were present in a greater percent (25.33; 15.66; 18.66 percent), but their influence was slow and indirect by haemorrheologic mechanism (the increasing aggregation of platelets, reduced flexibility of red and white blood cells, changed prostacycline-prostaglandin relation in endothelial and blood cells, viscosity of blood, LDL/HDL) [2, 3, 12, 13]. A prolonged psychogenic stress (8.66 percent in our group) was, also, a risk factor of stroke. It induced increase in catecholamine level, arterial hypertension, constriction of blood vessels, endothelial cell damages, increased aggregation of platelets, changed prostacycline-prostaglandin relation, metabolism of lipids and polysaccharides) [2, 3]. We found no abuse of ephedrine [16] or cocaine [15] as risk factors of stroke in our group, although it was described in litterature. Also, we found no postoperative thromboemolism (foramen ovale apertum). Ischaemic cerebrovascular insults dominated (77.34 percent) in our group of patients. In one article (Canada) [17] haemorrhagic insults were dominant in young adults. In our opinion, the number of our patients was not adequated, as haemorrhagic stroke is also treated in neurosurgical departments. The mor
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PMID:[Risk factors for stroke in young people]. 910 54

Animal models of autoimmune disease have been successfully used to explore peripheral stem cell transfusion and bone marrow transplantation. Allogeneic marrow transplants have been shown to suppress lupus-like disease and experimental allergic encephalomyelitis. Autologous transplantation has also been successful in adjuvant arthritis. Operationally, these may be considered as graft versus autoimmunity effects. In humans, adoptive autoimmunity, in which the donor becomes apparent in the recipient, has been documented for myasthenia gravis and insulin dependent diabetes mellitus. Of 9 allogeneic bone marrow transplants for rheumatoid arthritis, 4 patients have done well for many years while one relapsed after 2 years. In 2 cases, autologous marrow transplant has been used specifically to treat autoimmune disease: one patient with CREST had only a transient response and one patient with myasthenia gravis had remission. While allogeneic bone marrow transplant is the most rational procedure, its use in nonmalignant disorders must be very carefully considered secondary to its toxicity and potential morbidity. The use of peripheral blood CD34+ cells with T cell depletion, may promise complete or partial longterm remission but results of this therapy need to be compared with other immunosuppressive combinations.
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PMID:Stem cell transplantation for severe autoimmune disorders, with special reference to rheumatic diseases. 915 Jan 12

Autoimmune diseases cause significant and chronic morbidity and disability. The actual number of persons in the United States that are affected by autoimmune diseases and the resultant magnitude of their impact on the public's health are limited to a few specific diseases. In order to understand the clinical, public health and economic importance of these diseases it is necessary to have estimates of incidence and prevalence rates in the population. In this analysis, we estimate the number of persons affected by 24 autoimmune diseases in the United States by applying mean weighted prevalence and incidence rates obtained from published articles to U. S. Census data. The study was restricted to 24 autoimmune predefined diseases for which there was direct or indirect evidence for autoimmune pathogenesis. Subsequently, we used computerized search software and ancestry searching (bibliographies) to conduct a comprehensive search of articles published from 1965 to the present. Eligible studies included those which adhered to standard disease definitions and which included population-based estimates of incidence or prevalence rates. Mean weighted incidence and prevalence rates were calculated from eligible published studies with greater weight proportionately given to larger studies. The mean rates were then applied to the U.S. Census population figures to estimate the number of persons currently afflicted with each disease and the number of new cases occurring each year in the United States. Only U.S. and European studies were used to estimate prevalence and incidence rates when there were at least six eligible studies available for a disease. When there were fewer than six studies, all available studies were included, regardless of country of origin. The number of eligible incidence and prevalence studies found in the literature varied considerably between the 24 autoimmune diseases selected. The largest number of eligible prevalence studies were conducted on multiple sclerosis (MS), rheumatoid arthritis, and systemic lupus erythematosus (SLE) (>/=23), followed by insulin-dependent diabetes (IDDM), myasthenia gravis, primary biliary cirrhosis, and scleroderma (>/=7). There were only one to four eligible studies done on 11 other diseases, and no prevalence studies on 6 diseases. Incidence studies were less frequent but the largest number of studies were conducted on IDDM (n = 37) and MS (n = 28), followed by Graves' disease/hyperthyroidism, glomerulonephritis, primary biliary cirrhosis, rheumatic fever, rheumatoid arthritis, scleroderma, and SLE (>/=9). On the other 11 diseases, there were one to six eligible studies, and no studies on 5 diseases. There were no eligible incidence or prevalence studies on Goodpasture's syndrome, idiopathic thrombocytopenia purpura, or relapsing polychondritis. Overall we estimate that 8,511,845 persons in the United States or approximately 1 in 31 Americans are currently afflicted with one of these autoimmune diseases. The diseases with the highest prevalence rates were Graves'/hyperthyroidism, IDDM, pernicious anemia, rheumatoid arthritis, thyroiditis, and vitiligo, comprising an estimated 7,939, 280 people or 93% of the total number estimated. Glomerulonephritis, MS, and SLE added an estimated 323,232 people. The prevalence of the other diseases reviewed were rare, less than 5.14/100,000. Most diseases were more common in women. From the incidence data we estimate that 237,203 Americans will develop an autoimmune disease in 1996 and that approximately 1,186,015 new cases of these autoimmune diseases occur in the United States every 5 years. Women were at 2.7 times greater risk than men to acquire an autoimmune disease. After reviewing the medical literature for incidence and prevalence rates of 24 autoimmune diseases, we conclude that many autoimmune diseases are infrequently studied by epidemiologists. As a result the total burden of disease may be an underestimate. (ABSTRACT TRUNCATED)
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PMID:Epidemiology and estimated population burden of selected autoimmune diseases in the United States. 928 81

Human autoimmune diseases are thought to develop through a complex combination of genetic and environmental factors. Genome-wide linkage searches of autoimmune and inflammatory/immune disorders have identified a large number of non-major histocompatibility complex loci that collectively contribute to disease susceptibility. A comparison was made of the linkage results from 23 published autoimmune or immune-mediated disease genome-wide scans. Human diseases included multiple sclerosis, Crohn's disease, familial psoriasis, asthma, and type-I diabetes (IDDM). Experimental animal disease studies included murine experimental autoimmune encephalomyelitis, rat inflammatory arthritis, rat and murine IDDM, histamine sensitization, immunity to exogenous antigens, and murine lupus (systemic lupus erythematosus; SLE). A majority (approximately 65%) of the human positive linkages map nonrandomly into 18 distinct clusters. Overlapping of susceptibility loci occurs between different human immune diseases and by comparing conserved regions with experimental autoimmune/immune disease models. This nonrandom clustering supports a hypothesis that, in some cases, clinically distinct autoimmune diseases may be controlled by a common set of susceptibility genes.
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PMID:Clustering of non-major histocompatibility complex susceptibility candidate loci in human autoimmune diseases. 970 86

A single dose of pasteurized Mycobacterium bovis administered intravenously to prediabetic non-obese diabetic (NOD) mice prevented the onset of type 1 diabetes but precipitated a systemic 'autoimmune rheumatic disease' (ARD) similar to systemic lupus erythematosus. This syndrome was characterized by haemolytic anaemia, anti-dsDNA and anti-Smith antigen (Sm) antinuclear autoantibodies, increased severity of sialadenitis and glomerular immune complex deposition. Here, we examine the specificity of the autoantibody responses in M. bovis-treated NOD mice. Large amounts of antibody were detected to the Sm/ribonucleoprotein (RNP) complex, of which the 28 000 MW polypeptide appeared to be immunodominant. The IgG subclass involved in the anti-Sm response was primarily IgG2a. Antibodies against dsDNA were also detected, but the subclass of this response was mixed, with IgG2a and IgG2b being present in equal amounts. Together, these findings argue against a role for immune deviation towards T helper type 2 (Th2) responses in pathogenesis of the disease. The anti-dsDNA and anti-Sm reactivities were not mediated by polyreactive antibodies since neither antigen could cross-compete plasma antibody binding to the other in competitive enzyme-linked immunosorbent assay. The role of polyclonal B-cell activation was examined by measuring total gamma-globulin as well as IgG reactive with other nuclear antigens including Ro60, Ro52 and La, which although not a major component of the autoantibody responses in these mice, did show small but significant increases following immunization with M. bovis. Thus polyclonal stimulation, while likely to be occurring, was not directly responsible for production of anti-Sm antibodies.
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PMID:Characterization and specificity of B-cell responses in lupus induced by Mycobacterium bovis in NOD/Lt mice. 976 51

Since Morton and Siegel's epochal experiments 30 years ago animal models have been successfully utilized both for transfer and resolution of autoimmune diseases (AID). More recently human lymphocyte xenografts have reproduced clinical AID in SCID mice. Allogeneic stem cell transplantation demonstrated therapeutic potential in fully developed autoimmune disease. Mixed allogeneic chimerism induced by a sublethal approach has also been shown to prevent and even reverse autoimmune insulitis in nonobese diabetic (NOD) mice. More unexpectedly it was found that experimental adjuvant arthritis (AA) and experimental allergic encephalomyelitis (EAE) could be cured by means of total body irradiation (TBI) followed by autologous hemolymphopoietic stem cell (HSC) transplantation. It was postulated that the newly developing T cells might be tolerant to self antigens. The transfer of AID from affected donors to recipients of allogeneic HSC transplants has been reported for many organ-specific AID, including diabetes (IDDM), thyroiditis, myasthenia gravis and thrombocytopenic purpura (AITP); rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) were not transferred. Conversely patients with the combination of AID and a severe blood disease (leukemia, aplasia) were cured of both diseases following allogeneic BMT, with the notable exception of a relapse in a patient with RA despite full donor engraftment. Allogeneic transplants are certainly more promising as far as concerns a resolution of AID, because they may also exert a graft-versus-autoimmunity effect by gradually eradicating the recipient's lymphopoiesis, but transplant related mortality (TRM) is considered still too high to employ this procedure consistently. New non-myeloablative conditioning regimens, designed to allow the donor's immune system to take over, are already utilized for malignant and non-malignant hematologic diseases, and may become an attractive option for severe, refractory AID. For the time being, however, autologous procedures are still safer, and are being utilized in many projects worldwide. The EBMT/EULAR Registry has collected over 70 patient reports. The more numerous and favorable results have been obtained up to now in multiple scleosis and in systemic lupus erythematosus; the worst in refractory autoimmune thrombocytopenic purpura. No definite conclusions as to the efficacy of autologous HSC transplantation, from marrow or from blood, with or without T-cell depletion, may be drawn at this time, but the feeling is that real cures will be very difficult to obtain by this approach, and that corticosteroid-free remissions and a general lowering of the autoimmune potential will be more realistic goals. Accurate comparisons with already existing aggressive immunosuppressive protocols will become necessary, if possible by means of prospective randomized clinical studies.
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PMID:Stem cell transplantation for severe autoimmune diseases: progress and problems. 979 58

Vascular complications are the main cause of morbidity in diabetes mellitus. However, the risk factors for vascular disease remain incompletely elucidated. It has been previously suggested that factors other than glycemia may contribute to the development of vasculopathy. In this study we determined the prevalence of phospholipid-binding antibodies in uncomplicated and complicated diabetes. We studied 53 uncomplicated diabetic patients, with type 1 (n = 32) or type 2 (n = 21) diabetes; 23 diabetic patients with proliferative retinopathy; 28 diabetic patients with an overt nephropathy; 37 diabetic patients with macroangiopathy and 22 non diabetic control patients. Both lupus anticoagulant and anticardiolipin antibodies were determined. Other risk factors for macroangiopathy were analysed. The prevalence of phospholipid-binding antibodies was similar in uncomplicated diabetic patients and in controls (type 1 diabetes: 9.4%; type 2 diabetes: 9.5%; control group: 4.6%; P= 0.76). In complicated diabetes, the frequency of these antibodies was increased only in patients with overt nephropathy (32.1%, P=0.01) or with macroangiopathy (32.4%, P=0.01) while patients with isolated retinopathy were comparable with uncomplicated diabetic patients (4.3%, P= 0.66). Uncomplicated diabetes was not associated with phospholipid-binding antibodies. We found a higher prevalence of these antibodies in diabetic patients with macroangiopathy or nephropathy. These results suggest a potential role of phospholipid-binding antibodies in the progression of vascular complications in diabetes mellitus.
Lupus 1998
PMID:Vascular complications of diabetes mellitus: what role for phospholipid-binding antibodies? 979 49

Several investigators have reported the possibility of gene therapy for experimental autoimmune diseases such as type-1 insulin-dependent diabetes (IDDM), experimental allergic encephalomyelitis (EAE), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE). Although there are no reports about gene therapies for human autoimmune rheumatic diseases including RA and SLE, we reviewed these experimental therapies for model animals and discussed the possibility of gene therapy for human autoimmune rheumatic disorders as a new therapeutic strategy.
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PMID:[Gene therapy in autoimmune rheumatic diseases]. 1007 22

Although much is known about the pathology of human chronic atrophic (type A, autoimmune) gastritis, its cause is poorly understood. Mouse experimental autoimmune gastritis (EAG) is a CD4+ T cell-mediated organ-specific autoimmune disease of the stomach that is induced by neonatal thymectomy of BALB/c mice. It has many features similar to human autoimmune gastritis. To obtain a greater understanding of the genetic components predisposing to autoimmune gastritis, a linkage analysis study was performed on (BALB/cCrSlc x C57BL/6)F2 intercross mice using 126 microsatellite markers covering 95% of the autosomal genome. Two regions with linkage to EAG were identified on distal chromosome 4 and were designated Gasa1 and Gasa2. The Gasa1 gene maps within the same chromosomal segment as the type 1 diabetes and systemic lupus erythematosus susceptibility genes Idd11 and Nba1, respectively. Gasa2 is the more telomeric of the two genes and was mapped within the same chromosomal segment as the type 1 diabetes susceptibility gene Idd9. In addition, there was evidence of quantitative trait locus controlling autoantibody titer within the telomeric segment of chromosome 4. The clustering of genes conferring susceptibility to EAG with those conferring susceptibility to type 1 diabetes is consistent with the coinheritance of gastritis and diabetes within human families. This is the first linkage analysis study of autoimmune gastritis in any organism and as such makes an important and novel contribution to our understanding of the etiology of this disease.
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PMID:A major linkage region on distal chromosome 4 confers susceptibility to mouse autoimmune gastritis. 1022 80

Autism is an age-dependent neurologic disorder that is often associated with autoimmune disorders in the patients' relatives. To evaluate the frequency of autoimmune disorders, as well as various prenatal and postnatal events in autism, we surveyed the families of 61 autistic patients and 46 healthy controls using questionnaires. The mean number of autoimmune disorders was greater in families with autism; 46% had two or more members with autoimmune disorders. As the number of family members with autoimmune disorders increased from one to three, the risk of autism was greater, with an odds ratio that increased from 1.9 to 5.5, respectively. In mothers and first-degree relatives of autistic children, there were more autoimmune disorders (16% and 21%) as compared to controls (2% and 4%), with odds ratios of 8.8 and 6.0, respectively. The most common autoimmune disorders in both groups were type 1 diabetes, adult rheumatoid arthritis, hypothyroidism, and systemic lupus erythematosus. Forty-six percent of the autism group reported having relatives with rheumatoid diseases, as compared to 26% of the controls. Prenatal maternal urinary tract, upper respiratory, and vaginal infections; asphyxia; prematurity, and seizures were more common in the autistic group, although the differences were not significant. Thirty-nine percent of the controls, but only 11% of the autistic, group, reported allergies. An increased number of autoimmune disorders suggests that in some families with autism, immune dysfunction could interact with various environmental factors to play a role in autism pathogenesis.
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PMID:Familial clustering of autoimmune disorders and evaluation of medical risk factors in autism. 1038 47


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