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)

Lesions of the uteroplacental vasculature may be involved in the pathogenesis of "placental insufficiency" in pregnancies complicated by hypertension, diabetes, systemic lupus erythematosus, and idiopathic fetal growth retardation. The decidual arteries of the placental bed of normotensive, hypertensive, and diabetic women were studied by histologic examination and direct immunofluorescence for immunoglobulins and complement. Decidual tissue was obtained by curettage and snap frozen immediately after delivery of the placenta in 21 normal pregnant control subjects, 73 nondiabetic women with hypertensive disorders, and 41 women with insulin-dependent diabetes. Lesions of fibrinoid necrosis and/or atherosis were observed in some of the decidual arteries of 53% of women with preeclampsia (primary or superimposed) and also in a proportion of women with stable chronic hypertension or normotensive diabetes. Thus, fibrinoid necrosis/atherosis of the decidual arteries is not specific for preeclampsia. Immunoglobulins and complement were detected in arteries with lesions in subjects of all clinical groups. The findings do not support the concept that immunoprotein deposition in pathologic decidual arteries is related to a hypothetical immunologic reaction specific for preeclampsia. In preeclampsia, vascular deposition of immunoglobulin and complement may be related to local intravascular coagulation.
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PMID:Decidual arteriopathy in hypertension and diabetes in pregnancy: immunofluorescent studies. 703 98

The authors report the case of a 22-year-old Guatemalan in whom lupus was diagnosed 8 months after a second pregnancy. The diagnosis of lupus met the criteria of the ARA: Raynaud's syndrome, alopecia, arthralgia, thrombophlebitis, facial erythema, antinuclear factor at 1/100, Farr at 75 p. 100 and immunofluorescent demonstration of IgM binding in healthy skin. Two months after the beginning of the lupus, there was onset of insulin-resistant ketosic diabetes without overweight. The serum insulin was 1.140 mu U/ml. Acanthosis nigricans was noted and confirmed by a biopsy. Insulin-resistance can be attributed to anti-membrane receptor antibodies titrating at 1/200 (R. Khan). The short-term progress of the disease was favorable on corticosteroid treatment. Insulin could be stopped, but high insulin serum levels persisted. This case meets criteria for type B as defined by Flier, Khan and Roth, and is the first European case of lupus with a complete presentation. Short-term progress was favorable, and there is no evidence to affirm that there will be a tardive progression towards hypoglycemia which is, however, possible due to the persistence of elevated serum insulin levels.
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PMID:[Lupus, insulin-resistant diabetes and acanthosis nigricans (author's transl)]. 723 1

At some time in their lives one in a five persons is affected by urticaria and/or angioedema. The cause of urticaria may never be found in up to one quarter of patients with acute urticaria and in up to 90-95% with chronic urticaria. In this study we present results of our compounded approach (clinical follow up, laboratory findings, allergological testing) to patients with chronic urticaria and autoimmune diseases that progressed into chronic urticaria or started before the onset of the chronic urticaria. Our first case was a 56 year old woman with a 10 month history of chronic urticaria, angioedema and chronic gastritis before the diagnoses of insulin dependent Diabetes mellitus and Hypothyreoidismus primarius were established. Allergological testing reveals specific clinical significant immediate reaction to Balsam Peru. After adequate substitutional therapy was advocated and with specific clinical avoidance of offended allergen, remission was obtained. The second case was a 46 year old female suffering from chronic urticaria (with clinical features of urticaria like vasculitis) associated with hypocomplementemia (particularly C4 depressed) with negative antinuclear antibodies but positive circulating immune complexes after a 2 year follow up the patient developed Systemic lupus erythematosus. The third case was a 63 year old woman who developed chronic urticaria 3 years after total thyroidectomy, with pathological finding of Thyroiditis lymphocytaria-Hashimoto; after the allergological testing, positive lymphocyte transformation test revealed allergical sensitization to Vobenol was substituted with Thyvoral, complete remission was obtained.
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PMID:[Chronic urticaria from the aspect of autoimmune diseases]. 756 41

Immune-mediated diseases affect up to 5% of the population and are a major cause of morbidity and mortality. These diseases can be organ specific, such as insulin-dependent diabetes (IDDM) and non-organ specific, such as Rheumatoid Arthritis (RA). Identical and non-identical twins have been used to establish whether these diseases are determined by genetic or environmental factors. The results of these studies have been collated in a new section of the Mendel Institute in Rome. Diseases included in these studies included IDDM, RA, Systemic Lupus Erythematosus (SLE), Multiple Sclerosis (MS) and Myasthenia. Striking differences in concordance rates between identical and non-identical twins in all these studies suggest that genetic factors are important in causing these diseases. All the diseases are known to be associated with HLA genes on chromosome 6 which may account for some or all of the genetic susceptibility. However, in the majority of pairs the affected twin has an unaffected co-twin. These observations suggest that non-genetically determined factors, probably environmental factors and not somatic mutations, are critical. The study of unaffected co-twins, who are at high disease-risk, has allowed the identification of changes which precede and predict the clinical disease. The immune-mediated destruction in many of these diseases is probably caused by T-lymphocytes. Twin studies have shown the importance of genetic factors in determining T-cell responses. Identical twins should, therefore, provide the perfect test bed to assess the role of T-cells in immune-mediated diseases.
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PMID:Twin studies in auto-immune disease. 784 25

Physicochemical properties of immunoglobulin G of human blood serum under different states of the organism have been studied. Certain regularity of pH-distribution of IgG molecules which include different kinds of light chains has been first demonstrated using the method of isoelectrical focusing in a horizontal multicell apparatus of own construction in the system of ampholines (LKB, Sweden). This distribution changes directly depend on the peculiarities of the pathological process. The increase of a share of kappa-containing molecules of serum IgG in the alkali (by isopoints) fractions for the acute period of autoimmune thyroiditis, nodular toxic goiter, insulin depending diabetes mellitus, systemic lupus erythematosus is observed. The decrease of this parameter is characteristic under diffuse toxic goiter, gastric and duodenal peptic ulcer. IgG which takes direct part in immunocomplex processes differs from serum one by its physicochemical properties. In particular, this is manifested in the distribution of separate fractions in isospectrum, in the composition with other proteins and correlation of the types of light chains in them depending on concrete pathology.
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PMID:[Features of the isoelectric distribution of human immunoglobulin G depending on the type of light chains]. 787 93

Adrenal autoantibodies characteristic of autoimmune Addison disease are directed towards steroid 21-hydroxylase (21-OH; EC 1.14.99.10). We describe a new assay to measure 21-OH autoantibodies (21-OH Abs), based on immunoprecipitation by the antibodies of 35S-labeled human 21-OH. Using this immunoprecipitation assay (IPA), we detected 21-OH Abs in 42 of 64 (66%) patients with Addison disease and in 14 of 19 (74%) patients with autoimmune polyendocrine syndromes type I and type II. No 21-OH Abs were detected by the IPA in any patients with Addison disease attributable to tuberculosis (n = 9) or adrenoleukodystrophy (n = 9) or in patients with autoimmune thyroid disease (n = 28), systemic lupus erythematosus (n = 10), myasthenia gravis (n = 10), rheumatoid arthritis (n = 10), or insulin-dependent diabetes mellitus (n = 12). None of the 26 sera from healthy normal blood donors was positive for 21-OH Abs by the assay. We found good agreement between 21-OH Abs measured by IPA and by Western blotting (r = 0.83, n = 123, P < 0.001). The inter- and intraassay CVs for IPA were well < 10% at high, medium, and low concentrations of 21-OH Abs. Overall, our studies indicate that the IPA provides a specific, sensitive, and convenient system for measuring 21-OH Abs.
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PMID:Immunoprecipitation assay for autoantibodies to steroid 21-hydroxylase in autoimmune adrenal diseases. 788 6

The complement system is an important part of non clonal or innate immunity that collaborates with acquired immunity to kill pathogens and to facilitate the clearance of immune complexes. The complement is made up of 20 distinct plasma proteins and 9 different membrane proteins. Three components, factor B, C2 and C4 (with 2 isotypes), are coded by polymorphic HLA-linked genes and are sometimes referred to as class III antigens, inherited as compact units called complotypes. The C4 genes are the most polymorphic, including a common null allele (Q0) at both the C4A and C4B loci. Other polymorphic complement factors (not linked to HLA) are C3 (2 common alleles), C6 and C7 (closely linked, with 3 and 2 alleles, respectively). A certain degree of polymorphism has also been described for complement receptors and membrane control proteins. No differences in functional activity are usually detected among different alleles. Immune-mediated diseases are associated with C4Q0, in particular: systemic lupus erythematosus and discoid-systemic lupus erythematosus, insulin-dependent diabetes mellitus, liver cirrhosis, celiac disease and IgA/IgG4 deficiency. Even if optimal HLA markers do become available, genetic counselling is usually not the ultimate goal for dealing with most of the HLA-associated common diseases, although their study could help to better delineate disease pathogenesis.
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PMID:Polymorphism of the complement components in human pathology. 794 94

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

Epidemiological and experimental evidence suggested that denial of dietary cow milk protein early in life protects genetically susceptible children and animals from insulin-dependent diabetes (IDDM). Bovine serum albumin (BSA) was proposed as a candidate milk-borne mimicry antigen responsible for the diabetogenic cow milk effect. Elevated anti-BSA antibodies have been observed in patients and diabetic rodents, and these antibodies precipitate p69 from islet cell lysates. IDDM is a T cell mediated disorder but efforts to detect BSA-specific T cells in diabetic children have so far failed. We describe here a culture system which allowed the detection of BSA-specific T cells and we mapped this response to the ABBOS peptide (pre-BSA position 152-169) previously identified as a possible mimicry epitope. ABBOS-sensitized T cells were found in 28/31 children with recent onset IDDM but not in non-diabetic controls nor in children with SLE or JRA. T cell proliferative responses declined within the first few years of diabetes diagnosis. Although no effector cell role for BSA/ABBOS specific T lymphocytes has been demonstrated, the presence of BSA peptide-specific T cells strengthens the postulated link between a cow milk protein and IDDM.
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PMID:T cells from children with IDDM are sensitized to bovine serum albumin. 799 51

The particular histocompatability antigen (HLA) gene(s) that may confer systemic lupus erythematosus (SLE) susceptibility remains unknown. In the present study, 58 unrelated patients and 69 controls have been analyzed for their class I and class II serologic antigens, class II (DR and DQ) DNA restriction fragment length polymorphism, their deduced DQA1 and B1 exon 2 nucleotide sequences and their corresponding amino acid residues. By using the etiologic fraction (delta) as an almost absolute measure of the strongest linkage disequilibrium of an HLA marker to the putative SLE susceptibility locus, it has been found that the strength of association of the HLA marker may be quantified as follows: DQA1*0501 (associated to DR3) or DQB1*0201 (associated to DR3) > non Asp 57 beta DQ/Arg 52 alpha DQ > DR3 > non Asp 57 beta DQ. Thus, molecular HLA DQ markers tend to be more accurate as susceptibility markers than the classical serologic markers (DR3). However, dominant or recessive non Asp 57 beta DQ susceptibility theories, as previously postulated for insulin-dependent diabetes mellitus, do not hold in our SLE nephritic population; indeed, three patients bear neither Arg 52 alpha DQ nor Asp 57 beta DQ suscepibility factors. On the other hand, nonsusceptibility factors are included in our population in the A30B18CF130-DR3DQ2(Dw25) haplotype and not in A1B8CS01-DR3DQ2(Dw24); this distinctive association has also been recorded in type I diabetes mellitus and may reflect the existence of common pathogenic HLA-linked factors for both diseases only in the A30B18CF10DR3DQ2(Dw25) haplotype. Finally, the observed increase of deleted C4 genes (and not 'null' C4 proteins) in nephritic patients shows that C4 genes are disease markers, but probably without a pathogenic role.
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PMID:Differential contribution of C4 and HLA-DQ genes to systemic lupus erythematosus susceptibility. 810 32


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