Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003873 (rheumatoid arthritis)
 53,068 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to determine the effects of adrenal corticosteroids on regional adipose tissue cellularity groups of age-matched women subjected to long-term treatment with adrenal corticosteroids due to bronchial asthma or rheumatoids due to bronchial asthma or rheumatoid arthritis were compared with control of women. A small group of women suffering from Cushing's syndrome was also examined. Body composition, adipose cellularity in four major subcutaneous regions and metabolic variables were determined. The Cushing's syndrome patients weighed more than the other groups and seemed to have more fat cells while the patients with rheumatoid arthritis showed decreases in body cell mass, body fat and average fat cell size. These differences necessitated a body fat matching between patients and controls before analysis of regional depot fat differences. Body fat, average fat cell size and total fat cell number were similar in patients and controls. The Cushing's syndrome group was too small to allow this matching. All three groups exposed to increased levels of adrenal corticosteroids showed smaller fat cells in the gluteal region in comparison with controls, but no differences in fat cell size in the femoral, epigastrial or hypogastrial regions. This change also corresponded to a diminution of the thickness of subcutaneous plus skin layer in the gluteal region, measured with an ultrasonic technique. All the groups of patients had elevated fasting plasma insulin. The possibility was considered that the observed regional redistribution of fat is characteristic for adrenal corticosteroids.
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PMID:The effects of adrenal corticosteroids on regional adipocyte size in man. 124 97

Two new TCRV beta coding region polymorphisms were identified: V beta 6.9a/b and V beta 21.4a/b. In both cases, a single nucleotide difference gives rise to an amino acid exchange. Genomic typing by the PCR/sequence-specific oligonucleotide probing technique was performed to study a possible contribution of these two new polymorphisms in susceptibility to autoimmune diseases. However, there was no association with insulin-dependent diabetes mellitus, rheumatoid arthritis, juvenile rheumatoid arthritis, multiple sclerosis, myasthenia gravis or coeliac disease. On the other hand, significant differences were found between Caucasoid and Oriental populations in frequencies of the V beta 6.9 and V beta 21.4 alleles.
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PMID:Coding region polymorphisms of human T-cell receptor V beta 6.9 and V beta 21.4. 138 40

Two recent cases of cervical necrotizing soft-tissue infection are herein presented. Case 1. A 52-year-old man with uncontrolled diabetes was hospitalized because of an erythematous swelling of the left side of his neck and high grade fever. Fetid yellowish pus exuded from the left parotid area. The swelling extended from the left temporal area to the left supraclavicular fossa, with necrosis of the parotid gland, sternocleidomastoid, masseter and a portion of the strap muscles. Wound cultures revealed Staphylococcus aureus and alpha-hemolytic streptococcus. No anaerobic bacteria were detected. Treatment consisted of intravenous administration of antibiotics, control of diabetes with insulin, and debridement of the necrotic tissue, which left an epidermal defect in the initially swollen area. Transfer of a forearm free flap was done after the growth of healthy granulation tissue over the affected area. Case 2. A 55-year-old woman with rheumatoid arthritis was transferred to our hospital after tracheotomy performed in another hospital because of dyspnea due to severe crepitant swelling of her cheeks and submandibular areas bilaterally, and her left temporal area. A copious amount of fetid pus exuded from the incisions made in the left temporal area, left cheek, and right submandibular area. There were bilateral diffuse rales. Culturing the pus revealed alpha-hemolytic streptococci, while MRSA and Pseudomonas aeruginosa were detected from cultures of sputum. No anaerobic bacteria were found. After intravenous administration of antibiotics, infected wounds and pneumonia were ameliorated, and necrotic subcutaneous tissue and fascia were debrided. The patient was discharged with a residual depression in her left cheek and a scar on her left temporal area.
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PMID:[A report of two cases of cervical necrotizing soft-tissue infection]. 140 20

We investigated the effects of platelet-derived growth factor (PDGF), epidermal growth factor (EGF), and insulin on the cell proliferation of and the production of matrix metalloproteinases (MMPs) by rheumatoid synovial fibroblasts in order to determine the role of these agents in rheumatoid arthritis. PDGF stimulated rheumatoid synovial fibroblasts to increase DNA synthesis and the production of precursor forms of MMP-1 of M(r) = 53,000 and -3 of M(r) = 57,000. EGF and insulin also increased DNA synthesis and the production of these enzymes, but the amount of DNA or MMPs was smaller than that induced by PDGF. Since the production of matrix macromolecules and their degradation is essential for the remodelling of synovial tissue in rheumatoid arthritis, these data suggest that the production of MMP-1 and-3 by rheumatoid synovial fibroblasts in relation to cell proliferation plays an important role in the pathological process of rheumatoid arthritis.
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PMID:Cell proliferation-related production of matrix metalloproteinases 1 (tissue collagenase) and 3 (stromelysin) by cultured human rheumatoid synovial fibroblasts. 144 77

D-Penicillamine is a drug known to induce various immunological abnormalities. We used a competitive radiobinding assay, to evaluate the presence of insulin autoantibodies in 42 patients with rheumatoid arthritis (RA), under various treatment modalities. In 11/42 (26.2%) patients, the levels of insulin autoantibodies (range 59-1970 nU/ml) exceeded our upper limit of normal range (50 nU/ml). Nine of these 11 (81.8%) insulin autoantibodies positive patients had been treated with D-penicillamine. Out of 21 D-penicillamine treated patients, 9 (42.9%) were insulin autoantibodies positive (range 80 to 1970 nU/ml). An inverse correlation was found between the concentration of insulin autoantibodies and the time interval since the last drug administration, R = -0.58 (p < 0.05). No correlation was found between the autoantibodies levels and age, or duration of D-penicillamine treatment. In summary, elevated concentration of serum insulin autoantibodies are most probably induced by D-penicillamine therapy in patients with RA and tend to decrease after the drug withdrawal.
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PMID:Frequent induction of insulin autoantibodies by D-penicillamine in patients with rheumatoid arthritis. 146 63

It is now generally accepted that many cytokines are involved in the pathogenesis of autoimmune disease, either directly by causing tissue destruction or indirectly through the activation of autoreactive and inflammatory cells. Thus, cytokines, such as tumor necrosis factor-alpha, are implicated in the pathogenesis of rheumatoid arthritis based on in vitro studies on synovial tissue from patients with rheumatoid arthritis, which suggest that the effects of tumor necrosis factor-alpha are amplified by its potential to induce other pro-inflammatory cytokines, such as interleukin-1 and granulocyte-macrophage colony-stimulating factor. Transgenic mouse technology has shown that mice expressing the human tumor necrosis factor-alpha gene develop a polyarthritis. Interleukin-2 has also been identified by transgenic technology as a cytokine involved in the pathogenesis of insulin-dependent diabetes mellitus through the activation and stimulation of growth of autoreactive T cells.
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PMID:Cytokines in autoimmunity. 146 99

Generalized tendomyopathy (GTM), or fibromyalgia (FM), is a disease characterized by wide-spread pain in the musculoskeletal system which usually begins at a single site, e.g., as low-back pain or cervical syndrome, and develops into generalized pain over months or years. The disorder affects primarily women, beginning around the age of 35 and reaching its peak during or after the menopause. Its etiology is still unknown. Secondary forms are observed particularly in rheumatoid arthritis. In order to get more information on FM we determined the local metabolic rate of glucose in vivo in the skeletal muscle (lumbar region) with dynamic 18F-FDG positron emission tomography (PET). 2 healthy volunteers and 6 female patients with FM reaching in age from 31 to 53 years were scanned. As 18F-FDG PET scanning is a metabolic tool, it is crucial to observe standardized conditions of metabolic steady-state. We used, therefore, the hyperinsulinemic euglycemic insulin clamp technique to stimulate the myogenic glucose uptake under stable plasma-glucose levels. The local metabolic rates of glucose utilization were estimated with a non-linear least squares fit on the 3 compartment 18F-FDG-model. A lumped constant of 0.67 was assumed. Under glucose clamp conditions patients with FM showed a significantly (p < 0.001) lower metabolic rate of glucose (4.3 +/- 1.1) mumol/100 g tissue/min compared with normal volunteers (8.5 +/- 2.3 mumol/100 g/min). Due to a significantly (p < 0.005) increased glucose backflow from tissue into the vascular space (k2 in the kinetic model) the rate of phosphorylation was markedly reduced in patients with FM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Determination of regional rate of glucose metabolism in lumbar muscles in patients with generalized tendomyopathy using dynamic 18F-FDG PET]. 147 8

Autoimmune diseases result from the activation of self-reactive T cells induced by autoantigens or by foreign antigens cross-reactive with an autoantigen. A striking characteristic of autoimmune diseases is the increased frequency of certain HLA alleles in affected individuals. Moreover, as demonstrated for example in rheumatoid arthritis and insulin-dependent diabetes mellitus, class II alleles positively associated with autoimmune diseases share amino acid residues in the hypervariable HLA regions involved in peptide binding. Therefore, it is likely that disease-associated HLA class II molecules have the capacity to bind the autoantigen and present it to T cells, thereby inducing and maintaining, under appropriate conditions, the autoimmune disease. The data reviewed here demonstrate MHC-selective inhibition of antigen-induced T cell responses in vivo by parenterally administered soluble, MHC-binding peptide competitors, under conditions in which the competitor is not immunogenic. This suggests the feasibility of a therapeutic approach based on blockade of MHC class II molecules in the treatment of HLA-linked autoimmune diseases.
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PMID:Inhibition of T cell activation by MHC blockade: a possible strategy for immunointervention in autoimmune diseases. 150 37

Interleukin 6 (IL-6) is a potent cytokine, the biological activities of which include the stimulation of immunoglobulin secretion, T cell activation, induction of the acute phase response, activation of megakaryocytes, and pyrogenicity. These biological activities make it a plausible contributor to rheumatoid arthritis. The ability of synoviocytes to synthesise this potential mediator of inflammation was tested. Cultures of fibroblast-like cells were established from joint tissue from patients with rheumatoid arthritis, degenerative joint disease, or trauma. Supernatants from synoviocytes from each diagnostic category contained IL-6-like activity as detected in a B9 plasmacytoma cell proliferation assay. Supernatants from IL-1 stimulated synoviocytes from patients with rheumatoid arthritis (n = 5) contained an average of 70,000 U/ml IL-6. Western blot analysis confirmed that these supernatants contained peptides that reacted with a highly specific antibody to IL-6. A cDNA probe specific for IL-6 hybridised with mRNA derived from synoviocytes representative of each disease state. Interleukin 6 mRNA expression increased by culturing synoviocytes in the presence of 10% calf serum, IL-1 (30 U/ml), insulin (166 ng/ml), or basic fibroblast growth factor (16 ng/ml). In contrast, dexamethasone (10(-6) mol/l) suppressed the ability of IL-1 to increase the expression of IL-6 mRNA. Recombinant IL-6 itself did not detectably upregulate its own message. The regulation of production of IL-6 by synoviocytes may be important in the pathogenesis of joint inflammation.
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PMID:Production and modulation of interleukin 6 synthesis by synoviocytes derived from patients with arthritic disease. 155 Apr 4

The associations or linkages between the polymorphisms of the Gm and Km immunoglobulin allotypes and the susceptibility to autoimmune diseases, including diseases with immuno-pathological pathogenesis are reported in this review. These diseases include multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus, insulin-dependent diabetes mellitus, Crohn's disease, coeliac 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. Immunoglobulin allotypes are described as well as the statistical methods used to analyse the data.
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PMID:Gm and Km allotypes in autoimmune diseases. 162 73


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