Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 4851389 | Diffuse pulmonary alveolar fibrosis. | 1974 May | Scadding, J. G. (1974).Thorax, 29, 271-281. Diffuse pulmonary alveolar fibrosis. The problems of diagnostic categorization of diffuse pulmonary alveolar fibrosis are outlined, and attention is drawn to the different implications of categories defined aetiologically and histopathologically. The pattern of pulmonary insufficiency associated with changes of these sorts is described, and the importance of using a terminology of pulmonary insufficiency which refers unequivocally to disorders of function is emphasized. The usage of the word `interstitial' in the context of inflammations of the lung is critically examined. It seems to be used to imply predominant involvement of alveolar walls, which in other contexts would be regarded as `parenchyma'. This unresolved conflict which accepted anatomical usage can be avoided by general acceptance of complementary conventions that `pneumonia' refers to inflammations of the lung characterized by exudation into alveolar spaces leading to consolidation, and `alveolitis' to those affecting predominantly alveolar walls. Some cases of alveolitis, so defined, can be shown to be due to reactions with inhaled organic dusts in the gas-exchanging part of the lungs in specifically sensitized individuals, constituting a group of aetiologically defined categories `extrinsic allergic alveolitis'. A few are due to ingested toxic substances. Many remain of unknown cause and show a strong and early tendency to alveolar wall fibrosis: they constitute a histopathologically defined category `cryptogenic fibrosing alveolitis'. | |
| 6184896 | [Epidemiologic aspects of seronegative spondylarthritis]. | 1982 Oct 1 | In accordance with the prevailing trends of the development of science in rheumatology Wright, Moll and Haslock inaugurated the integrative conception of the seronegative spondarthritides in the middle of the seventies. The diseases which belong to the seronegative spondarthritides are the ankylosing spondylitis, the psoriasis-arthritis, the Reiter syndrome, the Behçet syndrome, the ulcerous colitis, Crohn's disease and Whipple's disease. Object of the representation is the determination of the notion of seronegative spondarthritis and its presence among the dwelling population. Furthermore, the authors deal more in detail with the distribution according to the demographic and ethnographic characteristics, the frequency of the presence of HLA B 27 as well as with the results of familial investigations (familial aggregation and association). The heuristic value of the classification scheme of the seronegative spondarthritides developed by clinics appears worth of discussion, since from the epidemiological point of view aggravating critical objections concerning the method must be raised. Clinico-epidemiological statements of investigation, prospective and multicentric longitudinal investigations concerning the more profound study of the "natural history" of the seronegative spondarthritides are hopeful and necessary within the future research strategy. | |
| 6435243 | Differences in the production of arachidonic acid metabolites between healthy and rheumati | 1984 | Production of various arachidonic acid metabolites from both endogenous and exogenous substrate was measured using cultures of synovial fibroblasts from healthy and rheumatic synovia. At first, the rheumatic cells showed retarded growth and an altered histological picture. Rheumatic cells produced more 6-keto-PGF1 alpha, the main metabolite of prostacyclin, and prostaglandin E2 than did normal cells, which synthesized more thromboxane B2. Later on these differences diminished or disappeared, except regarding 6-keto-PGF1 alpha. When fairly high concentrations of exogenous arachidonic acid were used, for 2-hour incubation of the cells, the production of identified metabolites, 6-keto-PGF1 alpha, PGF2 alpha, PGE2, PGD2, PGA + PGB and thromboxane B2, was slightly less in rheumatic cells. In general, the main metabolite formed was 6-keto-PGF1 alpha. Some kind of feedback mechanism between prostaglandins and cyclic nucleotides is suggested. | |
| 805770 | Effects of anesthesia, surgery and inflammation upon host defense mechanisms. I. Effects u | 1975 | Complement protein levels and C7 hemolytic activity were measured in four individuals following anesthesia and surgery, and in a group of 20 patients with inflammatory diseases. Seven of the eight complement components studied characteristically were elevated, most dramatically C1s and C3PA. Elevation of C1s often was greater than elevation of C1q, displaying an independent variation of C1s and C1q in both postoperative and inflammatory disease patient groupds. The major increases of C components were seen subsequent to the peak C-reactive protein response, as was the occurrence of the 'reactor state', a propensity to formation of C56 which surprisingly was associated with increased levels of C7. Levels of properdin frequently were reduced postoperatively. It is concluded that multiple complement components, with the notable exception of properdin, respond as acute phase reactants which are elevated and changed in proportion postoperatively and during inflammatory disease. | |
| 6386426 | Piroxicam. A reappraisal of its pharmacology and therapeutic efficacy. | 1984 Oct | Piroxicam is a chemically different non-steroidal anti-inflammatory drug with a long half-life which enables it to be administered once daily. This member of the oxicam series of compounds is now well established in the treatment of rheumatoid arthritis and osteoarthritis and has been shown to be a suitable alternative to aspirin, indomethacin, naproxen, ibuprofen, ketoprofen, sulindac, phenylbutazone and diclofenac in the treatment of rheumatic diseases. Open trials in many thousands of patients in hospital clinics and in general practice have demonstrated its analgesic and anti-inflammatory efficacy in a wide cross-section of patients with rheumatic diseases, when administered once daily either at night or in the morning, and recent studies have demonstrated its usefulness in musculoskeletal disorders, dysmenorrhoea and postoperative pain. Such studies have also demonstrated the generally good tolerability of piroxicam 20mg daily. As with other non-steroidal anti-inflammatory drugs, gastrointestinal complaints are the most frequently reported side effects. The frequency and severity of these effects are dose related. Thus, piroxicam is now well established in the treatment of rheumatic diseases and offers an alternative to other analgesics in various pain states. | |
| 6978375 | Complement receptor (CR1) deficiency in erythrocytes from patients with systemic lupus ery | 1982 May 1 | This study reports quantitative information on the concentration of complement receptor for C3b and C4b (CR1) on erythrocytes from normal individuals and patients with immune complex disease. The measurements were performed by an immunoradiometric assay using monoclonal antibodies against CR1. The antibody specificity was confirmed by immunoprecipitation of CR1 from extracts of surface-labeled cells, by inhibition of rosette formation between B lymphocytes and the erythrocytes intermediate EAC14oxy23b, and by the characteristic distribution of the antigen among cells of human peripheral blood. The number of CR1 molecules in erythrocytes from 52 normal individuals was estimated as 1,410 +/- 620. No significant differences in CR1 levels were observed when individuals were grouped by sex, age, or blood groups. In patients with SLE and rheumatoid arthritis, the number of CR1 molecules per RBC was significantly lower, i.e., 600 +/- 307 and 903 +/- 417, respectively. CR1 levels were normal in asthmatics undergoing long-term treatment with prednisone. In SLE patients, significant correlations were found between CR1 levels, C4 hemolytic titers, and levels of circulating immune complexes. In two out of four patients with SLE, CR1 levels increased significantly during remission, showing that the deficiency is, at least in part, reversible. The deficiency in CR1 could be genetically controlled or could represent an epiphenomenon caused by the interaction of the receptor with a ligand present in the circulation of patients. | |
| 2409682 | [Reactivation of the alpha 1-fetoprotein synthesis in systemic lupus erythematosus]. | 1985 Jun 1 | Serum concentrations of AFP have been determined in patients suffering from systemic lupus erythematosus (SLE) or other "collagenoses" using fluorescence ELISA adapted to the chamber analytical technique. 20% of the SLE patients showed elevated AFP levels (range 30-233 ng/ml), some of them repeatedly. Only 2 of the 14 patients without SLE had AFP levels above 30 ng/ml (37 resp. 40 ng/ml). In SLE sera there was a significant correlation of raised AFP to higher anti-dsDNA antibody concentrations (Mann-Whitney U-test: p = 0.042). The mean dosage of azathioprin and prednisone in patients with SLE did not significantly differ from the non-SLE group. We discuss the possible reactivation of AFP synthesis on account of SLE itself. | |
| 4587940 | Types of 'reticulin' antibodies detected in human sera by immunofluorescence. | 1973 Nov | Reticulin antibodies have been classified by immunofluorescence into five types reacting with distinct antigens of intra- and extracellular components in mesenchyme. Two types of fibrillar antigens can be distinguished on the basis of the staining patterns, anatomical distribution, and species specificity. A third antibody reacts with either small fibres, amorphous proteins, or mucopolysaccharides lining the hepatic sinusoids (ground substance antigens). In addition, at least two kinds of intrasinusoidal cells show cytoplasmic fluorescence, ie, Kupffer cells and glass-adherent, blood-borne cells antigenically related to peritoneal macrophages. Some sera may contain antibodies reacting with sinusoidal endothelial cells though this has not yet been proven. It has been confirmed that all these distinct antibodies related to reticulin antigens are most frequent in dermatitis herpetiformis and coeliac disease, but they are also found with increased frequency in chronic heroin addicts and in rheumatoid and Sjögren's syndromes. About 5% of normal individuals had such antibodies and no significant increase could be demonstrated in autoimmune disorders or in liver cirrhosis. The antibodies appear to be stimulated by bacterial or nutritional antigens and are likely to represent anamnestic responses rather than direct cross reactions with a multiplicity of foreign antigens. | |
| 6239742 | Auranofin. | 1984 Aug | It has been widely accepted for a number of years that chrysotherapy is a valuable therapeutic agent in the treatment of progressive rheumatoid disease. This therapeutic benefit has, to some extent, been offset by the potential toxicity associated with gold compounds. The development of a gold compound with a greater therapeutic to toxicity ratio would be of considerable interest and benefit, to both patients and physicians. Initial studies with auranofin suggested that this compound was a reliably absorbed agent and that its use would avoid regular gold thiol injections. Its initial therapeutic profile was considered to be similar to that of injectable gold compounds, but with a significantly greater safety margin. The further information that has accrued from the clinical studies reported so far would tend to support these early suggestions in that auranofin has compared very favourably with gold thiols and other disease-remittive agents and that the prevalence of side effects requiring withdrawal of therapy has been approximately 25-30 per cent less. In addition, the reasons for withdrawal have often been less potentially serious side effects, notably nephrotoxicity and haematological reactions. In a review of over 3000 patients treated with auranofin, compared to 465 patients treated with injectable gold, the frequency of withdrawal from studies due to inefficacy of auranofin was approximately two to three times higher than with the gold thiols. It would appear, therefore, that in those patients continuing on therapy, auranofin is similar to injectable gold, but that a higher proportion of patients will fail to get a response within three to six months to the therapy. This potential lack of therapeutic effect is offset by the increased safety margin. In time, it is possible that auranofin will be accepted for earlier treatment in the course of rheumatoid disease than perhaps would normally have been considered. The in vivo and in vitro studies of auranofin on its mechanism of action are of considerable interest. They provide theoretical and valuable information on the mechanism of action of gold compounds and the cellular functions and interactions which may be involved in the pathogenesis of rheumatoid disease. It is interesting to note that auranofin appears to be more potent and have different effects than gold thiols, despite the fact that in terms of clinical therapeutic profile the compounds are similar.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 1022412 | Changes in blood-serum enzymes in rheumatic myocarditis. | 1976 | Serum activity analyses of nine enzymes [CPK, HBDH, SDH, ALP, GPT, GOT, LDH, MDH, ALD] in patients with rheumaitc carditis revealed certain elevations of the mean values of LDH, GOT, HBDH, GPT, ALP and MDH. These changes have no particular diagnostic importance because similar findings were also obtained in patients with both rheumatic and nonrheumatic arthritis. The changes occurring during antirheumatic treatment are minimal and statistically not significant. Greater elevations of LDH, ALD, GOT, HBDH, GPT, MDH, and ALP are found in patients with decompensated rheumatic heart disease associated with active rheumatic carditis. | |
| 6602845 | A novel cell surface antigen (T305) found in increased frequency on acute leukemia cells a | 1983 Aug | Monoclonal antibody T305, prepared by immunizing mice with the T-ALL derived cell line RPMI-8402, immunoprecipitates a single chain glycoprotein with m.w. 160,000 daltons (under reducing conditions) or 180,000 daltons (under nonreducing conditions). In immunofluorescence assays, antibody T305 reacted with a subpopulation of T cells in normal blood (22 +/- 6%), thymus (28 +/- 11%), and lymph node (24 +/- 6%). Increased frequency of T cells reactive with antibody T305 was found in peripheral blood of patients with infectious mononucleosis (greater than 80%), graft-vs-host disease after bone marrow transplantation (65 +/- 11%), acquired immunodeficiency syndrome (53 +/- 12%). The T cells in synovial fluid of patients with rheumatoid arthritis had increased frequency of antibody T305 reactive cells (59 +/- 8%) as compared to their peripheral blood (18 +/- 7%). Two color immunofluorescent studies demonstrated that the T305+ T cells predominantly co-stained with antibody Leu 2a (suppressor/cytotoxic subset) in both normals and disease state blood. After cell sorting to obtain T305+ and T305- subpopulations, we demonstrated that a) natural killer and antibody-dependent cellular cytotoxicity activity in normal blood was in the T305+ but not T305- T cells; b) cytotoxic T cells induced by mixed lymphocyte reaction were predominantly T305+; c) T305- T cells could be induced in vitro to express T305 antigen by mitogens or allogeneic B cells; d) the DNA content of T305+ and T305- T cells in normal blood was similar (greater 95% of cells with G0/G1 level); e) after mitogen stimulation, T305 antigen induction on previously T305- cells occurs before S-phase; and f) significantly more [3H]-thymidine after mitogen stimulation was incorporated by originally T305- cells than by originally T305+ cells (p less than 0.001). The T305 antigen was not restricted to T cells because it was also found on myeloid precursors in bone marrow but was not present on polymorphonuclear leukocytes, red blood cells, platelets, muscle, liver, skin, kidney, lung, or brain. Antibody T305 was found on 24/25 cases of acute leukemia (6 T-ALL, 10/11 cALL, 7 AML, and 1 AMOL) but not on 18 cases of chronic leukemia (B-CLL, T-CLL, null CLL, CML). The importance of the T305 antigen is that it is present on a high number of T cells in certain autoimmune diseases and on virtually all acute leukemia cells. Its distribution on immature and in vitro activated cells suggests that it may represent a receptor for signals related to cellular replication or differentiation. | |
| 6723837 | Decreased glucose in RA-cell-positive pleural effusion: correlation of pleural glucose, la | 1984 May | A significant correlation between RA-cells in the pleural fluid and lowered concentration of glucose, increased LDH activity and protein content was demonstrated in pleural effusions of diverse etiology. The finding might suggest a common metabolic reaction of the pleura, the mechanism of which remains unexplained at present. | |
| 102587 | Binding of soluble immune complexes to Raji lymphocytes. Role of receptors for complement | 1978 Apr | We have found that, although the binding of particulate antigen-antibody complement complexes such as EAC to lymphoblastoid Raji cells is mediated largely through receptors for C3b, the binding of complement-containing soluble complexes such as those prepared with aggregated human IgG (AHG) occurs also via receptors for C1q. Evidence supporting this conclusion included: (1) Binding of AHG to Raji cells takes place after incubation in EDTA serum; (2) Binding of AHG does not occur in C1q deficient EDTA serum but does take place after addition of C1q; (3) The extent of binding of AHG in EDTA serum is a function of the amount of C1q present; (4) Raji cells can bind up to 5-4 times 10(5) molecules of 125I C1q per cell which can be blocked by unlabelled C1q; (5) AHG pre-incubated with C can bind to a T-cell line MOLT, which lacks receptors for C3b but possesses receptors for C1q to the same extent as Raji cells; (6) Immunoassays for immune complexes in human sera yield similar results whether Raji cells, MOLT cells or C1q precipitation is used for assay; (7) EAC-Raji cell rosettes can be inhibited with inulin-treated, C1q deficient serum containing C3b or C3d whereas binding of AHG or immune complexes in patient samples to Raji or MOLT cells is not inhibited by this reagent. We conclude that receptors for C1q on certain B and T lymphocytes may play an important role in physiologic functions of lymphocytes depending on binding of soluble immune complexes to their surfaces. | |
| 50844 | "A" protein of amyloidosis. Isolation of a cross-reacting component from serum by affinity | 1975 Jul | A nonimmunoglobulin protein (A protein) has been isolated from amyloidotic tissue of secondary type. Antisera prepared to this protein identified a cross-reacting substance in the sera of patients with secondary amyloidosis. Sera from 70 persons with amyloidosis, 120 normal adults, 20 aged persons, and 97 patients with chronic diseases were tested for this substance. One hundred percent of secondary amyloid sera had amounts of amyloid serum component detectable by double diffusion in agar, whereas only 19 percent of primary amyloid sera were positive. Approximately 60 percent of rheumatoid sera as well as 60 per cent of sera from aged individuals were positive. Only 3 percent or normal blood donors had detectable amounts of this circulating substance. Isolation of the serum component by affinity chromatography and partial characterization have shown that it is an alpha-globulins with a molecular weight of 100,000-120,000, that it is not related antigenically to immunoglobulin or amyloid P-compoment, and that it has an amino acid analysis that is markedly different from tissue A protein. The possible participation of this substance in the genesis of amyloid is discussed. | |
| 2996347 | Giant cell arteritis associated with mononeuritis multiplex and complement-activating 19S | 1985 Oct | Giant cell arteritis is a necrotizing granulomatous arteritis of large arteries, especially the aorta and its branches. Mononeuritis multiplex is a peripheral sensorimotor neuropathy usually producing foot or wrist drop, commonly associated with necrotizing arteritis of small and medium-sized arteries. Rheumatoid vasculitis is an example of the latter type of arteritis associated with high-titer 19S IgM rheumatoid factor typically occurring in patients with long-standing erosive rheumatoid arthritis. This report describes a 71-year-old man with biopsy-proved giant cell arteritis, mononeuritis (foot drop) multiplex, and high-titer complement-activating rheumatoid factor without rheumatoid arthritis. Possible pathogenic relationships are discussed. | |
| 6119051 | [Pulmonary alterations in collagenosis (author's transl)]. | 1981 Jul | Revision on the pulmonary alterations in the course of collagenosis. The respiratory tract participation in connective tissue disorders and the causes why they can appear are justified. A synthesis of the clinical, radiologic and functional alterations, with differential facts in each one of the main collagenosis, contrasting bibliographic facts with personal casuist is offered. | |
| 6375862 | Carcinogenicity of antineoplastic agents in man. | 1984 Mar | Review of the literature shows that: Anticancer drugs are in all probability mostly also carcinogenic. Alkylating agents such as melphalan, chlorambucil and cyclophosphamide seem to lead to the highest rate of second malignancies. Second malignancies after antitumour drugs are mostly acute leukaemias. Conditions which could influence the carcinogenicity of an antitumour drug are (a) its carcinogenic potency; (b) long-term administration; (c) the total dose used and (d) long-term survival of the patient. Irradiation and chemotherapy seem to have the greatest carcinogenic potential, e.g. in malignant lymphomas. The role of immunosuppression as a co-carcinogenic factor is difficult to estimate. Although transplant patients on anticancer drugs for immunosuppression have a higher risk of reticulosarcomas, but not of solid tumours, there is no evidence to suppose that in general immunosuppression and carcinogenicity are directly related. There is no reason to abandon intensive chemotherapy regimes if they lead to significant therapeutic results on the grounds of possible carcinogenicity of these drugs. | |
| 7235787 | Healing of aspirin-associated peptic ulcer disease despite continued salicylate ingestion. | 1981 May | Patients who have rheumatic disease and who are undergoing long-term aspirin therapy have a high incidence of peptic ulcer disease. Whether it is possible to heal long-term aspirin-related peptic ulcer disease if aspirin intake is continued is unknown. Nine patients with rheumatic disease who were receiving long-term aspirin therapy and who had 15 endoscopically verified gastric and/or duodenal ulcers were studied. Patients were treated daily with 1,200 mg of cimetidine plus at least 120 mL of antacid (Mylanta II), while continuing aspirin therapy at the same dose and type. By eight weeks, 14 ulcers had healed. This study shows that some aspirin-associated peptic ulcers can be healed, despite continued aspirin intake, by intensive medical therapy aimed at lowering intragastric acidity. | |
| 423 | Factors affecting the solubility of calcium pyrophosphate dihydrate crystals. | 1975 Dec | The solubility of triclinic calcium pyrophosphate dihydrate (CPPD) crystals was measured under varying conditions using 45Ca-labeled crystals, expressing solubility as micromoles per liter of 45Ca in solution. In a 0.1-M Tris-HC1 buffer pH 7.4, the solubility of accurately sized CPPD crystals (37-20mum) was 60muM with maximal solubility being attained after about 8 h incubation at 37degreeC. Reduction in crystal size, decrease in pH, increase in ionic strength, Mg++, citrate, and albumin all increased solubility. The most marked effects on solubility occurred when changing the calcium concentration or by enzymatic hydrolysis of inoganic pyrophosphate to orthophosphate. It was found that decreasing the ionized calcium level below 5 mg/100 ml resulted in a progressive enhancement of solubility. The observed solubility-enhancing effects of albumin could be explained solely on its calcium-binding ability and thereby, altered ionized calcium level. Diffusible calcium in synovial fluid was only 40% of the total calcium concentration, which means most joint fluids are normally near the critical concentration of 5 mg/100 ml of ionized calcium, below which solubility is enhanced. During surgery, especially parathyroidectomy, calcium levels fall, favoring dissolution of CPPD crystals. We speculate that the slight decrease in crystal size during dissolution frees them from their cartilaginous mold, resulting in a dose-dependent inflammatory reaction as they are "shed" into the joint space. Crystal shedding may be reinforced by the modest fall in joint fluid pH accompanying the inflammatory response. | |
| 4815078 | Bone marrow erythropoiesis in the anemia of infection, inflammation, and malignancy. | 1974 Apr | A major factor in the anemia of infection, inflammation, and malignancy is a relative failure of the bone marrow to increase erythropoiesis in response to a shortened red cell survival. The possible causes for this diminished marrow response are: (a) a reduced production of erythropoietin, or, (b) impaired bone marrow response to erythropoietin. In this report studies were performed on 6 normals, 13 patients with anemia from infection or inflammation, and 18 patients with anemia caused by advanced malignancy. Serum erythropoietin activity was measured using the posthypoxic, polycythemic mouse assay. Assessment of bone marrow response to erythropoietin was made by measuring (59)Fe-heme synthesis in bone marrow suspensions cultured for 3 days with and without the addition of erythropoietin. The results showed that marrow heme synthesis was increased in erythropoietin-treated cultures as compared with saline control cultures by 66+/-8% (mean +/-SE) in normals, 101+/-10% in patients with infection or inflammation, and 31+/-5% in malignancy. Serum erythropoietin levels were consistently diminished relative to expected levels for the degree of anemia in the infection-inflammatory group, but not in malignancy. In these patients, plasma inhibitors to the biological activity of erythropoietin were not detected in vitro. These studies suggest that another factor to consider in the anemia of malignancy is a decreased bone marrow response to erythropoietin. In the anemia of infection-inflammation, marrow response to erythropoietin is normal, but serum levels of erythropoietin are decreased relative to the degree of anemia. |