Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 7328565 | Felty's syndrome: response to parenteral gold. | 1981 Nov | Eight patients with Felty's syndrome who had associated fevers, cutaneous ulcers, or infections were treated with parenteral gold. A satisfactory response was noted in 7 of the 8 patients. Improvement in leukopenia (7/8), decrease in infections (5/8) and fevers (7/8), and healing of ulcers (4/5) were noted. We conclude that gold has a role in the treatment of this complication of rheumatoid arthritis. | |
| 6338718 | Endocytosis by the mononuclear phagocyte system and autoimmune disease. | 1983 Mar | The mononuclear phagocyte system, formerly called the reticuloendothelial system, is an important element in basic immunology, cell biology, and clinical disease. Secretory products participate in inflammation and immunoregulation. Endocytosis mediated by specific receptors for immunoglobulin and complement or by other opsonins is important in removal of damaged self or foreign particles. The ability to assess receptor-specific endocytosis has led to the recognition of Fc-receptor dysfunction in certain autoimmune diseases. This defect in membrane receptor function, whether inherited or acquired, may be important in the pathogenesis of these diseases. | |
| 6979449 | Complement-mediated solubilization of immune complexes in systemic lupus erythematosus. | 1982 Apr | The capacity of complement-mediated solubilization of immune complexes (complex releasing activity: CRA) was studied in 63 sera from eight systemic lupus erythematosus (SLE) patients. CRA in sera of active SLE (35 +/- 17.%) was significantly lower than that of inactive SLE (64.1 +/- 24.1%, P less than 0.001). In addition, 20 of 23 sera collected during active diseases demonstrated CRA values less than 50% of the control pooled serum. On the other hand, CRA of 29 of 40 sera from inactive disease exceeded the 50% level. CRA in SLE sera correlated with complement component levels and in particular with the CH50. Serial determination of CRA and of levels of circulating immune complexes (CIC), C4 and C3 in two active patients indicated that the correlation between CRA and the complement components was positive, while that between CRA and CIC was negative. These studies provide evidence that CRA may be useful for following the activity of SLE and that CRA reflects the levels of the complement components of both classical and alternative pathways. The possibility that CIC may be solubilized and opsonized by complement and cleared by the reticuloendothelial system was discussed. | |
| 6223411 | Natural and antibody-dependent cellular cytotoxicity of polymorphonuclear leukocytes. | 1983 May | Cytotoxic activity of polymorphonuclear leukocytes (PMN) in the peripheral blood of patients with various diseases was demonstrated to K562 cells (natural cytotoxicity, NC) and the antibody-coated P815 cells (antibody-dependent cellular cytotoxicity, ADCC), using a 51Cr-release method. The NC values of normal PMN were lower than those of normal lymphocytes with mean values of 5.0% and 30%, respectively. The NC values of patients' PMN were also lower in malignancy, chronic hepatitis and connective tissue diseases. The ADCC values of normal PMN were moderately high with a mean value of 16.0%, which was almost a half of normal lymphocytes. Higher ADCC values of PMN were found in patients with chronic hepatitis, SLE and Behcet's disease, and in these cases the ADCC values of their lymphocytes were extremely low. The supernatants of PMN mix-cultured with unlabeled K562 or the antibody-coated P815 cells were fairly cytotoxic to both cells, though the similar supernatants of lymphocytes were cytotoxic only to K562 cells, but not to the antibody-coated P815 cells. | |
| 803526 | The characterization of human anti-IgG autoantibodies by liquid isoelectric focussing. | 1975 Jan | A series of human anti-IgG autoantibodies (AGA) have been analyzed by liquid isoelectric focusing in order to a) determine their isoelectric points (pI) and b) assess their heterogeneity. The 13 AGA examined include five IgM, five IgA, and three three IgG AGA. All demonstrate a single major peak indicative of restricted heterogeneity and each is characterized by an acidic pI. This anodal pI is distinct from other immunoglobulins isolated from the same serum that do not exhibit anti-IgG activity. It is speculated that the acidic pI is the result of acidic amino acid substitutions in the variable regions of immunoglobulin chains. The restricted heterogeneity and distinctive pI of the AGA suggest the selection of structurally similar antibody molecules from the large repertoire available in the human genome. | |
| 1000085 | Fitzgerald factor (high molecular weight kininogen) clotting activity in human plasma in h | 1976 Dec | Fitzgerald factor (high molecular weight kininogen) is an agent in normal human plasma that corrects the impaired in vitro surface-mediated plasma reactions of blood coagulation, fibrinolysis, and kinin generation observed in Fitzgerald trait plasma. To assess the possible pathophysiologic role of Fitzgerald factor, its titer was measured by a functional clot-promoting assay. Mean +/- SD in 42 normal adults was 0.99+/-0.25 units/ml, one unit being the activity in 1 ml of normal pooled plasma. No difference in titer was noted between normal men and women, during pregnancy, or after physical exercise. Fitzgerald factor activity was significantly reduced in the plasmas of eight patients with advanced hepatic cirrhosis (0.40+/-0.09 units/ml) and of ten patients with disseminated intravascular coagulation (0.60+/-0.30 units/ml), but was normal in plasmas of patients with other congenital clotting factor deficiencies, nephrotic syndrome, rheumatoid arthritis, systemic lupus erythematosus, or sarcoidosis, or under treatment with warfarin. The plasmas of 21 mammalian species tested appeared to contain Fitzgerald factor activity, but those of two avian, two repitilian, and one amphibian species did not correct the coagulant defect in Fitzgerald trait plasmas. | |
| 6320933 | Effect of sera from patients with Hodgkin's disease on normal donor lymphocytes containing | 1984 Feb | Normal donor peripheral blood mononuclear cells incubated for 24 h with sera from patients with Hodgkin's disease were investigated by electron microscopy for the presence of parallel tubular structures (PTS) and/or amorphous electrondense granules (large granular lymphocytes = LGL). In comparison with normal human serum, 14 out of 29 sera of the patients induced a marked increase in the percentage of LGL. From a limited number of experiments it was likely that this increase is paralleled by an increase in Fcgamma receptor-bearing cells after the incubation. This serum effect did not show a correlation with the number of Fcgamma receptor-positive lymphocytes in the peripheral blood of the patients. A difference in the induction effect could be demonstrated between the sera from patients with a favourable and those with an unfavourable clinical course, but this distinction was not absolute. The presence or absence of splenic involvement by Hodgkin's disease does not apparently influence the effect of the sera. From experiments using sera positive for immune complexes or anti-Epstein-Barr virus antibodies, it seems unlikely that these factors are responsible for the observed increase in LGL. | |
| 1265236 | Routine tomography of the temporomandibular joint. | 1976 Apr | Routine lateral tomography of the temporomandibular joint has resulted in a three-fold increase in the detection of positive findings. The technique is easily accomplished, eliminates the problem of superimposition of unwanted structures, permits a true lateral view of the condyle and condylar fossa, and allows small articular surface abnormalities to be identified. Although the entrance skin dose to the patient's face in the beam is about two times greater per exposure than that for our previous conventional open and closed lateral views, we believe that the increased dose is reasonable and the resulting improved diagnostic accuracy outweighs this disadvantage. | |
| 807625 | Naturally-ocurring low molecular weight IgM in patients with rheumatoid arthritis, systemi | 1975 Jul | Some physicochemical properties of naturally occurring low molecular weight IgM (LMW IgM), IgM and their subunits obtained by reduction-alkylation were compared. On the basis of analytical ultracentrifugation, SDS polyacrylamide electrophoresis, analytical Sephadex chromatography, and heavy (H) and light (L) chain composition purified LMW IgM had an S20,W constant of approximately 8S, a molecular weight of 195,000 to 205,000 and a structural formula H2L2. Reduction and alkylation of IgM (IgM RA) by two techniques produces two components which could be distinguished by analytical ultracentrifugation, sucrose density ultracentrifugation, and gel filtration studies. IgM RA-cys had an estimated molecular weight similar to LMW IgM and IgM-2ME had physical properties similar to IgG. The molecular weights of H and L chains of IgM and LMW IgM were similar: 69,000 to 75,500 and 26,000 to 27,000, respectively. Unlike LMW IgM and IgM RA-cys, the less dense IgM RA reduced with 2ME dissociated into half subunits, and free H and L chains in SDS gel electrophoresis, indicating that it lacked intra-subunit disulfide bonds. J chain was not detected in LMW IgM or in the chromatographically purified reduced-alkylated subunits from a patient whose IgM contained J chain. Carbohydrate analyses of IgM, LMW IgM, and reduced-alkylated IgM products did not demonstrate differences in individual sugars or in the percentage of total carbohydrate. The different sedimentation and gel filtration properties of the two components obtained by reduction-alkylation of IgM could not be attributed to variations in peptide chain or carbohydrate content, rather they are probably dependent on conformational changes resulting from variable, reduction of intra-subunits disulfide bonds. | |
| 775436 | [The association of myasthenia and disseminated lupus erythematosus. 2 cases]. | 1976 May 1 | Two cases of the association myasthenia/systemic lupus erythematosus are described. This association is rare but of particular interest from a pathogenic point of view. The discussion includes the suggestion of an immunological disturbance which might be the common denominator of the two disorders. Recent data concerning the role of the thymus and of "suppressor" T cells support such a hypothesis. | |
| 6102955 | [Immunologic and allergic lung diseases. 2. Endogenous and exogenous immune complex diseas | 1980 Apr 3 | For the respiratory tract immunologic reactions of type I and type III according to Coombs and Gell are most important. The classical example for type-I-reaction is extrinsic (= "allergic") asthma. Mechanisms of sensitzation, of mediator release out of mast cells and of immunotherapy by specific hyposensitization are summarized. Immunologic type-III-reactions may lead to immune complex diseases of the lung. There are two different pathways: In the several forms of extrinsic alveolitis the interstitial lung tissue is involved, whereas the intrinsic forms of immune complex diseases mainly result in lung vasculitis. The diagnostic and therapeutical essentials of immunologic and allergic lung disease are discussed in detail. | |
| 5015291 | Toxicity of trimethoprim-sulphamethoxazole in patients with megaloblastic haemopoiesis. | 1972 Mar 11 | Four consecutive patients with megaloblastic anaemia who also received therapy with trimethoprim-sulphamethoxazole all showed poor responses to specific haematinic therapy. This was attributed to trimethoprim, which suppressed reticulocyte responses in three cases and produced a pancytopenia in two and a falling haemoglobin with neutropenia in a third. A fourth patient, with pernicious anaemia, had a satisfactory reticulocyte response but experienced no clinical benefit until after withdrawal of trimethoprim.Trimethoprim seems not to be a safe form of therapy in patients with a megaloblastic process; many of the toxic reactions reported with this drug may be on the basis of an unrecognized megaloblastic form of haemopoiesis. | |
| 6577245 | Glucocorticoid induced cytolysis of human normal and malignant lymphocytes. | 1983 Jul | Contrary to the general concept that man is a "glucocorticoid resistant species" this work demonstrates distinct human lymphoid subsets which are readily lysed in vitro by upper physiological and pharmacological concentrations of cortisol. These populations include the thymocyte precursor cells, i.e. prothymocytes, and immunoactivated T lymphocytes. Chronic lymphocytic leukemia cells and malignant cells from part of the acute lymphoblastic leukemia patients were also found to be highly sensitive to the in vitro cortisol induced lysis. The leukemic cells from all acute and chronic myeloid leukemias and from some acute lymphoblastic leukemia patients were found to be completely resistant to cortisol-induced lysis, even at the super pharmacological levels of the hormone. The lysis of the sensitive cell populations was specifically induced by glucocorticoids but not by other steroid hormones. Studies of the cytolic process showed high-affinity binding of the cortisol molecule to specific cytoplasmic receptor, and implied induction of "autolytic protein" synthesis. It is suggested that the observed in vitro cortisol-induced lysis accounts for part of the clinical effects of glucocorticoids. Furthermore this phenomenon may reflect a normal regulatory mechanism exerted by the corticoadrenal hormones on the immune system. | |
| 315771 | Iron deficiency anaemia--a prospective study. | 1979 Aug | A prospective study was performed over 15 months to determine the cause of iron deficiency in adult males and postmenopausal females attending a general hospital. The laboratory computer identified all subjects with a haemoglobin less than 10.6 g/dl and a mean corpuscular volume less than 86 fl. Patients becoming anaemic after trauma or recent surgery were excluded. The iron status of each patient was assessed by serum iron studies, serum ferritin or sternal marrow aspiration. Reduced red cell indices and blood film morphology were not diagnostic of iron deficiency. Of 215 patients assessed, about half (103) were found to be iron replete. This group had a variety of disorders--malignancy, chronic inflammation, chronic renal and non-malignant haematological diseases. The other group of 104 patients satisfied criteria for iron deficiency, and 100 of these were investigated further. The cause of iron deficiency was found in all but three subjects. Inadequate dietary intake was a contributing factor in over half of the patients and 40 regularly took salicylates. Investigation defined a source of chronic gastrointestinal blood loss in most instances. | |
| 6335023 | Clinical assessment of the renal toxicity of antirheumatic drugs. | 1984 | Antirheumatic drugs may cause a significant, although generally reversible, reduction of GFR, RPF, CNa and hyperkalemia in a wide range of extrarenal and renal disease states (severe liver disease, congestive heart failure, SLE, nephrotic syndrome, etc.); chronic ingestion has been associated with analgesic nephropathy. Recently cases have been reported of reversible acute renal failure with massive proteinuria and interstitial nephritis. The acute effects of a renal PG-inhibiting (ibuprofen) or a renal PG-sparing (sulindac) cyclo-oxygenase inhibitor on renal functional parameters (GFR, RPF, CNa, CK, urine volume) and proteinuria have been studied in 24 patients with clinically and biopsy proven chronic glomerular disease; in all patients ibuprofen significantly reduced GFR, RPF, CNa; these changes were fully reversible within a week of withdrawal of the drugs. A causal relationship exists between inhibited PG-synthesis and reduced renal function in these patients, since sulindac, which failed to reduce urinary PG excretion did not alter significantly the renal function. Moreover proteinuria is not reduced by ibuprofen at doses comparable, as far as concerns inhibition of PG-synthesis, to those of indomethacin. | |
| 4140267 | Ascorbic acid supplementation in the treatment of pressure-sores. | 1974 Sep 7 | In a prospective double-blind controlled trial the effect of large doses of ascorbic acid on the healing of pressure-sores has been assessed. 20 surgical patients were studied, the pressure areas being assessed by serial photography and ulcer tracings. The mean ascorbic-acid levels in treated and non-treated groups one month after the start of treatment were 65.6 and 25.8 mug per 10-8 white blood-cells. In the group treated with ascorbic acid there was a mean reduction in pressure-sore area of 84% after one month compared with 42.7% in the placebo group. These findings are statistically significant (P less than 0.005) and suggest that ascorbic acid may accelerate the healing of pressure-sores. | |
| 6774048 | Heterogeneity of human serum amyloid A proteins. | 1980 Sep 1 | Serum amyloid A proteins (SAA), presumed precursors of the tissue amyloid A proteins (AA) characteristic of secondary amyloidosis, have been isolated from the plasma high-density lipoproteins (HDL) of normals after etiocholanolone-induced inflammation and from patients with Wegener's granulomatosis, systemic lupus erythematosis, juvenile rheumatoid arthritis, Waldenström's macroglobulinemia, and Goodpasture's syndrome. At least six polymorphic forms of SAA wer identified among the low molecular weight proteins of HDL, and these comprosed up to 27% of the total HDL protein. Gel and ion-exchange chromatography permitted isolation of the SAA polymorphs in homogeneous form. Their amino acid compositions were very similar, they were indistinguishable in cationic and sodium dodecyl sulfate-polyacrylamide gel electrophoresis systems, and each had the terminal sequency COOH-Tyr-Lys-Phe-. Charge heterogeneity in anionic-urea polyacrylamide gel electropherograms was unaffected by neuaminidase treatment, and none of the SAA protein bands stained with the periodate-Schiff reagent. The two major SAA polymorphs, designated SAA4 and SAA5 according to their order of elution from DEAE-cellulose, had different NH2-terminal sequences. Manual Edman degradation demonstrated NH2-arg-ser-phe-phe- for SAA4 and NH2-ser-phe-phe- for SAA5. This NH2-terminal heterogeneity corresponds to that most frequently reported for AA and suggests that microheterogeneity in SAA may underlie that already documented in AA. Sufficient quantitites of the other SAA polymorphs were not available for similar analyses, but the amino acid compositions do not indicate that NH2-terminal heterogeneity accounts for all of the observed polymorphism. Artifactual polymorphism also appears unlikely, and the heterogeneiy of SAA may reflect origin from more than one cell type with or without posttranslational modificaton. We calculate from quantitative COOH-terminal analyses that SAA is of 11,000-11,900 mol wt. Primary structure studies have shown AA t be a single chain protein of 76 residues, and SAA, therefore, appears to contain a peptide of 33 amino acids that is missing from AA. | |
| 1218371 | Polymyositis: its presentation, morbidity and mortality. | 1975 Dec | A survey of 118 patients seen in the last twenty years in Newcastle upon Tyne forms the basis of this report. All of these 118 patients fulfilled clearly defined clinical, electrophysiological and pathological criteria for the diagnosis of polymyositis: muscle pain, weakness and characteristic EMG and/or muscle biopsy 55%; and characteristic muscle biopsy 17%; muscle weakness and characteristic EMG 7%; muscle weakness and pain, and raised serum CK activity in an established collagen-vascular disease 5%. A smaller group of 25 patients were selected in whom the clinical characteristics, EMG, muscle biopsy and serum enzyme levels were all completely diagnostic of polymyositis. The patients were followed for two months to twenty-six years, with a mean follow-up duration of six years. Analysis was made of the features at presentation and during the course of the illness, and of prognostic factors bearing upon the disability, response to treatment and mortality. Cases were classified according to the system of Rose and Walton (1966). Groups I, II, and III each constituted approximately one-third of the total cases, while only 8% of all cases were associated with carcinoma. The female to male ratio was 1.4:1. Though cases were seen in all age groups, the largest number was in the sixth decade. The sedimentation rate was raised in 55% of cases. Electromyography was characteristic of polymyositis in 45% of cases, and in only 11% was it normal. The serum creatine kinase activity was raised in 64% of cases. There was no correlation between the extent of these abnormalities and the degree of weakness or disability. 65% of muscle biopsies had changes with inflammatory infiltration virtually diagnostic of polymyositis. 17% of cases had a normal muscle biopsy. Most of the patients (89%) were treated with high-dose prednisone therapy, commencing with 30-100 mg/day, gradually reducing to a maintenance dose of 5-15 mg/day over two or three months. All clinical groups showed considerable improvement in average disability with time on "high dose" corticosteroid therapy, the maximum improvement occurring within the first three years. The degree of improvement in disability was considerably less in those inadequately treated, though the mortality rate was similar in the two groups. 66% of all survivors had essentially no functional disability at follow-up three or more years later, and in the majority of these cases the disease appeared to have burned itself out. 33% of cases had significant disability after three years, and in half of these the disease appeared to be still active. | |
| 6332160 | [Pathogenetic significance of adenosine deaminase in autoimmune diseases]. | 1984 Feb | Adenosine deaminase (ADA: E.C.3.5.4.4.) is one of the catabolic enzymes of purine nucleotide. In 1972 Gibllet has discovered two cases of ADA deficiency combined with severe immunodeficiency (ADA-. SCID) with remarkable dysfunction in both T and B cell. Thereafter, it has been believed by many investigators that deficiency of purine metabolic enzyme had played important role in immune function mechanism. Rheumatoid arthritis (RA) is one of the autoimmune diseases which is very frequently seen, but its pathogenesis is not distinct yet. This study has shown how the catabolic pathway of erythrocytes and lymphocytes in RA has been distorted. MATERIALS: Erythrocytes and lymphocytes in peripheral blood were obtained from patients with RA (48 cases), SLE (4), primary gout (55) and healthy control (23). 2. T cell and non-T cell in peripheral blood were obtained from patients with RA (5), gout (55) and healthy control (28). 3. T cell and non-T cell in joint fluid were obtained from patients with RA (19) and osteoarthritis (OA (9)). METHODS: Erythrocytes and lymphocytes were separated from peripheral blood by Ficoll-Conray (density 1,077) by use of gradient centrifugation method. The lymphocytes with PBS was mixed with sheep red blood cells. E rosette-positive (T cell) and E rosette-negative (non-T cell) populations were separated from lymphocytes in peripheral blood and joint fluid by human sodium metrizoate Ficoll mixed solution (density 1,090) by use of gradient centrifugation method. Erythrocytes bursted at -70 degrees C and lymphocytes were sonicated for 25 sec. at 20 kHz. The reaction mixture which consisted of 0.2 mM Tris-HCl buffer (pH 7.4), 30 mM [8-14C] adenosine and the samples was incubated at 37 degrees C for 30 min. After incubation, adenosine, inosine and the reaction mixture were applied on DEAE-cellulose paper. Radioactivity of the samples was measured with liquid scintillation counter. RESULTS: There was no significant difference in ADA activity of erythrocytes between normal male and female, but a significant difference was found in ADA activity of lymphocytes among its subpopulations. ADA activity of erythrocytes and lymphocytes in RA patients was much lower than the other groups (gout and normal subjects). Particularly, ADA activity in T cell was the lowest. In gouty patients, ADA activity of erythrocytes and T cell was higher. ADA activity of peripheral erythrocytes in RA patients was lower than that of joint fluid.(ABSTRACT TRUNCATED AT 400 WORDS) | |
| 6201111 | Anti-immunoglobulins and their idiotypes: are they part of the immune network? | 1983 | The anti-gamma globulins represent a very heterogeneous group of proteins with widely different specificities that might be considered a portion of the immune network. The hypothesis is presented that at least some of these proteins have other specificities, with the anti-gamma globulin reactivity being a secondary property. Anti-idiotypic antibodies are possible candidates. This is based on the low binding affinity for gamma globulin of many of these proteins and the results of CRI and sequence studies. All the proteins of the major CRI group have VKIIIb light chains, and these have a dominant but not total influence on this CRI. This has been evident from studies with rabbit antibodies and recently also with monoclonal hybridoma antibodies. Sequence studies have also demonstrated the similarity in light chains that, however, are not greater than with other VKIIIb chains; the heavy chains show little similarity except possibly in the J segment. The possibility is discussed that antibodies with secondary anti-gamma globulin binding properties might have selective advantages. |