Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 3296152 | Cyclosporin a therapy in patients with primary Sjögren's syndrome: results at one year. | 1986 | We present our experience with small doses of cyclosporine A (CyA), 5 mg/kg/day, in patients with primary Sjögren's syndrome treated for up to 12 months. Subjective improvement in xerostomia occurred at 6 months of treatment, without objective improvement in any sicca parameters. At 12 months, xerostomia improved slightly, but minor salivary gland histology worsened. We conclude that small doses of CyA in patients with primary Sjögren's syndrome for up to 12 months are rather ineffective. | |
| 2440945 | Specificity and molecular characteristics of monoclonal IgM rheumatoid factors from arthri | 1987 Aug 15 | Two-hundred twenty-four hybridomas secreting monoclonal IgM rheumatoid factor (hIgMRF) derived from MRL-lpr/lpr, MRL-+/+ and C57BL/6-lpr/lpr autoimmune mice were analyzed with regard to IgG subclass and domain specificity, and some for VH gene expression patterns. Among these mice, only MRL-lpr/lpr develop arthritis. Clonotypes specific for each of the four mouse IgG subclasses and clonotypes reacting with more than one IgG subclass were identified. Although each panel contained several clonotypes, the predominant one differed in each strain (MRL-lpr/lpr, anti-IgG2a; MRL-+/+, combined anti-IgG2a and 2b; C57BL/6-lpr/lpr, anti-IgG1 or combined anti-IgG1, 2a, and 3). The IgG domains recognized by these monoclonals were defined with mutant Ig carrying IgG1 heavy chains that lacked either the CH1 or CH3 domains, variant Ig carrying hybrid IgG2b-2a heavy chains, and IgG fragments. Inhibition of hIgMRF binding to IgG substrates by protein A was also assessed. Most determinants were assigned to the CH3 domain, but determinants in the hinge region, CH2 domain, and in some instances, even in the Fab portion, could also be identified. Hybridization of cytoplasmic RNA from 35 classes of diverse IgG subclass specificity with VH gene probes representing seven of the approximately 10 VH families (7183, S107, Q52, J558, J606, 36-60, X24) indicated that approximately 90% of these clones expressed VH genes belonging to the large J558 gene family. The results indicate that murine IgMRF are extremely heterogeneous in IgG subclass and domain specificities; the genetic background influences RF specificity characteristics that may relate to pathogenicity; and considering the complexity of the J558 VH gene family and reported RF heavy chain assignments to additional VH gene families, it appears that VH genes encoding RF are diverse. | |
| 3223742 | Multicentric reticulohistiocytosis. | 1988 Oct | This is a short report on the first case of a multicentric reticulohistiocytosis diagnosed at Middle Road Hospital in 1987. He presented with multiple reddish brown papules and nodules but without arthritis. Systemic review did not show any associated malignancies. Treatment with methotrexate has not been useful. Multicentric Reticulohistiocytosis is a proliferative histiocytic disorder that is benign. It is characterised by a dermatoarthritis, extensive red nodule and a rheumatoid-like arthritis. Histologically, multinucleated giant cells in ground glass cytoplasma and mononuclear histiocytes form the granulomatous infiltrate that invades the dermis, mucosa, synovium and others--bone, plasma, pericardium etc. | |
| 2787354 | Plasminogen activator and prostaglandin E2 levels in human synovial fibroblasts. Different | 1989 Aug 1 | Interaction between cells of the immune system and of the synovial tissue may be contributing to the pathogenesis of rheumatoid arthritis. Cytokines, produced by PBMC, were tested for their effects on plasminogen activator activity and PGE2 levels of a number of human synovial fibroblast-like cell lines. Evidence was obtained for a human monocyte polypeptide, synovial activator, which can stimulate synovial cell plasminogen activator activity but not PGE2 levels. Purified human rIL-1 alpha and IL-1 beta increased the levels of both products in the supernatants of the synovial cells; TNF-alpha raised the PGE2 levels but raised the plasminogen activator activity only weakly and inconsistently. Synovial activator was further distinguished from IL-1 alpha and IL-1 beta (and TNF-alpha) on biochemical, immunologic, and functional criteria. No other purified native or recombinant human cytokine tested was active on the synovial cells when judged by the criteria in question. Synovial activator could therefore be a novel monokine. The differences in the type of response elicited by the various cytokines in the synovial fibroblast-like cells could have implications for the understanding of the cellular interactions occurring in rheumatoid lesions. | |
| 2939541 | [D-penicillamine: mechanism of cellular action and induced autoimmune diseases]. | 1986 Jan | The fall in the IgM rheumatoid factors under treatment is not sufficient to explain the effectiveness of D-penicillamine in rheumatoid arthritis. The mechanism of action of D-penicillamine is still poorly elucidated. In vitro, in the presence of copper ions, D-penicillamine inhibits the lymphoblastic transformation induced by polyclonal mitogens; it decreases the production of immunoglobulins by lymphocytes stimulated by the Pokeweed mitogen. This inhibitory action is exerced on the helper T lymphocytes via the production of hydrogen peroxide (H2O2). Monocytes are capable of blocking the inhibitory action of D-penicillamine. The mechanism of the auto-immune complications induced by D-penicillamine is controversial. Two theories have been proposed:--a modification of the auto-antigens due to the presence of the highly reactive thiol group;--an interference with the lymphoid cells involved in suppressor or effector lymphocyte cellular co-operation. These auto-immune complications can be classified into two groups: organ-specific diseases such as myasthenia, polymyositis, thyroiditis, and non organ-specific diseases such as Sjögren's syndrome and lupus. The suspension of D-penicillamine generally leads to the resolution of the symptoms, but corticosteroid and immunosuppressant treatment is sometimes required. | |
| 2544985 | Expression of activation markers on CD4+ and CD8+ cells from synovial fluid, synovial tiss | 1989 Jun | We studied the expression of the Tac antigen, the transferrin receptor (Tfr-R), HLA class II antigens (DR, DQ, DP), CD30, and Act 1 on purified CD4+ and CD8+ cells isolated from synovial fluid (SF), synovial tissue (ST), and peripheral blood (PB) of patients with rheumatoid arthritis (RA) and with non-RA inflammatory arthritides (not ST). Subfractionated T cells of PB from healthy individuals served as controls. SF CD4+ cells from RA and non-RA arthritides expressed the Tac antigen much more frequently than corresponding CD8+ cells (54 and 58% versus 16 and 17%). In contrast, SF CD8+ cells of both patient groups expressed the HLA class II antigens rather more frequently than the corresponding CD4+ cells (88 and 68% versus 72 and 40%). Tfr-R expression was low on CD4+ and CD8+ SF T cells from both patient groups. SF T cells did not express CD30, and their expression of Act 1 did not differ from that of normal PB T cells. The RA ST findings were similar to those of RA SF. The overall expression of activation markers on PB T cells of patients was slightly higher than on those of normal controls, and the RA group was slightly higher than the non-RA group. The results show that intra-articular T cells in arthritis are activated and that CD4+ and CD8+ subsets differ in their expression of Tac antigen and HLA class II antigens. There were also similar patterns of activation markers on both CD4+ and CD8+ SF cells from RA and non-RA arthritis patients, suggesting that several types of arthritis display a similar immunopathogenesis in the joints. | |
| 3073313 | Radioimmunoassay for anti-actin antibody: application in viral and autoimmune diseases. | 1988 Dec | The development of a non-competitive, solid-phase radioimmunoassay for quantitating anti-actin antibody is described. Anti-actin antibody was captured on BSA-coated microspheres of polystyrene to which a synthetic peptide representing the fifteen amino acid N-terminus of human beta-actin was covalently attached. A rabbit antiserum against the actin peptide fragment was used as reference serum for the assay. Serums of 23 out of 28 (82%) patients with chronic active hepatitis, shown to have anti-actin antibodies (range 2-140 micrograms ml-1) by immunofluorescence and immunoblot assays, were used to validate the radioimmunoassay. Only 7 out of 130 (5%) control subjects exhibited anti-actin antibody serum concentrations above 14 micrograms ml-1 (range 2-20 micrograms ml-1), the 95% confidence interval. Anti-actin antibody serum concentrations were determined to be elevated in 28 out of 47 (60%) patients with juvenile rheumatoid arthritis (range 5-89 micrograms ml-1), 43 out of 64 (67%) patients with human immunodeficiency virus infection and AIDS (range 3-80 micrograms ml-1), and 17 out of 23 (74%) infants with Kawasaki Syndrome (range 7-138 micrograms ml-1). All of the differences observed between patient groups, either singly or collectively, and the control group are highly significant (P less than 0.001) as judged by chi-square analysis. Since all of these disease states contain elements of viral infection and autoimmune disease, it is possible that viral infection in these diseases triggers the production of anti-actin antibody, possibly by means of molecular mimicry in response to viral oncogenes or to abnormal expression of actin in host tissue. This radioimmunoassay for anti-actin antibodies may prove to be a useful tool for the detection and monitoring of certain forms of autoimmune disease. | |
| 1759042 | The clinical features, course, prognosis and treatment of juvenile arthritis. | 1991 Oct | The author's classification of juvenile arthritis (JA) differs from most by utilizing both the type of onset and the disease course separated into individual subgroups. The clinical aspects of each are described in detail, along with the special tests and studies to be done to differentiate them. Particular attention is given to the differences between the four subgroups of the pauciarticular onset group. There are different genetic factors for each subgroup and new data on HLA typing utilizing DNA techniques may be helpful in the prognosis of the disease course. The therapy of JA begins with non-steroidal anti-inflammatory drugs, continues with second-line drugs such as gold and penicillamine, and finally leads to the use of immunosuppressive agents. The range of doses, the maximal dose, and the frequency of administration is given for each medication. The long-term prognosis is generally good, with a low death rate, primarily seen in the systemic onset patients. The causes of death vary around the world. Prognosis for continued joint activity and joint function is determined significantly by the type of onset and is worse in the rheumatoid factor positive polyarticular onset group. | |
| 2794573 | Relationship between schistosomiasis and arthropathy. | 1989 Dec | This study was carried out to suggest criteria for diagnosing arthritis associated with schistosomiasis. 180 cases were classified into three clinical groups, 120 schistosomal arthritic group (I), 20 schistosomal non-arthritic (II), 20 arthritic non-schistosomal (III) and 20 controls (IV). Four tests were done to exclude other causes of arthritis namely, Erythrocyte sedimentation rate (ESR), Rose-Waaler test (RW) for rheumatoid factor (RF), antinuclear antibody test (ANA) and determination of serum uric acid (SUA) level. A history, clinical examination, urine and stool examination, intradermal test (IDT), indirect haemagglutination test (IHAT), circumoval precipitin test (COPT) and complete blood picture, were performed for all groups. 20 patients were selected randomly from group I and received praziquantel to be followed up 6 months later. Bilharzial ova were found in the excreta of group I and II. The percentage of positive IDT, IHAT and COPT in I & II was 90.8%, 90%, 88.3% and 85% respectively. Blood picture showed mild anaemia and from low to moderate eosinophilia. ESR was moderately raised. RF positivity was 6.6%, 10%, 65% and 5% in the four groups respectively. ANA positivity was 1.6%, 0%, 50% and 0% respectively. There was a marked improvement of arthritic manifestations after praziquantel in 90% of cases. | |
| 1925826 | Psychiatric morbidity in outpatients with systemic lupus erythematosus. | 1991 Sep 21 | A study group of 25 patients with systemic lupus erythematosus (SLE) and a control group of 25 with rheumatoid arthritis (RA) attending a routine outpatient clinic at Groote Schuur Hospital were psychiatrically evaluated. The patients were assessed using two structured interview tools: the Present State Examination and the Mini-Mental State Examination. The results showed a relatively high prevalence of neurotic depression in both groups (40% in SLE and 32% in RA). Ratings of tension, worry and social unease were high in both groups. No psychoses or organic disorders were found. Steroid usage did not appear to have contributed to psychiatric symptoms. It is suggested that the psychiatric morbidity in this group of SLE patients was due to psychosocial rather than organic factors. | |
| 1890830 | The physiological basis for a flexible condylar tibial plateau design. | 1991 Jul | Knee resurfacing is a successful treatment for osteo- and rheumatoid arthritis in elderly patients. The application of this treatment to younger more active and obese persons has the potential to produce premature wear, loosening, and undesirable bone remodelling. A new generation of more physiologically compatible components is required for these situations. This paper discusses the design and analysis of a prototype tibial base plate aimed at physiological load transfer. Incorporated in the design are mechanisms to alleviate lift-off phenomena, bone stress concentrations, stress shielding, and micromotion at the bone-implant interface. The design requires viable cancellous bone stock, so that the bone may respond by remodelling to the dynamic loading during normal ambulatory activities. | |
| 1370057 | Inhibitors of angiogenesis. | 1991 Jul | Angiogenesis, the formation of new capillaries, is essential to a number of important physiological events, both normal and pathological. Recently, increased attention has focused on the purification and characterization of inhibitors of this process, because of the potential therapeutic value of angiogenesis inhibitors in controlling such "angiogenic diseases" as proliferative retinopathy, solid tumors, rheumatoid arthritis, and neovascular glaucoma. We review the process of neovascularization and the assays that have been developed to study its inhibition in vivo and in vitro. We also discuss the properties of different angiogenesis inhibitors and examine the mechanisms by which such inhibitors could potentially intervene in the process of neovascularization. | |
| 1680093 | Vulvar pyoderma gangrenosum. | 1991 Jun | Pyoderma gangrenosum is an idiopathic dermatologic disease manifested by painful cutaneous ulceration. The ulcers are characterized by their undermined, violaceous borders and necrotic tissue at the ulcer base. The lesions may have an unusual response to physical manipulation known as pathergy, a phenomenon that is manifested by rapid progression following debridement. Pyoderma gangrenosum is frequently associated with systemic diseases such as inflammatory bowel disease, rheumatoid arthritis, chronic active hepatitis and hematologic malignancies. Conservative wound care and systemic corticosteroids are usually effective therapy. We report the second case in the gynecologic literature of a patient with vulvar pyoderma gangrenosum. | |
| 2015570 | Transgenic mice as models of hemopoiesis. | 1991 May 15 | A useful approach to establishing the biologic actions, in vivo, of granulocyte-macrophage colony-stimulating factor (GM-CSF) is to assess the consequences of long-term elevation of the factor in transgenic mice. Two lines of transgenic GM-CSF mice were analyzed. The major abnormality exhibited was an elevation in the number of macrophages, eosinophils, and polymorphs in the peritoneal and pleural cavities. Disease states exhibited by the lines were dependent on the insertion site of the GM-CSF gene. These disease states seem best explained on the basis of CSF-mediated macrophage activation and may provide valuable clues as to the cause of comparable human diseases such as malignant histiocytosis, polymyositis, or rheumatoid arthritis. | |
| 2043552 | Corneal complications of cataract surgery. | 1991 Jan | The intraoperative and postoperative complications of cataract surgery that affect the cornea vary in etiology and severity. Principal complications include epithelial disruption, infections, sterile corneal ulceration, stromal melt, mechanical or toxic injury of the endothelium, vitreous touch, stripped Descemet's membrane, and epithelial and fibrous downgrowth. Meticulous cataract surgery with careful attention to protecting the cornea can prevent most serious corneal complications. Certain clinical situations warrant special note; patients with rheumatoid arthritis and dry eyes require extra lubrication to the epithelium to prevent disruption during surgery; patients with low endothelial cell counts benefit from the least possible surgical trauma to minimize cell loss; surgical clean-up of vitreous from the anterior segment remains an important principle; clinically significant Descemet's membrane tears or areas of stripping should be repaired at the time of cataract surgery. The clinical judgment and skills of the cataract surgeon should be equal to the type of cataract operation performed. | |
| 2357506 | What do patients and rheumatologists regard as an 'acceptable' risk in the treatment of rh | 1990 Jun | A questionnaire designed to ascertain the risk of adverse effects which patients with rheumatic conditions would accept for a particular therapeutic outcome was administered to 50 patients. The same questionnaire together with 'potted' histories of five of the patients was sent to 10 consultant rheumatologists. The willingness of both patients and doctors to risk side-effects varied with both the severity of the side-effect and the potential therapeutic benefit. Doctors were more willing than patients to risk death or serious disability (Wilcoxon, P less than 0.01) for a particular expected benefit. Doctors were also more willing to risk side-effects in treating seropositive rheumatoid arthritis than in treating non-articular rheumatism. No correlation was seen for patients between acceptable risk and diagnosis, pain or smoking habits. The risks which both groups stated they were willing to accept were less than those apparently associated with antirheumatic therapy. The results disagreed markedly with those of a previous study, demonstrating the importance of the methods used in this type of work. | |
| 2254870 | [Protrusio acetabuli. An update on the primary and secondary acetabular protrusion]. | 1990 Jun | Acetabular protrusion refers to intrapelvic displacement of the medial wall of the acetabulum and is defined as inward movement of the acetabular line so that the distance between this line and the laterally located ilioischial line is 3 mm or more in adult men and 6 mm or more in adult women. As discussed in this article, acetabular protrusion may be found in many bone disorders such as degenerative joint disease, Paget's disease, rheumatoid arthritis, ankylosing spondylitis, osteomalacia, Marfan's disease and as an effect of irradiation. Protrusio acetabuli appearing in absence of any recognizable cause is termed primary acetabular protrusion or Otto pelvis. Primary acetabular protrusion usually affects both hips in young to middle aged women with a history of diminished abduction, rotation and hip pain since puberty. Radiographically one notes a bilateral axial migration of the femoral head without joint space loss and with moderate degenerative changes. | |
| 1967042 | Autoantibodies to chromosomal domains in rheumatic diseases. | 1990 Jun | Autoantibodies to chromosomal proteins are frequently found in the sera of certain patients with rheumatic diseases. In patients with scleroderma, especially in those with the CREST syndrome, autoantibodies to a specific chromosomal domain (centromere) have been found as a common feature. In this report we describe the results of a study that utilized chromosomes prepared from fibroblasts of an Asiatic deer, the Indian Muntjac (IM). This substrate is sensitive and allows a more precise localization of chromosomal antigens. Using IM chromosomes we provide evidence that antibodies directed against chromosomal components are present in patients with rheumatic diseases and in some normal controls. The titre of these antibodies is high in scleroderma patients and low in the normal controls. In a group of ankylosing spondylitis patients there is a greater frequency of moderately elevated tires of antibodies to the kinetochore domain than in patients with rheumatoid arthritis or systemic lupus erythematosus. | |
| 2111653 | Immunosuppressive mechanisms in pure red cell aplasia--a review. | 1990 May | Pure red cell aplasia (PRCA) has been associated with a variety of clinical disorders, and various autoimmune mechanisms have been described to account for the red cell suppression. Primary PRCA occurs via both humoral and cell mediated mechanisms. Recent evidence using gene rearrangement studies indicates PRCA with T-lymphocytosis is a clonal chronic T cell lymphoproliferative disorder in which the T cells suppress erythropoiesis. Called T cell lymphocytosis and cytopenia (TCLC), this disorder has unique features, such as frequent rheumatoid arthritis (RA) and neutropenia. A subset of this disorder with natural killer (NK) like cells also exists, though direct NK cell suppression has not been proven. In secondary PRCA, both humoral and cellular suppression of erythropoiesis have also been described, except in chronic lymphocytic leukemia (CLL) where T cell suppression primarily accounts for the red cell aplasia. A role for the cell-adherent layer of the bone marrow, including macrophages, has also been demonstrated. | |
| 3308303 | Monitoring of anti-inflammatory drugs. | 1987 Sep | Advances in analytic technology have allowed clinical laboratories to accurately measure plasma levels of NSAIDs. With the exception of salicylate, however, there is no relationship, or only a weak one, between plasma NSAID levels and clinical responses. Therefore, therapeutic drug monitoring of NSAIDs other than salicylate is of little value to clinicians in their management of patients with rheumatoid arthritis. On occasion, however, it may be helpful to monitor specific patients suspected of noncompliance by measuring plasma drug levels. Routine therapeutic drug monitoring of these NSAIDs must await further work on the refinement of quantitating clinical response and the possible relationship between free drug level and drug effects. |