Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
| ID | PMID | Title | PublicationDate | abstract |
|---|---|---|---|---|
| 3473638 | Differences between glycoprotein profiles of normal tear fluid and of tear fluid from pati | 1986 | We present a method for tear glycoprotein characterization using lectins as probes. SDS-page of samples is followed by electrophoretic transfer of proteins from gels onto nitrocellulose paper. Biotinylated lectin is overlayed and visualized with avidin-conjugated horseradish-peroxidase. With the use of 10 lectins, pooled samples of normal tears were assayed and compared to pooled samples of tears from patients with Sjögren's syndrome. Significant differences in number of bands, molecular weights and lectin binding capacity were observed between the two tear samples. | |
| 31952387 | The potential role of mycoplasmas as autoantigens and immune complexes in chronic vascular | 1991 | Many chronic degenerative diseases are suspected of resulting from autoimmune (AI) or immune complex (IC) mechanisms of unknown infectious etiology. Mycoplasmas have been associated with autoantibodies and tissue mimicry and with infertility and neonatal disorders, as well as with IC disorders. Their persistent colonization, which is clinically silent and common among healthy females, makes their etiopathogenic mechanisms difficult to assess. Finding the great apes to be colonized with and serologically expressing the human strains of mycoplasmas, as well as the anti-IgG rheumatoid factor (RF), provided us the ideal model of immunologically-related human disorders. In view of the etiopathologic role of IC in experimental vasculitis, especially collagen vascular diseases such as systemic lupus erythromatosus (SLE) with specific deposition on receptor sites of the vascular basement membranes, an investigation of IC's role in fetal and placental vascular disorders was initiated. The IgG-IC fractions isolated from solubilized human synovial and placental tissue extracts on affinity protein-A columns were further purified by pepsinization to minimize nonspecific Fc binding. Mycoplasmal antigens were identified in the F(ab)(2)-IC fractions by reacting the electroblots from SDS-PAGE with rabbit antisera to 6 IgG test serovars. Finding mycoplasmal and ureaplasmal antigens associated with the IgG-IC in synovial and placental tissues suggests their pathogenic role in collagen vascular and reproductive disorders of both humans and the great apes. Mycoplasma cells cultured in rabbit-serum-enriched broth bound rabbit IgG as indicated by their specific reaction with goat anti-rabbit IgG. Polyclonal rabbit antisera raised against the mycoplasma cells binding the gnotobiotic rabbit IgG expressed idiotypic antibodies reactive with heterologous mycoplasmas cultured with whole sera but not with gamma-free or fetal bovine sera. Immunoblot analysis of SDS-PAGE fractionated mycoplasmas with the anti-M. pneumoniae rabbit IgG recognized common IgG epitopes in heterologous mycoplasma cells cultures with whole horse serum. These results demonstrate a potential role and pathogenic mechanism of mycoplasmas acting as a ligand, binding and causing conformational changes of IgG that could also apply to other specific tissue proteins. Conformational changes of bound tissue components could produce "altered-self" antigens to initiate a variety of autoimmune disorders in both humans and the great apes. | |
| 2607901 | MRI of inflammatory synovial processes. | 1989 Sep | MRI was used to evaluate inflammatory synovial processes in 53 patients over a 4-year period. Multiple disease processes were imaged, including: rheumatoid arthritis [n = 12], osteochondromatosis [n = 6], bursal abnormalities [n = 17], ganglion cyst [n = 1], meniscal cyst [n = 5], hemophilia [n = 1], and septic arthritis [n = 11]. The soft tissue contrast resolution of MRI and its multiplanar capability makes it particularly suitable for evaluating masslike or fluid inflammatory processes for diagnostic purposes, to determine extent of disease, and in some cases, to determine the composition of the inflammatory processes. | |
| 3379620 | Factor structure of the Arthritis Helplessness Index. | 1988 Mar | The factor structure of the Arthritis Helplessness Index (AHI) was examined using principal components factor analysis with varimax rotation. Data for the initial factor analysis came from a longitudinal study of 368 patients with rheumatoid arthritis (RA). Two slightly negatively correlated (r = -0.21) subscales emerged: internality and helplessness. This analysis was cross-validated twice. Findings reveal that the 2 subscales of the AHI are more reliable and valid than the total score. The 5 item helplessness subscale, in particular, appears to be a highly valid indicator of the degree to which patients with RA feel overwhelmed by their disease. | |
| 3183675 | Long-term results of silicone trapezial implant arthroplasty. | 1988 | The senior author has performed the Swanson implant arthroplasty for arthritis of the basal joint of the thumb for the past 12 years. Fifty-two patients with a total of 64 arthroplasties of the thumb were reviewed, with follow-up periods of 12-156 months (average, 4.4 years). The majority (80%) of the arthroplasties were performed for osteoarthritis; 11% were performed for rheumatoid arthritis, 6% for traumatic arthritis, and 3% for mixed connective tissue disease. Subjective and objective hand functional measurements and radiographic examinations were performed in the majority of patients (77%). The overall results were good both subjectively and objectively. Although degenerative changes involving the implant occurred with increasing frequency as the follow-up period increased, these changes were not symptomatic in the majority of cases. | |
| 3941539 | Experimental arthritis in a nonhuman primate. I. Induction by bovine type II collagen. | 1986 Jan | Six squirrel monkeys immunized with native fetal bovine type II collagen (CII) in complete Freund's adjuvant developed arthritis 3 to 6 weeks later. None of three cebus monkeys given CII plus complete Freund's adjuvant or three control squirrel monkeys immunized with complete Freund's adjuvant alone developed arthritis. In four of the squirrel monkeys, arthritis was symmetrical and involved mainly the interphalangeal and metacarpal phalangeal joints. Two other monkeys had pauciarticular disease. Although three monkeys became cachetic and died, the others regained weight and their arthritis spontaneously remitted with minor residual deformities in digits and larger joints. Each squirrel monkey with arthritis had high titers of CII antibodies whereas the arthritis-resistant cebus monkeys had lower titers of CII antibodies whereas the arthritis-resistant cebus monkeys had lower titers of CII antibodies. As an animal model, experimentally induced arthritis in primates appears to resemble an acute arthropathy in man rather than chronic rheumatoid arthritis. | |
| 3499630 | [Etiology of bony bridges on the sides of the terminal phalanx of the great toe]. | 1987 Jun | Bony bridges along the sides of the terminal phalanx of the great toe occur not only in acromegaly but also in one third of cases with peripheral signs of diffuse idiopathic skeletal hyperostosis. Systemic diseases, such as rheumatoid arthritis or psoriatic arthritis with chronic inflammation of the interphalangeal joint of the great toe or extraarticular osseous changes in the terminal phalanx of the great toe do not influence the development of such bridges. | |
| 1930332 | Autoantibodies to human stress proteins. A survey of various rheumatic and other inflammat | 1991 Sep | Unselected sera from patients with various rheumatic, inflammatory bowel, and autoimmune skin diseases (n = 268) were examined against human cell lysate by immunoblotting procedures, to determine the prevalence of autoantibodies to stress proteins (heat-shock proteins) hsp60 (homolog of Escherichia coli groEL and mycobacterial 65K antigens), hsp73, and hsp90. Using standard, sensitive and specific assay conditions, IgG and IgM autoantibodies to these stress proteins were not demonstrable, or were detected infrequently, in sera from control subjects (n = 36) and from patients with rheumatoid arthritis, Sjögren's syndrome, ankylosing spondylitis, Reiter's syndrome, systemic lupus erythematosus, and systemic sclerosis. Autoantibodies to hsp60 were relatively more common (greater than or equal to 20% of sera) in patients with mixed connective tissue disease, polymyositis/dermatomyositis, psoriatic arthritis, inflammatory bowel disease, epidermolysis bullosa acquisita, and bullous pemphigoid. Anti-hsp73 autoantibodies were detected in 20% or more of the sera from patients with Lyme disease and ulcerative colitis. Taken together, these data extend the spectrum of autoimmune and inflammatory diseases in which humoral anti-stress protein autoreactivity develops. However, the paucity of humoral autoreactivity to stress proteins in patients with systemic lupus erythematosus and rheumatoid arthritis argues against a direct role of anti-stress protein autoantibodies in the pathogenesis of these disorders. | |
| 3047343 | Epidural hibernoma as a complication of corticosteroid treatment. Case report. | 1988 Oct | Centripetal fat deposition is a well-recognized consequence of excessive use of corticosteroids, either endogenous or exogenous. Recently, several patients receiving large doses of corticosteroids have suffered compressive myelopathies due to excessive epidural fat collections, labeled "epidural lipomatosis." Two of these have been children, and a third child is reported here. This child was receiving chronic steroids for juvenile rheumatoid arthritis when he presented with such a myelopathy, which was confirmed by metrizamide computerized tomography myelography as well as by surgical exploration. Histological examination revealed that the epidural tissue was a brown-fat tumor or "hibernoma." An epidural hibernoma has not been described previously. The histological and endocrine features of fat in Cushing's syndrome are discussed, and the literature concerning hibernoma and epidural lipomatosis is reviewed. | |
| 3688906 | Lipoatrophic panniculitis: a possible autoimmune inflammatory disease of fat. Report of th | 1987 Dec | We observed three children with a clinically similar presentation of erythematous nodules that expanded centrifugally leaving lipoatrophy. Areas of lipoatrophy coalesced, resulting in clinical pictures similar to partial or total lipodystrophy. Histologic study revealed a lobular panniculitis with a mixed infiltrate of lymphocytes and mononuclear phagocytes. Of these three children, one had insulin-dependent diabetes mellitus and Hashimoto's thyroiditis, one developed juvenile rheumatoid arthritis, and the third developed insulin-dependent diabetes mellitus, suggesting that the pathogenic mechanism may be an expression of autoimmunity. | |
| 2559906 | Testicular dysfunction in the adjuvant-induced arthritic rat. | 1989 Nov | Adjuvant-induced arthritis, an autoimmune disease similar to rheumatoid arthritis, was used to investigate possible mechanisms of immune system modulation of the reproductive system. This laboratory previously reported that arthritic male rats have reduced serum testosterone and elevated serum LH concentrations. In the experiments described here, serum prolactin levels were not significantly different in arthritic animals compared with non-injected control animals. Neither reduced food consumption of arthritic rats nor the injection vehicle appear to cause a reduction of serum testosterone. Serum corticosterone was significantly elevated in the arthritic group compared with both the non-injected or the vehicle-injected control animals. Testicular cells from arthritic animals secrete significantly less testosterone in vitro compared with cells from non-injected control animals, both basally and in response to dbcAMP and hCG. In summary, the reduced serum testosterone of arthritic animals appears to be the result of a testicular dysfunction. | |
| 3358393 | Naproxen nephrotoxicity in a 2-year-old child. | 1988 May | The development of acute renal failure and interstitial nephritis due to therapeutic doses of nonsteroidal anti-inflammatory drugs has been documented repeatedly in adult patients but is rare in children. We report the occurrence of this complication in a child. Acute renal failure and hyperkalemia developed in a 2-year-old boy with juvenile rheumatoid arthritis after one month of naproxen sodium therapy. The evidence of renal toxic effects became manifest after an episode of dehydration. A percutaneous renal biopsy specimen revealed interstitial nephritis. The patient recovered promptly after withdrawal of the drug. | |
| 2070569 | Expression of the major rheumatoid factor cross-reactive idiotype in pediatric patients wi | 1991 Aug | Rheumatoid factor cross-reactive idiotype (RF-CRI) is expressed in high concentrations in the sera of some patients with rheumatoid arthritis (RA) and juvenile rheumatoid arthritis (JRA). To determine if RF-CRI is specifically expressed in rheumatic disease or if it is secondary to polyclonal B-cell activation, we examined sera of 23 children with SLE, 16 adolescents with infectious mononucleosis (IM), and age-matched pediatric controls for RF-CRI expression. Concentrations of RF-CRI in serum, determined by an inhibition ELISA, were 24 +/- 17 micrograms/ml (mean +/- SD) in 25 normal children, 31 +/- 17 in 16 young adults with IM, and were significantly increased, 70 +/- 80 micrograms/ml, in the 23 children with SLE (p less than 0.036). Eleven of 23 SLE patients had serum RF-CRI greater than the mean +/- 2 SD for normal children. Ten of 23 SLE sera contained IgM rheumatoid factor (RF) activity. One patient with IM had a borderline elevated RF-CRI level, and 5 IM patients had RF in their sera. The serum IgM concentrations in sera were: SLE (192 +/- 93 mg/dl) and IM (234 +/- 77 mg/dl) sera. These levels were significantly elevated compared to controls (132 +/- 44 mg/dl), p less than 0.031 for SLE and p less than 0.001 for IM, suggesting that polyclonal activation of B cells was present in SLE and IM patient groups. Increased expression of RF-CRI in the SLE patients correlated directly with high titer anti-DNA antibody values (r = 0.3965, p less than 0.05) and RF activity when human IgG (r = 0.5026, p less than 0.05) was used as the RF binding substrate and inversely with serum C3 levels (r = 0.3925, p less than 0.05). RF-CRI expression did not correlate with RF that bound rabbit (r = 0.3123, p greater than 0.05). Increased serum RF-CRI expression is not a result of polyclonal B-cell activation. RF-CRI may be selectively up-regulated in patients with SLE. | |
| 3171300 | Rupture of flexor tendons to the little finger due to bony irregularities in the carpal tu | 1988 Aug | Rupture of a finger flexor tendon occurs most commonly in the patient with rheumatoid arthritis. We have treated two patients who suffered rupture of the flexor tendons to the little finger due to bony irregularities in the carpal tunnel unrelated to rheumatoid disease. Each irregularity was removed and the rough surface covered with a portion of the flexor retinaculum. This resurfacing affords protection against recurrent abrasion and rupture. Tendon function was restored by suturing the ruptured profundus tendon to the adjacent intact profundus tendon of the ring finger. Satisfactory function of the little finger was achieved in both patients. Neither patient has experienced recurrent rupture. | |
| 2679561 | Mass spectrometric quantitation of muramic acid, a bacterial cell wall component, in septi | 1989 Oct | This is the first report describing the use of gas chromatography-mass spectrometry for detection of muramic acid in infected synovial fluid (SF). Muramic acid is a ubiquitous component of bacterial cell walls, and it has been proposed that it could serve as a chemical marker for the presence of live bacteria or bacterial debris in rheumatoid joints. Our goal was to determine whether muramic acid was present at detectable levels in septic SF, since this would serve as a positive control for studies of reactive and rheumatoid arthritis. Muramic acid was found to be present at levels of less than 250-1,700 ng/ml in 12 septic SF samples (10 of which were culture positive for Staphylococcus aureus and 1 each for Escherichia coli and Streptococcus pneumoniae). Among these samples, those containing low bacterial colony counts did not contain detectable muramic acid. Muramic acid was also not detected in any SF samples from 20 control patients. We conclude that muramic acid can be used as a marker for the presence of bacterial peptidoglycan in SF. With further lowering of gas chromatography-mass spectrometry detection limits, determination of the quantities of bacterial debris present in joints of patients with rheumatoid or reactive arthritis will be attainable. | |
| 2784799 | Anchorage-independent growth of synoviocytes from arthritic and normal joints. Stimulation | 1989 Apr | Exuberant tumor-like synovial cell proliferation with invasion of periarticular bone is a feature of rheumatoid arthritis in humans and of streptococcal cell wall (SCW)-induced arthritis in rats. These histologic observations prompted us to examine synoviocytes from arthritic joints for phenotypic characteristics of transformed cells. The capacity to grow in vitro under anchorage-independent conditions is a characteristic that correlates closely with potential in vivo tumorigenicity. In medium supplemented with 20% serum or in basal media supplemented with platelet-derived growth factor (PDGF), early passage synoviocytes from both SCW-induced and rheumatoid arthritic joints formed colonies in soft agarose. Epidermal growth factor (EGF), interleukin 1 (IL-1), tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and transforming growth factor-beta (TGF-beta) did not support growth, although EGF enhanced PDGF-dependent growth. On the other hand, TGF-beta, as well as all-trans-retinoic acid, inhibited colony growth. Early passage normal rat and human synoviocytes also grew under the same conditions, but lung, skin, and late-gestation embryonic fibroblast-like cells did not. Considered in the context of other published data our findings provide cogent evidence that synoviocytes, but not other types of fibroblast-like cells, readily acquire phenotypic characteristics commonly associated with transformed cells. Expression of the transformed phenotype in the inflammatory site is likely regulated by paracrine growth factors, such as PDGF and TGF-beta. | |
| 2814294 | [Psoriatic onycho-pachydermo-periostitis of the big toe. Anatomo-clinical study and physio | 1989 Jul | The authors report 4 cases of rheumatoid psoriasis in which involvement of the great toe, associating psoriatic onychosis, thickening of the distal soft tissues and osteo-periostitis of the distal phalanx without lesions of the interphalangeal joint, is the result of a direct repercussion of the ungual lesion on the distal phalanx. This is explained by very close anatomic links between nail and distal phalanx. They advocate the term of psoriatic onycho-pachydermo-periostitis of the great toe or OP3GT, when referring to this radio-clinical syndrome highly evocative of rheumatoid psoriasis. | |
| 3722816 | Polymeric IgA rheumatoid factor in idiopathic IgA mesangial nephropathy (Berger's disease) | 1986 Jul 15 | A specific and sensitive enzyme-linked immunosorbent assay (ELISA) was used to detect IgA rheumatoid factor (RF) in sera from 88 patients with IgA nephropathy (IgA GN), a disease characterized by abnormalities of IgA production. Significantly higher levels of IgA antiglobulins were demonstrated in IgA GN patients than in normal healthy controls and patients with other forms of chronic primary glomerulonephritis (mean +/- SEM 28.4 +/- 6.6 vs 6.0 +/- 0.4 and 8.3 +/- 1.2 micrograms/ml respectively; p less than 0.002). Interestingly, in contrast to rheumatoid arthritis, IgA RF activity was not associated with IgM antiglobulins. Analysis of sera fractionated by gel chromatography at acid pH revealed that anti-IgG activity resided predominantly in the polymeric fractions of IgA as confirmed by the ability to bind "free" secretory component. Several findings in patients with IgA GN suggest that the IgA deposited in the glomeruli is polymeric, and levels of circulating macromolecular IgA are increased. Our findings confirm a general perturbation of IgA metabolism in this disease. Although the polymeric nature of the IgA RF is suggestive of a mucosal origin, additional evidence is needed to confirm this hypothesis. | |
| 2686766 | Orthopaedic complications of Lyme disease in children. | 1989 | Lyme disease is transmitted by the tick Ixodes dammini ("deer tick") or a related ixodid tick. Early diagnosis of children with Lyme disease is difficult because the bite of the ixodid tick often goes unnoticed. Furthermore, erythema chronicum migrans, the characteristic rash of the disease, occurs in less than 50% of cases. However, an awareness of orthopaedic complications of Lyme disease may facilitate an early diagnosis of this disease. Orthopaedic complications of Lyme disease include those which are oligoarticular in nature. Brief intermittent attacks of swelling and pain in one or more joints--primarily large ones--is the pattern of disease most frequently presented. The knee is the joint most commonly affected. In most cases, pain is not severe enough to debilitate the patient or prevent weight-bearing activity. An elevated sedimentation rate is the only consistently abnormal routine laboratory finding in Lyme disease. The only radiographic abnormalities noted in children are effusion and osteopenia. However, the radiograph of a patient known to have Lyme disease may not show any abnormalities at all. Lyme disease shares symptoms in common with septic arthritis and juvenile rheumatoid arthritis. Whenever a distinction between Lyme arthritis and septic arthritis is difficult to make, treatment should be directed at septic arthritis while serological tests for Lyme disease are pending. The physician should consider Lyme disease to be a possible diagnosis of any patient with arthritis and a history of rash or fever, idiopathic neurological disease, or a cardiac conduction defect--especially if there is a history of possible exposure to the carrier tick.(ABSTRACT TRUNCATED AT 250 WORDS) | |
| 1901422 | Mechanism of T-cell activation by mycobacterial antigens in inflammatory synovitis. | 1991 Mar | Earlier studies demonstrated enhanced proliferative responses to an acetone precipitable Mycobacterium tuberculosis (AP-MT) antigenic complex by T lymphocytes from the synovial fluid, compared with the peripheral blood, of patients with inflammatory synovitis, including rheumatoid arthritis. In contrast, decreased proliferation and interleukin 2 (IL-2) production in response to mitogens by synovial fluid lymphocytes from patients with rheumatoid arthritis has been demonstrated. In order to determine if IL-2 was produced in response to AP-MT, the peripheral blood and synovial fluid of patients with inflammatory arthritis were analysed by measuring proliferation and IL-2 production in response to AP-MT and tetanus toxoid. A reduction of IL-2 production relative to proliferation was observed in some, but not all, synovial fluids of patients who responded to the AP-MT. Nevertheless, antibodies to IL-2 as well as interleukin 4 (IL-4), significantly inhibited proliferation of synovial fluid lymphocytes by AP-MT. There was no inhibition by antibodies to interleukin 6 (IL-6). We conclude that AP-MT induced proliferation by synovial fluid lymphocytes is mediated by both IL-2 and IL-4. |