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PubMed1994

The T helper cell response in Lyme arthritis: differential recognition of Borrelia burgdorferi outer surface protein A in patients with treatment-resistant or treatment-responsive Lyme arthritis.

The host response to Borrelia burgdorferi is likely to play a role in the pathogenesis of Lyme arthritis. Whereas most patients with Lyme arthritis can be cured with antibiotic therapy, approximately 10% of the patients have persistent arthritis for months or even several years after antibiotic treatment. In this study, we tested the hypothesis that the T cell response to one or more antigens of B. burgdorferi is different in patients with treatment-responsive or treatment-resistant Lyme arthritis. For this purpose, 313 B. burgdorferi-specific T cell lines were derived from the synovial fluid or peripheral blood of four patients with treatment-responsive Lyme arthritis and five patients with treatment-resistant arthritis. 87 T cell lines from treatment-responsive Lyme arthritis and 112 lines from the treatment-resistant group were examined for the recognition of five recombinant. B. burgdorferi proteins: outer surface proteins A (OspA), B, C, p39, and p93. In both groups of patients, the T cell lines frequently recognized OspB, and only occasionally recognized OspC, p39, and p93. In contrast, OspA was preferentially recognized by T cell lines from patients with treatment-resistant arthritis, but only rarely recognized by T cell lines from patients with treatment-responsive arthritis (odds ratio 28.4, 95% confidence interval 9.2-87.8, p < 0.005). These results are compatible with the hypothesis that the T cell response to B. burgdorferi OspA is involved in the pathogenesis of treatment-resistant Lyme arthritis.

Adult↗
PubMed2006

Cia27 is a novel non-MHC arthritis severity locus on rat chromosome 10 syntenic to the rheumatoid arthritis 17q22-q25 locus.

Cia27 on rat chromosome 10 is a collagen-induced arthritis (CIA) severity quantitative trait locus originally identified in a study of (DA x ACI) F2. As an initial step towards the positional cloning of the Cia27 gene, a 17 cM (21 Mb) interval from the DA strain (arthritis-susceptible) containing the two-logarithm of odds support interval comprising Cia27 was introgressed into the ACI (arthritis-resistant) background through genotype-guided congenic breeding. ACI.DA(Cia27) congenics developed a significantly more severe form of arthritis (CIA), with a 5.9-fold increase in median arthritis severity index, a parameter known to correlate with synovial inflammation, and cartilage and bone erosions, compared with ACI (P< or =0.001). The arthritis severity enhancing effect could be detected from day 21 onwards. Rats heterozygous at the congenic interval developed a disease similar to ACI rats, suggesting that DA alleles operate in a recessive manner. Levels of autoantibodies anti-rat type II collagen did not correlate with arthritis severity. Synovial tissue mRNA levels of interleukin-1beta (IL-1beta) were significantly increased in ACI.DA(Cia27) congenics compared with ACI. These results demonstrate that Cia27 harbors a novel arthritis severity regulatory gene. The identification of this gene should facilitate the identification of the rheumatoid arthritis gene mapped to the human syntenic region on chromosome 17q22-q25.

Alleles↗
PubMed1984

Pathogenetic difference between collagen arthritis and adjuvant arthritis.

Daily treatment with cyclosporin at a dose of 25 mg/kg for 14 d gave complete suppression of the development of collagen arthritis and adjuvant arthritis in Sprague-Dawley rats during an observation period of 45 d. To study whether the immunologic unresponsiveness produced by cyclosporin is antigen specific, we rechallenged the cyclosporin-protected rats with either type II collagen or complete Freund's adjuvant (CFA) after discontinuation of cyclosporin treatment. Type II collagen-immunized, cyclosporin-protected rats did not develop arthritis in response to reimmunization with type II collagen, but, they did develop arthritis in response to a subsequent injection of CFA. Similarly, CFA-injected, cyclosporin-protected rats showed a suppressed arthritogenic reaction in response to reinjection of CFA, whereas their response to a subsequent immunization with type II collagen was unaffected. On the other hand, the rats that were treated with cyclosporin without any prior antigenic challenge could develop arthritis in response to a subsequent injection of CFA or type II collagen after cessation of cyclosporin treatment. These results indicate that specific immunologic unresponsiveness can be induced by cyclosporin in the two experimental models of polyarthritis, collagen arthritis and adjuvant arthritis, and that there is no cross-reactivity between type II collagen and the mycobacterial cell wall components. The results further indicate that immunity to type II collagen plays a critical role in the pathogenesis of collagen arthritis but that its pathogenetic role in adjuvant arthritis is insignificant.

Animals↗
PubMed1991

Septic arthritis as a non-surgical complication in rheumatoid arthritis: relation to disease severity and therapy.

More aggressive therapy including cytotoxic drugs is increasingly used in the treatment of rheumatoid arthritis (RA), and may confer increased susceptibility to infections. Septic arthritis is one infectious complication known to be overrepresented in RA. We studied the impact of disease severity and medication in a group of nine RA patients with proven septic arthritis, excluding those occurring as a complication of orthopaedic surgery. Two control groups were used for comparison. The septic arthritis patients were functionally more incapacitated and more often treated with cytotoxic drugs. Six of the nine septic arthritis patients had received an intra-articular injection into the infected joint within 3 months prior to the onset of the septic arthritis. Only one of these occurred immediately after arthrocentesis. The annual frequency of septic arthritis was approximately 0.2%. During the 4-year period studied the frequency was 0.5%. When related to the number of glucocorticosteroid injections, a frequency of 1 per 2000 injections was found when late septic arthritis was included. The high frequency of delayed septic arthritis after intra-articular glucocorticosteroid administration should alert physicians to this complication.

Administration, Oral↗
PubMed1998

Undifferentiated arthritis and reactive arthritis.

The terms undifferentiated arthritis and undifferentiated characterize arthritides that do not fit into well-known clinical disease categories (e.g., seronegative rheumatoid arthritis and reactive arthritis) and that are an early stage or forme fruste of a definite rheumatic disease, an overlap syndrome between such diseases, or an unknown, etiologically undefined disease that remains to be differentiated from other types of arthritis or spondylarthritis. Undifferentiated arthritis and undifferentiated spondylarthritis share some clinical features with reactive arthritides. Recent data suggest that, at least in Chlamydia-induced reactive arthritis, the triggering bacteria persist in affected joints for some time during the course of the disease in a viable but nonreplicative state, providing an antigenic stimulus for a bacteria-specific immune reaction in the joint. The clinical manifestations of reactive arthritis include not only Reiter's syndrome or clinically suspected postinfectious arthritis but also undifferentiated oligoarthritis and spondylarthritis. The optimal treatment remains to be defined, but there is increasing data that antibiotic therapy is not as effective in cases of well-established reactive arthritis as has been suggested.

Arthritis↗
PubMed1999

Pneumococcal polyarticular septic arthritis in a patient with rheumatoid arthritis.

Rheumatoid arthritis is the most commonly reported host-related risk factor for septic arthritis. This risk is highest in severe, seropositive, long-standing (mean, 10 years) rheumatoid arthritis responsible for extraarticular symptoms and treated with systemic glucocorticoids. The clinical presentation of the joint infection is often atypical, leading to diagnostic wanderings. In 25% of cases, the infection is polyarticular, with 3.5 involved joints on average. Staphylococcus aureus is the most common causative organism. Streptococcus pneumoniae causes 5% of all cases of septic arthritis and is more often responsible for polyarticular infections than other organisms. Polyarticular septic arthritis carries a poor prognosis, with a mortality rate of 50% in rheumatoid arthritis patients. Despite its low incidence, polyarticular septic arthritis should be routinely considered in the differential diagnosis of rheumatoid flares. We report a case of pneumococcal septic arthritis involving five joints in a patient with known rheumatoid arthritis. Three other cases with involvement of more than four joints have been published.

Anti-Bacterial Agents↗
PubMed1990

Radiographic changes in the temporomandibular joint of patients with rheumatoid arthritis, psoriatic, arthritis, and ankylosing spondylitis.

Sixty-one subjects with rheumatoid arthritis, 61 with psoriatic arthritis, 61 with ankylosing spondylitis, and 77 healthy controls were examined using orthopantomography to determine the frequency of radiographic changes in the condyle of the temporomandibular joint. Radiographic changes were found significantly more often in subjects with rheumatoid arthritis (66%), psoriatic arthritis (38%), and ankylosing spondylitis (30%) than in controls (12%). Subjects with rheumatoid arthritis also had significantly more radiographic changes, especially cortical erosions and subcortical cysts, than subjects with psoriatic arthritis or ankylosing spondylitis. It may be concluded that rheumatoid arthritis is a more severe disease than psoriatic arthritis or ankylosing arthritis regarding temporomandibular joint involvement.

Adult↗
PubMed2003

Induction of arthritis by single monoclonal IgG anti-collagen type II antibodies and enhancement of arthritis in mice lacking inhibitory FcgammaRIIB.

IgG anti-collagen type II (CII) antibodies (Ab) can induce arthritis in healthy mice. Here we have investigated if single monoclonal IgG anti-CII Ab can induce arthritis in CIA-susceptible DBA/1 mice and if there is an IgG subclass dependency. The involvement of Fc receptors for IgG (FcgammaR) in anti-CII Ab-mediated arthritis was also investigated by comparing the clinical outcome in DBA/1 mice to those in FcgammaR-deficient mice. We demonstrate for the first time that single mAb to naive DBA/1 mice can induce persistent arthritis. Histology of the inflamed joints revealed massive cellular infiltrate and cartilage and bone destruction. All IgG subclasses tested (IgG1, IgG2a and IgG2b) were arthritogenic, with the IgG1 and IgG2b isotypes as the dominating arthritogenic Ab. Pathogenicity was dependent on engagement of activating FcgammaR, as FcRgamma-deficient mice were completely resistant to Ab-mediated arthritis. The arthritis induced with the IgG1 and IgG2b Ab was also inhibited by FcgammaRIII disruption, whereas arthritis mediated by the IgG2a Ab was not substantially affected. The arthritic response of the IgG1 and IgG2b isotypes, but not of the IgG2a Ab, was further enhanced in mice lacking the inhibitory FcgammaRIIB. These results demonstrate that single IgG anti-CII mAb can induce erosive arthritis and that IgG anti-CII Ab mediate arthritis by engagement of FcgammaR.

Animals↗
PubMedDate not supplied

Cricoarytenoid arthritis: a cause of acute upper airway obstruction in rheumatoid arthritis.

PURPOSE: To report acute upper airway obstruction due to cricoarytenoid arthritis, a well known but uncommon complication of rheumatoid arthritis. CLINICAL FEATURES: We report the case of a 70-yr-old female scheduled for a colostomy who had been suffering from rheumatoid arthritis for 17 years. Preoperative history and physical examination revealed no cardiopulmonary compromise. Anesthesia was induced while an assistant immobilized the cervical spine and an atraumatic intubation was performed. Surgery was uneventful. Muscle paralysis was reversed, demonstrated by normalization of the train-of-four response, and the patient was extubated awake. Shortly postextubation, the patient developed inspiratory stridor, which disappeared after a second dose of neostigmine. The patient was transported to the postanesthesia care unit. Just prior to arrival the patient once again developed inspiratory stridor, became distressed, and oxygen saturation decreased. Direct laryngoscopy followed by a nasal fibreoptic examination of the larynx was performed. Cricoarytenoid arthritis secondary to rheumatoid arthritis with airway compromise was diagnosed. An uneventful awake tracheostomy was performed. The patient was discharged on day ten with a colostomy and a tracheostomy in place. One month postdischarge the patient's trachea was decannulated. On follow-up, a normal voice and mobile cords were observed. CONCLUSION: Cricoarytenoid arthritis is an infrequent complication of rheumatoid arthritis. A thorough history and physical examination are necessary to recognize signs and symptoms of cricoarytenoid arthritis. Prompt recognition of airway obstruction due to cricoarytenoid arthritis is essential for appropriate management.

Aged↗
PubMed2006

Clinical assessment and core outcome variables are poor predictors of hip arthritis diagnosed by MRI in juvenile idiopathic arthritis.

OBJECTIVES: To compare the diagnostic performance of clinical assessment against magnetic resonance imaging (MRI) diagnosed hip arthritis in a juvenile idiopathic arthritis (JIA) population. To determine the clinical and serological predictors of MRI diagnosed hip arthritis. METHODS: A total of 34 JIA patients with established disease (mean disease duration 6.3 yrs) had their hip MRIs scored for features of active hip arthritis and hip damage. Results were compared with clinical variables (disease subtype, history of hip pain, core outcome variables (COV)) and the clinician's assessment of active hip arthritis. RESULTS: MRI features of active hip arthritis were found in 45 hips (70%) and hip damage in 36 hips (56%). Clinical assessment had fair agreement with MRI scoring of active arthritis in patients with disease duration <4 yrs (kappa score 0.38, P = 0.045). Clinical assessment had a sensitivity of 25.7% and specificity of 91% for detecting MRI diagnosed arthritis. Of the core outcome variables only erythrocyte sedimentation rate predicted inflammation detected on MRI (r = 0.44, P = 0.014). CONCLUSIONS: The association between the clinician's assessment, core outcome variables and MRI findings in this study was limited. This indicates that clinical and laboratory findings are inadequate diagnostic tools for the assessment of hip arthritis when compared with MRI as the gold standard.

Adolescent↗
PubMed2004

Bone marrow cells carrying the env-pX transgene play a role in the severity but not prolongation of arthritis in human T-cell leukaemia virus type-I transgenic rats: a possible role of articular tissues carrying the transgene in the prolongation of arthritis.

Transgenic rats carrying the env-pX gene of human T-cell leukaemia virus type-I (env-pX rats) were immunized with type II collagen (CII), and chronological alterations of arthritis were compared with findings of collagen-induced arthritis (CIA) in wildtype Wistar-King-Aptekman-Hokudai (WKAH) rats. Arthritis induced by CII in env-pX rats was more severe and persisted longer than CIA in WKAH rats. To determine whether the phenomenon is caused mainly by the transgene-carrying lymphocytes or articular tissues, we immunized lethally irradiated env-pX and WKAH rats with reciprocal bone marrow cell (BMC) transplantation. A severe but transient arthritis was induced by CII in WKAH rats reconstituted by env-pX BMC (w/tB/CII rats). On the other hand, in env-pX rats reconstituted by WKAH BMC, arthritis persisted longer than in w/tB/CII rats, although the degree was less at an early phase after CII immunization. These findings suggest that articular tissues rather than the BMCs carrying the env-pX transgene play a role in the prolongation of arthritis in env-pX rats, although BMCs carrying the transgene are associated with the severity of arthritis. When inflammatory cytokines in synovial cells isolated from env-pX rats before they developed arthritis were examined, interleukin-6 (IL-6) was detected at a higher level than in synovial cells from WKAH rats, thus suggesting the critical role of IL-6 in env-pX arthritis.

Animals↗
PubMed1995

Type XI and II collagen-induced arthritis in rats: characterization of inbred strains of rats for arthritis-susceptibility and immune-responsiveness to type XI and II collagen.

To determine the relationship between susceptibility to bovine type XI and II (BXI and BII) collagen-induced arthritis, we immunized 14 inbred and one outbred strains of rats with BXI and BII. Susceptibility to BXI-arthritis corresponded largely with susceptibility, or resistance, to BII-arthritis. LEW, BB, WF, DA, and WKY were readily susceptible to BXI- and BII-arthritis. Likewise, BII-resistant F344 and BN rats were BXI-resistant. Some strains responded differently to BXI and BII. BUF and COP, which are moderately susceptible to BII, were BXI-resistant, whereas the BII-resistant rats, DA.1N and WF.1N, were partially susceptible to BXI. (F344 x BN) F1 hybrids responded to both collagens suggesting gene complementation. Arthritis occurred in all strains producing the highest titer antisera (LEW, WF and BB). Antibody responses to BXI and BII were generally commensurate within individual strains. DA were susceptible to arthritis but produced low levels of antibody comparable to BN rats which were arthritis-resistant. BXI and BII-susceptibility was variable in rats producing intermediate antibody responses. Antibodies to RXI were detected in all BXI-immunized rats, whereas antibodies to RV and RII were uniformly weaker. DTH to RXI and RII was strong in both groups of rats, correlating poorly with arthritis and antibody responses. These studies show that phenotypic susceptibility to BXI- and BII-arthritis are largely concordant among inbred rat strains but clear differences exist in certain strains; multiple genes are likely involved.

Animals↗
PubMedDate not supplied

[Hepatitis C virus infection and arthritis. A clinico-serological investigation of arthritis in patients with or without cryoglobulinemic syndrome].

OBJECTIVE: To compare the clinico-serological features of arthritis from two HCV+ patient groups characterized by mixed cryoglobulinemia (MC) or chronic hepatitis (CH). METHODS: We retrospectively studied 157 MC patients (119 females, mean age 64.8 yrs, range 36-88) and 155 CH patients (103 females, mean age 58.8 yrs, range 30-81). Patients with HBV and/or HIV co-infections and a follow-up shorter than 1 year were excluded. MC was classified according to standard criteria, while CH classification was based on Desmet's criteria. RESULTS: No differences in epidemiology were demonstrated between the two series of patients. Although significantly prevalent in MC patients, extra-hepatic manifestations including nephropathy, neuropathy, pneumopathy, mixed cryoglobulins, RF positivity and hypocomplementemia were detected in both patient groups. Arthritis was present in 23 CH (15%) and 12 MC (8%) patients. A symmetrical polyarthritis was observed in 87% of 23 CH patients, while cryoglobulinemic arthritis was invariably asymmetrical and pauciarticular. Unlike MC patients, who had a constantly non-erosive arthritis, in 7/23 CH patients arthritis was erosive. Steroids and/or hydroxycloroquine or D-penicillamine were safe and useful in controlling the arthritis over the short-medium time, although clinical response was more evident in MC patients. Instead, in 5/23 CH and 3/12 MC patients, interferon-alpha treatment was able to trigger or exacerbate the arthritis despite a good control of liver function. CONCLUSIONS: HCV infection seems to be, possibly in genetically predisposed patients, responsible for arthritis at times similar to rheumatoid arthritis. In these patients a careful assessment of the interferon-alpha treatment is mandatory owing to the potential "arthritogenic effect" due to its immunoregulatory properties.

Adult↗
PubMed2005

Effects of telephone intervention on arthritis self-efficacy, depression, pain, and fatigue in older adults with arthritis.

PURPOSE: Arthritis self-efficacy (ASE) characterizes individuals' confidence in managing their arthritis. This study's purpose was to examine the effects of a telephone intervention on ASE, depression, pain, and fatigue in older adults with arthritis. METHODS: Eighty-five elders with arthritis were randomly assigned to the intervention or control group. Participants in both groups: (a) completed baseline assessments of ASE, depression, pain, and fatigue; (b) received written information on arthritis management; and (c) received individualized action plans for achieving their own arthritis management goal over the 6-week study. Participants in the intervention group received a telephone intervention including instruction on managing arthritis and encouragement to pursue their goal. In the sixth week the assessment tools were re-administered. Quantitative and qualitative data analysis methods were employed. RESULTS: Quantitative analyses showed a significant increase in ASE and a significant reduction in depression and pain over time for both groups. Qualitative analyses revealed several themes related to benefits of telephone intervention. CONCLUSION: Study results suggest that minimal intervention (ie, written information, goal-setting, and action plans) may produce positive changes in ASE, depression, and pain in some older adults with arthritis. Furthermore, telephone intervention may assist older patients in managing their arthritis.

Aged↗
PubMed2000

Treatment with leflunomide slows radiographic progression of rheumatoid arthritis: results from three randomized controlled trials of leflunomide in patients with active rheumatoid arthritis. Leflunomide Rheumatoid Arthritis Investigators Group.

OBJECTIVE: To determine whether treatment with leflunomide (LEF), methotrexate (MTX), or sulfasalazine (SSZ) for 6-12 months retards progression of radiographic damage and to identify clinical variables that correlate with radiographic progression. METHODS: Radiographs of the hands and feet were performed at baseline and at the end of study or early exit in 3 randomized controlled trials. Protocol US301 was a 12-month controlled trial of LEF or MTX treatment compared with placebo in 482 patients randomized in a 3:3:2 ratio. Protocol MN301 compared 6 months of LEF or SSZ treatment with placebo in 358 patients, randomized in a 3:3:2 ratio, with continued blinded treatment in the active control arms for 12 months. Protocol MN302 compared 12 months of LEF treatment with MTX in 999 patients. Radiographs were blinded for sequence and treatment and were scored for erosions and joint space narrowing. All analyses were by intent-to-treat. Sensitivity analyses were performed to account for missing data. RESULTS: LEF, MTX, and SSZ treatment resulted in statistically significantly less radiographic progression compared with placebo at 6 and 12 months: for protocol US301, LEF versus placebo P = 0.0007 and MTX versus placebo P = 0.0196; for protocol MN301, LEF versus placebo P = 0.0004 and SSZ versus placebo P = 0.0484. The effect of LEF treatment was similar to that of MTX and SSZ. CONCLUSION: These are the first 6- and 12-month randomized placebo- and active drug-controlled trials to demonstrate retardation of radiographic progression by a new disease-modifying antirheumatic drug (DMARD), LEF, as well as 2 commonly used DMARDs, MTX and SSZ.

Anti-Inflammatory Agents, Non-Steroidal↗