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Results for “Arthritis, Reactive”

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PubMed2005

[Quality of life and psychosocial adaptation in children and adolescents with juvenile idiopathic arthritis and reactive arthritis].

OBJECTIVE: We sought to measure self-reported health related quality of life (HRQOL) and psychosocial adaptation in children and adolescents with juvenile idiopathic arthritis (JIA) and reactive arthritis and to determine factors associated with these outcomes. METHODS: We interviewed 72 children and adolescents with chronic arthritis, age 8-16, about HRQOL (KINDL-R-Questionnaire) and functional ability in activities of daily living (Childhood Health Assessment Questionnaire-CHAQ). Mothers reported behavior problems (Child Behavior Checklist-CBCL). RESULTS: Children and adolescents with juvenile idiopathic arthritis and reactive arthritis reported lower HRQOL compared to normative data in several areas. Children reported lower QOL in the dimensions self-esteem; adolescents reported lower QOL in the dimensions physical well being and total QOL. Almost 20% of the sample appeared to have serious behavior problems, mostly social isolation and depression/anxiety. Functional limitations affected HRQOL and behavior problems. Inpatient children and adolescents and those with shorter disease duration reported lower QOL than outpatient children and adolescents and those with longer disease duration. Best predictors for impaired HRQOL were functional limitations, social isolation and depression/anxiety. CONCLUSIONS: Self-reported HRQOL and behavior problems may be relevant outcome measures in children and adolescents with chronic arthritis and useful to monitor psychosocial support in this population.

Activities of Daily Living↗

PubMed1990

[Nosologic concept and new developments in the etiopathogenesis of reactive arthritis].

Reactive inflammatory arthritis is caused by extraarticular infection with different arthritogenic microorganisms. The causative bacteria can not be cultured from synovial specimens, but bacterial antigens have been demonstrated in cells of synovial fluid and synovial membrane, respectively. Thus, latent intraarticular infection may be the cause of reactive arthritis. A model of the etiopathogenesis of reactive arthritis is described on the basis of recent immunological and microbiological findings.

Antibodies, Bacterial↗

PubMed1998

Analysis of the cellular infiltrates and expression of cytokines in synovial tissue from patients with rheumatoid arthritis and reactive arthritis.

The cellular infiltrates and cytokine patterns in synovial tissue (ST) from patients with rheumatoid arthritis (RA) and reactive arthritis (ReA) were compared in order to determine the mechanisms responsible for the chronic and destructive course of RA. Since the results could be influenced by differences in disease duration, ST was studied from patients in both early and late stages of the disease. Ten patients had early RA (< 1 year), ten long-standing RA (> 1 year), six early ReA (< 1 year), and five long-standing ReA (> 1 year). Histological analysis demonstrated that the scores for infiltration by lymphocytes and plasma cells, and the scores for inflammation, were significantly higher in RA than in ReA. Immunolabelling studies showed that in particular, the scores for infiltration by CD38+ plasma cells, granzyme B+ cells, and interferon-gamma (IFN gamma)+ cells were significantly higher in RA than in ReA. The results were independent of the disease duration. The increased number of lymphocytes, plasma cells, and granzyme B+ cells in rheumatoid synovial tissue supports the paradigm that RA is the result of specific immune recognition in the joint and that granzyme B+ cells play an important role in joint destruction.

Adolescent↗

PubMed2002

Inadequately low serum levels of steroid hormones in relation to interleukin-6 and tumor necrosis factor in untreated patients with early rheumatoid arthritis and reactive arthritis.

OBJECTIVE: To compare levels of steroid hormones in relation to cytokines and to study levels of cortisol or dehydroepiandrosterone (DHEA) in relation to other adrenal hormones in untreated patients with early rheumatoid arthritis (RA) and reactive arthritis (ReA) compared with healthy controls. METHODS: In a retrospective study with 34 RA patients, 46 ReA patients, and 112 healthy subjects, we measured serum levels of interleukin-6 (IL-6), tumor necrosis factor (TNF), adrenocorticotropic hormone (ACTH), cortisol, 17-hydroxyprogesterone (17-OH-progesterone), androstenedione (ASD), DHEA, and DHEA sulfate (DHEAS). RESULTS: RA patients had higher serum levels of IL-6, TNF, cortisol, and DHEA compared with ReA patients and healthy subjects, but no difference was noticed with respect to ACTH and DHEAS. However, in RA and ReA patients compared with healthy subjects, levels of ACTH, cortisol, ASD, DHEAS, and 17-OH-progesterone were markedly lower in relation to levels of IL-6 and TNF. Furthermore, the number of swollen joints correlated inversely with the ratio of serum cortisol to serum IL-6 in RA (R(Rank) = -0.582, P = 0.001) and, to a lesser extent, in ReA (R(Rank) = -0.417, P = 0.011). In RA patients, the mean grip strength of both hands was positively correlated with the ratio of serum cortisol to serum IL-6 (R(Rank) = 0.472, P = 0.010). Furthermore, in these untreated patients with RA and ReA, there was a relative decrease in the secretion of 17-OH-progesterone, ASD, and DHEAS in relation to DHEA and cortisol. This indicates a relative predominance of the nonsulfated DHEA and cortisol in relation to all other measured adrenal steroid hormones in the early stages of these inflammatory diseases. CONCLUSION: This study indicates that levels of ACTH and cortisol are relatively low in relation to levels of IL-6 and TNF in untreated patients with early RA and ReA compared with healthy subjects. The study further demonstrates that there is a relative increase of DHEA and cortisol in relation to other adrenal hormones, such as DHEAS. This study emphasizes that adrenal steroid secretion is inadequately low in relation to inflammation. Although changes in hormone levels are similar in RA and ReA, alteration of steroidogenesis is more pronounced in RA patients than in ReA patients.

Adrenal Cortex Hormones↗

PubMed1999

Diagnostic evaluation of classification criteria for rheumatoid arthritis and reactive arthritis in an early synovitis outpatient clinic.

OBJECTIVE: To evaluate the diagnostic performance of classification criteria for rheumatoid arthritis (RA) and reactive arthritis (ReA) in an early synovitis outpatient clinic. METHODS: In a prospective two year survey consecutive patients with early synovitis of less than one year duration were documented using a standardised registry and were classified after an expert diagnosis. Of a total of 320 patients 39 (19%) were diagnosed as having RA, 24 (11%) patients had ReA, 117 (54%) patients did not have an unequivocal diagnosis, and were considered as undifferentiated arthritis. RESULTS: The retrospective application of the revised 1987 ACR criteria for the classification of RA in this data set revealed a sensitivity of 90% and a specificity of 90%. The positive predictive value was 0.67, the negative predictive value 0.98. Similarly, the criteria for ReA of the French Society of Rheumatology (FSR) showed a sensitivity of 80% and a specificity of 90% with a positive predictive value of 0.55 and a negative predictive value of 0.97. Both criteria sets had a satisfying likelihood ratio of 9 and 10, respectively. CONCLUSION: Both the 1987 ACR criteria for RA and the criteria of the FSR for ReA have a reasonable diagnostic validity in patients with early synovitis, including a large portion of undifferentiated arthritis.

Arthritis, Reactive↗

PubMed1989

Synovial T lymphocyte recognition of organisms that trigger reactive arthritis.

Reactive arthritis (ReA) is believed to be "triggered' by infection with certain bacteria. When the proliferative responses of mononuclear cells (MC) obtained from the synovial fluid (SF) of ReA patients were examined, it was found that they responded maximally to the specific organism responsible for the preceding infection. The response was shown to be due to Class II MHC-restricted T cells by inhibition experiments using cyclosporin A and monoclonal antibodies. Significant SFMC responses to additional organisms associated with ReA were also recorded; since there was no serological evidence of preceding infection by these organisms, this finding suggests that these bacteria share common T cell-recognized antigenic epitopes. The corresponding responses by peripheral blood mononuclear cells (PBMC) were much lower and often barely detectable, whereas their responses to PHA were consistently higher than those of SFMC. These results, combined with evidence that bacterial antigens localize in the joint, indicate that a bacteria-specific, T-cell-mediated response may play a central role in the pathogenesis of ReA.

Antigens, Bacterial↗

PubMed1989

[The state of humoral immunity to enterobacterial antigens in juvenile rheumatoid arthritis and reactive arthritis in children].

Investigation findings are generalized based on quantitation of antibodies against the antigens of intestinal microorganisms of Enterobacteriaceae family conducted in 66 children with various joint disease using the enzyme-linked immunoassay (ELISA) methodology. High antibody titres were revealed in 77.1% juvenile rheumatoid arthritis cases and in 80% cases with chronic juvenile arthritis which was not defined nosologically. All the patients with reactive arthritis associated with intestinal infection showed high tension of immunity to all tested enterobacteriaceae antigens with cross reactions to them. Patients with reactive arthritis associated with oral infection, with Reiter's disease and other disorders exhibited high antibody titres at the same rate as in the control.

Antibody Formation↗

PubMed1997

[The comparative clinico-laboratory characteristics of Lyme arthritis and reactive arthritis].

The paper presents comparative clinical and laboratory characteristics of 17 cases of Lyme-arthritis (LA) and 28 cases of reactive arthritis (RA). LA and RA patients differed by age and sex. LA arose after the tick bite followed by erythema migrans or infection symptoms. In RA patients the above symptoms were absent. In LA patients arthritis was associated with typical symptoms of neuroborreliosis. The articular syndrome manifested similarly in LA and RA: arthritis was preceded by arthralgias, low limb joints and periarticular tissues were involved most frequently. The differences were: monoarthritis, elbow and shoulder joints, muscles lesions occurred more frequently in LA; polyarthritis, arthritis of hand and foot joints, talalgia were more common in RA. RA ran more actively, joint syndrome more frequently gave rise to fever. Prevalence of chlamydial infection in LA was close to that in RA. LA may run as RA, is frequently combined with Chlamydia trachomatis infection.

Aged↗

PubMed2002

Ankylosing spondylitis, psoriatic arthritis, and reactive arthritis show increased bone resorption, but differ with regard to bone formation.

OBJECTIVE: To test if markers of bone metabolism are altered in patients with seronegative spondyloarthropathies (SSpA). METHODS: We studied biochemical markers of bone resorption and bone formation, osteoprotegerin (OPG), and bone mineral density (BMD) in patients with psoriatic arthritis (PsA), ankylosing spondylitis (AS), and reactive arthritis (ReA) and healthy volunteers. RESULTS: The bone resorption markers urinary deoxypyridinoline and crosslinked telopeptide of collagen-I were significantly increased in patients with AS, PsA, and ReA; in PsA they correlated with the acute phase response (C-reactive protein and erythrocyte sedimentation rate). The bone formation markers were divergent: bone-specific alkaline phosphatase was increased in PsA, but not in AS or ReA. Osteocalcin levels were only elevated in AS. Serum levels of OPG were significantly increased in both AS and PsA. Dual energy x-ray absorptiometry (DEXA) measurements of lumbar spine and femoral neck revealed osteopenia in patients with AS, whereas the DEXA distribution was within normal range in PsA. CONCLUSION: Our data indicate high and, particularly in AS, unbalanced bone turnover in SSpA, consistent with the decrease in BMD found in patients with AS.

Absorptiometry, Photon↗

PubMed1985

Difference in cartilage proteoglycan level in synovial fluid in early rheumatoid arthritis and reactive arthritis.

Cartilage proteoglycans were measured, by the use of an enzyme-linked immunosorbent assay, in synovial fluids obtained from 109 unselected patients attending an outpatient rheumatology clinic because of inflammation of the knee. The content of proteoglycans in synovial fluid was inversely related to the degree of joint destruction shown on X-ray. The proteoglycan concentrations in knee-joint exudates were higher in patients with reactive arthritis than in patients with rheumatoid arthritis having synovitis of corresponding duration and lacking radiological evidence of cartilage destruction. The measurement of proteoglycan levels may therefore be useful in differentiating between the two conditions.

Arthritis↗

PubMed2006

When is arthritis reactive?

Reactive arthritis is an important cause of lower limb oligoarthritis, mainly in young adults. It is one of the spondyloarthropathy family; it is distinguishable from other forms of inflammatory arthritis by virtue of the distribution of affected sites and the high prevalence of characteristic extra-articular lesions. Many terms have been used to refer to this and related forms of arthritis leading to some confusion. Reactive arthritis is precipitated by an infection at a distant site and genetic susceptibility is marked by possession of the HLA-B27 gene, although the mechanism remains uncertain. Diagnosis is a two stage process and requires demonstration of a temporal link with a recognised "trigger" infection. The identification and management of "sexually acquired" and "enteric" forms of reactive arthritis are considered. Putative links with HIV infection are also discussed. The clinical features, approach to investigation, diagnosis, and management of reactive arthritis are reviewed.

Anti-Bacterial Agents↗

PubMed1998

Detection of bacterial DNA in joint samples from patients with undifferentiated arthritis and reactive arthritis, using polymerase chain reaction with universal 16S ribosomal RNA primers.

OBJECTIVE: Bacteria are considered to be important in the pathogenesis of several forms of arthritis. The goal of this study was to apply the 16S ribosomal RNA (rRNA)-polymerase chain reaction method for the detection of bacterial DNA in synovial fluid (SF) and synovial tissue (ST) from inflamed joints. METHODS: Samples from 5 patients with septic arthritis and from 7 with osteoarthritis or arthritis secondary to joint trauma were used as controls. Samples from 6 patients with spondylarthropathy (SpA) and from 20 with undifferentiated arthritis (UA) were analyzed for the presence of bacterial DNA using universal 16S rRNA primers. Automated sequencing and comparative data analysis were performed to identify the species. RESULTS: In the positive control group, the bacterial species cultured from the synovium could be identified in all cases. No bacterial DNA was detected in the SF and ST from patients in the negative control group. In 4 of 6 patients with SpA and 7 of 20 with UA, the analysis of joint samples revealed the presence of bacterial DNA. Sequence analysis indicated the presence of multiple species, which was confirmed by sequencing of cloned products. CONCLUSION: When the the above techniques were used with a stringent regimen, we were able to demonstrate that it is possible to collect and analyze joint samples without contaminating bacterial DNA. The accumulation of phagocytic cells that contain bacterial DNA of various species could play a role in the pathogenesis of both SpA and UA.

Adolescent↗

PubMed1998

Reactive arthritis associated with group C and group G beta-hemolytic streptococci.

OBJECTIVE: Group A beta-hemolytic streptococci (GAS) are known to be capable of evoking sterile arthritis. Reactive arthritis (ReA) has been reported sporadically following primary infection with group C and group G beta-hemolytic streptococci (GCS, GGS). We prospectively studied 4 cases of ReA secondary to throat infection with GCS and GGS. METHODS: Four patients with arthritis secondary to throat infection were seen. Three patients were Dutch, one was Indonesian; female/male ratio was 1/3; mean age was 30 years (range 18-46). Diagnostic evaluation included culture of throat swab and serological screening. RESULTS: All patients presented with a nonmigratory asymmetrical arthritis: monoarthritis in one patient, oligoarthritis in 3. Culture of throat swab was positive in all. Antistreptolysin-O (ASO) titer rose significantly in 2 patients, and anti-DNase-B rose in 2 patients. ASO was maximal (mean 1000 U/ml; range 890-1110) and anti-DNase-B was 395 U/ml (range 290-500). Treatment consisted of feneticillin for 5 days; nonsteroidal antiinflammatory drugs were prescribed on demand. All patients recovered fully in 3 to 12 weeks. CONCLUSION: These cases provide evidence of a benign non-group A streptococcal ReA, i.e., secondary to GCS or GGS. The presence of the organism in the throat along with the elevation of antibody to streptococcal products is important for the diagnosis of GCS/GGS associated ReA. A positive throat culture is needed for differentiation from GAS associated poststreptococcal ReA, because prophylactic measures are effective only in GAS associated sequelae, but not in GCS/GGS associated ReA.

Adolescent↗

PubMed2002

Chlamydial conjunctivitis (in adults), uveitis, and reactive arthritis, including SARA. Sexually acquired reactive arthritis.

This chapter deals with Chlamydia -induced ocular and rheumatic diseases of the adult. All of these may follow a primary urogenital infection with Chlamydia trachomatis in genetically predisposed patients. Besides the infection with Chlamydia trachomatis, infections with Chlamydia pneumoniae and Chlamydia psittaci are also discussed as possible causative agents. Chlamydial conjunctivitis is frequently a secondary infection, and the organism is transferred from the urogenital tract to the eye by autoinoculation. Uveitis and reactive arthritis are believed to be triggered - among other infections - by a preceding urogenital infection. Both of them are closely associated with HLA-B27 positivity. The simultaneous occurrence of uveitis and reactive arthritis is termed Reiter's syndrome. We report on clinical characteristics, diagnosis and the role of Chlamydia in the pathogenesis of chlamydial conjunctivitis, uveitis and reactive arthritis as well as on the currently recommended treatment regimens.

Adult↗

PubMed1988

Serum and synovial fluid adenosine deaminase activity in patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis.

Adenosine deaminase activity was determined in paired samples of serum and synovial fluid taken from patients with rheumatoid arthritis (n = 12), reactive arthritis (n = 13), and osteoarthritis (n = 7), and the value of this investigation in the diagnosis of synovial swellings was assessed. Increased activity was found in the synovial fluid taken from patients with rheumatoid disease and reactive arthritis, though values were less raised in the latter. Synovial fluid taken from patients with osteoarthritis did not show significantly raised adenosine deaminase activity as compared with that of normal controls (n = 3).

Adenosine Deaminase↗

PubMed1989

Bowel infection predisposing to reactive arthritis.

Postenteric reactive arthritis is one of several syndromes in which arthritis appears to be secondary to gastrointestinal tract pathology. A wide range of microbes may trigger this type of arthritis. On the other hand, there are differences between strains in their arthritogenic potential. Two possible mechanisms, not mutually exclusive, can be forwarded to explain these findings: first, particular characteristics of the infective organisms are necessary to initiate events leading to reactive arthritis and, second, particular anatomical locations and a certain degree of mucosal involvement are needed to initiate the process. Studies on humoral and cellular immune responses have not revealed any unifying feature that could explain the pathogenesis of reactive arthritis. The HLA allele B27 plays some kind of key role. Yet the elucidation of the fine structure of B27 specificity has not led to any immediate breakthrough in the understanding of the pathogenetic pathways. Experience of reactive arthritis associated with acquired immunodeficiency syndrome suggests that helper T cells are not involved. Antigen persistence may be connected with continuation of the inflammation. Recent developments in the serology of enteric bacterial infections will provide additional tools for uncovering the triggering agents in reactive arthritis. 'Idiopathic reactive arthritis' associated with clinically silent terminal ileitis is an interesting disease entity requiring further characterization.

Arthritis↗

PubMed2005

Chemokine and chemokine receptor expression in paired peripheral blood mononuclear cells and synovial tissue of patients with rheumatoid arthritis, osteoarthritis, and reactive arthritis.

BACKGROUND: Chemokine receptors and chemokines have a crucial role in leucocyte recruitment into inflamed tissue. OBJECTIVE: To examine the expression of an extensive number of chemokines and receptors in a unique bank of paired samples of synovial tissue (ST) and peripheral blood (PB) from patients with different forms of arthritis to assist in identifying suitable targets for therapeutic intervention. METHODS: Synovial biopsy specimens were obtained from 23 patients with rheumatoid arthritis (RA), 16 with osteoarthritis, and 8 with reactive arthritis. ST chemokine (CCL2/MCP-1, CCL5/RANTES, CCL7/MCP-3, CCL8/MCP-2, CCL14/HCC-1, CCL15/HCC-2, CCL16/HCC-4), chemokine receptor (CCR1, CCR2b, CCR5, CXCR4), and CD13 expression was analysed by immunohistochemistry and two colour immunofluorescence. Chemokine receptor expression (CCR1, CCR3, CCR5, CCR6, CCR7) on PB cells was studied by flow cytometry. Non-parametric tests were used for statistical analysis. RESULTS: Abundant expression of CCR1, CXCR4, and CCR5 was found in all forms of arthritis, with a specific increase of CCL5 and CCL15 in RA. CCL7, CCL8, CCL14, CCL15, and CCL16 were detected for the first time in ST. The results for PB analysis were comparable among different arthritides. Interestingly, compared with healthy controls, significantly lower expression of CCR1 (p<0.005) and CCR5 (p<0.05) by PB monocytes in the patient groups was seen. DISCUSSION: A variety of chemokines and receptors might have an important role in several inflammatory joint disorders. Although other receptors are involved as well, migration of CCR1(+) and CCR5(+) cells towards the synovial compartment may play a part in the effector phase of various forms of arthritis.

Adolescent↗

PubMed1988

Synovial lymphocyte responses to microbial antigens differentiate the arthritis of enteric reactive arthritis from the arthritis of inflammatory bowel disease.

Synovial lymphocyte responses to microbial antigens were measured by the 3H-thymidine uptake method in 5 patients with bacteriologically defined enteric reactive arthritis and 7 patients with arthritis associated with inflammatory bowel disease. All the patients with enteric reactive arthritis had maximal synovial lymphocyte responses to the relevant enteric antigen; in contrast, the synovial lymphocytes of the patients with inflammatory bowel disease all responded maximally to nonenteric antigens.

Antigens, Bacterial↗