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PubMed2005

Does systemic-onset juvenile idiopathic arthritis belong under juvenile idiopathic arthritis?

'Science is the systematic classification of experience' George Henry Lewes (1817-78), English philosopher, critic, dramatist, scientist. Juvenile idiopathic arthritis (JIA) is prevalent in about 1 in 1000 children. The earliest formal description of this disease was by Sir George Frederick Still in 1897. This work was done when he was a registrar at the Hospital for Sick Children, Great Ormond Street, London. In this initial description of 19 patients he identified three patterns of arthritis, one of which came to be known later as Still's disease [now known as systemic-onset juvenile idiopathic arthritis (SoJIA)]. Over the next few decades it came to be appreciated that one form of arthritis in children is very different and dominated by the presence of systemic manifestations. Over the last two decades several paediatric rheumatologists have come together to classify juvenile arthritis for purposes of better disease identification and research. All along, the systemic form of juvenile arthritis was always recognized as belonging to a distinct group; in fact for several decades (and even now in some countries) the systemic form of juvenile arthritis was referred to as Still's disease. In this article we will attempt to highlight the reasons why we feel that SoJIA is perhaps not best retained in the company of JIA.

Arthritis, Juvenile↗
PubMed2005

Antibodies to cyclic citrullinated peptide in patients with chronic arthritis attending an arthritis-monitoring clinic.

BACKGROUND: Early diagnosis of rheumatoid arthritis allows prompt initiation of antirheumatic therapy, which is associated with improved outcome. The use of IgM rheumatoid factor, the most widely used serologic test in assisting the diagnosis of rheumatoid arthritis, is limited by low specificity. An enzyme-linked immunosorbent assay test detecting antibodies to cyclic citrullinated peptide (CCP) has been developed with apparently higher specificity for rheumatoid arthritis. AIM: We aimed to evaluate an assay for anti-CCP antibodies by determining the prevalence and titer of antibodies to CCP in a group of patients with chronic arthritis. METHOD: Thirty-four sera were collected from outpatients attending an arthritis-monitoring clinic and tested for anti-CCP and IgM rheumatoid factor. RESULTS: Anti-CCP and rheumatoid factor were detected in 86% and 72% of patients with rheumatoid arthritis, respectively. Six patients negative for rheumatoid factor were positive for anti-CCP. CONCLUSION: Anti-CCP antibodies are frequently detectable in high titer in patients with longstanding rheumatoid arthritis. This assay may be especially helpful in such cases when positive in rheumatoid factor-negative patients.

Antibodies↗
PubMed1990

Adjuvant-induced arthritis in rats. Evidence that autoimmunity to homologous collagens types I, II, IX and XI is not involved in the pathogenesis of arthritis.

We examined the sera of arthritic outbred Wistar and Sprague-Dawley rats and inbred Fisher 344 and Wistar-Lewis rats for autoantibodies to rat type I, II, IX and XI collagens following the induction of arthritis with mycobacteria (MTB). Although many sera collected over an extended time were assayed in addition to acid eluates of arthritic joints, convincing evidence for autoimmunity to collagen could not be demonstrated. Instead, modest non-specific reactions were observed to collagen, irrelevant proteins, and buffer-treated plastic microtitre wells. In contrast, antibodies to purified protein derivative (PPD) were detected in the sera of rats developing adjuvant-induced arthritis, and antibodies to type II collagen, in the sera and joint eluate of rats developing experimental collagen-induced arthritis. Lastly, delayed-type hypersensitivity responses to collagen could not be detected, nor could adjuvant-induced arthritis be attenuated by soluble collagen injected intravenously before challenge with MTB. We conclude that adjuvant-induced arthritis and experimental collagen-induced arthritis are distinct models of rheumatic disease and that autoimmunity to collagen is neither prevalent in adjuvant-induced arthritis nor necessary for its pathogenesis.

Animals↗
PubMed2006

Arthritis of the large joints - in particular, the knee - at first presentation is predictive for a high level of radiological destruction of the small joints in rheumatoid arthritis.

OBJECTIVE: To investigate the predictive value of the distribution of inflamed joints at first presentation for the severity of the disease course in rheumatoid arthritis (RA). METHODS: Of the 1009 consecutive patients included in the Leiden Early Arthritis Clinic (Leiden, The Netherlands), 285 patients fulfilled the American College of Rheumatology criteria for RA within 1 year of follow-up. Of these, 28 patients achieved remission. Radiographs of hands and feet were scored according to the Sharp-van der Heijde method, and the 28 patients with the most destructive disease were selected. The distribution of inflamed joints of the patients with the extreme disease courses was compared. The association between the distribution of inflamed joints and the level of destruction of the joints of hands and feet in the whole group of patients with RA was assessed using regression analysis. RESULTS: Comparison of patients with extreme disease courses using univariate and logistic regression analyses showed that arthritis of the large joints - in particular, the knee - was associated with severe RA. In the whole group of patients with RA, the total number of swollen joints and the presence of knee arthritis were associated independently with the level of destruction of the small joints. Patients with RA with knee arthritis had higher C reactive protein (CRP) levels than patients without knee arthritis, and investigating the distribution of inflamed joints together with other variables yielded the number of swollen joints, CRP, presence of anti-cyclic citrullinated peptide antibodies and symptom duration as predictors for severity of RA. CONCLUSION: Arthritis of large joints - in particular, the knee - at first presentation is associated with a destructive course of RA.

Aged↗
PubMed1999

A clinical and serological comparison of group A versus non-group A streptococcal reactive arthritis and throat culture negative cases of post-streptococcal reactive arthritis.

OBJECTIVE: To identify clinical and serological differences of patients with reactive arthritis after infection with Lancefield group A beta-haemolytic streptococci (GAS), compared with non-group A-that is, group C or G streptococci (NGAS:GCS/GGS), and a group of culture negative or unidentified streptococci (GUS). METHODS: A prospective study of consecutive patients with reactive arthritis after serologically or culture confirmed infection with beta-haemolytic streptococci, presenting to the outpatient department of rheumatology from January 1992 until January 1998. Alternative causes for reactive arthritis were excluded. Main outcome measures were clinical and serological characteristics including antistreptolysine-O (ASO) and antideoxyribonuclease-B (antiDNase-B) antibody titres. RESULTS: 41 patients (female/male ratio 22/19; mean (SD) age 38 (13) years) with reactive arthritis were included. Culture of throat swab was positive in 13 cases (32%): 6 (15%) GAS, 7 NGAS (17%), that is, 5 (12%) GCS, 2 (5%) GGS. In 28 cases throat culture remained negative resulting in a group of unidentified streptococci; antibiotic pre-treatment had been given by the general practitioner in 18 cases (64%). Arthritis was non-migratory, the number of arthritic joints in GAS and NGAS was similar, whereas in NGAS patients fewer joints were involved than in GUS: mean (SEM) 36 swollen joint index: 3.3 (1.0) in NGAS v 5.6 (1.0) in GUS (p<0.005); 28 swollen joint index: 2.9 (1.0) in NGAS v 4.3 (0.8) in GUS (p<0.05). Extra-articular manifestations-that is, erythema nodosum/ multiforme, AV conduction block or hepatitis-were observed after GAS or GUS infection, but not after NGAS infection. ASO and/or antiDNase-B rose significantly in all patients. The maximal titres for ASO and antiDNase-B in 41 PSRA patients were: mean (SEM) 1242 (232) U/l and 890 (100) U/l respectively; the maximal ASO titres were similar in the three groups: mean (SEM) 1125 (185) in GAS, 625 (160) in NGAS (GAS v NGAS: p=0.17), and 1430 (320) U/l in GUS (NGAS v GUS: p=0.10). AntiDNase-B titres were: mean (SEM) 1075 (180) in GAS, 375 (105) in NGAS (GAS v NGAS: p<0.01), and 995 (125) U/l in GUS (NGAS v GUS: p<0.005). ASO: antiDNase-B ratios were: mean (SEM) 0.89 (0.21) in GAS, 2.60 (0.76) in NGAS (GAS v NGAS: p<0.05), and 1.43 (0.28) in GUS (NGAS v GUS: p=0.12). CONCLUSION: Post-streptococcal reactive arthritis occurs not infrequently. Differentiation of PSRA based on the causative streptococcal strain is frequently thwarted by negative throat cultures. Sometimes extra-articular manifestations are present that exclude NGAS as the causative organism. Serologically, lower antiDNase-B titres may be indicative for primary NGAS infection; the ASO/antiDNase-B ratio may be of additive value for differentiation in cases of a negative throat culture: the higher ASO/antiDNase-B ratios suggesting primary NGAS infection. In reactive arthritis, serological monitoring consisting of a simultaneous titration of antiDNase-B and ASO, seems to be of clinical importance to trace GAS induced cases, especially when throat cultures remain negative.

Adult↗
PubMed2005

The role of regulatory T cells in antigen-induced arthritis: aggravation of arthritis after depletion and amelioration after transfer of CD4+CD25+ T cells.

It is now generally accepted that CD4+CD25+ Treg cells play a major role in the prevention of autoimmunity and pathological immune responses. Their involvement in the pathogenesis of chronic arthritis is controversial, however, and so we examined their role in experimental antigen-induced arthritis in mice. Depletion of CD25-expressing cells in immunized animals before arthritis induction led to increased cellular and humoral immune responses to the inducing antigen (methylated bovine serum albumin; mBSA) and autoantigens, and to an exacerbation of arthritis, as indicated by clinical (knee joint swelling) and histological scores. Transfer of CD4+CD25+ cells into immunized mice at the time of induction of antigen-induced arthritis decreased the severity of disease but was not able to cure established arthritis. No significant changes in mBSA-specific immune responses were detected. In vivo migration studies showed a preferential accumulation of CD4+CD25+ cells in the inflamed joint as compared with CD4+CD25- cells. These data imply a significant role for CD4+CD25+ Treg cells in the control of chronic arthritis. However, transferred Treg cells appear to be unable to counteract established acute or chronic inflammation. This is of considerable importance for the timing of Treg cell transfer in potential therapeutic applications.

Animals↗
PubMed1995

Collagen-induced arthritis in mice: synergistic effect of E. coli lipopolysaccharide bypasses epitope specificity in the induction of arthritis with monoclonal antibodies to type II collagen.

DBA/1 mice develop a chronic peripheral arthritis after immunization with type II collagen termed collagen-induced arthritis. We have localized the main arthritogenic determinants of CB11, a CNBr-generated arthritogenic fragment of chick type II collagen (CII), using 3 smaller peptide fragments of CB11 generated by endoproteinase LysC, LysC1 (CII 124-290), LysC2 (CII 291-374) and LysC3 (CII 375-402) and a panel of monoclonal antibodies (mAb) specific to CB11. MAb specific to the arthritogenic region of CB11 were also used to study the synergistic effect of E. coli lipopolysaccharide (LPS) on antibody-mediated arthritis in naive DBA/1 mice. LysC2 contained a minimum essential arthritogenic fragment of type II collagen: LysC2 induced arthritis by active immunization, also, a combination of four mAb specific to LysC2 passively transferred arthritis to naive mice. A single i.p. injection of LPS (50 micrograms/mouse) reduced the threshold values of the arthritogenic dose of mAb from 1 mg to 50 micrograms/clone per mouse, and decreased the number of mAb required for inducing arthritis from 4 to 2 clones. These observations suggest that LysC2, an 84 amino acid residue fragment, contains the main arthritogenic determinants within chick CB11. Importantly, LPS, a strong inducer of pro-inflammatory cytokines, negates the required multiple epitope specificity of autoantibodies in the passive transfer model and acts synergistically in the induction of arthritis by autoantibody.

Animals↗
PubMedDate not supplied

Prevalence of uveitis in an outpatient juvenile arthritis clinic: onset of uveitis more than a decade after onset of arthritis.

PURPOSE: To determine the prevalence and severity of uveitis in an outpatient pediatric arthritis clinic in the midwestern United States during the 1990s. METHODS: The prevalence and clinical characteristics of uveitis were studied retrospectively for all children diagnosed with arthritis at Shriner's Hospital for Crippled Children and followed by the pediatric rheumatology and ophthalmology units of the St Louis Children's Hospital between 1992 and 1995. RESULTS: Seven children (9%) developed uveitis in a population of 78 patients with juvenile arthritis. Six of the seven children were female, and all six females had anti-nuclear antibody (ANA)-positive, juvenile rheumatoid arthritis (JRA). The prevalence of anterior uveitis in females with ANA-positive, pauciarticular JRA was 20%, and in polyarticular JRA, 17%. One of the girls with uveitis had combined JRA and sarcoidosis; the boy with uveitis had juvenile spondylitis. Arthritis preceded the onset of uveitis in each child by 1 to 13 years (average, 6.4 years). Progression of the uveitis in three of the children resulted in band keratopathy and cataract, causing significant visual loss in two (i.e., in 29% of the children who developed uveitis). CONCLUSION: The prevalence and ocular morbidity of uveitis in juvenile arthritis appears to have remained relatively stable over the last 2 decades. Onset of the uveitis in several of the children in our study population occurred more than a decade after the diagnosis of arthritis. Girls with ANA-positive JRA and boys with juvenile spondylitis may need to be followed by periodic slit-lamp examination for longer periods than recommended previously.

Adolescent↗
PubMed2000

Prominent expression of mRNA for proinflammatory cytokines in synovium in patients with juvenile rheumatoid arthritis or chronic Lyme arthritis.

OBJECTIVE: To examine the cytokine profiles in synovium of patients with juvenile rheumatoid arthritis (JRA) or Lyme arthritis, 2 chronic inflammatory arthritides that affect children. METHODS: We used in situ hybridization with specific riboprobes to determine the expression of mRNA for proinflammatory or antiinflammatory cytokines in synovial samples from 5 patients with early, untreated JRA, 15 patients with late, treated JRA, and 9 patients with chronic Lyme arthritis. For comparison, synovia were examined from 6 patients with rheumatoid or psoriatic arthritis, and from 9 patients with various orthopedic conditions. RESULTS: Among the children with early, untreated JRA, a median of 3 to 8% of inflammatory cells in synovial samples expressed mRNA for the proinflammatory cytokines interleukin 1beta (IL-1beta), tumor necrosis factor-alpha(TNF-alpha), or interferon-gamma (IFN-gamma). Although a median of 3.9% of the cells expressed mRNA for the antiinflammatory cytokine IL-10, none had IL-4 mRNA. Most of the patients with late, treated JRA, chronic Lyme arthritis, rheumatoid, or psoriatic arthritis had mRNA for each of these proinflammatory cytokines in about 1% of the cells, whereas mRNA for the antiinflammatory cytokines was less frequent. The inflammatory cell density was much less in the synovium of patients with various orthopedic conditions, but about 1% of the infiltrating cells expressed mRNA for at least one of the proinflammatory cytokines. CONCLUSION: Patients with early or late JRA or chronic Lyme arthritis have expression of mRNA in synovial tissue primarily for proinflammatory cytokines, with less expression of antiinflammatory cytokines.

Adult↗
PubMed2000

On the difficulties of establishing a consensus on the definition of and diagnostic investigations for reactive arthritis. Results and discussion of a questionnaire prepared for the 4th International Workshop on Reactive Arthritis, Berlin, Germany, July 3-6, 1999.

OBJECTIVE: There is no agreement on how to classify and diagnose reactive arthritis (ReA) and it is also unclear what kind of specific clinical and laboratory investigations are appropriate. We define relevant points of agreement and identify points of disagreement among an international group of experts in the field. METHODS: Prior to the 4th International Workshop on Reactive Arthritis, Berlin, July 1999, we sent questionnaires to 42 experts identified by personal knowledge and recent publications. RESULTS: The response rate was 81% (n = 34). There was agreement on the nomenclature and recommendation to use the term "reactive arthritis" only if the clinical picture and the microbes involved are HLA-B27 and spondyloarthropathy (SpA) associated, whereas the term "infection related arthritis" is used for all other arthritides related to or associated with infections. A differentiation between acute and chronic ReA with a cutoff of 6 months is recommended. The history of a preceding symptomatic infection is thought to be most relevant for a diagnosis of ReA. The minimal interval between preceding symptoms and arthritis is proposed to be 1-7 days, maximally 4 weeks. The joint pattern in ReA is asymmetrical, with predominance of the lower limbs. SpA related symptoms may contribute to the diagnosis. A search for chlamydia in urine/urethra/cervix is recommended, while in the case of diarrhea enterobacteria should be searched for in stool and antibodies against them in serum. There were also areas of disagreement, such as: Is arthritis essential for the diagnosis of ReA?, Is it oligoarthritis or any arthritis?, What are the role and value of polymerase chain reaction investigation?, The role and value of serology?, Is the diagnostic sensitivity of microbiological tests for ReA increased by HLA-B27 determination? CONCLUSION: The points of agreement will support better communication in this area, and clarification of the disagreements will lead to further studies and discussion.

Arthritis, Reactive↗
PubMed2001

The contribution of arthritis and arthritis disability to nonparticipation in the labor force: a Canadian example.

OBJECTIVE: To examine the factors affecting labor force participation and understand how arthritis affects labor force participation in a Canadian working population. METHODS: Data from the 1990 Ontario Health Survey population (n = 35,221) were used. Labor force participation was dichotomized as in the labor force and not in the labor force. Stratified logistic regression analyses by sex were carried out to identify factors associated with not being in the labor force, including arthritis, chronic disorders, and sociodemographic and family composition variables. RESULTS: Overall, 6.7% of men and 23.0% of women were not in the labor force compared with 18.6% and 36.0%, respectively, of men and women with arthritis. After controlling for other covariates, disability caused by arthritis was significantly associated with increased risk of being out of the labor force, with odds ratios of 2.70 for men and 1.91 for women. Low education, pain, and nonarthritis disability were also significantly associated with being out of the labor force. The effects of age and family structure on employment were sex dependent. Women were at higher risk at all age groups. Men with dependent children were more likely to work, as were women who lived alone. For women, having dependent children increased the likelihood of not being in the labor force. CONCLUSION: People with arthritis disability were more likely to be out of the labor force. It was not arthritis per se that limited people in labor force participation, but rather the arthritis disabilities.

Adult↗
PubMed2002

Rheumatoid factor and antibodies to cyclic citrullinated Peptide differentiate rheumatoid arthritis from undifferentiated polyarthritis in patients with early arthritis.

OBJECTIVE: To study the diagnostic value of IgM rheumatoid factor (RF), IgA-RF, antibodies to cyclic citrullinated peptide (anti-CCP), and combinations of these antibodies, measured at baseline, to discriminate rheumatoid arthritis (RA) from undifferentiated polyarthritis (uPA) in patients with recent onset arthritis. METHODS: Patients with early arthritis with peripheral arthritis of 2 or more joints and symptom duration less than 3 years were clinically diagnosed as having RA or uPA by an experienced rheumatologist during the first year. Patients with bacterial, psoriatic, or crystal induced arthritis or spondyloarthropathy were excluded. Optimal cutoff values for serum IgM RF, IgA RF, and anti-CCP were deduced from receiver operating characteristics curves in order to predict the diagnosis of RA in early arthritis. RESULTS: A total of 379 patients (69% female, median age 57 yrs, range 17-86 yrs) were studied; 258 patients were clinically diagnosed as RA and 121 as uPA. Both IgM-RF > 40 IU/ml and anti-CCP > 50 AU/ml showed high specificity, but the sensitivity of these tests was low. In many RA patients the occurrence of IgM-RF and anti-CCP antibodies was independent. Thus the optimal criterion proved to be the combination of IgM-RF > 40 or anti-CCP > 50, which yielded sensitivity of 55.4% and specificity of 96.7%. CONCLUSION: The criterion IgM-RF > 40 or anti-CCP > 50 is able to predict the diagnosis of RA in early arthritis patients with high specificity and acceptable sensitivity. Anti-CCP testing combined with IgM-RF testing has additional value over IgM-RF testing alone in patients with early undifferentiated oligo and polyarthritis.

Adolescent↗
PubMed2003

All-cause mortality and vascular events among patients with rheumatoid arthritis, osteoarthritis, or no arthritis in the UK General Practice Research Database.

OBJECTIVE: To compare all-cause mortality rates and the incidence of major vascular events among patients with rheumatoid arthritis (RA), osteoarthritis (OA) without RA, or no arthritis using the UK General Practice Research Database (GPRD) while adjusting for age and sex. Clinic-based studies have found that patients with RA have higher all-cause and cardiovascular (CV) mortality than those without RA, after adjusting for age and sex. Much smaller elevations in risk have been found in the few community-based studies that have addressed this question. METHODS: After excluding patients with a history of myocardial infarction or cerebrovascular events, we followed a retrospective cohort of patients 40 years and older from GPRD practices until the earliest of death, disenrollment, or the occurrence of an incident vascular event. Using Poisson regression we compared age and gender adjusted incidence rates for RA, OA, or no arthritis. RESULTS: Five hundred and ninety-four practices contributed 2.37 million patients (1.11 million men and 1.26 million women) to the analysis. Over a mean duration of followup of almost 5 years, age and gender adjusted all-cause mortality rates were 60 to 70% higher in patients with RA compared to patients with OA and those with no arthritis. For the various vascular endpoints, the age and gender adjusted incidence rates were 30 to 60% higher in patients with RA compared to both patients with OA and those with no arthritis during the study period. The rates in patients with OA and those with no arthritis were essentially the same. CONCLUSION: Compared to patients with OA and those with no arthritis, patients with RA had a higher age and gender adjusted incidence of all-cause mortality and of major vascular events during almost 5 years of followup.

Adult↗
PubMed2006

Prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation--United States, 2003-2005.

Arthritis is highly prevalent among U.S. adults, the leading cause of disability, and associated with substantial activity limitation, work disability, reduced quality of life, and high health-care costs. As the population ages, arthritis is expected to affect an estimated 67 million adults in the United States by 2030. This report updates estimates of the national prevalence of doctor-diagnosed arthritis and arthritis-attributable activity limitation in the adult U.S. population, using data from the National Health Interview Survey (NHIS) for 2003-2005. The findings indicated that an estimated 21.6% of the adult U.S. population (46.4 million persons) had doctor-diagnosed arthritis, and 8.3% (17.4 million) had arthritis-attributable activity limitations. Public and private health agencies should promote measures to increase the availability of evidence-based arthritis prevention and management interventions.

Activities of Daily Living↗
PubMedDate not supplied

Type II collagen-induced murine arthritis. II. Genetic control of arthritis induction is expressed on L3T4+ T cells required for humoral as well as cell-mediated immune responses to type II collagen.

The present study investigates the cellular and molecular mechanisms responsible for expressing genetic control of type II collagen-induced murine chronic arthritis. Analyses were made for both humoral and cellular immune responses, since the induction of arthritis required synergy between both types of immunities. Immunization of high (DBA/1) and low (C57BL/6, C3H/He, BALB/c) responder mice with native bovine type II collagen resulted in the production of the respective high and low levels of anti-collagen antibody. However, polyclonal in vitro stimulation of normal spleen cells from high or low responder mice with lipopolysaccharide (LPS) induced a comparable magnitude of anti-collagen antibody responses, indicating the localization of the genetic defect at cellular levels other than B cells themselves. In contrast to immunization with native collagen, sensitization of DBA/1 mice with heat-denatured collagen failed to stimulate B cells, but resulted in selective generation of L3T4+ T cell-mediated immunity. These included anti-collagen delayed-type-hypersensitivity (DTH) responses and the generation of various interleukins (IL) responsible for antibody production as well as DTH responses. It was demonstrated that there was appreciable difference in the magnitudes of these responses between lymphoid cells from high and low responder mice. Differential effects of sensitization with heat-denatured collagen in high versus low responders were reflected on the genetic difference in the development of chronic arthritis. A typical arthritis was induced neither in denatured collagen-sensitized DBA/1 mice nor in unsensitized mice transferred with anti-collagen antiserum. However, the antiserum transfer into denatured collagen-sensitized DBA/1 mice induced chronic perpetuating arthritis. This sharply contrasted with the failure of the same aliquot of the antiserum to induce a chronic arthritis when inoculated into denatured collagen-sensitized low responder mice. These results indicate that the genetic control of the induction of arthritis is expressed on L3T4+ T cells which are required for generating anti-collagen humoral as well as cell-mediated immunities as assessed by DTH responses in vivo or lymphokine productions in vitro.

Animals↗
PubMedDate not supplied

Meeting the needs of people with arthritis: quality of life programs of the Arthritis Foundation.

The Arthritis Foundation's Quality of Life Action Plan (Brady et al., 1993) is a strategic planning document that provides direction for service and education initiatives through the year 2000. This plan is a guide for the fulfillment of the quality of life aspect of the Arthritis Foundation's Mission Statement: "To support research to find the cure for and prevention of arthritis and to improve the quality of life for those affected by arthritis." The plan is based on documented needs and challenges that affect the quality of life of people with arthritis, with a focus on physical, psychosocial, and economic issues. This article provides a review of these issues and describes the types of services that the Arthritis Foundation provides to help people with arthritis effectively deal with these problems.

Arthritis↗
PubMed1996

[Blood prolactin under the effect of protirelin in spondylarthropathies. Treatment trial of 4 cases of reactive arthritis and 2 cases of psoriatic arthritis with bromocriptine].

Prolactin radioimmunoassay was carried out before and 15, then 30 min after intravenous infusion of protireline (0.2 mg) in 3 groups of male patients: 7 with reactive arthritis (HLA B27: 6; age: 25 +/- 6.3 yr), 13 with ankylosing spondylitis (HLA B27: 11; age: 33.2 +/- 14.7 yr), 5 with psoriatic arthritis (HLA B27: 1; age: 28.8 +/- 6.3 yr). The same test was carried out in sex-age-body mass index matched controls. Only the patients with reactive arthritis presented dynamic hyperprolactinaemia 15 and 30 min after protireline infusion and none of ankylosing or psoriatic arthritis groups. A complete failure of bromocriptine was observed in reactive arthritis. In 2 cases of psoriatic arthritis, adding bromocriptine to gold salts and nonsteroidal anti-inflammatory drug was followed by a drastic efficacy with spectacular improvement in clinical, biological and occupational status. Because none of the cases had hyperprolactinaemia, bromocriptine acted probably had an intrinic anti-inflammatory effect independent of its antiprolactinic effect.

Adult↗
PubMed2004

The Short Arthritis Assessment Scale: a brief assessment questionnaire for rapid evaluation of arthritis severity in research and clinical practice.

OBJECTIVE: To develop a short, 4-item arthritis severity questionnaire that is simple to score, clinically useful and meaningful, and suitable for use in primary care, where osteoarthritis (OA) is the primary prevalent arthritis illness. METHODS: Data and items from the Medical Outcomes Study Short Form 36 (SF-36), the Western Ontario McMaster Osteoarthritis Index (WOMAC(c)), and visual analog scales (VAS) for pain and patient global severity were studied in 16,519 patients with arthritis. The Short Arthritis Assessment Scale (SAS) was developed by performing multivariable analyses that involved individually adding/subtracting items in differing regression models. The candidate items and scales were then studied by Rasch analysis, and tested for effect size, sensitivity to change, and reliability. The resultant scale was validated using data from a recent OA clinical trial. RESULTS: The VAS pain and VAS global severity scales and 2 items from the WOMAC in the VAS format, difficulty going down stairs and difficulty shopping, were found to be the best predictors of change in health status. The 4-item SAS was reliable (Cronbach's alpha = 0.87), demonstrated good test-retest reliability (Lin's concordance coefficient = 0.85), was unidimensional, and was strongly correlated with other important clinical measures, indicating good construct validity. Using data from a recent randomized clinical trial in OA, the SAS performed better than the WOMAC pain scale and the SF-36 physical component score in detecting change, and at least as well as the clinical trial VAS pain scale. CONCLUSION: The SAS is a 4-item arthritis severity questionnaire that can be easily administered in primary care for patients with OA, but is suitable for use across all arthritis illnesses. Scoring is simple, requiring only the addition of four 10-point scales, and interpretation is straightforward. The SAS may have a role in rapid assessment of the arthritis patient in primary care practice.

Adult↗