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ID PMID Title PublicationDate abstract
18004573 [Interleukin-17 in chronic inflammatory and autoimmune diseases: rheumatoid arthritis, Cro 2008 Feb Data from recent animal experiments and clinical studies show that interleukin-17 (IL-17A, B, C, D, E, and F) plays an important role as proinflammatory cytokine in the host response to extracellular bacteria and in chronic inflammatory and autoimmune diseases. These findings have led to a revision of the well-known T(H)1/T(H)2 hypothesis. In rheumatoid arthritis elevated IL-17 serum levels, Th-17 cells in synovial fluid and in T-cell-rich areas of inflamed synovia are found. In Wegener's granulomatosis, IL-17D is expressed in nasal granulomas. In Crohn's disease IL-17 as well as IL-17 plus IFN-gamma producing CD4(+) T-cells are detected in peripheral blood and inflamed intestinal mucosa. So far, CD4(+)IL-17(+)IFN-gamma(+) T-cells have been described only in humans. These and other findings indicate a number of differences in the cytokine response between murine models and human beings.
17465339 Prolactin and autoimmune diseases in humans. 2007 Prolactin has been shown to have immunomodulatory as well as lactogenic effects. Generally less well known is that prolactin may also play a role in the activity of autoimmune diseases such as systemic lupus erythematosus and rheumatoid arthritis. Studies have shown decreasing prolactin production to be beneficial in animal models of autoimmune disease. Thus far, double-blinded, placebo-controlled studies of dopamine agonist treatment in humans with autoimmune disease have been done only in lupus patients, and support the potential efficacy of such agents. Small, open-label trials have also suggested potential benefit in patients with rheumatoid arthritis, Reiter's syndrome, and psoriasis. More studies are required to further delineate the mechanisms by which prolactin affects autoimmune disease activity, to determine in which specific diseases prolactin plays a significant role, and to test the efficacy of prolactin-lowering agents as therapy for such diseases.
17254342 The rheumatoid arthritis shared epitope increases cellular susceptibility to oxidative str 2007 We have recently demonstrated that the rheumatoid arthritis (RA) shared epitope (SE) acts as a ligand that triggers nitric oxide (NO) signaling in opposite cells. Given the known pro-oxidative effect of NO and the proposed role of oxidative stress in the pathogenesis of RA, this study explores whether SE-triggered signaling can increase cellular oxidative stress. cAMP levels, adenylyl cyclase activity, and protein kinase A activity were measured using commercial kits. Generation of reactive oxygen species (ROS) was quantified using the fluorochrome dichlorofluorescein diacetate. Oxidative DNA damage was quantified using the single-cell electrophoresis technique. Here, we report that cells exposed to cell surface SE-positive HLA-DR (human leukocyte antigen-DR) molecules, to cell-free recombinant proteins genetically engineered to express the SE motif, or to SE-positive synthetic peptide showed diminished cAMP-dependent signaling, increased ROS levels, and higher vulnerability to oxidative DNA damage. Introduction of single amino acid substitutions into SE-positive peptides revealed a consensus five-amino acid sequence motif of Q/R-K/R-X-X-A that is necessary and sufficient for SE-triggered signaling. The pro-oxidative effect of the SE could be reversed by inhibiting NO production. We conclude that the SE acts as a signaling ligand that activates an NO-mediated pro-oxidative pathway. The potential contribution of this signaling aberration to RA pathogenesis is discussed.
18839195 The analysis of genetics and associated autoimmune diseases in Chinese vitiligo patients. 2009 Feb Vitiligo is a common skin and hair depigmentary disorder that results from selective destruction of melanocytes. It occurs in a typical multifactorial, polygenic inheritance. Several studies have indicated that vitiligo is associated with some autoimmune diseases. In this paper we examined 6,516 vitiligo patients including clinical characteristics, familial involvement, and their association with other autoimmune diseases. Compared with sporadic vitiligo probands, familial vitiligo probands have earlier age onset and longer disease duration. The prevalences of four autoimmune diseases namely rheumatoid arthritis, chronic urticaria, alopecia areata and psoriasis, were significantly elevated in generalized vitiligo probands and their first-degree relatives. The prevalences of chronic urticaria, rheumatoid arthritis, psoriasis were much higher in familial generalized vitiligo probands. In addition, the prevalences of diabetes mellitus and asthma were also higher in familial vitiligo probands. These findings indicate that generalized vitiligo may share common genetic aetiologic links with other autoimmune diseases, and the genetic component of familial generalized vitiligo is stronger.
18278547 Serum pro-hepcidin levels in rheumatoid arthritis and systemic lupus erythematosus. 2008 Jun Hepcidin is a principal iron regulatory hormone and its expression is stimulated by cytokines. The aim of this study was to determine serum levels of the prohormone form of hepcidin, pro-hepcidin, in rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). The study included 72 RA and 28 SLE patients and 33 healthy controls (HC). Serum iron status, tumor necrosis factor (TNF)-alpha, interleukin (IL)-6 and pro-hepcidin levels were determined. Pro-hepcidin levels in the RA group was higher than SLE and HC groups (p < 0.05, p < 0.001, respectively). Pro-hepcidin levels did not correlate with disease activity scores, cytokine levels and serum iron status in the RA and SLE groups, while it correlated with TNF-alpha, IL-6 and ferritin levels in the HC group (r = 0.459, p < 0.01, r = 0.374, p < 0.05, r = -0.603, p < 0.01, respectively). Pro-hepcidin levels show extremely wide variations within the groups as do iron status and cytokines. Despite these wide variations correlation analysis do not reveal anything.
17365805 Necrotising anterior scleritis in a late-onset rheumatoid arthritis (LORA) patient. 2007 Jan Late-onset rheumatoid arthritis (LORA) is a clinically distinct entity from rheumatoid arthritis of younger onset (YORA). We present a case of necrotising anterior scleritis in an elderly lady with new-onset LORA that was initially thought to be infective. Oestrogen receptors have been identified on B cells, T cells, and macrophages with oestrogens demonstrated to increase their activation and enhance RA synovial inflammation. The presence of long-term oestrogen supplementation may have contributed to the development and perpetuation of her RA, thereby necessitating awareness of the possible immunomodulatory role of the sex steroids in immune-mediated diseases which affect the eye.
16249227 Anchorage on fibronectin via VLA-5 (alpha5beta1 integrin) protects rheumatoid synovial cel 2006 Jun BACKGROUND: Rheumatoid synovial cells are resistant to apoptosis induction in vivo, whereas, fibroblast-like synovial cells in rheumatoid arthritis (RA-FLS) are vulnerable to Fas-induced apoptosis in vitro. OBJECTIVE: To clarify this discrepancy by studying the contribution of the interaction between cellular integrin and matrix fibronectin (Fn), which is significantly increased in the rheumatoid joints, to the induction of apoptosis in RA-FLS. METHODS: Integrin and Fas mRNAs were measured by reverse transcription-polymerase chain reaction in RA-FLS. Integrins expressed in rheumatoid synovial tissues were analysed by immunohistochemistry. RA-FLS plated either on Fn or on control poly-L-lysine were incubated with agonistic anti-Fas monoclonal antibodies (mAbs). Apoptosis induction was evaluated using terminal deoxynucleotidyl transferase mediated UTP nick end labelling (TUNEL) and immunoblotting for caspase-3 and poly (ADP-ribose) polymerase in the presence or absence of anti-VLA-5 mAb. RESULTS: VLA-5 (alpha5beta1 integrin), a major integrin expressed on RA-FLS, was required for the adhesion of RA-FLS on Fn. RA-FLS plated on Fn were more resistant to Fas-induced apoptosis than those plated on control poly-L-lysine. This protection by Fn was reversed by anti-VLA-5 mAb. CONCLUSION: Anchorage of RA-FLS on matrix Fn via VLA-5 protects RA-FLS from Fas-induced apoptosis, and Fn abundantly present in rheumatoid synovium appears to afford RA-FLS resistance against apoptosis induction in vivo.
18784373 Mechanisms and pathologic significances in increase in serum interleukin-6 (IL-6) and solu 2008 Nov 15 Interleukin-6 (IL-6) plays pathologic roles in immune-inflammatory diseases such as rheumatoid arthritis (RA) and Castleman disease. By inhibiting IL-6 receptors (IL-6Rs), tocilizumab (a humanized anti-IL-6R antibody) ameliorates the symptoms of these diseases and normalizes acute-phase proteins, including C-reactive protein (CRP). We found that tocilizumab treatment increased serum levels of IL-6 and soluble IL-6R (sIL-6R). To investigate the pathologic significance of these increases, we analyzed the kinetics of serum IL-6 and sIL-6R and the proportion of sIL-6R saturated with tocilizumab after tocilizumab administration in patients with RA and Castleman disease and then compared the results with the CRP values. Serum IL-6 and sIL-6R markedly increased after tocilizumab administration in both RA and Castleman disease. As long as free tocilizumab was detectable, sIL-6R was saturated with tocilizumab and IL-6 signaling was completely inhibited. We concluded that it is likely that sIL-6R increased because its elimination half-life was prolonged by the formation of tocilizumab/sIL-6R immune complex, and that free serum IL-6 increased because IL-6R-mediated consumption of IL-6 was inhibited by the unavailability of tocilizumab-free IL-6R. We also concluded that the increased level of free IL-6 during tocilizumab treatment closely reflects the actual endogenous IL-6 production and true disease activity.
18434750 Measurement of the kidney function in patients with rheumatoid arthritis: plasma cystatin 2008 BACKGROUND/AIM: Knowledge of the usefulness of cystatin C measurement in the detection of chronic kidney disease in patients with rheumatoid arthritis (RA) is scant. The purpose of this study was to evaluate the ability of plasma cystatin C- and creatinine-based methods to predict glomerular filtration rate (GFR) and classify chronic kidney disease in RA patients. METHODS: The study population consisted of 64 RA patients aged 41-86 years. Comparisons were made between measured plasma creatinine, cystatin C, creatinine clearance and GFR estimated by the Cockcroft-Gault (CG) and the Modification of Diet in Renal Disease (MDRD) formulas. The plasma clearance of (51)Cr-EDTA served as a reference. RESULTS: The Pearson correlation coefficients between plasma clearance of (51)Cr-EDTA and the markers of GFR were calculated. The correlation coefficients were 0.800 for plasma creatinine, 0.863 for cystatin C, 0.866 and 0.904 for GFR values estimated by MDRD and CG and 0.922 for plasma creatinine clearance. Statistically significant differences were detected between the correlation coefficients of plasma creatinine and GFR estimated by CG (p = 0.0412) and plasma creatinine and creatinine clearance (p = 0.0099). Creatinine clearance and the MDRD and CG formulas proved to be better at identifying GFR <90 ml/min than plasma creatinine or cystatin C. CONCLUSION: We recommend using the CG formula or creatinine clearance for the estimation of the GFR of RA patients instead of solely creatinine or cystatin C in clinical work.
18253737 Serum IgG activity against cyclic citrullinated peptide in patients evaluated for rheumato 2008 Jul The purpose of this study was to evaluate the frequency of seric antibodies against cyclic citrullinated peptide (a-CCP) in patients tested for rheumatoid factor (RF) reactivity, and to analyze the correlation between their titers. We obtained serum from 112 consecutive patients (85 female), aged 47.2 +/- 13.4 years and from 46 clinically healthy subjects (CHS). Patients where stratified into four subgroups: rheumatoid arthritis (RA), probable RA (PRA), spondylarthropathies and other diagnosis. The a-CCP antibodies were determined by enzyme linked immunoassay (ELISA), RF by nephelometric test (IgM) and ELISA (IgG and IgM). Analysis of variance (ANOVA) showed statistically that a-CCP antibodies differs among RA versus CHS and other diagnosis; PRA versus CHS and other diagnosis. A significant Rho value of 0.84 (P < 0.05, Spearman's correlation) was identified between a-CCP antibodies and RF in PRA subgroup. When a correlation of a-CCP antibodies with RF (both isotypes) was done, the higher correlation was observed against IgM RF. The data suggests different pathways and times for each antibody generation.
16935544 Retention of the patella in total knee arthroplasty for rheumatoid arthritis. 2006 Oct AIM: To determine whether retention of the native patella during total knee arthroplasty is appropriate in patients with rheumatoid arthritis. METHODS: All patients undergoing total knee arthroplasty with a diagnosis of rheumatoid arthritis were identified between January 1997 and December 2000. Subsequently, each individual underwent both radiological and clinical assessments at a designated follow-up clinic. RESULTS: A total of 30 total knee arthroplasties were studied in 28 patients. Twenty-six patients (93%) were female with a mean age of 74.7 years (range 60-83 years). The average post-operative interval was 59.4 months (range 46-82 months). All individuals were noted to have satisfactory patellar tracking and bone stock at the time of surgery. No patient subsequently underwent revision surgery during follow-up and no episodes of implant sepsis were identified. The mean Patellar Score at final follow-up was 26.2 (range 22-30) with an average anterior knee pain score of 14.2 (range 10-15). The mean Oxford Knee Score was 18.7 (range 16-23) with a mean pain score component of 5.9. Patients were finally assessed with respect to the Knee Society Score. The mean Knee Score was 83.8 (range 71-96) with a mean Function Score of 79.7 (range 40-90). CONCLUSION: By retaining the native patella we were still able to obtain highly satisfactory medium-term results in terms of pain relief and function. In addition, the potential complications associated with prosthetic replacement of the patella were avoided.
16508940 Sphingosine kinase 1-mediated inhibition of Fas death signaling in rheumatoid arthritis B 2006 Mar OBJECTIVE: It is becoming increasingly apparent that B cells play an important role in the pathogenesis of rheumatoid arthritis (RA). Due to the scarcity of B cells in RA, it has been technically difficult to functionally characterize B cell apoptosis in this disease. As a necessary first step to identify candidate aberrations, we investigated Fas-mediated signaling events in immortalized peripheral blood B lymphoblastoid cell lines (LCLs) from patients with RA and controls. METHODS: Cell death was determined by the MTS assay, and apoptosis was detected by the TUNEL assay and DNA laddering. Proteolytic activation of caspase 3 was determined by immunoblotting, and its enzymatic activity was determined by a fluorometric technique. Messenger RNA (mRNA) expression was quantified by real-time polymerase chain reaction (PCR) analysis. The functional role of sphingosine kinase (SPHK) was determined by measuring its enzymatic activity, by quantifying the levels of its product, sphingosine 1-phosphate (S1P), and by investigating the ability of the SPHK inhibitor N,N-dimethylsphingosine and isozyme-specific small interfering RNA (siRNA) oligonucleotides to reverse signaling aberrations. RESULTS: LCLs from patients with RA displayed disease-specific Fas-mediated signal transduction impairment with consequent resistance to cell death. RA LCLs displayed high constitutive SPHK activity and increased levels of S1P. Real-time PCR analysis showed higher SPHK-1 mRNA expression levels in RA patients compared with paired controls. Increased SPHK-1 (but not SPHK-2) mRNA levels were observed in synovial tissue from RA patients. Competitive inhibitors of SPHK reversed the resistance of RA LCLs to Fas-induced apoptosis. Additionally, resistance to Fas-mediated signaling was reversed by siRNA oligonucleotides specific for SPHK-1 but not by oligonucleotides specific for SPHK-2. CONCLUSION: These findings demonstrate disease-specific resistance to Fas-mediated death signaling in patients with RA and implicate increased SPHK-1 activity as the cause of this aberration.
17328044 Proinflammatory mediator-induced reversal of CD4+,CD25+ regulatory T cell-mediated suppres 2007 Mar OBJECTIVE: We previously demonstrated that CD4+,CD25+ regulatory T (Treg) cells are present in increased numbers in the synovial fluid (SF) of rheumatoid arthritis (RA) patients and display enhanced suppressive activity as compared with their peripheral blood (PB) counterparts. Despite the presence of these immunoregulatory cells in RA, chronic inflammation persists. The purpose of the present study was to investigate whether particular proinflammatory mediators that are associated with RA could abrogate CD4+,CD25+ Treg-mediated suppression. METHODS: Monocyte phenotype was determined by flow cytometry and cytokine levels by enzyme-linked immunosorbent assay. Magnetically sorted CD4+,CD25- and CD4+,CD25+ T cells derived from the PB and SF obtained from RA patients were stimulated alone or in coculture with anti-CD3 monoclonal antibody (mAb) and autologous antigen-presenting cells, in the absence or presence of anti-CD28 mAb or the proinflammatory cytokines interleukin-6 (IL-6), tumor necrosis factor alpha (TNFalpha), or IL-7. RESULTS: Monocytes from the SF of RA patients displayed increased expression of HLA class II molecules, CD80, CD86, and CD40 as compared with PB-derived monocytes, indicating their activated status. Mimicking this increased costimulatory potential, addition of anti-CD28 mAb to cocultures of CD4+,CD25- and CD4+,CD25+ T cells resulted in reduced CD4+,CD25+ Treg-mediated suppression in both PB and SF. Furthermore, IL-7 and, to a limited extent, TNFalpha, both of which are produced by activated monocytes and were detected in SF, abrogated the CD4+,CD25+ Treg-mediated suppression. In contrast, IL-6 did not influence Treg-mediated suppression. CONCLUSION: Our findings suggest that the interaction of CD4+,CD25+ Treg cells with activated monocytes in the joint might lead to diminished suppressive activity of CD4+,CD25+ Treg cells in vivo, thus contributing to the chronic inflammation in RA.
18432408 Epigenetics in human autoimmunity. Epigenetics in autoimmunity - DNA methylation in system 2008 May Epigenetic mechanisms are essential for normal development and function of the immune system. Similarly, a failure to maintain epigenetic homeostasis in the immune response due to factors including environmental influences, leads to aberrant gene expression, contributing to immune dysfunction and in some cases the development of autoimmunity in genetically predisposed individuals. This is exemplified by systemic lupus erythematosus, where environmentally induced epigenetic changes contribute to disease pathogenesis in those genetically predisposed. Similar interactions between genetically determined susceptibility and environmental factors are implicated in other systemic autoimmune diseases such as rheumatoid arthritis and scleroderma, as well as in organ specific autoimmunity. The skin is exposed to a wide variety of environmental agents, including UV radiation, and is prone to the development of autoimmune conditions such as atopic dermatitis, psoriasis and some forms of vitiligo, depending on environmental and genetic influences. Herein we review how disruption of epigenetic mechanisms can alter immune function using lupus as an example, and summarize how similar mechanisms may contribute to other human autoimmune rheumatic and skin diseases.
17105853 Evaluation of a modified ACR20 scoring system in patients with rheumatoid arthritis receiv 2006 Dec OBJECTIVE: To evaluate a modified American College of Rheumatology 20 (mACR20) scoring system for patients with rheumatoid arthritis. METHODS: The data were evaluated from one study on patients with methotrexate (MTX)-naive early rheumatoid arthritis (ERA) and another study on patients with DMARD-refractory late rheumatoid arthritis (LRA). For mACR20 scoring, acute-phase reactant measurements were excluded, and 20% improvement from baseline was determined by 2 or 3 of the 4 remaining ACR components. RESULTS: For full joint counts with data from patients with ERA, marked differences favoured 25 mg etanercept (ETN) over 10 mg ETN by using the unmodified ACR20 (69% v 55%), the mACR20(3 of 4) (63% v 49%) and the mACR20(2 of 4) (72% v 58%). An assessment of 28 joints showed similar findings. In the trial on patients with LRA, considerably more patients in both ETN groups achieved a clinical response compared with placebo by using the ACR20, the mACR20(3 of 4) and the mACR20(2 of 4), whether using full or 28 joint counts. The mACR20(3 of 4) and full joint counts with data on patients with ERA showed a marked difference between the MTX and 10 mg ETN groups (63% v 49%), which was not observed with the ACR20. CONCLUSION: Patterns of improvement indicated by mACR20 scores were consistent with standard ACR20 scores.
19210871 Basal anti-cyclic citrullinated peptide (anti-CCP) antibody levels and a decrease in anti- 2008 Nov OBJECTIVE: To investigate the effect of adalimumab treatment on anti-cyclic citrullinated peptide antibodies (anti-CCP) in patients with rheumatoid arthritis (RA). METHODS: 70 RA patients who failed treatment with disease modifying antirheumatic drugs (DMARDs) received 40 mg adalimumab subcutaneously every other week during 24 weeks. Serum samples were collected at baseline and at weeks 8, 16 and 24 before the corresponding adalimumab dose. The serum anti-CCP levels were tested by enzyme linked immunosorbent assay. RESULTS: At baseline, 52 of the 70 patients (74.3%) were positive for anti-CCP antibodies. 60 % of the anti CCP positive patients and 44.4% of the anti CCP negative patients were ACR 20 responders at week 24 (p<0.049). The serum levels of anti-CCP antibodies decreased significantly after 24 weeks of adalimumab treatment only in those patients who met ACR 20 response criteria at week 24 (p<0.00044). Differences between baseline anti-CCP titers and those at 8, 16 and 24 weeks were all statistically significant (p<0.014, 0.003 and 0.019 respectively). No statistically significant changes in the anti-CCP levels were observed in patients who did not meet the ACR 20 response criteria. CONCLUSION: Basal anti-CCP antibodies levels correlate with clinical response to adalimumab. A decrease in anti-CCP levels on time was observed in patients showing also clinical improvement, suggesting that serum anti-CCP antibodies determination may be useful in assessing treatment efficacy in RA patients.
18180875 Femoral nerve palsy caused by a huge iliopectineal synovitis extending to the iliac fossa 2008 We report on a 54-year-old woman with rheumatoid arthritis who had severe femoral nerve palsy affected by a distended synovium in the hip joint. Surgical exploration demonstrated a perforation of the iliopectineal bursa connecting with the hip joint. The patient fully recovered from femoral nerve palsy after surgery. It was considered that synovitis of the hip joint had developed following huge iliopectineal bursitis.
18220555 Periodontal diseases and rheumatoid arthritis: a coincident model for therapeutic interven 2007 Dec There are remarkable similarities in the pathogenesis of periodontal diseases and rheumatoid arthritis. The mechanisms that drive antigen induced sequelae of oxidative stress are discussed in this review. A poorly modulated inflammatory response drives both diseases resulting in oxidative stress induced tissue injury. Immune complex formation in response to the periodontal pathogen Porphyromonas gingivalis triggering the production of ROS in both gingivae and synovium of RA patients has been reported. Elevated antibody levels to several periodontal pathogens in RA patients has implications on both RA and periodontal diseases. Periodontal patients are challenged individuals representing a multifactorial aetiopathogenesis with potential for therapeutic intervention in the context of free radical damage. Subjects with moderate to severe periodontal bone loss are significantly more likely than healthy individuals to have several co-existing systemic conditions resulting in ROS mediated damage. There is potential for dual induction of periodontal disease by existing inflammatory mechanisms of systemic diseases rather than exacerbation of low grade inflammation only; emphasizing the relevance of reducing inflammatory burden for disease control. Therapeutic strategies based on disease mechanisms include combined low dose non-steroidal anti-inflammatory drugs and doxycycline for synergistic reduction of matrix metalloproteinase activity in periodontal tissues and RA; sub-optimal dosing with CMT-8 and a biphosphonate clodronate to reduce pathologically elevated levels of MMPs, elastase and to restore alveolar bone in experimental periodontits demonstrating dual applications. Therapeutic interventions relevant to both diseases discussed in this review, have scope for a double hit in periodontal patients with co-existing RA and vice versa.
17457739 Predictors of functional disability in rheumatoid arthritis: results from a 13-year prospe 2007 May 30 PURPOSE: To explore the role of distress and social support as modifiers of functional disability in rheumatoid arthritis (RA). We hypothesized that: (a) higher inflammatory activity, more joint tenderness and more pain lead to more disability, and (b) that more distress and less social support lead to more disability and accelerate the disablement process by moderating the effects of inflammatory activity, joint tenderness and pain. METHODS: The study is a Dutch extension of the European Research on Incapacitating Diseases and Social Support (EURIDISS) which started with 292 patients. After five waves of data collection 129 still participated. Correlational and hierarchical regression analyses were performed. RESULTS: In short-term RA, 68% of the variance in disability could be explained primarily by mean disability over the prior years. Other important predictors were inflammatory activity and pain. In long-term RA, 56% of the variance in disability could be explained primarily by mean disability over the prior years. Other important predictors were joint tenderness and pain. No clear moderator effects of distress and social support were found in short-term or long-term RA. CONCLUSIONS: The results confirm the main pathway from pathology to disability in short-term and long-term RA, but do not provide support for the influence of distress and social support on the disablement process.
18565260 Professional practice assessment in ambulatory private rheumatology: a pilot evaluation of 2008 Mar OBJECTIVE: Professional Practice Assessment (PPA) has become an obligation for all physicians in France, however its modalities remain unclear. The objective of this work was to evaluate the feasibility and accuracy of a PPA for private practice rheumatologists performed in the context of a network. METHODS: A list of items considered mandatory to collect during an outpatient visit for rheumatoid arthritis, was prepared by the network. Non hospital-based rheumatologists, members of the network then evaluated some of their patient files selected by chronological order over a one-month period of time using this list. These files were then assessed by another private rheumatologist, member of the group, randomly allocated, using the same list of items. RESULTS: Eighty percent of the private-practice doctors accepted to participate. The mean time to evaluate 15 patient files was 2 hours. Agreement between auto-evaluation and external evaluation for each file was good (agreement statistic, 0.75-1.0). Items mandatory to collect were collected in a high proportion of cases (84.6%). CONCLUSION: PPA can be performed in the context of a network, auto-evaluation is a valid method and when the list of items is decided on by the network, the data are collected satisfactorily.