Browse

Search for: rheumatoid arthritis    methotrexate    autoimmune disease    biomarker    gene expression    GWAS    HLA genes    non-HLA genes   

ID PMID Title PublicationDate abstract
10364907 Effects of nabumetone compared with naproxen on platelet aggregation in patients with rheu 1999 Apr OBJECTIVE: To test the hypothesis that nabumetone (a partially selective cyclooxygenase-(COX)-2 inhibitor) has less effect on platelet aggregation than naproxen (a non-selective COX-inhibitor) in patients with rheumatoid arthritis (RA). METHODS: A crossover study in 10 RA patients was performed, using either nabumetone or naproxen for two weeks, and, after a washout period of two weeks, the other drug during another two weeks. Platelet aggregation studies were performed and bleeding time was assessed before and after each treatment period. RESULTS: Maximum platelet aggregation induced by epinephrine and by collagen was significantly more reduced after the use of naproxen than of nabumetone; secondary aggregation induced by ADP and epinephrine disappeared more often by naproxen than by nabumetone. Bleeding times were not influenced. CONCLUSION: COX dependent platelet aggregation in RA patients seems to be more inhibited by naproxen than by nabumetone. This may be relevant for patients requiring non-steroidal anti-inflammatory drug treatment but who have an increased risk of bleeding as well.
10577971 The function of tumour necrosis factor and receptors in models of multi-organ inflammation 1999 Nov There is now good evidence to demonstrate that aberrations in tumour necrosis factor (TNF) production in vivo may be either pathogenic or protective and several plausible mechanisms may explain these contrasting activities. According to the classic pro-inflammatory scenario, failure to regulate the production of TNF at a site of immunological injury may lead to chronic activation of innate immune cells and to chronic inflammatory responses, which may consequently lead to organ specific inflammatory pathology and tissue damage. However, more cryptic functions of this molecule may be considered to play a significant part in the development of TNF mediated pathologies. Direct interference of TNF with the differentiation, proliferation or death of specific pathogenic cell targets may be an alternative mechanism for disease initiation or progression. In addition to these activities, there is now considerable evidence to suggest that TNF may also directly promote or down regulate the adaptive immune response. A more complete understanding of the temporal and spatial context of TNF/TNF receptor (TNF-R) function and of the molecular and cellular pathways leading to the development of TNF/TNF-R mediated pathologies is necessary to fully comprehend relevant mechanisms of disease induction and progression in humans. In this paper, the potential pathogenic mechanisms exerted by TNF and receptors in models of multi-organ inflammation, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease are discussed. Elucidating the nature and level of contribution of these mechanisms in chronic inflammation and autoimmunity may lead to better regulatory and therapeutic applications.
11136419 The development of an instrument to measure the compliance of adolescents with a chronic d 2000 Dec The purpose of this paper was to describe the process of developing an instrument for measuring the compliance of adolescents with a chronic disease. The aim was to develop an instrument that could be used in a clinical setting to evaluate the compliance of young people with a chronic disease and to test a theoretical model of compliance, which had been developed along with the instrument. The instrument was originally developed to measure the compliance of adolescents with diabetes and later adjusted to measure the compliance of adolescents with asthma, rheumatoid arthritis and epilepsy. To test and develop the instrument, face and criterion validity, factor analyses, linear structural relations (LISREL) analyses, correlation coefficients and Cronbach's alpha were used. The instrument has 13 background questions and 41 items to measure compliance and factors connected to it.
11254249 Distal extremity swelling with pitting oedema in rheumatoid arthritis. 2001 Distal extremity swelling with pitting oedema due to altered lymphatic drainage has been reported in some patients with rheumatoid arthritis (RA). The resistant-to-therapy oedema usually affected the upper limbs in an asymmetrical pattern. Until now, extensor tenosynovial involvement has not been described in RA patients suffering from distal extremity swelling with pitting oedema. Three patients are described: two of them had predominant extensor tenosynovial involvement in their hands, with impaired lymphatic drainage demonstrated by (MRI) and lymphoscintigraphy, respectively. In both cases the oedema was chronic and not responsive to treatment. One patient had extensor tenosynovial involvement without impaired lymphatic drainage. In this case, the oedema remitted completely after a few days of corticosteroid therapy. None of them showed differences in serum levels of vascular endothelial growth factor (VEGF), whether they were RA patients with no pitting oedema or healthy volunteers.
9018238 Interleukin-15 mediates T cell-dependent regulation of tumor necrosis factor-alpha product 1997 Feb Tumor necrosis factor-alpha occupies a central role in rheumatoid arthritis (RA) pathogenesis. We now report that interleukin-15 (IL-15) can induce TNF-alpha production in RA through activation of synovial T cells. Peripheral blood (PB) T cells activated by IL-15 induced significant TNF-alpha production by macrophages via a cell-contact-dependent mechanism. Freshly isolated RA synovial T cells possessed similar capability, and in vitro, IL-15 was necessary to maintain this activity. IL-15 also induced direct TNF-alpha production by synovial T cells. In contrast, IL-2 induced significantly lower TNF-alpha production in either cell-contact-dependent or direct culture, and IL-8 and MIP-1 alpha were ineffective. Antibodies against CD69, LFA-1 or ICAM-1 significantly inhibited the ability of T cells to activate macrophages by cell contact.
9132933 [Autoimmune diseases: frequent misdiagnosis]. 1997 Mar 1 False diagnosis of autoimmune diseases may have many different reasons. It may be caused by the relative rareness of these rather complicated diseases, by sometimes mono- or oligosymptomatic courses, and by the highly variable clinical presentations. In addition, many physicians lack experience in the treatment of these rheumatologic-immunological diseases. A first shot diagnosis, inadequate technique in obtaining a correct history or in performing a physical examination, as well as an incomplete evaluation of differential diagnosis, are possible causes of wrong diagnosis in the context of autoimmune diseases and may delay effective therapy. To illustrate these problems, three examples of patients with autoimmune diseases are discussed, namely a patient with polyarthritis and fever, a patient with polymyalgia rheumatica, and a patient with an ulcerative skin lesion. These examples serve to discuss the difficulty of correct diagnosis in complicated courses of autoimmune diseases, which are also relatively common in general practice.
11469452 Autoantibodies to osteopontin in patients with osteoarthritis and rheumatoid arthritis. 2001 Jul OBJECTIVE: Osteopontin (OPN), secreted mainly from chondrocytes, is suggested to be involved in the ossification and remodeling of bone and also in regulation of cytokine profiles. We investigated whether patients with osteoarthritis (OA) and rheumatoid arthritis (RA) display autoimmunity against OPN. METHODS: Recombinant human OPN (rhOPN) was prepared as a fusion protein with beta-galactosidase using E. coli. Serum samples from patients with OA or RA and from age matched healthy donors were tested for autoantibodies to rhOPN using ELISA and Western blotting. Reactivity of the same samples to purified native human OPN (nhOPN) was investigated by ELISA separately, to evaluate conformational epitopes. RESULTS: By ELISA, autoantibodies to rhOPN were found in one (0.95%) of 105 patients with OA and 2 (2.3%) of 88 patients with RA. These autoantibodies to rhOPN were confirmed by Western blotting. In contrast, 11 (9.5%) of 105 OA serum and 13 (15%) of 88 RA serum samples reacted to nhOPN. The anti-OPN positive RA patients showed high serum levels of rheumatoid factor and C-reactive protein and accelerated erythrocyte sedimentation rate compared to the anti-OPN negative group, although the differences did not achieve statistical significance. CONCLUSION: Our data showed that OPN is one of the autoantigens in OA and RA. Preferential recognition of nhOPN to rhOPN indicates that major epitope(s) of OPN would be conformational. Clinically, existence of the anti-OPN antibodies may be linked to disease severity in RA.
10631383 Additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, sulfasala 1999 Dec To evaluate the efficacy and safety of additive triple disease modifying anti-rheumatic drug (DMARD) combination therapy of a low dose of sulfhydryl compounds ¿D-penicillamine, bucillamine or tiopronin¿, sulfasalazine (SSZ) and methotrexate (MTX) as a treatment for rheumatoid arthritis (RA) patients, we studied a total of 33 Japanese RA patients (6 males, 27 females). At 1 or 2 months after simultaneous administration of the 3 above-mentioned DMARDs was begun, significant improvements were seen in markers of joint inflammation, i.e., erythrocyte sedimentation rate and C-reactive protein in sera. At 6 months, clinical improvement judged by the physicians' overall assessment of joint symptoms and laboratory data was observed in 29 (88%) of the 33 RA patients. No marked effect was observed in the other 4 (12%) patients, however. We observed no significant adverse reaction to this therapy. This suggests that additive triple DMARD combination therapy of a low dose of sulfhydryl compounds, SSZ and MTX could be a useful drug therapy for the treatment of RA patients, even those who are refractory.
9536387 Analysis of the NF-kappa B p65 subunit, Fas antigen, Fas ligand and Bcl-2-related proteins 1998 Mar OBJECTIVE: To investigate the nuclear localization of the transcription factor NF-kappa B, the status of apoptosis and the expression of the Fas antigen, Fas ligand, Bcl-2, Bcl-xL and Bax by synovial cells. METHODS: Electrophoresis mobility shift assay (EMSA), immunohistochemical staining, two colour-flow cytometry and the terminal deoxynucleotidyl transferase (TDT)-mediated dUTP nick end labelling (TUNEL)-technique were used. RESULTS: The NF-kappa B p65 subunit appears to be present in the nuclei of synovial tissue and fluid cells as detected by EMSA and immunohistochemical staining. Fas antigen and Fas ligand (L) are expressed on up to 90% and 11% of CD3+ synovial fluid (SF) cells, respectively. Both the Fas antigen and its ligand are also expressed by synovial tissue cells. Interestingly, freshly isolated SF T cells upregulated the expression of Bcl-xL as compared to Bcl-2. An overexpression of Bax compared to Bcl-xL was seen in the synovial tissues (ST) of patients with ongoing apoptosis, but not in patients with few apoptotic cells. CONCLUSIONS: NF-kappa B appear to be activated in vivo, both Fas and its ligand being expressed by synovial cells. Apoptosis is ongoing in the ST with significant patient variations. Such variations could be in part due to the level of Bax expression. Finally, the upregulation of Bcl-xL expression may contribute to the accumulation of SF infiltrating T cells.
11814236 Serum autoantibodies profile and increased levels of circulating intercellular adhesion mo 2001 The clinical manifestation of systemic vasculitis may be postulated as a consequence of immune response abnormalities in the course of connective tissue diseases (CTD). The aim of this study was to elucidate the significance of the different autoantibodies and soluble intercellular adhesion molecule 1 (sICAM-1) being shed into the circulation in the diagnosis of vasculitis in rheumatic diseases. Sera of 86 patients with rheumatic diseases (54 with rheumatoid arthritis (RA) and 32 with CTD) were analyzed for the concentrations of sICAM-1 levels by the enzyme-linked immunosorbent assay (ELISA). Control sera were obtained from 30 healthy individuals. Anti-nuclear antibodies (ANA), anti-double-stranded DNA (anti-dsDNA) antibodies and anti-proteinase 3 (PR-3) antibodies (cytoplasmic specific anti-neutrophil cytoplasmic autoantibodies, cANCA) were assessed by the ELISA method. Fifty out of the 86 patients had systemic lesions. A pathological picture of the vascular loop under nailfold capillary microscopy was found in 84 patients. In 19 patients the microvascular changes were advanced, in 35 moderate and in 30 mild. All patients with articular manifestations had pathological changes under capillary microscopy. Patients with advanced changes under capillary microscopy had longer disease durations than patients with a mild intensity of vasculitis. The serum concentrations of sICAM-1 were significantly increased in RA and CTD patients compared with 30 controls (in both cases p<0.001). Moreover, RA and CTD patients with systemic vasculitis showed significantly higher levels of sICAM-1 than those without vascular involvement (p<0.001 and p<0.005 respectively). ANA were observed in significantly elevated concentration among RA and CTD patients with the systemic damage compared with patients without organ injury (p<0.001 and p<0.05 respectively). Also, cANCA levels were two-fold higher, but only among CTD patients with systemic damage (p<0.05). Serum concentrations of sICAM-1 were elevated in the patients showing the presence of ANA antibodies (p<0.05). Significant correlations between ANA level and disease duration and hemoglobin concentration were observed. The concentrations of cANCA correlated with those of rheumatoid factor and of dsDNA with patient age. We conclude that systemic lesions in the course of RA and CTD are accompanied by the microvascular injury observed under nailfold capillary microscopy. Our data suggest that sICAM-1, ANA and cANCA serum levels may reflect the extent of the vascular involvement in RA and CTD patients.
10752495 Prediction of creatinine clearance from serum creatinine in patients with rheumatoid arthr 2000 The estimation of glomerular filtration rate is important for the medical treatment of patients with rheumatoid arthritis (RA). However, the determination of endogenous creatinine clearance (Clcr) from a 24-h urine collection is an unreliable and time-consuming procedure. We therefore tested the accuracy of six equations and one nomogram for the prediction of Clcr from serum creatinine (Scr) in 38 patients with RA and 20 controls. A positive correlation was found for all methods in the controls (r = 0.83-0.94) and RA patients (r = 0.51-0.69). The methods did not overestimate Clcr in RA. In the RA group the simple formula published by Cockcroft [Clcr = ((140 - age) x body weight)/(72 x Scr), x 0.85 for females] showed the best correlation with the measured Clcr. In RA the Cockroft formula can reliably be used to predict Clcr from Scr.
9678682 Diffuse panbronchiolitis and rheumatoid arthritis-associated bronchiolar disease: similari 1998 Jun There is a considerable overlap between diffuse panbronchiolitis (DPB) and bronchiolar disease associated with rheumatoid arthritis. The present study assessed how these conditions could be differentiated. The subjects included 25 DPB patients and 15 RA patients with bronchiolar disease (RA-BD). Patients with either condition had chronic cough, purulent sputum, dyspnea and coarse crackles. Most patients with either DPB or RA-BD had a history of sinusitis as well as elevated cold hemagglutin titers and decreased levels in partial pressure of oxygen (PaO2), forced expiratory volume in one second (FEV1.0) and V 25/Ht. On histological examination, both conditions also shared various histological patterns although panbronchiolitis lesions were more common in DPB than RA-BD (68% vs 20%) and bronchiolar obliteration appeared to occur at more proximal sites in RA-BD than DPB. However, there were important differences: long-term treatment with erythromycin had less effect in RA-BD than DPB, and the frequency of HLA B54 tended to be higher in DPB than RA-BD (50.0% vs 22.2%), suggesting that they are distinct conditions.
10229403 Phenotypic characteristics of B cells in Behçet's disease: increased activity in B cell s 1999 Apr OBJECTIVE: Increased numbers of spontaneous Ig secreting B cells and elevated immunoglobulin levels have been described in Behçet's disease (BD), in addition to changes in numbers and activities of T cells, natural killer cells, and monocyte-macrophages. We investigated other characteristics of B cells in BD. METHODS: B lymphocyte subsets (CD19+CD5+, CD19+CD13+, CD19+CD28+, CD19+CD33+, CD19+CD80+, CD5+CD19+CD45RA+, CD5+CD19+CD45RO+) were phenotypically evaluated in 50 patients with BD, 80 healthy subjects, and 20 other patients with rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), and sepsis. RESULTS: Although the B cell number (CD19+) was normal, CD13 and CD33 positive B cells were more numerous in BD and sepsis compared to healthy controls and patients with RA and SLE. The percentage of CD45RO positive B cells was higher in both BD and sepsis, while the percentage of CD80 positive B cells was high only in BD. There was no increase in the CD5+CD19+ B cell subset, previously shown to be increased in several autoimmune diseases. Naive (CD45RA) and memory (CD45RO) status of CD5+CD19+ and CD5-CD19+ B cells showed that CD45RA expression was higher in CD5+CD19+ B cells, whereas expression of both CD45RA and CD45RO was higher in the CD5-CD19+ B cell group compared with healthy controls. CONCLUSION: Although the total B cell number was normal, increased levels of activated and memory B cell subsets suggest a modified B cell function in BD, which may be related to a weak stimulus by an unknown external antigen.
9040015 A wide spectrum of collagen vascular and autoimmune diseases in transgenic rats carrying t 1997 Feb To investigate the pathogenesis of human T lymphocyte virus type I (HTLV-I)- related diseases, the env-pX gene of HTLV-I was introduced into the germline of inbred Wistar-King-Aptekman-Hokudai rats. A wide spectrum of collagen vascular diseases was evident in the transgenic rats, including chronic destructive arthritis similar to rheumatoid arthritis, necrotizing arteritis mimicking polyarteritis nodosa, polymyositis, myocarditis, dermatitis, and chronic sialoadenitis and dacryoadenitis resembling Sjögren's syndrome in humans. Thymic atrophy with the depletion of CD4 and CD8 double-positive thymocytes was also observed. In these animals, a number of autoantibodies, including high titers of rheumatoid factor, were present in the serum. We propose that the HTLV-I env-pX gene region may play a pathogenetic role in the development of collagen vascular and autoimmune diseases associated with autoimmune phenomenon.
9844764 Anti-agalactosyl IgG antibodies and isotype profiles of rheumatoid factors in Sjögren's s 1998 Nov OBJECTIVE: Rheumatoid factors (RFs) in sera from rheumatoid arthritis (RA) patients bind better to agalactosyl IgG [gal(-) IgG] than to native IgG. Recently, a novel lectin-enzyme immunoassay (LEIA) which can detect all isotypes of the immunoglobulins was developed in Japan. Since RFs are also detectable in Sjögren's syndrome (SS), we determined anti-gal(-) IgG antibodies and RF isotypes in sera from primary or secondary SS and RA patients to elucidate the clinical significance of these antibody profiles. METHODS: A series of 128 patients with primary SS (35 pts.), RA (57 pts.), or secondary SS [n = 36 pts., the SS being associated with RA (RA-SS) in 12 pts., systemic lupus erythematosus (SLE-SS) in 17 pts., and mixed connective tissue disease (MCTD-SS) in 7 pts.] and 38 healthy females were examined. Anti-gal(-) IgG antibodies were measured with a LEIA kit (ED055) using human gal(-) IgG as antigen. IgG-, IgA- and IgM-RF were determined with an enzyme-linked immunosorbent assay kit using human IgG-Fc as antigen. RFs were also examined by a conventional assay (laser nephelometry; LN-RF). RESULTS: Serum anti-gal(-) IgG antibody titers were higher in RA than in primary SS, SLE-SS or MCTD-SS, but the incidence of the antibodies did not differ between RA and primary SS. In both RA and primary SS, the antibodies were positive in half of the LN-RF-negative patients, and were also detected in almost all of those patients who had at least one of the RF isotypes. LN-RF, IgG-RF, IgA-RF and IgM-RF were present more frequently and their titers were higher in RA than in primary SS, but IgA-RF levels were similar in both groups. In RA-SS, all of the antibody titers were notably higher than in RA or primary SS. In RA and primary SS, IgA-RF and IgM-RF were common RF isotypes, and anti-gal(-) IgG antibody levels correlated well with LN-RF, IgA-RF and IgM-RF levels. These antibody profiles did not relate to any of the clinical parameters in RA, but all the antibody titers correlated with anti-SS-A/Ro antibody levels in primary SS. CONCLUSIONS: The anti-gal(-) IgG antibodies are not specific for RA; they are also frequent in SS. Our LEIA for antibodies is a very sensitive method to detect all RF isotypes in both RA and SS. Most of the antibody profiles are common to both diseases, although antibody titers are higher in RA, especially in RA-SS.
9367409 Specificities of anti-neutrophil autoantibodies in patients with rheumatoid arthritis (RA) 1997 Nov The objective of this study was to characterize antigens recognized by neutrophil-specific autoantibodies from patients with RA. Sera from 62 RA patients were screened by indirect immunofluorescence (IIF). Positive sera were further tested by ELISAs for antibodies against various granule proteins and by immunoblotting of electrophoretically separated cell, granule or nuclear extracts. Forty-two sera (68%) reacted with ethanol-fixed neutrophils. In the ELISAs 32% of the 28 medium to strongly IIF-positive sera were negative, while 43% were weakly positive for more than one antigen. Immunoblots of whole neutrophils showed IgG reactions at 25-35 kD, in the 55-kD region, at 80 kD, and at 110 kD. Most sera reacted with more than one band. Except for the 55-kD antigen, none of the antigens appeared in lymphocytes. The most notable reactivity in subcellular fractions was with lactoferrin and with bands of 25-35 kD from nuclei. In conclusion, anti-neutrophil autoantibodies from RA patients recognize different antigens in the cytoplasm and in the nucleus. Lactoferrin is one of the common antigens recognized, but also unknown nuclear antigens of 25-35 kD mol. wt are involved.
9586675 Relations between surface expression of the interleukin-2 receptor and release of the solu 1998 The relationship between surface expression of the interleukin-2 receptor (IL-2R) and release of the soluble form of the receptor (sIL-2Ralpha or sCD25) was investigated with peripheral blood mononuclear cells (PBMCs) from individuals with rheumatoid arthritis (RA) or systemic lupus erythematosus (SLE). The spontaneous release of sCD25 was significantly increased in PBMCs from RA patients and decreased in cells from SLE patients, compared with normal controls. However, the extent of sCD25 release from phytohaemagglutinin (PHA)-stimulated PBMCs did not differ between RA or SLE patients and normal controls. The serum concentration of sCD25 was significantly increased in SLE or RA patients compared with the normal controls. Whereas the surface expression of CD25 by unstimulated PBMCs did not differ among the three groups of subjects, this parameter was significantly reduced for PHA-stimulated PBMCs from RA patients relative to those from normal controls. The surface expression of CD25 showed a positive correlation with sCD25 release for PBMCs from SLE patients under either basal or stimulated conditions. No such relation was apparent for cells from RA patients. The surface expression of IL-2Rbeta (CD 122) under basal or stimulated conditions was significantly reduced in PBMCs from RA or SLE patients, compared with cells from normal controls. Thus, the increased concentration of sCD25 in the serum of individuals with these autoimmune rheumatic diseases may result from two different mechanisms: an increase in the spontaneous release of sCD25 in RA, and reduced clearance of this protein in SLE.
11229464 Development of fulminant hepatitis B (precore variant mutant type) after the discontinuati 2001 Feb A 75-year-old female rheumatoid arthritis patient who was positive for hepatitis B surface antigen and for antibodies to hepatitis Be antigen showed liver dysfunction, and therefore methotrexate (MTX) therapy was discontinued. Her drug lymphocyte stimulation test indicated positivity for MTX. Her liver dysfunction improved briefly, but she developed fulminant hepatitis with elevated levels of hepatitis B virus (HBV)/DNA polymerase and subsequently died. HBV/DNA analysis performed with polymerase chain reaction-mutation site-specific assay revealed that the fulminant hepatitis was caused by a precore mutant virus. Sudden reactivation of the immune system by discontinuation of MTX may have led to the attack on infected cells. Even when hepatitis Be antibodies are present, MTX should not be used in patients who have chronic infection with HBV.
11391029 Adverse reactions to disease-modifying anti-rheumatic drugs in clinical practice. 2001 Jun We analysed computerized records of disease-modifying anti-rheumatic drug (DMARD) monotherapy to determine how long rheumatoid arthritis (RA) patients continued on five commonly prescribed DMARDs, and the incidence and time-course of adverse drug reactions (ADRs) they experienced. We studied the records for 3923 courses of DMARDs given to a cohort of 2170 patients monitored for a total of 9378 treatment-years. Methotrexate (MTX) was the DMARD most likely to be continued long-term; <45% of patients had discontinued the drug after 96 months. For the other DMARDs, the time until 50% discontinued due to ADRs or inefficacy was 43.3 months for sulphasalazine (SAS), 33.9 months for D-penicillamine (DPN) and 26 months for myocrisin. Most monitored ADRs requiring drug discontinuation were seen early in therapy, with a median time to onset of <6 months; the important exceptions to this were haematological ADRs to MTX, where the median delay to neutropenia was 16.9 months, and that to thrombocytopenia was 9.4 months. Monitored ADRs (identified by blood or urine tests) were seen least frequently with SAS (one ADR in every 35 patient-years of monitoring) but this apparent advantage was offset by a high incidence of gastrointestinal ADRs and inefficacy. Overall, one toxicity reaction requiring drug discontinuation was identified for every 15.9 patient-years of monitoring.
9490122 [The development of a finger joint phantom for the optical simulation of early inflammator 1997 Nov In the field of rheumatology, conventional diagnostic methods permit the detection only of advanced stages of the disease, which is at odds with the current clinical demand for the early diagnosis of inflammatory rheumatic diseases. Prompted by current needs, we developed a finger joint phantom that enables the optical and geometrical simulation of an early stage of rheumatoid arthritis (RA). The results presented here form the experimental basis for an evaluation of new RA diagnostic systems based on near infrared light. The early stage of RA is characterised mainly by a vigorous proliferation of the synovial membrane and clouding of the synovial fluid. Using a double-integrating-sphere technique, the absorption and scattering coefficients (mua, mus') are experimentally determined for healthy and pathologically altered synovial fluid and capsule tissue. Using a variable mixture of Intralipid Indian ink and water as a scattering/absorption medium, the optical properties of skin, synovial fluid or capsule can be selected individually. Since the optical and geometrical properties of bone tissue remain constant in early-stage RA, a solid material is used for its simulation. Using the finger joint phantom described herein, the optical properties of joint regions can be adjusted specifically, enabling an evaluation of their effects on an optical signal--for example, during fluorography--and the investigation of these effects for diagnostically useful information. The experimental foundation for the development of a new optical system for the early diagnosis of RA has now been laid.