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

ID PMID Title PublicationDate abstract
9523389 Bronchiolitis obliterans organizing pneumonia in a patient with rheumatoid arthritis. 1998 Jan A 75-year old man with rheumatoid arthritis developed bronchiolitis obliterans organizing pneumonia (BOOP), which responded to treatment with prednisolone (1 mg/kg/d) and cyclophosphamide (100 mg/d).
9590651 Interprosthetic fracture of the femoral shaft. 1998 Apr Experience in the management of a complication of ipsilateral hip and knee arthroplasty is described. The cases of four female patients who sustained a femoral shaft fracture after ipsilateral hip and knee arthroplasty are reported. All fractures were treated operatively, and in all cases internal fixation devices failed. This complication of multiple joint arthroplasty presents a difficult management problem. Rigid fixation has a high failure rate for this type of fracture. Surface knee arthroplasty provides a better opportunity for internal fixation than a knee arthroplasty with a stemmed femoral component.
9972960 The posterior tibial tendon and the tarsal sinus in rheumatoid flat foot: magnetic resonan 1999 Feb OBJECTIVE: To investigate the role of the posterior tibial tendon in the flat foot deformity of rheumatoid arthritis (RA). METHODS: Eleven patients with hyperpronated feet and 9 without hyperpronation underwent magnetic resonance imaging (MRI) of the feet and ankles. Radial oblique double echo images provided cross sectional views of the posterior tibial tendon as it coursed behind and under the medial malleolus and inserted beneath the midfoot. RESULTS: Complete tears (Type III) of the posterior tibial tendon were seen in one patient with hyperpronation and in one without hyperpronation. However, partial tears (Types I and II) of the posterior tibial tendon were common, and when Type I-III posterior tibial tendon tears were grouped together, they were seen in 68% of flat feet and in 43% of feet that were not flat. Abnormalities of the tarsal sinus, including cortical erosions and replacement of the normal fat signal with intermediate signal soft tissue, were seen in 74% of flat feet and in 5% of feet that were not flat. CONCLUSION: Posterior tibial tendon tears are common in RA flat feet, but are usually incomplete and are not solely responsible for the flat foot deformity.
10446859 Linkage of a marker in intron D of the estrogen synthase locus to rheumatoid arthritis. 1999 Aug OBJECTIVE: To test for the presence of linkage of the estrogen synthase (CYP19) locus to rheumatoid arthritis (RA) in affected sibling pair (ASP) families. METHODS: Two data sets of RA ASPs (225 ASPs and 107 ASPs) were genotyped for a polymorphic tetranucleotide marker at the CYP19 locus using fluorescence-based semiautomated genotyping technology. Evidence of linkage was assessed by estimating allele sharing (identical by descent) in affected sibling pairs. The effect of this locus was also examined in patient subgroups stratified by sex and by age at disease onset. RESULTS: An increase in allele sharing at the CYP19 locus was observed in the first data set of 225 ASPs (logarithm of odds [LOD] 0.8; P = 0.04). There was also an increase in allele sharing in a second data set, but this did not reach statistical significance (LOD 0.34; P = 0.1). The highest increase in allele sharing was seen in patients with an age at disease onset that was >50 years (LOD 1.1; P = 0.02). CONCLUSION: An increase in allele sharing at the CYP19 locus has been demonstrated in 2 large samples of RA ASPs. The evidence for linkage was strongest in patients with an age at onset that was >50 years, which suggests that this locus may be a susceptibility locus for developing RA later in life. These data provide preliminary evidence that CYP19 may have a role in RA susceptibility.
9256607 [Cyclophosphamide pulse therapy for refractory rheumatic diseases]. 1997 Jun We studied the efficacy of cyclophosphamide pulse therapy (CYP) for refractory rheumatic diseases except for lupus nephritis. Thirty-five patients were included in all, that is 9 patients with systemic lupus erythematosus (SLE), 10 with rheumatoid arthritis (RA), 7 with polymyositis/dermatomyositis (PM/DM), 2 with progressive systemic sclerosis (PSS), 2 with anti-phospholipid antibody syndrome (APS), 1 with mixed connective tissue disease (MCTD), 1 with juvenile rheumatoid arthritis (JRA), 1 with Behcet's disease (BD), 1 with Wegener's granulomatosis (WG) and 1 with allergic granulomatous angiitis (AGA). Moderate to marked improvement was noted in 4 patients with SLE (2 with CNS-lupus and 2 with vasculitis), 7 with RA (2 with interstitial pneumonia:IP, 2 with vasculitis and 2 with refractory arthritis), 4 with PM/DM (2 with IP and 2 with refractory myositis), 1 PSS with IP, 2 APS with thrombocytopenia, 1 JRA with vasculitis and BD with CNS disturbance. On the other hand, adverse reactions were observed in 9 out of 35 patients (25.8%). CYP should apply in the treatment for such refractory rheumatic diseases as CNS disturbance, vasculitis, IP and autoimmune thrombocytopenia.
11208277 Soluble interleukin-6 receptor in plasma and in lymphocyte culture supernatants of healthy 2000 Jan The soluble IL-6 receptor (sIL-6R) occurring in various body fluids of healthy persons and patients with various diseases is an agonist since its complex with IL-6 binds to gp130 making IL-6 receptor negative cells responsive for IL-6. The generation as well as the functional role of soluble IL-6 receptor is poorly understood. We measured the sIL-6R levels by ELISA sandwich technology in sera and in supernatants of lymphocyte cultures without and after incubations with dexamethasone. Our results indicate, that the sIL-6R levels in sera of patients with inactive systemic lupus erythematosus (SLE) and active rheumatoid arthritis (RA) were higher than those of the control group, active SLE and inactive RA. In vitro dexamethasone treatment stimulated generation of sIL-6R in both healthy persons and in active SLE, however it strongly suppressed sIL-6R in both RA groups. At mRNA level, we found that in SLE both the mRNA coding the cell-bound and an alternatively spliced variant corresponding to soluble IL-6R transcript increases, however the strong decrease of sIL6R protein in RA was not found at mRNA level.
10745935 [Role of anti-TNF therapy in rheumatoid arthritis]. 2000 Mar 11 TUMOR NECROSIS FACTOR: TNF is a cytokine produced by several types of cells, but mainly by monocyte-macrophages, activated endothelial cells, fibroblasts, and joint cartilage chondrocytes. The circulating form of TNF alpha (homotrimere) is derived from its membrane form by cleavage induced by a metalloprotease called TACE. This cytokine plays a pivotal role in the inflammatory reaction in conjunction with IL-1 and IL-6. The effect of TNF alpha is mediated by two membrane receptors carried on the surface of target cells (TNF-RI p55 and TNF-RII p75) which are released into the biological fluids (synovial fluid and plasma). ARGUMENTS FOR A PATHOGENIC ROLE: Transgenic mice carrying the human gene for TNF alpha develop polyarthritis suggesting this cytokine is directly implicated in the pathogenesis. In diverse cell types in rheumatoid joints, TNF alpha and its receptors can be identified by immunohistochemistry techniques as can TNF alpha mRNA by RT-PCR. THERAPEUTIC POSSIBILITIES: Anti-TNF alpha antibodies can effectively attenuate or prevent arthritis in the main experimental models. TNF alpha can also be neutralized with soluble receptors, TNF alpha RI or TNF alpha RII. The efficacy of these two therapeutics has been proven in rheumatoid arthritis, but with a short-term though remnant effect, leading to iterative injections and/or combinations with methotrexate. Short-term side effects are mild but the long-term infectious and oncogenic adverse effects remain to be determined. Is this simply a powerful antiinflammatory treatment or a real curative treatment? A precise examination of radiographic scores will be required to provide the answer to this question.
11282995 Decreased expression of signaling lymphocytic-activation molecule-associated protein (SAP) 2001 Apr The function of Epstein-Barr virus (EBV)-specific cytotoxic T cells is disturbed in rheumatoid arthritis (RA) patients but the mechanism for this disturbance has remained unknown. In a recent study searching for the causative gene of X-linked lymphoproliferative syndrome, the gene possibly linked to EBV-specific cytotoxic T cells or NK cell-mediated cytotoxic activity to EBV-infected cells was discovered, and its product is now referred to as signaling lymphocytic-activation molecule-associated protein (SAP) or Src homology 2 domain-containing protein (SH2D1A). In the present study, we attempted to investigate the involvement of the SAP gene in RA using a quantitative real-time PCR; the expression level of SAP transcripts in peripheral leukocytes or T cells was examined for patients with RA. The expression level of SAP transcripts in peripheral leukocytes of 21 RA patients was significantly lower than that of 13 normal individuals (P = 0.0007), four patients with palindromic RA, 11 with inactive systemic lupus erythematosus (SLE) or 17 with chronic renal diseases. The decreased expression of SAP transcripts in RA patients was also observed in peripheral CD2(+) T cells compared with normal individuals. There was no mutation in the coding region of SAP cDNAs derived from peripheral leukocytes of five RA patients. The decreased expression of SAP transcripts in peripheral leukocytes or T cells of RA patients might lead to the failure of the immune system to eliminate the EBV-infected synovial lining cells in joints of RA patients. Our findings have suggested that decreased expression of the SAP gene might be involved in the onset or progress of RA.
11034605 Immunoglobulin heavy chain variable region gene replacement As a mechanism for receptor re 2000 Oct 16 Mature B cells can alter their antibody repertoires by several mechanisms, including immunoglobulin heavy chain variable region (V(H)) replacement. This process changes the antigen combining site by replacing a portion of the original V(H)/diversity/heavy chain joining region (V(H)DJ(H)) rearrangement with a corresponding portion of a new V(H) segment. This exchange can involve cryptic heptamer-like sequences embedded in the coding regions of V(H) genes. While studying the B lymphocytes that expand in the synovial tissues of patients with rheumatoid arthritis (RA), clones with V(H)DJ(H) variants that were apparently generated by V(H) replacement were identified with surprising frequency (approximately 8%). Examples of multiple independent V(H) replacement events occurring in distinct progeny clones were also identified. These secondary V(H) rearrangements were documented at both the cDNA and genomic DNA levels and involved several heptamer-like sequences at four distinct locations within V(H) (three sites in framework region 3 and one in complementarity determining region 2). The identification of blunt-ended double-stranded DNA breaks at the embedded heptamers and the demonstration of recombinase activating gene (RAG) expression suggested that these rearrangements could occur in the synovial tissues, presumably in pseudo-germinal centers, and that they could be mediated by RAG in a recognition signal sequence-specific manner. The presence of V(H) mutations in the clones that had undergone replacement indicated that these B cells were immunocompetent and could receive and respond to diversification signals. A relationship between these secondary V(H) gene rearrangements and the autoimmunity characteristic of RA should be considered.
9415633 Fluoride therapy in prevention of rheumatoid arthritis induced bone loss. 1997 Dec OBJECTIVE: To determine the efficacy of sodium fluoride (40 mg/day) in preventing rheumatoid arthritis (RA) induced bone loss, which may lead to osteoporosis. METHODS: We conducted an 18 month, randomized, double blind, placebo controlled trial in 38 patients with RA. The primary outcome measure was the difference in the percentage change between groups in lumbar spine bone mineral density (BMD) from baseline values after 18 months of therapy. The secondary outcome measures were the differences in the percentage change between groups in femoral neck, Ward's triangle, trochanter, and total body BMD from baseline after 18 months of therapy. RESULTS: There was a significant percentage difference (SD) between groups of 6.2% (7.3%) (p = 0.0005) in lumbar spine BMD after 18 months of treatment in favor of the fluoride group. The fluoride group experienced a 5.2% (8.4%) (p = 0.0125) increase, whereas the placebo group showed a 1.0% (4.8%) (p = 0.8015) decrease in lumbar spine BMD after treatment. No significant differences were found for the femoral neck, Ward's triangle, trochanter, and total body BMD in terms of the percentage changes from baseline within each treatment group or in the differences in the degree of change between groups after therapy. Lumbar spine BMD increased in about 80% of patients treated with fluoride (responders) compared to 44% of patients treated with placebo. CONCLUSION: The results showed that fluoride therapy was well tolerated and increased vertebral bone mass in patients with RA.
11127335 Levels of plasma lipid peroxide products and antioxidant status in rheumatoid arthritis. 2000 Jun Oxygen free radicals have been implicated as mediators of tissue damage in patients with rheumatoid arthritis. The aim of our study was to assess the lipid peroxide products and antioxidant status in rheumatoid arthritis patients (RA). The study involved determination of two plasma lipid peroxide products, malondialdehyde (MDA) and conjugated dienes (CD), two plasma antioxidant vitamins (C and E) in 91 RA patients and 26 healthy subjects. The results showed that rheumatoid patients had increased plasma CD but not MDA and decreased plasma vitamin E, when properly expressed per unit cholesterol and triglyceride. This finding suggested that RA patients had increased oxidant stress that might play a role in the tissue damage and inflammation process of this disease.
10440507 Giant cell arteritis associated with rheumatoid arthritis monitored by magnetic resonance 1999 Aug A 57-year-old Japanese woman with well controlled rheumatoid arthritis visited our hospital with a severe bitemporal headache and marked fatigue. Based on the classification criteria by the American College of Rheumatology, she was diagnosed as having giant cell arteritis. Magnetic resonance (MR) angiography was performed, from which stenotic changes in the bilateral superficial temporal arteries were strongly suspected. Corticosteroid therapy was quickly started. The patient followed an uneventful course with no complications. Therapeutic effect was confirmed by MR angiographic findings obtained 4 weeks after the initiation of therapy.
9144848 A potential new treatment for rheumatoid arthritis: thunder god vine. 1997 Apr Various extracts of the vinelike plant Tripterygium wilfordii Hook f have been widely used in China to treat patients with a number of autoimmune diseases. Although most of the clinical experience has derived from uncontrolled trials, one placebo-controlled double-blind trial has clearly demonstrated efficacy in rheumatoid arthritis. Studies in laboratory animals have indicated that extracts of Tripterygium wilfordii Hook f suppress both immune and inflammatory responses and also effectively treat a number of models of autoimmune disease. More detailed in vitro analysis has indicated that components of Tripterygium wilfordii Hook f suppress immune responses by inhibiting transcription of cytokine genes, including interleukin-2 and gamma interferon. The current status of knowledge of the potential clinical benefit of this herbal remedy and possible mechanisms accounting for its utility are considered in this review.
10902765 Expression of osteopontin messenger RNA and protein in rheumatoid arthritis: effects of os 2000 Jul OBJECTIVE: Osteopontin (OPN) is an extracellular matrix protein that has been implicated in the interactions between tumor cells and host matrix, including those involved in invasion and spread of tumor cells. Because joint destruction in rheumatoid arthritis (RA) is mediated by the invasive growth of synovial tissue through its attachment to cartilage, we examined the expression of OPN in the synovia of patients with RA and the effect of OPN on the production of collagenase 1 in rheumatoid synovial fibroblasts and articular chondrocytes. METHODS: The expression of OPN messenger RNA (mRNA) and protein in synovia from 10 RA patients was examined by in situ hybridization and immunohistochemistry. Synovial fibroblasts from RA patients and articular chondrocytes from patients without joint disease were cultured in the presence of various concentrations of OPN, and levels of collagenase 1 in the culture supernatants were measured by enzyme-linked immunosorbent assay. RESULTS: The expression of OPN mRNA and protein was observed in 9 of 10 specimens obtained from patients with RA. OPN was expressed in the synovial lining and sublining layer and at the interface of cartilage and invading synovium. Double labeling revealed that the majority of OPN-expressing cells were positive for the fibroblast-specific enzyme prolyl 4-hydroxylase and negative for the macrophage marker CD68, while only a few, single OPN-expressing cells were positive for CD68 at sites of synovial invasion into cartilage. OPN staining was not observed in lymphocytic infiltrates or leukocyte common antigen (CD45)-positive cells. Three of 3 cultures of human articular chondrocytes secreted detectable basal amounts of collagenase, with a dose-dependent increase upon OPN stimulation, while synovial fibroblast cultures produced much lower levels of collagenase, with only 2 of 4 fibroblast cultures responding in a dose-dependent manner. CONCLUSION: These findings suggest that OPN produced by synovial fibroblasts in the synovial lining layer and at sites of cartilage invasion not only mediates attachment of these cells to cartilage, but also contributes to matrix degradation in RA by stimulating the secretion of collagenase 1 in articular chondrocytes.
9877192 Expression of heat-shock proteins in Streptococcus pyogenes and their immunoreactivity wit 1998 Aug The heat-shock response of Streptococcus pyogenes following exposure to elevated growth temperatures, and the immunological reactivity of heat-shock proteins (HSPs) in streptococcal infections were studied. Two major proteins of 65 and 75 kDa were expressed when a S. pyogenes strain was shifted from 37 degrees C to heat-shock temperatures of 40, 42 and 45 degrees C. Such proteins are members of the GroEL and DnaK families recognised in a Western blot assay with polyclonal antibodies against Escherichia coli GroEL and E. coli DnaK, respectively. Two-dimensional autoradiograms of polypeptides labelled at 37 or 42 degrees C showed an increased intensity of three spots at 42 degrees C. A monoclonal antibody (MAb) against HSP 63 of Bordetella pertussis also recognised the 65-kDa inducible protein, although MAbs against Mycobacterium tuberculosis HSP 65 failed to recognise this protein. Immunoblot analysis of sera from individuals with rheumatic fever or uncomplicated streptococcal diseases revealed seven major immunogenic protein bands, two of which also reacted with anti-E. coli GroEL and DnaK polyclonal antibodies. Furthermore, antibodies to the GroEL and DnaK proteins were also detected in sera from patients with either rheumatoid arthritis or systemic lupus erythematosus. These results demonstrated a heat-shock response of S. pyogenes, and indicated the presence of an immune response against HSPs in streptococcal diseases.
9851263 Autoantibodies against human calpastatin in rheumatoid arthritis: epitope mapping and anal 1998 Nov Autoantibodies against calpastatin have recently been described to be highly prevalent in sera of patients with rheumatoid arthritis (RA). When the sera of 45 patients with RA were analysed for autoantibodies against calpastatin by a newly developed enzyme-linked immunosorbent assay (ELISA), only four sera (8.9%) tested positive, which is not significantly different from the frequency observed in healthy controls. Since the ELISA is based on a synthetic peptide containing the C-terminal 27 amino acids of calpastatin bound to the solid phase, this negative result might be the consequence of the small antigen used. Therefore, a systematic analysis of the epitopes for autoantibodies in calpastatin was performed using sera from RA patients and healthy individuals. Recombinant fusion proteins containing fragments of calpastatin or the complete protein were produced and sera analysed by Western blots. In the N-terminal portion (amino acids 1-369), at least two major epitopes exist, against which 65% of normal sera as well as 76% of RA sera show reactivity in Western blot assays. These epitopes are not useful for clinical diagnostics. Only five out of 45 (11.1%) RA sera reacted against the C-terminal portion (amino acids 363-708) of calpastatin, while four out of 52 (7.7%) control sera showed reactivity. Three of the five RA sera and two out of four control sera had autoantibodies against the C-terminal 27 amino acids of calpastatin. These three patient sera had already been tested positive in the ELISA. The fourth patient positive in the ELISA was Western blot negative. The differences between the group of RA patients and controls are not statistically significant. When the clinical characteristics of the four patients with autoantibodies against the carboxyl end of calpastatin were analysed, it became apparent that all four had significantly elevated C-reactive protein (>50 mg/l). This observation might indicate that calpastatin autoantibodies are found in RA patients with more active disease. Thus, while the majority of RA patients do not have an increased prevalence of calpastatin autoantibodies, it cannot be ruled out definitively that a small subgroup may be characterized by autoantibodies to the C-terminus of calpastatin.
11393663 Mannose-binding lectin gene: polymorphisms in Japanese patients with systemic lupus erythe 2001 Apr Mannose-binding lectin (MBL) is a key element of the innate immunity, with a structure similar to complement C1q. Serum MBL levels are greatly affected by the polymorphisms of the MBL gene. In particular, codon 54 mutation of the MBL gene results in a significant reduction of serum MBL. To determine whether polymorphism of the MBL gene is associated with occurrence of systemic lupus erythematosus (SLE), rheumatoid arthritis and Sjögren's syndrome in the Japanese population, we analyzed the MBL gene polymophisms of these patients and controls, by polymerase chain reaction-restriction fragment length polymorphism methods. We found that patients studied had a significantly higher frequency of having homozygous codon 54 mutation compared to controls. In particular, patients with SLE or Sjögren's syndrome showed higher probabilities of being homozygous for this mutation. Among subjects with the same genotype, SLE patients tended to have higher serum MBL concentration than controls. Analysis of the promotor region suggested that SLE patients heterozygous for the codon 54 mutation have a higher probability of having a low producing haplotype for the gene without the codon 54 mutation. We conclude that persons homozygous for codon 54 mutation of the MBL gene may be prone to occurrence of autoimmune disorders including SLE, in the Japanese. MBL may have protective effects on occurrence and progression of SLE.
9551411 Involvement of interleukin-8 in dialysis-related arthritis. 1998 Apr To elucidate the role of interleukin (IL)-8, a chemotactic factor for neutrophils, in dialysis-related arthritis (DRA) of patients on long-term hemodialysis, the concentration of IL-8 was measured in the synovial fluids of DRA patients with acute arthralgia and joint swelling, and was compared with those in patients with rheumatoid arthritis (RA) and patients with osteoarthritis (OA). We noted a marked elevation of IL-8 in the joint fluids of patients with DRA and RA as compared with OA. Furthermore, to determine the role of IL-8 in synovitis, we examined the in vivo effect of intra-articular injection of human recombinant IL-8 on leukocyte infiltration into the joint space of rabbits. A single injection of IL-8 to the joints of rabbits induced rapid infiltration of neutrophils into the joint space and synovial tissues, which reached a maximum in four hours. The oral administration of indometacin farnesil (a prodrug that is converted to indomethacin after intestinal absorption) before the injection of IL-8 alleviated the infiltration of neutrophils. When human synovial cells were incubated with tumor necrosis factor (TNF)-alpha, the expression of IL-8 mRNA and IL-8 production in the cultured synovial cells were increased. The TNF-alpha-stimulated expression of IL-8 mRNA and IL-8 production in the cultured synovial cells were markedly inhibited by dexamethasone. In conclusion, IL-8 levels were markedly elevated in the joint fluids of patients with DRA. Interleukin-8 released from synovial cells may be an important factor to induce acute inflammation in DRA. Dexamethasone and indomethacin may be effective for DRA by inhibiting the production and chemotactic actions of IL-8, respectively.
10555912 Comorbidity in arthritis. 1999 Nov OBJECTIVE: To describe the relative frequency of selected comorbidities in 2 population based prevalence cohorts of patients with rheumatoid arthritis (RA) and osteoarthritis (OA) compared to age and sex matched community controls. METHODS: Using the population based data resources of the Rochester Epidemiology Project, we assembled 3 prevalence cohorts of all residents of Olmsted County, Minnesota, with RA (1987 American College of Rheumatology criteria) and age and sex matched controls without arthritis on January 1, 1965, January 1, 1975, and January 1, 1985. Cases and controls were followed longitudinally through their complete (inpatient and outpatient) medical records beginning 10 years prior to the prevalence (or index) date until death, migration from the county, or January 1, 1995. Comorbidity was assessed yearly using the Charlson Comorbidity Index and the Index of Co-existent Diseases (ICED). Descriptive statistics were used to illustrate the baseline characteristics of the study population and the frequency of individual comorbidities in each of the 3 groups over the followup period. Cox proportional hazards modeling was used to assess the risk for each individual comorbidity among patients with arthritis compared to controls and to identify significant predictors of an increase in comorbidity level over time. RESULTS: Our study population included 450 RA, 441 OA, and 891 control subjects. The age and sex distributions of cases and their controls were similar. Over the followup period, patients with RA had a higher likelihood of developing congestive heart failure, chronic pulmonary disease, dementia, and peptic ulcer disease, while cases with OA had a significantly higher risk of developing peptic ulcer disease and renal disease. Among patients with either RA or OA, age, male sex, and baseline comorbidity were significant predictors of a rise in comorbidity. The presence of RA was a highly significant predictor of a rise in comorbidity from one year to the next, even after controlling for the effects of age, sex, and baseline comorbidity (p = 0.0004 for the Charlson and p = 0.006 for the ICED). CONCLUSION: These data indicate that the burden of illness among people with arthritis is higher than for nonarthritics and that this burden appears to be increasing over time, particularly in RA. These results suggest that specialized chronic disease care will be increasingly important for the future health care needs of people with RA.
11845435 A purified green barley extract with modulatory properties upon TNF alpha and ROS released 1998 Jul Based on the finding that reactive oxygen species (ROS) play important roles in mediating proinflammatory cytokine production (e.g. TNF alpha) and that many plant extracts contain substances with antioxidant properties, we examined the antiinflammatory action of a green barley extract, commercially available as "Natural SOD". The results obtained in this study demonstrate that the antiinflammatory properties of "Natural SOD" due to its micromolecular substances, able to scavenge ROS and to down-regulate TNF alpha production, main inflammation mediators produced by specialised cells from peripheral blood (PB) and synovial fluid (SF) of patients with rheumatoid arthritis (RA). We prepared and tested a purified green barley extract (PE) containing micromolecular substances under 1 kDa, able to inhibit TNF alpha releasing--measured by an bioassay--from LPS stimulated human mononuclear cells (MNC) isolated both from PB and SF of RA patients. Luminol-dependent chemiluminescence has been used to measure the scavenging activity of PE on ROS releasing from activated neutrophils isolated from PB of RA patients. PE, containing high concentrations of substances with antioxidant and antiinflammatory properties, could be a more efficient natural drug for human use than "Natural SOD" in the treatment of RA patients.