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

ID PMID Title PublicationDate abstract
21084245 Treatment failure with antagonists of TNF-α: mechanisms and implications for the care of 2010 Dec The use of TNF-α antagonists has substantially improved the care of many patients with inflammatory and autoimmune diseases. However, approximately one third of such patients fail to respond well to treatment, regardless of the antagonist used or of the underlying disease. The mechanisms underlying these failures are analyzed in this review, and proposals made concerning how best to adapt therapeutic decisions in these instances.
19261095 Vesicular thick-walled swollen hyphae in pulmonary zygomycosis. 2009 Mar An autopsy case of pulmonary zygomycosis in a patient with rheumatoid arthritis on immunosuppressive therapy is presented herein. There was a pulmonary cavitated infarct caused by mycotic thrombosis. Thin-walled narrow hyphae and vesicular thick-walled swollen hyphae were found on the pleural surface and in the necrotic tissue at the periphery of the cavity. Findings of such shaped fungal elements may cause erroneous histopathological diagnosis because pauciseptate broad thin-walled hyphae are usually the only detectable fungal elements in zygomycosis tissue. Although immunohistochemistry confirmed these unusual elements to be zygomycetous in the present case, it is important for the differential diagnosis to be aware that zygomycetes can form thin narrow hyphae and vesicular thick-walled swollen hyphae.
20436077 Clinical significance of serum levels of vascular endothelial growth factor, angiopoietin- 2010 Jun OBJECTIVE: To evaluate the clinical significance of serum levels of vascular endothelial growth factor (VEGF), angiopoietin-1 (Ang-1), and angiopoietin-2 (Ang-2) in patients with rheumatoid arthritis (RA). METHODS: The subjects were 70 patients with RA. Serum VEGF, Ang-1, and Ang-2 levels were determined by ELISA. As indices of disease activity, serum levels of C-reactive protein (CRP) and matrix metalloprotease (MMP)-3 were examined, and the 28-joint count Disease Activity Score (DAS28)-CRP was calculated. Power Doppler ultrasonography was performed in the bilateral wrists, elbows, shoulders, knees and ankles. The synovial blood flow signals were scored using a 3-grade scale (0-2), and the total of the scores in the 10 joints was regarded as the total signal score (TSS). RESULTS: Serum VEGF level showed significant correlations with serum CRP and MMP-3 levels, DAS28-CRP, and TSS. Serum Ang-1 level showed significant correlations with serum MMP-3 level and DAS28-CRP. Serum Ang-2 level showed significant correlations with serum CRP level and TSS. CONCLUSION: The serum VEGF level is important as an index of the activity of RA based on angiogenesis and a prognostic factor regarding joint destruction. Serum Ang-1 level may be useful as an index of sustained arthritis based on the maintenance of newly formed vessels. Serum Ang-2 level may reflect a state of marked angiogenesis.
19589891 A pilot risk model for the prediction of rapid radiographic progression in rheumatoid arth 2009 Sep OBJECTIVES: Identifying patients with RA at high risk of rapid radiographic progression (RRP) is critical for making appropriate treatment decisions. We developed an exploratory prediction model for the risk of RRP using an RA study population undergoing either conservative or aggressive disease management. METHODS: Using data from the active-controlled study of patients receiving infliximab for the treatment of rheumatoid arthritis of early onset (ASPIRE) early RA study, RRP was defined as a threshold change in modified Sharp/van der Heijde score (SHS) of > or =5 U/year. Spearman's rank analysis was used to identify baseline risk factors for RRP. Logistic regression was used to calculate the probability of RRP in 1 year. The results were combined into a matrix model that consisted of risk factors and initiated treatment arranged in increasing risk of RRP. Data from the anti-TNF trial in rheumatoid arthritis with concomitant therapy (ATTRACT) established RA study were applied to the model to test its generalizability in another population. RESULTS: The 28 swollen joint count, RF, CRP and ESR are included as trichotomous variables and initiated treatment (monotherapy or combination therapy) as a dichotomous variable. Two models, one incorporating all risk factors except CRP and another incorporating all risk factors except ESR, were developed to adjust for collinearity. These models identify subpopulations of RA patients at higher predicted risk for RRP. CONCLUSIONS: These preliminary matrix models predict the risk of RRP using initiated treatment and easily accessible clinical and laboratory variables. Further testing in other populations and with other therapies is needed to obtain a definitive risk model that will guide rheumatologists in making treatment decisions for individual RA patients.
20707220 Functional polymorphisms of PTPN22 and FcgR genes in Tunisian patients with rheumatoid art 2009 To investigate a possible association between functional polymorphisms of the protein tyrosine phosphatase nonreceptor type 22 (PTPN22-R620W) and receptors for the Fc fragment of IgG (FcgRIIa-H131R, FcgRIIIa-F158V FcgRIIIb-NA1/NA2), and rheumatoid arthritis (RA), 133 Tunisian patients with RA and 100 controls were genotyped. We found strong evidence of an association of PTPN22 620W allele and RA. However, analysis does not detect an association between auto-antibodies seropositivity, presence of nodules or erosions and this allele. No significant skewing of any of the three FcgR polymorphisms was seen in this RA group. Nevertheless, we identified FcgRIIIa-V/V158 as the most important FcgR genotype for severe disease subset with joint erosions and observed that patients with FcgRIIIb-NA2/NA2 genotype had an earlier incidence of clinical symptoms. In conclusion, we have confirmed that PTPN22 620W allele is associated with Tunisian RA but does not constitute a factor influencing clinical manifestations. Conversely, this study supports that the FcgRIIa/IIIa and IIIb polymorphisms could influence the course and the severity of this disease. A large number of samples are required to provide independent confirmation of these findings.
20107818 [Pathogenesis of parodontitis in rheumatic diseases]. 2010 Mar Inflammatory periodontal disease (PD) is a common disease worldwide that has a primarily bacterial aetiology and is characterized by dysregulation of the host inflammatory response. The degree of inflammation varies among individuals with PD independently of the degree of bacterial infection, suggesting that alteration of the immune function may substantially contribute to its extent. Factors such as smoking, education, and body mass index (BMI) are discussed as potential risk factors for PD. Most PD patients respond to bacterial invaders by mobilizing their defensive cells and releasing cytokines such as interleukin (IL)-1beta, tumour necrosis factor (TNF)-alpha, and IL-6, which ultimately causes tissue destruction by stimulating the production of collagenolytic enzymes, such matrix metalloproteinases. Recently, there has been growing evidence suggesting an association between PD and the increased risk of systemic diseases, such ateriosclerosis, diabetes mellitus, stroke, and rheumatoid arthritis (RA). PD and rheumatologic diseases such as RA share many pathological aspects and immunological findings.
19876631 Complementary and alternative medicine use in rheumatoid arthritis: proposed mechanism of 2010 Mar Complementary and alternative medicine (CAM) has become popular in patients with rheumatoid arthritis (RA) worldwide. The objective of this study is to systematically review the proposed mechanisms of action and currently available evidence supporting the efficacy of CAM modalities in relieving signs and symptoms of RA. The prevalence of CAM usage by RA patients is anywhere from 28% to 90%. Many published studies on CAM are based on animal models of RA and there is often insufficient evidence for the efficacy of CAM modalities in RA. The existing evidence suggests that some of the CAM modalities, such as acupuncture, herbal medicines, dietary omega-3 fatty acids, vitamins, and pulsed electromagnetic field show promising efficacy in reducing pain. While the use of CAM modalities for the treatment of RA continues to increase, rigorous clinical trials examining their efficacy are necessary to validate or refute the clinical claims made for CAM therapies.
19059533 The role of homocysteine as a significant risk factor for white matter lesions in Japanese 2009 Jan The presence of white matter lesions (WML) is an important prognostic factor for the development of stroke. Plasma total homocysteine (tHcy), which increases with diabetes, has been flagged as a novel predictor for cerebrovascular events. We tested the hypothesis that the presence of WML correlates with tHcy in rheumatoid arthritis patients. Based on brain magnetic resonance imaging findings, 65 rheumatoid arthritis patients were divided into 2 groups: WML-positive group (61 +/- 6 years, mean +/- SD; n = 25) and WML-negative group (60 +/- 7 years, n = 40). The level of metabolic parameters was assessed by total cholesterol, triglycerides, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, fasting plasma glucose, and homocysteine (tHcy). The duration of rheumatoid arthritis was longer in the WML-positive group than in the WML-negative group (P < .05). Plasma levels of triglyceride was higher whereas high-density lipoprotein cholesterol was lower in the WML-positive group than in the WML-negative group (P < .05 and P < .01, respectively). Fasting plasma glucose (P < .05) and tHcy (<.0001) levels were higher in the WML-positive group than in the WML-negative group. Multivariate logistic analysis revealed that WML was independently predicted by the tHcy (odds ratio, 1.35; 95% confidence interval, 1.12-1.63; P < .0001). Our findings indicate that the presence of WML was associated with the tHcy in Japanese patients with rheumatoid arthritis.
20030816 Active immunization to tumor necrosis factor-alpha is effective in treating chronic establ 2009 INTRODUCTION: Passive blockade of tumor necrosis factor-alpha (TNF-alpha) has demonstrated high therapeutic efficiency in chronic inflammatory diseases, such as rheumatoid arthritis, although some concerns remain such as occurrence of resistance and high cost. These limitations prompted investigations of an alternative strategy to target TNF-alpha. This study sought to demonstrate a long-lasting therapeutic effect on established arthritis of an active immunotherapy to human (h) TNF-alpha and to evaluate the long-term consequences of an endogenous anti-TNF-alpha response. METHODS: hTNF-alpha transgenic mice, which spontaneously develop arthritides from 8 weeks of age, were immunized with a heterocomplex (TNF kinoid, or TNF-K) composed of hTNF-alpha and keyhole limpet hemocyanin after disease onset. We evaluated arthritides by clinical and histological assessment, and titers of neutralizing anti-hTNF-alpha antibody by enzyme-linked immunosorbent assay and L929 assay. RESULTS: Arthritides were dramatically improved compared to control mice at week 27. TNF-K-treated mice exhibited high levels of neutralizing anti-hTNF-alpha antibodies. Between weeks 27 and 45, all immunized mice exhibited symptoms of clinical deterioration and a parallel decrease in anti-hTNF-alpha neutralizing antibodies. A maintenance dose of TNF-K reversed the clinical deterioration and increased the anti-hTNF-alpha antibody titer. At 45 weeks, TNF-K long-term efficacy was confirmed by low clinical and mild histological scores for the TNF-K-treated mice. Injections of unmodified hTNF-alpha did not induce a recall response to hTNF-alpha in TNF-K immunized mice. CONCLUSIONS: Anti-TNF-alpha immunotherapy with TNF-K has a sustained but reversible therapeutic efficacy in an established disease model, supporting the potential suitability of this approach in treating human disease.
19538721 Negative association of the chemokine receptor CCR5 d32 polymorphism with systemic inflamm 2009 INTRODUCTION: Chemokines and their receptors control immune cell migration during infections as well as in autoimmune responses. A 32 bp deletion in the gene of the chemokine receptor CCR5 confers protection against HIV infection, but has also been reported to decrease susceptibility to rheumatoid arthritis (RA). The influence of this deletion variant on the clinical course of this autoimmune disease was investigated. METHODS: Genotyping for CCR5d32 was performed by PCR and subsequent electrophoretic fragment length determination. For the clinical analysis, the following extra-articular manifestations of RA were documented by the rheumatologist following the patient: presence of rheumatoid nodules, major organ vasculitis, pulmonary fibrosis, serositis or a Raynaud's syndrome. All documented CRP levels were analyzed retrospectively, and the last available hand and feet radiographs were analyzed with regards to the presence or absence of erosive disease. RESULTS: Analysis of the CCR5 polymorphism in 503 RA patients and in 459 age-matched healthy controls revealed a significantly decreased disease susceptibility for carriers of the CCR5d32 deletion (Odds ratio 0.67, P = 0.0437). Within the RA patient cohort, CCR5d32 was significantly less frequent in patients with extra-articular manifestations compared with those with limited, articular disease (13.2% versus 22.8%, P = 0.0374). In addition, the deletion was associated with significantly lower average CRP levels over time (median 8.85 vs. median 14.1, P = 0.0041) and had a protective effect against the development of erosive disease (OR = 0.40, P = 0.0047). Intriguingly, homozygosity for the RA associated DNASE2 -1066 G allele had an additive effect on the disease susceptibility conferred by the wt allele of CCR5 (OR = 2.24, P = 0.0051 for carrier of both RA associated alleles) CONCLUSIONS: The presence of CCR5d32 significantly influenced disease susceptibility to and clinical course of RA in a German study population. The protective effect of this deletion, which has been described to lead to a decreased receptor expression in heterozygous patients, underlines the importance of chemokines in the pathogenesis of RA.
19247707 Stabilization of lung function and clinical symptoms in a patient with cystic fibrosis (CF 2009 May The most characteristic feature of airway inflammation in cystic fibrosis (CF) is the persistent infiltration of massive numbers of neutrophils. Although inflammation is primarily a protective response to injury, it has the potential to cause considerable harm when it is excessive. Recent recognition of the prominent role of inflammation has prompted the investigation of treatments designed to control inflammation in the CF lung. We report a 35-year-old man with abrupt stabilization of his rapidly progressive CF and forced expiratory volume (FEV1) after starting infliximab for his rheumatoid arthritis. This effect was sustained for 8 years while continuing to use twice-monthly infliximab.
20238216 FK506 inhibition of gliostatin/thymidine phosphorylase production induced by tumor necrosi 2011 Jul Gliostatin/thymidine phosphorylase (GLS/TP) is known to have angiogenic and arthritogenic activities. The purpose of this study was to determine the inhibitory effects of FK506 (tacrolimus) on GLS production in rheumatoid arthritis (RA). We investigated the modulation of serum GLS by FK506 therapy and the effect of FK506 on the production of GLS in fibroblast-like synoviocytes (FLSs). Serum samples were collected from 11 RA patients with active disease at baseline and after 12 weeks of FK506 treatment. Serum concentrations of GLS and matrix metalloproteinase (MMP)-3 were measured by ELISA and found to be down-regulated in responders evaluated with a disease activity score. Patient FLSs were cultured and stimulated by tumor necrosis factor (TNF)-α with or without FK506. The expression levels of GLS were determined using reverse transcription-polymerase chain reaction (RT-PCR) and enzyme immunoassay and shown to be significantly increased. GLS levels in TNF-α-stimulated FLSs were reduced by FK506 treatment. Our data show a novel mechanism for the action of physiological concentrations of FK506 in RA that regulates the production of GLS in FLSs.
20610442 Clinical synovitis in a particular joint is associated with progression of erosions and jo 2010 Dec OBJECTIVES: To assess the relationship between joint tenderness, swelling and joint damage progression in individual joints and to evaluate the influence of treatment on these relationships. METHODS: First-year data of the Behandel Strategieën (BeSt) study were used, in which patients recently diagnosed as having rheumatoid arthritis (RA) were randomly assigned into four different treatment strategies. Baseline and 1-year x-rays of the hands and feet were assessed using the Sharp-van der Heijde score (SHS). With generalised estimating equations, 3-monthly assessments of tender and swollen joints of year 1 were related to erosion progression, joint space narrowing (JSN) progression and total SHS progression at the individual joint level (definition > 0.5 SHS units) in year 1, corrected for potential confounders and within-patient correlation for multiple joints per patient. RESULTS: During year 1, 59% of all 13 959 joints analysed were ever tender and 45% ever swollen, 2.1% showed erosion progression, 1.9% JSN progression and 3.6% SHS progression. Swelling and tenderness were both independently associated with erosion and JSN progression with comparable OR, although with higher OR in the hands than in the feet. Local swelling and tenderness were not associated with local damage progression in patients initially treated with infliximab. CONCLUSION: Clinical signs of synovitis are associated with erosion and JSN progression in individual joints after 1 year in RA. A disconnect between synovitis and joint damage progression was observed at joint level in patients who were treated with methotrexate and infliximab as initial treatment, confirming the disconnect between synovitis and the development of joint damage in tumour necrosis factor blockers seen at patient level.
20149318 Citrullinated antigens as C1q-binding and monoclonal rheumatoid factor (mRF)-binding pepti 2009 Nov OBJECTIVE: Previous studies have demonstrated that immune complexes (ICs) may be involved in the pathogenesis of rheumatoid arthritis (RA). However, autoantigens contained in rheumatoid ICs remain to be elucidated. In the present study, we investigated whether the peptides captured by C1q and monoclonal rheumatoid factor (mRF), presumably associated with ICs, were citrullinated in synovial fluids from patients with RA. METHODS: Sixteen rheumatoid arthritis synovial fluids (RASFs), 7 osteoarthritis synovial fluids (OASFs), and 20 sera from RA patients were used for experiments. ICs were measured using commercially available kits based on the C1q-binding (C1q-IC) and mRF-binding (mRF-IC) assays. Citrullination of the peptides captured by C1q and mRF was detected by anti-modified citrulline antibody (Senshu Ab) after chemical modification. RESULTS: There was a significant correlation between levels of citrullination of C1q-binding peptides and those of mRF-binding peptides in RASFs (r=0.77), both of which were significantly higher than those in OASFs. No citrullinated Ags captured by C1q and mRF were detected in sera from patients with RA. CONCLUSIONS: We have demonstrated the presence of citrullinated Ags as C1q- and mRF-binding peptides in RASF. We suggest that citrullinated Ags may contribute to the pathogenesis of RA through IC formation in the joint.
19950268 DNA hypomethylation in rheumatoid arthritis synovial fibroblasts. 2009 Dec OBJECTIVE: Rheumatoid arthritis synovial fibroblasts (RASFs) are phenotypically activated and aggressive. We undertook this study to investigate whether the intrinsic activation of RASFs is due to global genomic hypomethylation, an epigenetic modification. METHODS: Global genomic hypomethylation was assessed by immunohistochemistry, flow cytometry, and L1 promoter bisulfite sequencing. The levels of Dnmt1 were determined in synovial tissue and cultured SFs by Western blotting before and after treatment with cytokines and growth factors. Normal SFs were treated for 3 months with a nontoxic dose of the DNA hypomethylation drug 5-azacytidine (5-azaC), and changes in gene expression were revealed using complementary DNA arrays. The phenotypic changes were confirmed by flow cytometry. RESULTS: In situ and in vitro, RASF DNA had fewer 5-methylcytosine and methylated CG sites upstream of an L1 open-reading frame than did DNA of osteoarthritis SFs, and proliferating RASFs were deficient in Dnmt1. Using 5-azaC, we reproduced the activated phenotype of RASFs in normal SFs. One hundred eighty-six genes were up-regulated>2-fold by hypomethylation, with enhanced protein expression. These included growth factors and receptors, extracellular matrix proteins, adhesion molecules, and matrix-degrading enzymes. The hypomethylating milieu induced irreversible phenotypic changes in normal SFs, which resembled those of the activated phenotype of RASFs. CONCLUSION: DNA hypomethylation contributes to the chronicity of RA and could be responsible for the limitation of current therapies.
20716297 Detection of hydrogen sulfide in plasma and knee-joint synovial fluid from rheumatoid arth 2010 Aug Blood concentrations of hydrogen sulfide (H(2)S) are markedly elevated in several animal models of inflammation. Pharmacological inhibition of H(2)S synthesis reduces inflammation and swelling, suggesting that H(2)S is a potential inflammatory mediator. However, it is currently unknown whether H(2)S synthesis is perturbed in human inflammatory conditions or whether H(2)S is present in synovial fluid. We analyzed paired plasma and synovial fluid (SF) aspirates from rheumatoid arthritis (RA; n= 20) and osteoarthritis (OA; n= 4) patients and plasma from age matched healthy volunteers (n= 20). Median plasma H(2)S concentrations from healthy volunteers and RA and OA patients were 37.6, 36.6, and 37.6 microM, respectively. In RA patients, median synovial fluid H(2)S levels (62.4 microM) were significantly higher than paired plasma (P= 0.002) and significantly higher than in synovial fluid from OA patients (25.1 microM; P= 0.009). SF H(2)S levels correlated with clinical indices of disease activity (tender joint count, r= 0.651; P < 0.05) and markers of chronic inflammation; Europhile count (r=-0.566; P < 0.01) and total white cell count (r=-0.703; P < 0.01). Our study shows for the first time that H(2)S is present in synovial fluid and levels correlated with inflammatory and clinical indices in RA patients.
20110488 Immunology. Arsonists in rheumatoid arthritis. 2010 Jan 29 Inflammation associated with rheumatoid arthritis is stoked by platelets, expanding their roles into the immune system.
20019779 [Clinical characteristics of rheumatoid arthritis with interstitial pulmonary fibrosis]. 2009 Dec 18 OBJECTIVE: To analyze the clinical characteristics of interstitial pulmonary fibrosis (IPF) in patients with Rheumatoid arthritis (RA). METHODS: We retrospectively analyzed 198 RA patients with or without IPF. Characteristics of RA-IPF in clinical and lab data were analyzed. Age, duration of disease, clinical and laboratory parameters, history of smoking and medicine were compared between the patients with and without IPF. RESULTS: (1) Among the 198 RA patients, 15.2% (30/198) were found with IPF. 100% RA-IPF patients had HRCT findings. However, 63.3% (19/30) had positive findings in chest X-ray, and only 46.7% (14/30) had the complaints of cough and short breath. Velcro rales were found in 50.0% (15/30) patients with IPF and no acropachy occurred. Only one patient suffered from hypoxemia. IPF presented after the joint symptoms in most patients. (2) RA-IPF patients were older than those without IPF [(65.50 +/- 9.71) vs (55.22 +/- 12.98) years, P<0.01]; Higher positivity of anti-keratin antibodies (AKA) were found in RA-IPF compared to patients without IPF (61.5% vs 35.9%, P=0.014). Furthermore, the levels of anti-cyclic citrullinated peptide (CCP) antibody were significantly higher in RA-IPF [(4.38 +/- 2.08) vs (3.20 +/- 2.12), P=0.01]. No differentiation of duration of disease, history of smoking and medicine, IgM rheumatoid factor, IgG rheumatoid factor, anti-nuclear antibody, anti-SSA antibody and levels of immunoglobins and complements were found between the two groups of RA patients with and without IPF. CONCLUSION: The clinical symptoms of IPF in RA patients are mild and more common in older patients. AKA and anti-CCP antibody might be important antibodies associated with RA-IPF.
19229584 Are fibromyalgia patients as inactive as they say they are? 2009 Jun Both fibromyalgia and rheumatoid arthritis (RA) patients self-report similar disability. These diseases are viewed differently by the medical profession as one has ample evidence of tissue damage and inflammation and the other does not. We were interested to see if an objective measure produced similar results. Twelve patients with RA were matched with 12 fibromyalgia patients by sex, age, and Health Assessment Questionnaire (HAQ) score. The 24-h ambulatory activity of these patients was recorded using the Numact monitor. Statistical analysis was performed using independent group t test for the ambulatory activity data and Spearman's correlation coefficients for HAQ and total energy. There were no significant differences found between the two groups in terms of total activity. Other compared analyses for activity included the number of steps taken, vigor of steps, and time spent standing, which were not statistically different. The correlation coefficients of HAQ and total ambulatory activity for the fibromyalgia group were rho = -0.638 (p = 0.026). Patients with RA and fibromyalgia displaying similar levels of self-reported disability have objective evidence of similar levels of total ambulatory activity. There is a statistically significant correlation between self-reported and objective measurements of disability for the fibromyalgia patients. Either of these measures merits further study as outcome measures for fibromyalgia.
19529880 Peripheral bone density in patients with rheumatoid arthritis. 2009 Oct Bone loss in patients with rheumatoid arthritis (RA) varies at different skeletal sites. The aim of the study was to evaluate whether bone mineral density (BMD) of the forearm is significantly different in patients with RA and controls and may correlate to BMD or other parameters of inflammation or bone resorption. We included 421 patients (357 women: mean age 58.4 +/- 12.87 years and 64 men: mean age 56.11 +/- 12.80 years) with RA in the study. BMD values of the ultradistal forearm (0.381 +/- 0.052 g/cm(2)) and middistal forearm (0.519 +/- 0.091 g/cm(2)) were significantly (p < 0.01) lower in women with RA than controls (0.395 +/- 0.043 and 0.535 +/- 0.052 g/cm(2), respectively). In contrast, there was no difference in bone density at the lumbar spine (women 0.921 +/- 0.1570 g/cm(2), men 0.941 +/- 0.144 g/cm(2)) or hip (women 08.11 +/- 0.140 g/cm(2), men 0.895 +/- 0.143 g/cm(2)) in patients with RA in comparison to controls (lumbar spine: women 0.930 +/- 0.146 g/cm(2); men 0.960 +/- 0.146 g/cm(2); hip: women 0.820 +/- 0.122 g/cm(2); men 0.899 +/- 0.144/cm(2)). Patients with increased inflammatory activity (elevated C-reactive protein) presented with significantly lower BMD of the hip (0.7533 +/- 0.144 versus 0.825 +/- 0.138 g/cm(2)) and ultradistal forearm (0.366 +/- 0.09 versus 0.390 +/- 0.07 g/cm(2)). This was not the case for the lumbar spine. BMD of the forearm is precise and, in contrast to BMD of the lumbar spine, significantly lower in patients with RA. It is related to inflammatory activity, grip strength, and treatment with glucocorticoids in patients with RA.