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ID PMID Title PublicationDate abstract
16371767 Acute coronary syndrome after infliximab infusion. 2006 Jan The TNFalpha inhibitor infliximab is widely used in the treatment of rheumatoid arthritis and Crohn disease. Mild infusion reactions consisting of low-grade fever, headache, nausea, and fatigue are common, but we describe for the first time the occurrence of an acute coronary syndrome during infliximab administration. This case alerts infusion centers to consider the possibility that chest pain and dyspnea during infliximab infusion can represent a myocardial infarction, even in younger patients without a history of cardiac disease.
18854346 C-reactive protein: the underlying cause of microvascular dysfunction in rheumatoid arthri 2008 Dec OBJECTIVE: RA is a chronic autoimmune inflammatory condition associated with increased cardiovascular morbidity and mortality. Endothelial dysfunction, a marker of early atherosclerotic disease, occurs in some inflammatory diseases but this relationship has not been previously explored within the microvasculature of patients with RA. We therefore assessed forearm microvascular endothelial function in patients with RA and determined its relationship to RA disease activity and inflammation. METHODS: A total of 128 RA patients with no previous history of cardiovascular disease were evaluated. Endothelium-dependent and -independent forearm skin microvascular function was measured using laser Doppler imaging after iontophoretic delivery of acetylcholine (ACh) and sodium nitroprusside (SNP), respectively. Parameters of RA disease activity and inflammation were also checked. RESULTS: There was a significant negative correlation between the level of inflammation measured by log(10)CRP and maximum vasodilatation measured by peak ACh response (r(2) = -0.209, P = 0.018, Pearson correlation test). In a multiple regression model, age (beta = -0.449, P < 0.0001) and log(10)CRP (beta = -0.193, P = 0.026) were independently negatively associated with ACh responses. When RA patients were sub-divided according to their systemic inflammatory status (CRP > 10 mg/l vs CRP
17178671 Application of flow cytometry in detection of red-cell-bound IgG in Coombs-negative AIHA. 2006 Aug Coombs negative autoimmune hemolytic anemia (AIHA) is characterized by laboratory evidence of in vivo hemolysis along with a negative direct antiglobulin test (DAT) performed by conventional tube technique (CTT) in clinically suspected AIHA patients. The sensitive gel test (GT) and flow cytometry (FC) can effectively diagnose such patients where CTT does not detect low level of red cell autoantibodies. We investigated the use of FC in the serological evaluation of CTT DAT negative AIHA and its comparison with GT DAT. Of the 50 patients with suspected AIHA, CTT DAT was negative in 5 patients (Coombs negative AIHA). GT DAT could detect red cell autoantibodies in 4 of these 5 patients. Monospecific GT DAT showed IgG and/or C3d as the responsible autoantibody. FC was considered as reactive when MFI was >3.6 (mean of 20 healthy negative volunteers +2SD). FC was reactive in all five Coombs negative AIHA patients. The mean MFI in five known CTT DAT positive samples taken for comparison was significantly higher compared to 5 DAT negative AIHA (18.3 +/- 7.78 vs. 7.88 +/- 1.35, p < 0.05). There was poor correlation between strength of GT DAT and MFI by FC. We conclude that FC is more sensitive test than the CTT and helps in the serological diagnosis of Coombs negative AIHA. However, in resource poor settings, GT DAT can be a good alternative to FC.
19095472 Resistin is elevated following traumatic joint injury and causes matrix degradation and re 2009 May OBJECTIVE: Resistin is a secreted factor that is elevated in rheumatoid arthritis (RA) and believed to drive joint inflammation in vivo. This study was undertaken to determine if resistin is present in the joint following joint injury and to elucidate the role of resistin in cartilage degradation. METHODS: The level of resistin was measured in paired synovial fluid (SF) and serum samples from patients following joint injury (anterior cruciate ligament, ACL or meniscus tear). Localization of resistin was visualized by immunohistochemistry of synovial tissue and cartilage from healthy and OA donors. Mouse and human cartilage cultures were used to assess the effect of resistin on cartilage metabolism. RESULTS: In trauma patients, resistin levels declined with increasing time post injury. The resistin levels were highest in samples collected up to 1 week following traumatic injury (SF: 2980 pg/ml, serum: 7901 pg/ml) and lowest in samples collected 6-26 years post injury (SF: 686 pg/ml, serum: 5682 pg/ml). Resistin was shown to be expressed in macrophage-like cells in both healthy and OA synovial tissue. Treatment of mouse cartilage cultures with recombinant resistin led to a dose dependent loss of proteoglycan and induction of inflammatory cytokine and PGE(2) production. Recombinant resistin inhibited proteoglycan synthesis in human cartilage explants. CONCLUSION: Resistin is elevated both systemically and locally in the weeks immediately following joint injury and has a direct effect on cartilage matrix turnover and cytokine production. Resistin may play a role in the early stages of trauma-induced OA and may represent a new therapeutic target to slow joint destruction in OA.
18503089 Assessment of anti-TNF-alpha efficacy in rheumatoid arthritis: is 3 months sufficient? 2008 Jul OBJECTIVES: The optimal therapeutic trial duration of anti-TNF-alpha therapy is currently unknown. The British Society for Rheumatology (BSR) guidance states that non-response at 3 months warrants re-evaluation of treatment and recommends not to persist beyond 6 months. The National Institute for Health and Clinical Excellence (NICE) specifies treatment continuation if response is achieved by 6 months, yet the European League against Rheumatism (EULAR) and the American College of Rheumatology (ACR) maintain a 3 month cut-off. No evidence exists to support a 6 month therapeutic trial over 3 months. Thus, we undertook a study to evaluate the proportion of patients who failed to meet NICE response criteria at 3 months but obtained this by 6 months, and to identify predictive factors for this. METHODS: Patients who commenced anti-TNF-alpha therapy for RA were studied, counting those who switched to a second or third agent separately for each instigation of therapy (n = 244). Response at 3 and 6 months was defined according to NICE criteria as a >or=1.2 reduction in Disease Activity Score (DAS28). RESULTS: Of the 189 patients with available 3 month DAS28 responses, 149 fulfilled response criteria. Of the 40 who failed, 27 continued treatment, of whom 21 were available for follow-up at 6 months. Out of the 21 patients, 12 (57%; 95% CI 36, 78) achieved a response at this time. This data set was too small to investigate predictors of response at 6 months. CONCLUSIONS: A substantial proportion of patients who fail NICE response criteria at 3 months and continue on treatment to 6 months achieve a response. These results support a 6 month therapeutic trial over 3 months.
16483568 Stem cell factor and its receptor c-Kit as targets for inflammatory diseases. 2006 Mar 8 Stem cell factor (SCF), the ligand of the c-Kit receptor, is expressed by various structural and inflammatory cells in the airways. Binding of SCF to c-Kit leads to activation of multiple pathways, including phosphatidyl-inositol-3 (PI3)-kinase, phospholipase C (PLC)-gamma, Src kinase, Janus kinase (JAK)/Signal Transducers and Activators of Transcription (STAT) and mitogen activated protein (MAP) kinase pathways. SCF is an important growth factor for mast cells, promoting their generation from CD34+ progenitor cells. In vitro, SCF induces mast cells survival, adhesion to extracellular matrix and degranulation, leading to expression and release of histamine, pro-inflammatory cytokines and chemokines. SCF also induces eosinophil adhesion and activation. SCF is upregulated in inflammatory conditions both in vitro and in vivo, in human and mice. Inhibition of the SCF/c-Kit pathway leads to significant decrease of histamine levels, mast cells and eosinophil infiltration, interleukin (IL)-4 production and airway hyperresponsiveness in vivo. Taken together, these data suggest that SCF/c-Kit may be a potential therapeutic target for the control of mast cell and eosinophil number and activation in inflammatory diseases.
16960897 Prevalence of antiphospholipid antibodies in Chilean patients with rheumatoid arthritis. 2006 Antiphospholipid (aPL) antibodies found in patients with autoimmune diseases are also detected in those with inflammatory diseases. The purpose of this study was to examine the prevalence of these antibodies in patients with rheumatoid arthritis (RA), and to evaluate the association of these antibodies with thrombosis and/or other clinical characteristics of this inflammatory disorder. Eighty-four patients with RA and 82 normal controls were studied. Anticardiolipin (aCL), anti-beta(2) glycoprotein I (anti-beta(2)GPI), and antiprothrombin (aPT) antibodies and the lupus anticoagulant (LA) activity were determined. Seven out of 84 (8.3%) patients were positive for aCL, six out of 84 (7.2%) for anti-beta(2)GPI, and six out of 84 (7.2%) for aPT, while in controls the overall prevalence of aPL antibodies was 3.6% (3 out of 82). All patients and controls were LA negative. There was no correlation between the presence of aPL with thrombosis and/or other clinical features of the antiphospholipid syndrome. We found aPL antibodies in 19.1% (16 out of 84) of the patients with rheumatoid arthritis and this prevalence was statistically higher than in normal controls (P<0.003). In this study, the presence of aPL antibodies was not associated with the development of thrombosis and/or thrombocytopenia. Whether the presence of aPL antibodies implies an increased risk for thrombosis and atherosclerosis in these patients should be studied further.
16146738 Beneficial autoimmunity participates in the regulation of rheumatoid arthritis. 2006 Jan 1 Antigen specific T cells and B cells recognize their target determinants by antigen specific receptors that are being rearranged in a random manner. These cells then undergo negative and positive selection processes that limit, albeit not eliminate, the escape of self-reactive T and B cells capable of eliciting autoimmune responses. The above processes are referred to as "central selection", and their outcome is the "central tolerance". Auto-reactive T and B cells escaping central tolerance are then subjected to peripheral mechanisms that restrain their auto-aggressive behavior. Different types of regulatory T cells are key players in maintaining actively induced peripheral tolerance. In patients suffering from various autoimmune disorders autoreactive T and/or B cells that escaped central tolerance also circumvented regulatory T cells that could, potentially, eradicate their pathogenicity in the periphery. We have found an additional regulatory mechanism that restrains the harmful activity of these cells at that time. It includes autoimmune B cells that produce neutralizing autoantibodies against numerous inflammatory mediators, mostly cytokines and chemokines, which participate in destructive autoimmunity. These autoantibodies restrain the harmful consequences of inflammatory autoimmune conditions such as in rheumatoid arthritis. Interestingly, this antibody production is elicited during autoimmune diseases, and to a much lesser extent during local inflammation. The specificity of this response is highly restricted to determinants with minimal cross reactivity to other known gene products. Thus, the immune system allows selective breakdown of tolerance in autoimmune conditions. The findings that this beneficial response is turned on by the autoimmune condition, and then regulated by its progression further imply for the existence of a programmed regulatory response of "beneficial autoimmunity". In the current review we describe how this mechanism was discovered in experimental models of rheumatoid arthritis and multiple sclerosis, demonstrate its importance in the natural regulation of these diseases, and finally explore its relevance to human diseases.
17426623 Upper-airway obstruction after short posterior occipitocervical fusion in a flexed positio 2007 Apr 15 STUDY DESIGN: Case report. OBJECTIVE: To stress the importance of the fusion angle of the occipitocervical spine based on an unusual case of upper-airway obstruction after a posterior fusion from the occipital bone to the second cervical vertebra (O-C2) in a flexed position. SUMMARY OF BACKGROUND DATA: It is well known that cervical malalignment after occipito-cervicothoracic fusion may cause dysphagia or, rarely, dyspnea. However, to the best of our knowledge, there have been no previous English reports of prolonged upper-airway obstruction after an O-C2 fusion. METHODS: We present the case of a 77-year-old woman with rheumatoid arthritis, who developed an upper-airway obstruction immediately after an O-C2 fusion. She was reintubated immediately and extubated the next day. She again suffocated suddenly 3 days after surgery, and a tracheotomy was performed. Suspecting that the main cause of the airway obstruction was not only pharyngeal edema, but also the fixture of the upper cervical angle in a flexed position, we changed the angle to the neutral position 14 days after surgery. RESULTS: After revision surgery, the upper-airway obstruction disappeared. CONCLUSION: An adequate fixation angle is necessary to avoid airway obstruction after an occipitocervical fusion, even for short upper cervical fusions, especially in patients with rheumatoid arthritis.
19083035 GPs as citizens' agents: prescription behavior and altruism. 2009 Oct To curb the heavily increasing drug budgets some Danish counties have introduced voluntary agreements between general practitioners (GPs) and health authorities. We extend the models of generic prescription by Hellerstein (Rand J Econ 29(1):108-136, 1998) and Lundin (J Health Econ 19:639-662, 2000) to allow for substitution between analogues and use difference-in-difference models to assess the effect on two drug groups (lipid-lowering and rheumatism drugs). For both drug groups we find evidence of a significant effect of the intervention. In the case of lipid-lowering drugs, we found a significant larger impact on GPs with low loyalty to the insurer and with indication of low prescription quality. In contrast we found that the intervention had a significantly lower impact on this group of GPs in the case of rheumatism drugs. We conclude that the effectiveness of the voluntary approach may partly be due to its indirect effect on GPs' altruistic motivation, which makes the GPs and the authorities collide in a common agency role.
18547834 Osseous changes and condyle position in TMJ tomograms: impact of RDC/TMD clinical diagnose 2008 Aug OBJECTIVE: The objective of this study was to evaluate the impact of clinical TMJ diagnosis, gender, and age on the agreement between expected and actual radiographic findings. STUDY DESIGN: A total of 204 patients with TMJ symptoms were examined using the Research Diagnostic Criteria (RDC/TMD). Expected radiographic findings were recorded. TMJ tomograms in closed and open mouth position were assessed for osseous changes and condyle position. Expected and actual findings were compared. Logistic regression analyses were performed with agreement on radiographic findings as the dependent variable and with clinical RDC/TMD diagnoses, gender and age as the independent variables. RESULTS: The number of radiographic findings was mostly underestimated. A clinical diagnosis of osteoarthritis and age increased the chance of overestimating osseous changes. Disc displacement and age decreased the chance of agreement on certain condyle positions. CONCLUSION: Tomography often revealed unexpected findings. It was not possible to select particular patient groups who would benefit more or less from a radiographic examination.
17604286 Microscopic measurement of inflammation in synovial tissue: inter-observer agreement for m 2007 Dec OBJECTIVES: To evaluate inter-observer agreement for microscopic measurement of inflammation in synovial tissue using manual quantitative, semiquantitative and computerised digital image analysis. METHODS: Paired serial sections of synovial tissue, obtained at arthroscopic biopsy of the knee from patients with rheumatoid arthritis (RA), were stained immunohistochemically for T lymphocyte (CD3) and macrophage (CD68) markers. Manual quantitative and semiquantitative scores for sub-lining layer CD3+ and CD68+ cell infiltration were independently derived in 6 international centres. Three centres derived scores using computerised digital image analysis. Inter-observer agreement was evaluated using Spearman's Rho and intraclass correlation coefficients (ICCs). RESULTS: Paired tissue sections from 12 patients were selected for evaluation. Satisfactory inter-observer agreement was demonstrated for all 3 methods of analysis. Using manual methods, ICCs for measurement of CD3+ and CD68+ cell infiltration were 0.73 and 0.73 for quantitative analysis and 0.83 and 0.78 for semiquantitative analysis, respectively. Corresponding ICCs of 0.79 and 0.58 were observed for the use of digital image analysis. All ICCs were significant at levels of p<0.0001. At each participating centre, use of computerised image analysis produced results that correlated strongly and significantly with those obtained using manual measurement. CONCLUSION: Strong inter-observer agreement was demonstrated for microscopic measurement of synovial inflammation in RA using manual quantitative, semiquantitative and computerised digital methods of analysis. This further supports the development of these methods as outcome measures in RA.
18621096 Unexpected finding of a marked non-neuronal cholinergic system in human knee joint synovia 2008 Sep 12 The cholinergic anti-inflammatory pathway is a newly discovered pathway. Another recent concept is the existence of a non-neuronal cholinergic system that has, so far, been defined for human tendons, intestine, airways and urinary bladder. The existence of such a system in joint synovial tissue is yet to be described. We therefore aimed to investigate the expression of choline acetyltransferase (ChAT) at both the protein and mRNA level using immunohistochemistry and in situ hybridisation, in human knee synovial tissue from rheumatoid arthritis (RA) and osteoarthritis (OA) patients. The biopsy samples were collected from patients undergoing knee prosthetic surgery. Our results show that both ChAT protein and mRNA is expressed in fibroblast-like and mononuclear-like cells, and to some extent in blood vessel walls in the synovial tissue. The mononuclear-like cells showing ChAT expression were scattered throughout the synovial tissue or located in association with lymphoid aggregates. Thus, we present the first evidence of the existence of a marked non-neuronal cholinergic system in human synovial tissue. The existence of this system could lead to the development of alternative medications to those currently in use. The system might function as a cholinergic anti-inflammatory pathway in synovial tissue. Our observations show that synovial tissue of patients with marked RA or OA, a tissue in which cholinergic innervation is not proven to exist, is supplied with acetylcholine via production in non-neuronal cells within the tissue.
17938029 Reversal of multifocal cutaneous lymphoproliferative disease associated with Epstein-Barr 2007 Nov Patients treated with immunosuppressive agents are prone to developing lymphoproliferative disorders, in particular Epstein-Barr virus-associated lymphoproliferative disease. This complication was reported first in post-transplanted patients treated with cyclosporine, and, more recently, in patients receiving long-term methotrexate therapy for inflammatory disease. We describe the case of a 70-year-old female patient with multifocal cutaneous lymphoproliferative disease occurring in the course of long-term, weekly methotrexate therapy for rheumatoid arthritis. Immunohistochemical study revealed the presence of latent membrane protein within neoplastic cells. Cutaneous lesions initially continued to increase in number and size in the first 2 months and finally disappeared completely within 5 months after discontinuation of methotrexate. The patient is now in complete remission with 12-months' follow-up. Despite initial progression after cessation of immunosuppressive therapy, Epstein-Barr virus-induced lymphoproliferative disease may disappear completely within months, thus avoiding pointless chemotherapy.
16632481 Inhibitory characteristics of citrullinated telopeptides of type I and II collagens for au 2006 Nov OBJECTIVE: To study how soluble citrullinated telopeptides of type I and II collagens inhibit the binding of autoantibodies to the respective antigens immobilized onto solid phase, and to use modifications of previous methods to re-analyse rheumatoid arthritis (RA) and control serum samples. METHODS: Autoantibody binding was inhibited with normal or citrullinated carboxytelopeptides using enzyme-linked immunosorbent assay (ELISA) methods. Serum samples were available from 120 patients with RA and 81 controls. RESULTS: Autoantibodies that bind normal C-telopeptides were not inhibited with soluble normal or citrullinated telopeptides. However, the antibodies that bind only citrullinated telopeptides could be inhibited with corresponding citrullinated telopeptides. Thus, it is not necessary to study the binding of autoantibodies to normal collagens if the specificity of their binding is assessed by immunological inhibition. For type I telopeptide, there are two arginines, the latter of which, when citrullinated, is important for binding. For type II telopeptide, there is one arginine, which is important when citrullinated. The other amino acids, e.g. the last alanine, have only a slight effect on binding. These improved methods differentiate better between RA patients, who have specific citrullinated autoantibodies, and controls than previous ELISA methods. CONCLUSIONS: Based on inhibition assay, it is possible to measure the autoantibodies binding specifically to citrullinated telopeptides of type I and II collagens. When only one assay is involved, variance is decreased and the overall performance is easier than before.
16799778 Anti-tumour necrosis factor-alpha therapy over conventional therapy improves endothelial f 2006 Oct Rheumatoid arthritis (RA) is associated with cardiovascular morbidity and mortality and inflammation contributes to related endothelial dysfunction. We aimed to investigate the effect of anti-TNFalpha therapy on endothelial function in subjects with rheumatoid arthritis. We measured flow-mediated (FMD) and GTN-mediated dilation of the brachial artery before and following 36 weeks of anti-TNFalpha therapy in nine RA patients and in a group of RA patients on conventional therapy. Thirty-six weeks of anti-TNFalpha therapy improved FMD relative to those on conventional therapy (8.65 +/- 1.50 vs. 1.70 +/- 1.36%, P = 0.02). No significant changes in GTN responses were evident. Significant improvements in tender (P = 0.03) and swollen (P = 0.02) joint counts, patients' global self-assessment (P = 0.01) and DAS-28 scores (P = 0.04) were observed in the anti-TNFalpha treated group. The addition of anti-TNFalpha treatment to conventional therapy, in those with severe RA, reduces inflammatory symptoms and improves endothelial function, potentially lowering future atherosclerotic risk.
18432273 STAT4 but not TRAF1/C5 variants influence the risk of developing rheumatoid arthritis and 2008 Jun The aim of this study was to determine the influence of STAT4 (rs7574865) and TRAF1/C5 (rs10818488 and rs2900180) gene polymorphisms on the risk of developing rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) in a Colombian population. This was a case-control study in which 839 individuals with RA (N=274) and SLE (N=144) and matched healthy controls (N=421) were included. Genotyping was performed by using a polymerase chain reaction system with pre-developed TaqMan allelic discrimination assay. STAT4 rs7574865T allele disclosed a significant influence on the risk of developing SLE (P=0.0005; OR 1.62, 95% CI 1.22-2.16) and RA (P=0.008; OR 1.36; 95% CI 1.08-1.71), whereas no effect on these autoimmune diseases was observed for the TRAF1/C5 polymorphisms examined. Our data strengthen STAT4 rs7574865 polymorphism as a susceptibility factor for RA and SLE and provide further evidence for a common origin of autoimmune diseases.
18249124 Outcome following knee arthroplasty beyond 15 years. 2008 Mar There is a paucity of information detailing functional outcome following total knee arthroplasty for this length of follow-up. We collected data from 187 knees in 150 surviving patients, beyond 15 years from implantation. Survival of the implant was confirmed and a patient administered questionnaire including WOMAC, SF-36 and patient satisfaction was used, data was scrutinised for differences between primary and revision knee surgery. Seventy knees were revised at a mean of 10.8 years. The mean WOMAC Pain score was 72 indicating predominantly mild pain. The mean WOMAC Function scores were lower at 55 indicating moderate limitation of most activities. No significant differences were found between revised and un-revised patients. Long-term pain and satisfaction scores in this population were good illustrating the benefits of TKA in the long term even in patients who have undergone revision surgery.
17905725 ADAM-15: a metalloprotease that mediates inflammation. 2008 Mar Cell-cell and cell-matrix interactions are of utmost importance in the pathogenesis of inflammatory diseases. For example, cell-cell and cell-matrix interactions are crucial for leukocyte homing and recruitment to inflammatory sites. The discovery of the disintegrin and metalloprotease (ADAM) proteins, which have both adhesive and proteolytic activities, raised the question of their involvement in inflammatory processes. More interestingly, the presence of the RGD integrin-binding sequence in the disintegrin domain of ADAM-15 (MDC-15; metargidin) highlighted ADAM-15 as a protein particularly involved in cell-cell interactions. These findings therefore prompted authors to investigate the roles of ADAM-15 in inflammatory diseases. Because of the early description of ADAM-15 expression in endothelial cells, work first focused on the roles of ADAM-15 in vascular diseases, and ADAM-15 was found to be associated with atherosclerosis. Other studies also pointed at ADAM-15 as a mediator of rheumatoid arthritis and intestinal inflammation as well as inherent angiogenesis. The roles of ADAM-15 in these diseases appear to involve mechanisms as different as cell-cell interactions, cell-extracellular matrix (ECM) interactions, and shedding activity. Here we review and discuss these recent discoveries pointing to ADAM-15 as a mediator of mechanisms underlying inflammation and as a possible therapeutic target for prevention of inflammatory diseases.
17962947 The differentiation of anaemia in rheumatoid arthritis: parameters of iron-deficiency in a 2008 Apr Iron deficiency anaemia (IDA) is common in Indian patients with rheumatoid arthritis (RA). We evaluated red blood cell indices, serum iron related and bone marrow iron stores measurements in diagnosing iron deficiency in patients with RA. Fifty consecutive anaemic patients with RA had their complete blood counts, red cell indices, serum iron, serum ferritin and serum total iron binding capacity (TIBC) measured and underwent posterior iliac crest bone marrow aspiration. Fixed smears were stained for iron with Perl's Prussian blue and patients who had no (grade 0) or minimal stainable iron (grade I) were regarded as iron deficient and rest iron replete (grade II-IV) and hence as having anaemia of chronic disease (ACD). To determine diagnostic power of tests used for diagnosing iron deficiency in addition to positive likelihood ratio, sensitivity, specificity and negative predictive values; receiver operating characteristics (ROC) curves were plotted and areas under the receiver-operating curves were compared. Eighteen patients (36%) had IDA and 32 (64%) had ACD. Correlation between the bone marrow iron stores and serum ferritin was poor in the IDA group (r = -0.09, P = 0.57) and significant in the ACD group (r = 0.79, P < 0.0001). Areas under the ROC curves for mean corpuscular haemoglobin (MCV), serum iron, TIBC and mean corpuscular haemoglobin concentration (MCHC) were relatively low (0.52, 0.71, 0.75 and 0.77, respectively) and these tests had low positive likelihood ratios (1.08, 2.13, 4.62 and 1.5, respectively). Both area under ROC curve [0.98, 95% confidence interval (0.94, 0.99)] and negative predictive value (97%) were highest when cut off serum ferritin was <82 microg/l. In patients with RA serum iron, TIBC, MCV and MCHC have limited value in diagnosing iron deficiency. In this study compared to American and European studies a much higher cut off value of serum ferritin had most diagnostic power for detecting iron deficiency. Bone marrow iron stores measurements appears to be the most reliable method for diagnosing IDA however, it needs to be taken in conjunction with other laboratory findings and the clinical scenario.