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ID PMID Title PublicationDate abstract
12073264 [Treatment of anemia in rheumatoid arthritis with transplantation of hemopoietic stem cell 2002 The article describes chief links of pathogenesis of anemia in rheumatoid arthritis (RA). These include the blood hyperviscosity syndrome, abnormalities of iron metabolism, blockade of iron in the reticuloendothelial system, hemolysis, depression of erythropoiesis. Indices for the hemoglobin peripheral blood, erythrocytes, reticulocytes, platelets in the group of RA patients were analysed together with their changes under exposure to transplantation of hemopoitic stem cells of human embryional liver.
14767710 Retroodontoid pseudotumor resected by a high cervical lateral approach in a rheumatoid art 2004 A retroodontoid pseudotumor is a nonneoplastic mass arising posterior to the odontoid process. We describe a 67-year-old woman admitted to our hospital with numbness of the left upper extremity, dysbasia, and impairment of fine motor movement of the fingers. She was diagnosed with myelopathy due to a retroodontoid pseudotumor underlying rheumatoid arthritis. According to previously published reports, reduction of the pseudotumor was achieved by posterior fusion alone. However, in the present report, the tumor was very large, and there was no instability at the atlantoaxial segment. Therefore we managed the patient by resection of the mass through a high lateral cervical approach without fusion. The spinal cord symptoms diminished rapidly.
15184703 Psychiatric comorbidity and work disability in patients with inflammatory rheumatic diseas 2004 May OBJECTIVE: To determine the relative contribution of psychiatric comorbidity to work disability in patients with inflammatory rheumatic diseases (IRD). Parallel analyses were also performed in a matched control group with no diagnosis of IRD to investigate if predictors of work disability in medical patients are independent from the presence of IRD. METHOD: The patient group with IRD (73.9% female; mean age, 42.7 years) and the control group (73.9% female; mean age, 42.2 years) consisted of 356 outpatients each. Psychiatric comorbidity was diagnosed using the Patient Health Questionnaire (PHQ), functional disability was measured with the 12-item Short-Form Health Survey (SF-12), and severity of illness was assessed by the treating physicians. Stepwise logistic regression analyses were performed to identify independent predictors of work disability controlling for psychiatric comorbidity, functional disability, severity of illness, additional clinical variables, and demographics. RESULTS: Psychiatric comorbidity increased work disability in patients with severe IRD from 25% to 50%, and from 5% to 17% in mild disease. Physical functioning (OR = 0.6; p <.0001), depression severity (OR = 1.6; p =.005), and illness severity (OR = 1.8; p =.006) were identified as independent predictors of work disability in patients with IRD. Similar predictors of work disability were identified in the control group, but depression severity did not meet statistical significance at the 5% level. CONCLUSIONS: This study provides evidence that depression is an independent risk factor of work disability in patients with IRD, but this result cannot be generalized to other medical conditions. Improved diagnosis and treatment of depressive disorders in patients with IRD may help avoid work disability.
15146416 Expression of interleukin-21 receptor, but not interleukin-21, in synovial fibroblasts and 2004 May OBJECTIVE: To determine the role and expression of the cytokine/receptor pair interleukin-21 (IL-21)/IL-21 receptor (IL-21R) in rheumatoid arthritis (RA). METHODS: The expression of IL-21R and IL-21 was analyzed by TaqMan real-time polymerase chain reaction (PCR) and in situ hybridization of synovial biopsy samples from patients with RA and osteoarthritis (OA). Double labeling by immunohistochemistry after in situ hybridization was performed with anti-CD68 antibodies. The expression of IL-21R at the protein level was confirmed by Western blotting. Stimulation experiments were performed with recombinant IL-1beta, tumor necrosis factor alpha (TNFalpha), platelet-derived growth factor (PDGF), and transforming growth factor beta (TGFbeta). The role of IL-21R in cartilage destruction was analyzed in the SCID mouse coimplantation model of RA. RESULTS: IL-21R was found in total RNA extracts and in synovial biopsy samples from RA patients, whereas no expression or only minimal expression was seen in samples from OA patients. Double labeling indicated that both synovial macrophages and synovial fibroblasts expressed IL-21R. Western blotting with anti-IL-21R antibodies confirmed the expression of IL-21R protein in RA synovial fibroblasts (RASFs). Of note, IL-21 was not detectable by real-time PCR and in situ hybridization in the same samples in vivo as in vitro. The level of expression of IL-21R messenger RNA (mRNA) was not altered by stimulation with IL-1beta, TNFalpha, PDGF, or TGFbeta. Interestingly, in the SCID mouse coimplantation model, RASFs did not maintain their expression of IL-21R at sites of invasion into the cartilage. Similarly, IL-21R mRNA was not expressed at sites of invasion into cartilage and bone in RA synovium. CONCLUSION: Our data demonstrate that IL-21R is expressed in RA synovium by RASFs and synovial macrophages. IL-21R is associated with the activated phenotype of RASFs independently of the major proinflammatory cytokines IL-1beta and TNFalpha, but correlates negatively with the destruction of articular cartilage and bone.
15251133 Inhibition of IL-6 for the treatment of inflammatory diseases. 2004 Aug Interleukin-6 (IL-6) is a pleiotropic cytokine with various biological activities. Deregulated overproduction of IL-6 has been found to play pathological roles in chronic inflammatory diseases such as rheumatoid arthritis, Castleman's disease, juvenile idiopathic arthritis and Crohn's disease. Humanized anti-IL-6 receptor antibody has been developed as a therapeutic agent for these diseases, and therapeutic benefits have been revealed in clinical studies.
12528108 The effect of HLA-DR on susceptibility to rheumatoid arthritis is influenced by the associ 2003 Jan OBJECTIVE: HLA-DRB1, a major genetic determinant of susceptibility to rheumatoid arthritis (RA), is located within 1,000 kb of the gene encoding tumor necrosis factor (TNF). Because certain HLA-DRB1*04 subtypes increase susceptibility to RA, investigation of the role of the TNF gene is complicated by linkage disequilibrium (LD) between TNF and DRB1 alleles. By adequately controlling for this LD, we aimed to investigate the presence of additional major histocompatibility complex (MHC) susceptibility genes. METHODS: We identified 274 HLA-DRB1*04-positive cases of RA and 271 HLA-DRB1*04-positive population controls. Each subject was typed for 6 single-nucleotide polymorphisms within a 4.5-kb region encompassing TNF and lymphotoxin alpha (LTA). LTA-TNF haplotypes in these unrelated individuals were determined using a combination of family data and the PHASE software program. RESULTS: Significant differences in LTA-TNF haplotype frequencies were observed between different subtypes of HLA-DRB1*04. The LTA-TNF haplotypes observed were very restricted, with only 4 haplotypes constituting 81% of all haplotypes present. Among individuals carrying DRB1*0401, the LTA-TNF 2 haplotype was significantly underrepresented in cases compared with controls (odds ratio 0.5 [95% confidence interval 0.3-0.8], P = 0.007), while in those with DRB1*0404, the opposite effect was observed (P = 0.007). CONCLUSION: These findings suggest that the MHC contains genetic elements outside the LTA-TNF region that modify the effect of HLA-DRB1 on susceptibility to RA.
12714388 Tumour necrosis factor alpha and interleukin 6 gene expression in keratocytes from patient 2003 May BACKGROUND/AIMS: Ultrastructural alterations in the stroma adjacent to corneal perforations have previously been reported in patients with longstanding rheumatoid arthritis. Since patients with rheumatoid arthritis often present upregulation of proinflammatory cytokines in serum and in synovial fluid, it was of interest to analyse the gene expression of these cytokines-for example, tumour necrosis factor alpha (TNF-alpha) and interleukin 6 (IL-6), in corneal samples from patients with corneal ulcerations and/or perforations associated with rheumatoid arthritis. METHODS: Corneal samples from seven patients with corneal ulcerations and/or perforations associated with rheumatoid arthritis were collected in 4% paraformaldehyde in "RNAse-free" conditions. Paraffin sections were fixed on silan coated slides and further analysed by systematic non-radioactive in situ hybridisation, using specific gene probes for TNF-alpha and IL-6 labelled with digoxigenin (DIG). Detection of hybrids was carried out by using a commercially available DIG detection system. RESULTS: Whereas an extended TNF-alpha gene expression could be clearly observed in the keratocytes surrounding the corneal ulcerations and/or perforations from five of the seven analysed patients, all seven patients presented clearly positive results for an extended IL-6 gene expression in the analysed tissue samples. CONCLUSIONS: Alterations in corneal cells surrounding ulcerations and/or perforations in patients with rheumatoid arthritis may occur with implication for inflammatory processes. Upregulation of the proinflammatory cytokines TNF-alpha and IL-6 may modify the production of metalloproteinases in the corresponding cells resulting in collagenolytic corneal damage.
12064825 Immunoglobulin G fc-receptor (FcgammaR) IIA, IIIA, and IIIB polymorphisms related to disea 2002 Jun OBJECTIVE: Fc receptors for IgG (FcyR) modulate immune responses. FcyR are expressed on various leukocytes and contain allelic polymorphisms with different capacity for IgG binding and phagocytosis. We investigated the distribution of FcgammaRIIA, FcgammaRIIIA, and FcgammaRIIIB polymorphisms in rheumatoid arthritis (RA) and whether they were related to disease expression and severity. METHODS: Ninety-six controls and 114 patients fulfilling American College of Rheumatology (ACR) criteria for RA were genotyped for FcgammaRIIA, IIIA, and IIIB using polymerase chain reaction. Physician's global assessment of RA type estimated RA disease expression. In addition, usual measures of disease activity were recorded. RESULTS: The genotype and allele frequencies did not differ significantly between the RA patients and the controls. Patients homo or heterozygous for the FcgammaRIIA arginine (R) allele had significantly more aggressive RA and swollen joints than patients homozygous for the FcgammaRIIA histidine (H) allele. Although there was a tendency of more severe disease among patients homo or heterozygous for the FcgammaRIIIA valine allele, there were no significant findings with the disease activity for the FcgammaRIIIA and FcgammaRIIIB genotypes. CONCLUSION: FcgammaRIIA is implicated as a possible disease modifying gene in RA. Individuals homozygous for the FcgammaRIIA R allele have less efficient binding of IgG2 subclasses than individuals homozygous for the H allele. Less effective processing of circulating immune complexes in RA patients homozygous for the FcgammaRIIA R allele may therefore contribute to a more unfavorable course.
12010564 Joint disease caused by defective gp130-mediated STAT signaling. 2002 IL-6 is a multifunctional cytokine produced by lymphoid and nonlymphoid cells; it regulates immune responses, acute-phase reactions, and inflammation. IL-6 signaling is mediated exclusively by the common signal-transducing component gp130, which is also essential for signal transduction of other cytokines of the leukemia inhibitory factor (LIF)/IL-6 family. M Ernst and colleagues generated and studied knock-in mice (gp130DeltaSTAT/DeltaSTAT), in which all STAT-binding sites (sites binding signal transducers and activators of transcription) were deleted from their gene encoding gp130 but binding sites for both Janus kinases (JAKs) and for the protein tyrosine phosphatase-2 (SHP-2) were preserved. They found that this mutant mouse displayed a blastocyst implantation defect, gastrointestinal ulceration, and, interestingly, severe joint disease with representative features of rheumatoid arthritis. Synovial cells from this mouse exhibited mitogenic hyper-responsiveness to cytokines of the LIF/IL-6 family, a phenomenon that was caused by sustained gp130-mediated SHP-2/Ras/Erk activation due to a defect in the induction of SOCS-1 (suppressor of cytokine signaling-1; also known as SSI or JAB). This suppressor, induced by STAT signaling, regulates cytokine signaling. It is, therefore, conceivable that the disturbance of the balanced activation between the STAT and SHP-2/Ras/Erk signal pathways causes the joint disease in the gp130DeltaSTAT/DeltaSTAT mouse. These findings may be beneficial in the elucidation of the cause and the treatment of rheumatoid arthritis in humans.
12209029 Blocking the effects of IL-1 in rheumatoid arthritis protects bone and cartilage. 2002 Sep Destruction of articular joints occurs progressively in patients with rheumatoid arthritis (RA). Although the exact aetiology of RA has not been fully elucidated, a large body of evidence supports a role for interleukin-1 (IL-1) in cartilage and bone erosion. In vitro studies suggest that IL-1 can cause cartilage destruction by stimulating the release of matrix metalloproteinases and other degradative products, and it can increase bone resorption by stimulating osteoclast differentiation and activation. In animal models of RA, blocking the effects of IL-1 with either IL-1 receptor antagonist (IL-1Ra; endogenous), anti-IL-1 monoclonal antibodies, or soluble IL-1 type II receptors significantly reduced cartilage destruction and bone erosion. Gene therapy with IL-1Ra was also effective in reducing joint destruction in experimental RA and osteoarthritis (OA) models. In clinical studies, anakinra, a human recombinant IL-1 receptor antagonist (IL-1ra; exogenous), significantly slowed radiographic progression of RA relative to placebo and significantly reduced clinical symptoms when used as monotherapy or in addition to existing methotrexate therapy. These results demonstrate that blocking IL-1 protects bone and cartilage from progressive destruction in RA.
15310421 The role of social support in coping with daily pain among patients with rheumatoid arthri 2004 Sep Using a daily process methodology, the current study examined the role of social support in coping and pain severity among patients with rheumatoid arthritis (RA). Seventy-three adults with RA completed a structured record twice daily for one week on pain severity, pain coping, satisfaction with support and disappointment in support. Findings suggested that support influenced pain indirectly, by encouraging the use of specific coping strategies, as well as impacting coping effectiveness. Satisfaction with support was associated with adaptive and maladaptive coping, while disappointment was associated with maladaptive coping. Findings highlight the importance of close others in promoting adaptive coping strategies.
12086162 Comparison of gastroduodenal, renal and abdominal fat biopsies for diagnosing amyloidosis 2002 May The aim of the study was to determine the frequency of amyloidosis detected by gastroduodenal biopsy in rheumatoid arthritis (RA) patients, and to investigate correlations between the results of gastroduodenal biopsy and abdominal fat and renal biopsies. A total of consecutive 1006 RA patients underwent gastroduodenal biopsy. The 71 patients who tested positive for gastrointestinal (GI) amyloidosis were asked to undergo renal and abdominal fat biopsies, and 21 did so. Renal biopsies were also performed on 12 patients with no amyloidosis but indicators of drug-induced renal damage, and abdominal fat biopsies were performed on 50 RA patients with no indication of amyloidosis. The prevalence of GI amyloidosis was 7.1%. Urinary abnormalities and GI symptoms were common in GI amyloidisis, and inflammatory markers were elevated. Sixty-one (86%) had either depressed creatinine clearance or urinary symptoms. Nineteen of the 21 patients (91%) with GI amyloidosis who underwent renal biopsies also had renal amyloid deposits. Eleven of the 21 (52%) had amyloidosis on abdominal fat biopsy. None of the 12 patients without GI amyloidosis had renal amyloidosis on renal biopsy, and none of the 50 patients without GI amyloidosis had amyloidosis on abdominal fat biopsy. Gastroduodenal biopsy reveals a high prevalence of amyloidosis in RA patients. Amyloidosis is often associated with signs of renal impairment. Results of GI biopsy are highly correlated with those of renal biopsy, but the results of fat biopsy are not. We recommend GI biopsy for RA patients for the screening of systemic amyloidosis.
12519286 Two-year follow-up of a randomized controlled trial of a clinical nurse specialist interve 2003 Jan AIM: To compare the long-term effectiveness of care delivered by a clinical nurse specialist (CNS) with inpatient team care and day patient team care in patients with rheumatoid arthritis and increasing functional limitations. Background. The role of CNSs in the management of patients with rheumatoid arthritis (RA) is evolving, and their effectiveness in comparison with care provided by a rheumatologist alone has been established. However, long-term controlled studies showing how the effectiveness of CNSs compares with that of other forms of co-ordinated care, such as multidisciplinary team care, are lacking. METHODS: Two hundred and ten patients rheumatoid arthritis patients were randomized to care delivered by a CNS in a rheumatology outpatient clinic (12 weeks), inpatient team care (2 weeks) and day patient team care (3 weeks). Clinical assessments recorded on study entry, weeks 12, 26, 52, 78 and 104 comprised the health assessment questionnaire (HAQ) and MacMaster Toronto Arthritis (MACTAR) patient preference interview as primary outcome measures. Grip strength, walk test, RAND-36, Rheumatoid Arthritis Quality of Life questionnaire and disease activity score (DAS) were applied as secondary outcome measures. RESULTS: No significant differences in medical treatment, use of services of other health professionals, introduction of adaptive equipment or number of hospitalizations were observed between the three treatment groups during 2 year follow-up, except that visits to nurse specialists were more frequent and home help was less frequent in the CNS group. A comparison of clinical outcomes among the three groups and a comparison between the nurse specialist and inpatient and day patient care groups together did not show any significant differences. Within all three groups functional status, quality of life and disease activity improved significantly (P < 0.05). In general, the results obtained after 12 weeks remained stable until 104 weeks after the start of the study. CONCLUSION: Care provided by a CNS in an outpatient rheumatology clinic has a similar long-term clinical outcome to inpatient and day patient team care in patients with rheumatoid arthritis. A CNS intervention appears to be an effective innovation in the care for patients with rheumatoid arthritis.
11980132 [Pharmacokinetic of prednisolone in patients with rheumatoid arthritis]. 2002 AIM: To study pharmacokinetics of prednisolone in patients with rheumatoid arthritis (RA). MATERIAL AND METHODS: The examination of 10 RA patients included blood tests for glucocorticoids 1, 2, 4 and 6 hours after the drug intake. Serum steroids were measured using high performance liquid chromatography. Pharmacokinetic parameters were estimated in one-chamber model with absorption. RESULTS: In spite of the same dose of prednisolone, its serum concentration as well as pharmacokinetic parameters were individual in each patient. CONCLUSION: Pharmacokinetic indices of prednisolone in RA patients provide more reliable information for design of treatment scheme for each patient individually.
15459815 An elevated level of IL-10- and TGFbeta-secreting T cells, B cells and macrophages in the 2004 Oct A relative high secretion level of IL-10 and a low secretion of TNF-alpha has been described in the synovial fluid and peripheral blood of patients with reactive arthritis (ReA), possibly contributing to the persistence of bacteria. The role of TGF-beta is less clear. We investigated these cytokines in the synovial membrane of patients with ReA and rheumatoid arthritis (RA) and tried to identify their cellular source. We used sections from the synovial membrane of 4 ReA and 4 RA patients which were double stained with immunofluorescence antibodies against cell surface markers for T cells (CD3), macrophages (CD68) and B cells (CD20) in combination with antibodies against intracellular cytokines TNF-alpha, IFN-gamma, TGF-beta, IL-4 and IL-10, and quantified these using a fluorescence microscope. A lower number of TNF-alpha-secreting cells were found in ReA compared to RA: CD3+: 1.78 +/- 0.54% versus 5.02% +/- 0.47% (p = 0.034). CD68+: 2.86 +/- 0.52 versus 5.37 +/- 0.53% (p = 0.034), CD20+ : 3.02 +/- 0.42% versus 3.58 +/- 0.48% (p > 0.05). A higher number of IL-10 positive cells were found in ReA compared to RA: CD3+: 3.27 +/- 1.5% versus 1.13 +/- 0.50% (p = 0.034), CD68+ 1.23 +/- 0.75% versus 0.83 +/- 0.35% (p > 0.05), CD20+: 3.70 +/- 1.6% versus 1.6 +/- 1.1% (p > 0.05). A difference between ReA and RA was also found for TGF-beta+ T cells: CD3+ 7.86 + 1.5% versus 1.78 + 0.35% (p = 0.032); CD20+: 7.91 + 2.1% versus 2.1 + 2.8% (p > 0.05), CD68+: 7.81% + 1.24% versus 2.12 + 0.28% (p = 0.032). In conclusion, we saw a different cytokine secretion pattern in the synovial membrane of ReA and RA. For T cells in ReA we found a cytokine secretion profile typical for T regulatory cells 1 (Tr1), with an elevated level of IL-10- and TGF-beta-secreting cells. Whether this is due to a more general difference in TNF-alpha, IL-10 or TGF-beta production which is genetically determined or regulated by T cells remains to be determined.
14984815 Heart failure in rheumatoid arthritis: rates, predictors, and the effect of anti-tumor nec 2004 Mar 1 PURPOSE: We sought to determine the frequency of heart failure in patients with rheumatoid arthritis, and to determine its predictors, particularly the use of anti-tumor necrosis factor (TNF) therapy. METHODS: Rheumatoid arthritis (n = 13,171) and osteoarthritis (n = 2568) patients were studied during a 2-year period ending in June 2002. The diagnosis of heart failure was based on self-report or review of medical records. Propensity scores were used to adjust for the risk of anti-TNF (infliximab and etanercept) prescription. RESULTS: Heart failure was more common among patients with rheumatoid arthritis (3.9% [n = 461]) than in those with osteoarthritis (2.3% [n = 87]), after adjusting for differences in demographic characteristics. Patients with rheumatoid arthritis had similar risk factors for heart failure (e.g., hypertension, prior myocardial infarction, diabetes, advanced age) as persons in population-based studies. Heart failure was significantly (P <0.05) less common in anti-TNF-treated patients (3.1% [180/5832]) than in the remaining patients (3.8% [281/7339]), even after adjusting for baseline differences. In the absence of pre-existing cardiovascular disease, the risk of heart failure was low (0.4% [24/6251]) and was not related to anti-TNF therapy. CONCLUSION: Our results suggest that rheumatoid arthritis increases the risk of heart failure, which may be ameliorated by anti-TNF therapies.
15231512 Influence of anti-tumour necrosis factor therapy on cardiovascular risk factors in patient 2005 Feb BACKGROUND: Tumour necrosis factor (TNF) is known to increase the concentrations of interleukin (IL) 6 and C reactive protein (CRP) and to induce proatherogenic changes in the lipid profile and may increase the cardiovascular risk of patients with rheumatoid arthritis (RA) and other inflammatory disorders. OBJECTIVE: To assess whether anti-TNF therapy modifies the cardiovascular risk profile in patients with RA. METHODS: The lipoprotein spectrum and the inflammation markers CRP and IL6 were investigated in 33 patients with RA treated with human anti-TNF monoclonal antibodies (D2E7, adalimumab, Humira) and 13 patients with RA given placebo, before and after 2 weeks' treatment. RESULTS: In the anti-TNF treated group, the mean (SD) concentrations of HDL-cholesterol were significantly higher after 2 weeks' treatment (0.86 (0.30) mmol/l v 0.98 (0.33) mmol/l, p<0.01), whereas LDL and triglyceride levels were not significantly changed. Additionally, a significant decrease in CRP (86.1 (54.4) mg/l v 35.4 (35.0) mg/l, p<0.0001), and IL6 (88.3 (60.5) pg/ml v 42.3 (40.7) pg/ml, p<0.001) concentrations was seen in this group. No changes in lipid profile, IL6, or CRP levels were seen in the placebo group. CONCLUSIONS: TNF neutralisation with monoclonal anti-TNF antibodies increased HDL-cholesterol levels and decreased CRP and IL6 levels after 2 weeks. Therefore this treatment may improve the cardiovascular risk profile of patients with RA.
12784387 Leflunomide for the treatment of rheumatoid arthritis: a systematic review and metaanalysi 2003 Jun OBJECTIVE: To systematically review the evidence from clinical trials on the efficacy and toxicity of leflunomide for the treatment of active rheumatoid arthritis (RA). METHODS: We searched Medline, Embase, Current Contents, and the Cochrane Controlled Trial Register for human randomized controlled trials (RCT) and controlled clinical trials up to December 2001. We also hand-searched reference lists and conference proceedings and consulted content experts. Relative benefit (RB), and weighted mean differences or standardized mean differences with their 95% confidence interval (95% CI) were calculated. RESULTS: Six RCT totaling 2044 patients with RA were included in this review. Using specific criteria, all trials were considered of high methodological quality. Leflunomide improved the ACR20 response rate roughly 2 times over placebo both at 6 months (RB = 1.93, 95% CI 1.51, 2.47) and at 12 months (RB = 1.99, 95% CI 1.42, 2.77). Other clinical outcomes of disease activity and function and radiological scores were also significantly better for leflunomide patients than those taking placebo. No significant differences for most of the outcomes were observed between leflunomide and sulfasalazine (SSZ) or methotrexate (MTX). Adverse events were more common in the leflunomide group, but withdrawal rates were fewer than for placebo. Overall, withdrawal rates and adverse events in the leflunomide group were not different from SSZ or MTX. CONCLUSION: Leflunomide improves all clinical outcomes and delays radiographic progression at 6 and 12 months of RA treatment compared to placebo. Its efficacy and adverse events at 2 years of treatment are comparable to SSZ and MTX. Longterm efficacy and toxicity remain to be established.
15301237 The prevalence of rheumatoid arthritis in an urban population of Izmir-Turkey. 2004 Jul OBJECTIVE: To estimate the prevalence of rheumatoid arthritis (RA) in an urban area in Izmir, Turkey. METHODS: The study was conducted in the Balcova and Narlidere districts of Izmir and a total of 2,887 people aged 20 years or older were contacted with a 98.2% acceptance rate. Nine medical doctors administered an RA questionnaire by face-to-face interview. Subjects reporting a history of swelling in at least 2 joints lasting more than 4 continuous weeks or a history of a diagnosis of rheumatoid arthritis, inflammatory joint rheumatism or joint rheumatism were considered as screening positive and they were invited to come in for an examination. RA cases were defined by the 1987 American College of Rheumatology (ACR) criteria modifiedfor use in population studies. RESULTS: A total of 301 subjects (243 women, 58 men), or 10.6% of those who received the questionnaire were screening positive. 240 (79.7%) of these agreed to undergo a clinical examination either in the clinic or at home. Among these, 14 (12 female, 2 male) patients fulfilled the ACR criteria for RA. The prevalence of RA was 0.49% (95% CI 0.27-0.83) in the total population interviewed, 0.77% (95% CI 0.40-1.35) in women and 0.15% (95%CI 0.02-0.60) in men. The age- and sex-adjusted prevalence for the general population was estimated as 0.36%. Five of the 14 RA (36%) cases had not been diagnosed previously CONCLUSION: These data are consistent with the results of other Mediterranean countries. A significant proportion of RA cases remain undiagnosed in the community.
12376608 Interstitial lung diseases associated with collagen vascular diseases: radiologic and hist 2002 Oct Collagen vascular diseases that demonstrate features of interstitial lung disease include systemic lupus erythematosus, rheumatoid arthritis, progressive systemic sclerosis, dermatomyositis and polymyositis, ankylosing spondylitis, Sjögren syndrome, and mixed connective tissue disease. At histopathologic analysis, interstitial lung diseases associated with collagen vascular diseases are diverse and include nonspecific interstitial pneumonia, usual interstitial pneumonia, bronchiolitis obliterans organizing pneumonia (BOOP), apical fibrosis, diffuse alveolar damage, and lymphocytic interstitial pneumonia. Although proportions of interstitial pneumonias vary, nonspecific interstitial pneumonia accounts for a large proportion, especially in progressive systemic sclerosis, dermatomyositis and polymyositis, and mixed connective tissue disease. The more favorable prognosis in interstitial pneumonia associated with collagen vascular diseases than in idiopathic interstitial pneumonias may be explained by the larger proportion of nonspecific interstitial pneumonia than of usual interstitial pneumonia. High-resolution computed tomography seems to help characterize and determine the extent of interstitial lung disease in collagen vascular diseases.