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ID PMID Title PublicationDate abstract
11886466 Thrombotic stroke associated with the use of porcine factor VIII in a patient with acquire 2002 Jan Porcine factor VIII (pFVIII), which is used to control bleeding in patients with congenital or acquired haemophilia who have high-titre neutralizing antibodies to human FVIII, is not known to increase the risk of arterial or venous thrombosis. We have recently encountered a patient with acquired haemophilia who developed a thrombotic left middle cerebral artery distribution stroke while being treated with pFVIII. To our knowledge, this is the first such reported thrombotic event. We speculate that platelet activation induced by pFVIII may have contributed to thrombosis and suggest that pFVIII be used with caution in elderly patients with pre-existing cardiovascular risk factors.
15471596 [Prescribing patterns of rofecoxib in the primary care setting: results of a French survey 2004 Oct OBJECTIVES: To assess the prescribing patterns of rofecoxib, a selective cyclo-oxygenase-2 inhibitor or coxib relative to those of conventional non steroidal anti-inflammatory drugs (NSAIDs) in the primary care setting in France. METHODS: A representative sample of 1010 French general practitioners participated in the study. They recorded the demographic, medical and pharmaceutical characteristics of all patients for whom they prescribed an NSAID between July 1, 2001 and June 30, 2002. RESULTS: The prescribing patterns of rofecoxib were similar for both available dosages (12.5 and 25 mg). The proportion of patients aged 65 years and older was significantly higher among those receiving rofecoxib (48%) than among those receiving a traditional NSAID (37.3%). A history of peptic ulcer or gastrointestinal bleeding was more frequent in the former (4.8%) than in the latter (2.1%). Low dose aspirin and antihypertensive agents were being taken in 6.1% and 34.8%, respectively, of the patients in the rofecoxib group versus 2.3% and 15.6%, respectively, in the conventional NSAID group. Concurrent use of a proton pump inhibitor (PPI) was marginally less frequent in the rofecoxib group (16.9%) than in the conventional NSAID group (18.6%). However, a significantly higher proportion of patients were given a PPI prior to rofecoxib therapy (10.4%) than prior to conventional NSAID therapy (3.7%). CONCLUSION: Our findings show that French general practitioners are more likely to prescribe rofecoxib for patients who have risk factors of NSAID gastropathy.
12652077 Structural studies on IgG oligosaccharides of patients with primary Sjögren's syndrome. 2002 Jan Sjögren's syndrome (SS) is an autoimmune disease, and some patients have been found to have SS complicated with rheumatoid arthritis (RA), in which IgG is known to carry abnormal N-linked oligosaccharides. In order to investigate the relationship between SS and RA, the structures of N-linked oligosaccharides of IgG from 12 primary SS patients without RA, 9 RA patients, and 8 healthy individuals were analyzed using reversed-phase high-performance liquid chromatography, in combination with sequential exoglycosidase treatment and matrix-assisted laser desorption ionization time-of-flight mass spectrometry. All of the IgG samples obtained from primary SS patients, RA patients, and healthy individuals contained the same series of biantennary complex-type oligosaccharides, but the ratio of each oligosaccharide differed among these 3 groups. The incidence of galactose-lacking N-linked oligosaccharides obtained from the IgG of RA patients was significantly higher than that from healthy individuals, but that from the serum IgG of primary SS patients varied among individuals. The patients with primary SS were classified into two groups based on the galactosylation levels of IgG oligosaccharides; one group exhibits galactosylation levels as low as those of RA patients and another exhibits levels similar to those of healthy individuals. Measurement of levels of rheumatoid factor (RF) revealed that primary SS patients with a high incidence of RF belonged to the low galactosylation group, as did RA patients. These results suggest that appearance of IgG carrying abnormal N-linked oligosaccharides in primary SS may be related to future complication with RA.
12086151 Correlation between the numbers of gammadelta T cells and CD4+ HLA-DR+ T cells in broncho- 2002 Apr CD4+ HLA-DR+ T cells are known to be increasing in broncho-alveolar lavage fluid (BALF) from patients with sarcoidosis, and related to disease activity. Although there are several reports that the number of gammadelta T cells in peripheral blood from patients with sarcoidosis are increasing, contradictory assertions can be seen about the number of gammadelta T cells in BALF, and the clinical significance on the presence of gammadelta T cells in disease site of patients with diffuse lung disease including sarcoidosis. The absolute number of gammadelta T cells and CD4+ HLA-DR+ T cells in BALF were determined by flow cytometry in 107 patients with diffuse lung diseases; 56 with sarcoidosis, 36 with collagen vascular diseases with lung involvement and 15 with idiopathic pulmonary fibrosis. We also measured the number of the transferrin receptor-positive macrophages in BALF. The correlation between gammadelta T cells and activated (maybe antigen-specific) T cells and macrophages were evaluated. Sarcoidosis patients were also evaluated from the data of the number of gammadelta T cells in peripheral blood by flow cytometry and clinical backgrounds. A significant correlation between the numbers of these two cell types was detected in each of the three patient groups. The percentage of peripheral gammadelta T cells was markedly increased in 7 sarcoidosis patients, each of whom also showed affected organs other than lung, however, 5 individuals did not show an increased number of gammadelta T cells in BALF. The number of gammadelta T cells in BALF did not correlate with the number of transferrin receptor-positive macrophages in all three patient groups. These results suggest that the increased number of gammadelta T cells in diffuse lung diseases likely plays a role in immunosurveillance and contributes to the activation of antigen-specific alphabeta T cell.
15170938 Antiagalactosyl IgG antibodies in juvenile idiopathic arthritis, juvenile onset Sjögren's 2004 Jun OBJECTIVE: To determine the normal range of antiagalactosyl IgG antibodies in healthy children, and to investigate the utility of determination of antiagalactosyl IgG antibodies in patients with juvenile idiopathic arthritis (JIA) and juvenile onset Sjögren's syndrome (SS). METHODS: Serum concentrations of antiagalactosyl IgG antibodies were measured in 225 healthy children, 68 patients with JIA (systemic arthritis in 21, polyarthritis in 29, oligoarthritis in 18), and 15 patients with juvenile onset SS, using a lectin-enzyme immunoassay employing prepared human agalactosyl IgG as antigen. A comparison was made between the prevalence and utility of antiagalactosyl IgG antibodies in patients and those of conventional rheumatoid factors (RF) determined by laser nephelometry. RESULTS: The average serum concentration of antiagalactosyl IgG antibodies for healthy controls was 2.41 +/- 0.93 arbitrary units (AU)/ml, and the cutoff value of the normal range was set at 4.3 AU/ml (mean + 2 SD). As a result, antiagalactosyl IgG antibodies were positive in 25 (37%) of 68 patients with JIA, and 14 (93%) of 15 patients with juvenile onset SS, in whom values were much higher than the frequencies of RF positivity. The serum concentrations of antiagalactosyl IgG antibodies in patients were closely correlated with those of RF. Thirteen patients with JIA and 6 patients with juvenile onset SS were positive for antiagalactosyl IgG antibodies despite being negative for RF. With regard to prognosis during followup periods of at least 5 years, JIA patients positive for antiagalactosyl IgG antibodies, even if negative for RF, were resistant to treatment. However, positivity for antiagalactosyl IgG antibodies had no relation to joint destruction. CONCLUSION: Our data suggest that antiagalactosyl IgG antibodies, compared with RF, show higher sensitivity to detect immunological disorders in JIA and juvenile onset SS.
12436372 [Gastrointestinal side effects in the therapy of rheumatologic diseases]. 2002 Nov Antirheumatic drugs may lead to a number of relevant gastrointestinal complications. Symptomatical treatments with glucocorticoids and non steroidal antirheumatic drugs (NSAD) are known to induce gastric or duodenal ulcers, above all under combination therapies. Side effects of DMARD's (methotrexate, leflunomide, hydroxy/chloroquine, sulfasalazine) include unspecifical gastrointestinal symptoms like nausea, vomiting and diarrhea as well as induction of ulcerative mucosal lesions (methotrexate) and occurrence of a hepatopathy. The latter may appear as an asymptomatical elevation of liver transaminases or cholestase parameters, but can also lead, in some cases of a monothera-py (hydroxy-/chloroqine, sulfasalazine) or combination therapy (methotrexate + leflunomide) to a fulminant hepatitis. TNF-alpha-inhibiting drugs (etanercept, infliximab) as a new generation of anti-inflammatory therapeutics don't have relevant gastrointestinal side effects according recently published data.
12846049 Five-year follow-up of 665 Hungarian patients with undifferentiated connective tissue dise 2003 May OBJECTIVE: To determine the clinical symptoms and the panel of autoantibodies of patients with early undifferentiated connective tissue disease (UCTD) followed for at least 1 year. METHODS: 716 UCTD patients with manifestations suggestive but not diagnostic of specific connective tissue disease (CTD) were recruited and followed up between 1994-1999. The patients with early UCTD were subdivided into those with isolated Raynaud's phenomenon (RP) (50 patients), unexplained polyarthritis (31 patients) and "true" UCTD (665 patients). UCTD was diagnosed on the basis of clinical manifestations suggestive of a connective tissue disease and the presence of at least one non-organ specific autoantibody. The patients' sera were tested for anti-nuclear (ANA), as well as for nine different specific autoantibodies (anti-dsDNA, -Sm, -RNP, -SSA, -SSB, -Scl-70, -centromere, -Jo1 and -PM-Scl). RESULTS: The most common clinical manifestations of UCTD included RP, arthritis/arthralgias, pleuritis/pericarditis, sicca symptoms, cutaneous involvement (photosensitivity, rash), central nervous symptoms, peripheral neuropathy, fever, vasculitis, less pulmonary involvement and myositis. 230 of the 665 true UCTD patients (34.5%) developed a defined CTD (28 systemic lupus erythematosus [SLE], 26 mixed connective tissue disease [MCTD], 19 progressive systemic sclerosis [PSS], 45 Sjögren's syndrome, 3 polymyositis/dermatomyositis [PM/DM], 87 rheumatoid arthritis [RA], and 22 systemic vasculitis. 435 of 665 patients (65.4%) remained in the UCTD state, and 82 of 665 patients (12.3%) achieved complete remission with symptoms not reappearing within the 5-year period. The highest probability of evolution to a defined CTD was during the first 2 years after onset: of 230 UCTD patients 183 (79.5%) developed major organ symptoms and signs. In particular skin and cardiac complications seemed to spread during the follow-up period in those patients who progressed to SLE. The condition of 18/50 patients with isolated RP evolved to UCTD and 3 of 31 patients with unexplained polyarthritis progressed to definite CTD (2 patients RA and one MCTD). CONCLUSION: In our study most of the UCTD patients did not develop a definite CTD, but during the follow-up period we found new clinical and serological manifestations. One-third of the UCTD patients showed progress into different types of specific CTD.
15380044 Increased circulating levels and salivary gland expression of interleukin-18 in patients w 2004 IL-18, an immunoregulatory and proinflammatory cytokine, has been shown to play an important pathogenic role in Th1-driven autoimmune disorders. In this study, we evaluated the circulating levels and salivary-gland expression of IL-18 in patients with Sjögren's syndrome (SS), a mainly Th1-mediated disease. IL-18 serum levels were measured by ELISA in 37 patients with primary SS, 42 with rheumatoid arthritis, and 21 normal controls. We demonstrated high IL-18 serum levels in SS, similar to those in rheumatoid arthritis patients and significantly higher than in controls (P < 0.01). In addition, IL-18 serum concentrations were significantly higher in anti-SSA/Ro+ and anti-SSB/La+ than in anti-SSA/Ro- and anti-SSB/La- SS patients (respectively, P = 0.01, P < 0.01). Serum IL-18 correlated strongly with anti-SSA/Ro (P = 0.004) and anti-SSB/La (P = 0.01) titers. Salivary gland IL-18 expression was investigated by single/double immunohistochemistry in 13 patients with primary SS and in 10 with chronic sialoadenitis, used as controls. The expression of IL-18 was also examined in periductal inflammatory foci in relation to the acquisition of features of secondary lymphoid organs such as T-B compartmentalization, formation of follicular dendritic cell networks, and presence of germinal-center-like structures. IL-18 expression in SS salivary glands was detected in 28 of 32 periductal foci of mononuclear cells (87.5%), while no IL-18 production by infiltrating cells was detected in patients with chronic sialoadenitis. Within the inflammatory foci, IL-18 immunoreactivity co-localized almost exclusively with CD68+ macrophages. In addition, IL-18 was found in 15 of 19 foci (78.9%) with no evidence of T-B cell compartmentalization (nonsegregated) but in 100% of the segregated aggregates, both in T- and B-cell-rich areas. Strikingly, IL-18 was strongly expressed by CD68+ tingible body macrophages in germinal-centre-like structures both in SS salivary glands and in normal lymph nodes. IL-18 expression was observed in the ducts of all SS biopsies but in only 4 of 10 patients with nonspecific chronic sialoadenitis (P < 0.01). This study provides the first evidence of increased circulating levels and salivary gland expression of IL-18 in SS, suggesting an important contribution of this cytokine to the modulation of immune inflammatory pathways in this condition.
12632414 Heterogeneity of response of rheumatoid synovium cell subsets to interleukin-18 in relatio 2003 Mar OBJECTIVE: To examine the differential response of rheumatoid arthritis (RA) synovium cell subsets to interleukin-18 (IL-18), the effect of IL-18 on Th1-cytokine production, and the regulation of IL-18 by IL-18 binding protein (IL-18BP). METHODS: RA fibroblast-like synoviocytes were stimulated with IL-1 beta, IL-12, and IL-18, and levels of IL-6 were measured by enzyme-linked immunosorbent assay (ELISA). Expression of IL-18 receptor alpha and beta chains (IL-18R alpha and IL-18R beta, respectively), interferon-gamma (IFN gamma), and IL-17 messenger RNA (mRNA) by peripheral blood mononuclear cells, by total RA synovium cells containing T cells obtained after collagenase digestion, and by RA fibroblast-like synoviocytes was determined by reverse transcription-polymerase chain reaction. Levels of IFN gamma were measured by ELISA. RESULTS: IL-1 beta and, less effectively, IL-12 could induce RA fibroblast-like synoviocytes to produce IL-6, but IL-18 failed to have an effect. Although IL-18R alpha mRNA was constitutively expressed by RA fibroblast-like synoviocytes, IL-18R beta could not be detected, either with or without stimulation with IL-1 or IL-12. Total RA synovium cells containing T cells showed a strong expression of both IL-18R alpha and IL-18R beta mRNA, and only IL-18R beta was up-regulated by IL-12. The combination of IL-12 and IL-18 synergistically up-regulated IFN gamma mRNA expression by total RA synovium cells containing T cells, but down-regulated that of IL-17. IL-12-induced IFN gamma production by total RA synovium cells containing T cells was increased by additional IL-18 and decreased by IL-18BP. CONCLUSION: These results indicate that IL-18 plays an important role in RA inflammation and joint destruction via T cells and macrophages, but it does not have a direct effect on fibroblast-like synoviocytes. IL-18BP may be a tool for RA therapy because of its ability to neutralize endogenous IL-18.
14994395 Sensitivity and specificity for primary Sjögren's syndrome of IgA and IgG anti-alpha-fodr 2004 Mar OBJECTIVE: To investigate the sensitivity and specificity of anti-alpha-fodrin antibodies in patients with primary Sjögren's syndrome (pSS). METHODS: IgA and IgG anti-alpha-fodrin antibodies were measured in the sera of 80 patients with pSS, 60 blood donors matched for age and sex, 50 patients with systemic lupus erythematosus (SLE), 30 with rheumatoid arthritis (RA), 20 with systemic sclerosis (SSc), and 10 with polymyositis or dermatomyositis (PM/DM) by an ELISA method employing recombinant human alpha-fodrin as antigen. RESULTS: The sensitivity of IgA and IgG anti-alpha-fodrin antibodies for pSS was 32.50% and 21.25%, respectively. When the prevalence of these antibodies in patients with SLE, RA, SSc, and PM/DM was evaluated, we observed specificity of these antibodies of 68.18% and 79.09%, respectively. The sensitivity and specificity for pSS of the combined determination of IgA and IgG anti-alpha-fodrin antibodies were 40% and 58.18%, respectively. CONCLUSION: The prevalences of IgA and IgG anti-alpha-fodrin antibodies in our patients with pSS and other chronic autoimmune diseases have induced us to doubt their use as diagnostic markers of pSS.
15043120 Septic arthritis in a patient with juvenile rheumatoid arthritis. 2004 Jan The acute flare of joint inflammation in the child with known juvenile rheumatoid arthritis causes concern primarily regarding the need for additional or modified medical treatment. Acute joint inflammation in an otherwise healthy child creates concern regarding the existence of joint infection. In the early phase of disease, the clinical findings and symptoms of an inflamed joint attributable to juvenile rheumatoid arthritis or infection may be similar and difficult to differentiate from the other. Juvenile rheumatoid arthritis usually is well controlled by medical interventions, however, the initiation of specific treatment is more urgent in children with joint sepsis. The following case report is presented to emphasize the difficulty in evaluation of patients with known juvenile rheumatoid arthritis and coexistent septic arthritis, and to discuss the methods used to differentiate between the two conditions.
12114303 The use of pupillometry in joint and connective tissue diseases. 2002 Jun The central and peripheral nervous systems are variably affected in the rheumatic diseases. Automated standardized infrared pupillometry allows the safe, noninvasive assessment of the pupillary innervation. Pupillometry has already been used in studying the autonomic nervous system (ANS) in various rheumatic diseases. In systemic lupus erythematosus, the irideal parasympathetic branch of ANS was more affected then the sympathetic branch. In Sjögren's syndrome, signs of pupillary parasympathetic denervation have been reported. In rheumatoid arthritis, pupil parasympathetic dysfunction has been shown to correlate with ocular dryness. In systemic sclerosis (SSc), both sympathetic and parasympathetic irideal impairment have been demonstrated. Beside providing autonomic innervation, sensory nerves fibers are able to control iris diameter. Exogenous ocular instillation of substance P (SP), a sensory neuropeptide, can determine an omathropine-resistant, non-cholinergic myosis, acting on specific receptors present on the iris sphincter muscle. We first studied pupillary SP-ergic responsiveness in SSc, evaluating substance P (SP)-stimulated pupillary diameters by pupillometry. A higher basal and SP-stimulated myosis was found in lSSc versus both dSSc and controls, whereas no differences existed between dSSc and controls. From the literature, the pupillary parasympathetic nervous system seems to be more affected than the sympathetic branch of ANS in the rheumatic diseases characterized by an inflammatory status. However, we found in SSc both sympathetic and parasympathetic pupil control to be equally impaired. From our experience, we conclude that pupillary nervous control is differently affected in the two subsets of SSc, and that the SP-ergic system seems to be impaired only in lSSc.
12133752 Low Fcgamma receptor III and high granulocyte colony-stimulating factor serum levels corre 2002 Aug 1 PURPOSE: To determine whether serum levels of soluble Fcgamma receptor III and granulocyte colony-stimulating factor (G-CSF) are associated with the risk of infection in patients with neutropenia due to Felty's syndrome or systemic lupus erythematosus. SUBJECTS AND METHODS: Serum levels of G-CSF and soluble Fcgamma receptor III were measured by enzyme-linked immunosorbent assays in 13 patients with neutropenia due to Felty's syndrome, 10 patients with neutropenia due to systemic lupus erythematosus, and 41 controls with normal leukocyte counts (25 with systemic lupus erythematosus, 16 with rheumatoid arthritis). We calculated the area under the receiver operating characteristic (ROC) curves for the absolute neutrophil count, soluble Fcgamma receptor III levels, and G-CSF levels. RESULTS: Nine of the neutropenic patients (7 with Felty's syndrome, 2 with lupus) had one or more infections within 3 months before and after blood samples were obtained. Absolute neutrophil counts were similar in neutropenic patients who did or did not have infections. However, the median level of soluble Fcgamma receptor III (63 vs. 126 arbitrary units, P = 0.005) was significantly lower among patients who developed infections, whereas the median level of G-CSF (90.9 vs. 53.3 pg/mL, P = 0.04) was significantly higher compared with patients without infections. The area under the ROC curve was 0.58 (P = 0.49) for the absolute neutrophil count, 0.84 (P = 0.007) for soluble Fcgamma receptor III levels, and 0.73 (P = 0.03) for G-CSF levels. CONCLUSION: In patients with chronic neutropenia due to rheumatic diseases, low soluble Fcgamma receptor III levels and elevated G-CSF levels are better indicators of the risk of infection than is the neutrophil count.
11928375 [The antisynthetase syndrome: a subgroup of inflammatory myopathies not to be unrecognized 2002 Mar PURPOSE: Antisynthetase syndrome (AS) is frequently revealed by interstitial lung disease and arthritis. There are mechanic's hand, Raynaud's phenomenon and anti aminoacyl t-RNA synthetase antibodies. The anti JO-1 antibody is the most frequently identified. We report five cases of antisynthetase syndrome with particular clinical features and good response to corticosteroids. METHODS: There are three women and two men with a median age of 59 years at presentation (range: 44-77). Three patients progressively developed AS: the symptoms are dyspnea (three). Raynaud's phenomenon (one), purpura (one) and hyperkeratosis, scaling and fissuring on the lateral sides of the fingers (two). Patients always had skin signs: hyperkeratosis and scaling (five), purpura (one), Raynaud's phenomenon with normal capillaroscopy (two). Lung disease is present in the five cases with interstitial lesions in CT scans (five), trouble of CO diffusion (three/three) and lymphocytic alveolitis (two/two). Moderate muscular disorders are present in five cases (moderate elevated muscular enzyme: five, positive muscle histology: two). Anti-JO-1 antibodies are present in five cases. AS is associated with connective tissue diseases: rheumatoid polyarthritis in one case and Gougerot-Sjögren in three cases. No malignant tumour is associated. Patients have received oral corticosteroid treatment (five/five) with high doses of intravenous perfusions (three/five) with, initially, a good response. For only one patient, immunosuppressive treatment was necessary because of the articular relapse. The interstitial lung disease had a good response to corticosteroids therapy alone in four cases. Because of the relapse during the tapering off of corticosteroids, corticosteroids were increased in one case and immunosuppressive therapy was required in one case. CONCLUSION: The prognosis of AS depends of the interstitial lung disease. High doses of corticosteroids are required. In our study, the response to corticosteroids is good. Immunosuppressive agents must be added in severe and progressive form of interstitial lung disease in AS.
12436177 Immunoglobulin E-rheumatoid factor in juvenile rheumatoid arthritis. 2002 Sep OBJECTIVES: To determine the presence of immunoglobulin E-rheumatoid factor in patients with juvenile rheumatoid arthritis and to correlate it with clinical and laboratory parameters. METHODS: A multicenter prospective study was carried out from January 1993 to January 1999 with the enrollment of 3 centers of pediatric rheumatology. Ninety-one children with juvenile rheumatoid arthritis diagnosed according to the American College of Rheumatology criteria were studied: 38 (42%) with systemic, 28 (31%) with pauciarticular, and 25 (27%) with polyarticular onset. Ages ranged from 2.1 years to 22.6 years (mean 10.5 +/- 4.7), with 59 (65%) girls. The control group consisted of 45 healthy children. The detection of immunoglobulin E-rheumatoid factor was carried out utilizing an enzyme-linked immunosorbent assay. Associations of immunoglobulin E-rheumatoid factor with immunoglobulin M-rheumatoid factor (latex agglutination test), total serum immunoglobulin E, erythrocyte sedimentation rate, antinuclear antibody, and functional and radiological classes III or IV were analyzed. RESULTS: Positive immunoglobulin E-rheumatoid factor was found in 15 (16.5%) of the 91 children with juvenile rheumatoid arthritis: 7 (18.5%) with systemic, 5 (18%) with pauciarticular, and 3 (12%) with polyarticular onset. A significant correlation was observed between immunoglobulin E-rheumatoid factor and total serum immunoglobulin E in the juvenile rheumatoid arthritis patients. No correlation was found between immunoglobulin E-rheumatoid factor and positive latex agglutination slide test, erythrocyte sedimentation rate, antinuclear antibody, or the functional and radiological classes III or IV in any disease onset group. In 4 out of 45 control children (8.9%), immunoglobulin E-rheumatoid factor was positive but with no correlation with total serum immunoglobulin E levels. CONCLUSIONS: Immunoglobulin E-rheumatoid factor could be detected in 16.5% of juvenile rheumatoid arthritis patients, particularly in those with high levels of total serum immunoglobulin E, and immunoglobulin E-rheumatoid factor appears not to be associated with disease activity or severity.
15383405 Risk of connective tissue disorders among breast implant patients. 2004 Oct 1 In a US retrospective cohort study (1960-1996), 351 (4.8%) of 7,234 patients with breast implants and 62 (2.9%) of 2,138 patients who had undergone other types of plastic surgery reported subsequent rheumatoid arthritis (RA), scleroderma, systemic lupus erythematosus, or Sjögren's syndrome (relative risk = 2.0, 95% confidence interval (CI): 1.5, 2.8). Risks of RA, scleroderma, and Sjögren's syndrome were elevated both before and after 1992, when the Food and Drug Administration changed the status of breast implants to investigational. When records for these diseases were retrieved (35-40% retrieval rate) and blindly reviewed, two expert rheumatologists assessed only a minority of the cases as being "likely" (e.g., regarding RA, 16.5% for implant patients and 23.5% for comparison patients). Recalculation of incidence rates using "likely" diagnoses found relative risks of 2.5 (95% CI: 0.8, 7.8) for RA, scleroderma, and Sjögren's syndrome combined and 1.9 (95% CI: 0.6, 6.2) for RA only. When the proportions deemed "likely" were applied to all self-reports, the estimated relative risks were 2.0 (95% CI: 0.7, 5.4) for the three disorders combined and 1.3 (95% CI: 0.5, 3.8) for RA. These results indicate that self-reports of connective tissue disorders are influenced by reporting and surveillance biases. Given the diagnostic complexities of these diseases, excess risks, if they exist, may be beyond detection even in a study of this size.
17041479 Rheumatoid nodulosis: is it a different subset of rheumatoid arthritis? 2003 Oct Rheumatoid nodulosis is an entity that describes a particular variant of polyarthritis associated with early manifestations of palindromic rheumatism, radiologic subchondral bone cysts, and subcutaneous rheumatoid nodules. This study describes the clinical, radiologic, histologic, crystallographic, and laboratory findings, as well as the outcome in a group of 16 patients with rheumatoid nodulosis that were followed for a period of 1-12 years. Six of these patients had an aggressive course and developed classic erosive polyarticular rheumatoid arthritis, while the others continued having episodic arthritis without erosive disease. Seven patients had cholesterol crystals in olecranon bursae containing nodules. Second-line drugs used to control the articular manifestations did not improve the nodulosis, erosive, or cystic subchondral bone changes. Rheumatoid nodulosis mimics several other rheumatic diseases, and in about 40%, classic erosive rheumatoid arthritis develops. The presence of cholesterol crystals in rheumatoid nodules or affected bursae can increase the confusion with other crystal-induced arthritis, in particular, tophaceous monosodium urate gout or xanthomatosis.
18033994 Role of interleukin-17 in cartilage and bone destruction in rheumatoid arthritis. 2004 Apr 30 Interleukin 17 is a newly discovered inflammatory cytokine produced by T cells. Although pathogenesis of rheumatoid arthritis is still unknown more and more data show that IL-17 has an influence in this process. The concentration of this interleukin is very high locally in the joint fluid and synovium of the patients with rheumatoid arthritis. The most recent studies show, that IL-17 is situated at the top of inflammatory cascade and stimulates fibroblasts, synovial cells and macrophages to higher production of proinflammatory cytokines. Moreover IL-17 initiates the loss of proteoglycans and stimulates increased production of enzymes in chondrocytes causing degradation of collagen. Rheumatoidal synovial fibroblasts produce metalloproteinases, which can be regulated by IL-17 in the presence of proinflammatory cytokines. It is suggested, that IL-17 stimulates osteoblasts to synthesis of prostaglandin E2 (PGE2) and expression of receptor gene NF - kappa ss (RANK), which induces osteclastogenesis. Probably IL-17 is responsible for intensive resorption of bone tissue in rheumatoid arthritis. It seems, that IL-17 plays an important role in the immunological response and in the destruction of cartilage and bone tissue in rheumatoid arthritis. The deeper understanding of the mechanism of IL-17 action on the cartilage and bone cells may help to introduce the new methods of treatment in rheumatoid arthritis.
11992763 Acute lethal encephalopathy in systemic juvenile rheumatoid arthritis. 2002 Apr Macrophage activation syndrome is the most common cause of death in children with systemic juvenile rheumatoid arthritis. We present a first patient with systemic juvenile rheumatoid arthritis in which acute necrotizing encephalopathy developed as a complication of macrophage activation syndrome but not of Reye's syndrome. The suspected mechanism of this lethal complication is discussed.
15690560 Acute hypoxic respiratory failure as the first manifestation of systemic-onset juvenile rh 2004 Dec Systemic onset juvenile rheumatoid arthritis is the most common rheumatologic disorder of childhood. Pleuropulmonary manifestations are rare in children in this multiorgan disease, and are usually not severe. The diagnosis of systemic onset juvenile rheumatoid arthritis is made by exclusion, in the presence of clinical findings constellation. We present the case of an 8-year-old girl who developed acute hypoxic respiratory failure as the first manifestation of systemic onset juvenile rheumatoid arthritis, then severe respiratory relapse 16 months later. Clinical and radiological improvement were achieved at both times after high dose pulse methylprednisolone therapy.