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ID PMID Title PublicationDate abstract
16827378 [Analysis of short-term results of post total knee arthroplasty using TC-Dynamic posterior 2006 Jun OBJECTIVE: To assess the feasibility, safety, and validity of the TC-Dynamic posterior stabilized prostheses implanted in the total knee arthroplasty (TKA). METHODS: Twelve knees of 10 patients (the TC-Dynamic group) were followed up, who had been implanted with the TC-Dynamic posterior stabilized prostheses from September 2003 to March 2004. Preoperative KSS knee scores were 16.08 +/- 11.58, function scores 13.75 +/- 19.79, and the range of motion (ROM) of the knee 75.00 +/- 26.46 degrees. Meanwhile, 50 knees of 30 patients (the Scorpio group) were followed up, who had undergone TKA with the Scorpio posterior stabilized prostheses. Preoperative KSS knee scores were 19.48 +/- 9.67, function scores 3.16 +/- 19.82, and the ROM of the knee 80.80 +/- 22.82 degrees. The anteroposterior and lateral X-ray films of each knee were examined before and after operation. The statistical Z-test was used to analyze the differences between the 2 groups in the improvement of the KSS knee scores, function scores, and ROM after operation. RESULTS: The average of the 130 days' follow-up revealed that the patients implanted with the TC-Dynamic prostheses had an excellent result. In the TC-Dynamic group, the KSS knee scores were 88.83 +/- 4.04 with improved scores of 72.75 +/- 14.47 compared with those before operation; function scores were 79.17 +/- 5.15 with improved scores of 65.42 +/- 19.47; the ROM of the knee was 107.92 +/- 11.57 degrees with increased degrees of 32.92 +/- 32.22 degrees. Meanwhile, in the Scorpio group, the KSS knee scores were 85.68 +/- 7.36 with improved scores of 66.20 +/- 10.44 compared with those before operation; function scores were 71.40 +/- 12.70 with improved scores of 68.24 +/- 25.35; the ROM of the knee was 109.20 +/- 11.13 degrees with increased degrees of 28.40 +/- 26.41 degrees. There was no significant difference in the improvement of the KSS knee scores, function scores, and ROM after operation between the 2 groups (P > 0.01). All the X-ray films of the knees implanted with both the Scorpio prostheses and the TC-Dynamic prostheses were analyzed. No mal-alignment or lucent line with the prostheses was seen in all these X-ray films. CONCLUSION: The short-term follow-up indicates that the patients implanted with the TC-Dynamic prostheses have an excellent result. The TC-Dynamic prostheses with a scientific and proper design is more suitable for the Chinese. However, the long-term outcome of the patients implanted with the TC-Dynamic prostheses should be observed in a larger number of TKA operations. The basic surgical principles, including excision of both the cruciate ligaments and correction of the bone deformity with the proper balancing of the soft tissues in flexion and extension, are still crucial to successful TKA and to the long-term high survival rate of the knee prostheses.
15751084 Accelerating effect of an MRL gene locus on the severity and onset of arthropathy in DBA/1 2005 Mar OBJECTIVE: To analyze the influence of the genetic background of an arthritis-prone strain of mice, MRL, on the spontaneous development of arthropathy in DBA/1 mice, which histopathologically resembles enthesopathy in humans, and to clarify the strain-specific gene loci and their interactions that confer susceptibility to arthropathy. METHODS: MRL, DBA/1, (MRL x DBA/1)F(1), and (MRL x DBA/1)F(2) intercross mice were prepared, and the severity and onset of arthropathy of the ankle joints in individual mice were quantified (0-3 and 0-5 scale, respectively). A genome-wide scan of 271 male F(2) intercross mice with polymorphic microsatellite markers was performed. RESULTS: Only male DBA/1, (MRL x DBA/1)F(1), and (MRL x DBA/1)F(2) mice developed arthropathy. The macroscopic and histopathologic findings of arthropathy in the F(2) mice were similar to those in the parental DBA/1 mice, but the onset was significantly earlier. In the quantitative trait locus analysis of male F(2) mice, 1 susceptibility locus for both the severity and early onset of the disease in the region of an MRL allele, Amd1, was located at marker D10Mit259 (map position 40.0 cM), which was common to 1 of the sialadenitis susceptibility loci in MRL mice, Asm1. Another susceptibility locus for the severity and early onset of arthropathy in the region of a DBA allele, Amd2, was located at D3Mit46 (29.5 cM). These loci manifested an additive effect on the development of arthropathy. CONCLUSION: Arthropathy in DBA/1 mice is under the control of an allelic combination of gene loci, one of which is common to the locus for sialadenitis in MRL/MpJ-lpr/lpr mice.
16277677 Raloxifene reduces urokinase-type plasminogen activator-dependent proliferation of synovio 2005 Extracellular fibrinolysis, controlled by the membrane-bound fibrinolytic system, is involved in cartilage damage and rheumatoid arthritis (RA) synovitis. Estrogen status and metabolism seem to be impaired in RA, and synoviocytes show receptors for estrogens. Our aims in this study were to evaluate in healthy and RA synoviocytes the effects of Raloxifene (RAL), a selective estrogen receptor modulator (SERM), on: proliferation; the components of the fibrinolytic system; and chemoinvasion. The effects of RAL were studied in vitro on synoviocytes from four RA patients and four controls. Proliferation was evaluated as cell number increase, and synoviocytes were treated with 0.5 microM and 1 microM RAL with and without urokinase-plasminogen activator (u-PA) and anti-u-PA/anti-u-PA receptor (u-PAR) antibodies. Fibrinolytic system components (u-PA, u-PAR and plasminogen activator inhibitor (PAI)-1) were assayed by ELISA with cells treated with 0.5 microM and 1 microM RAL for 48 h. u-PA activity was evaluated by zymography and a direct fibrinolytic assay. U-PAR/cell and its saturation were studied by radioiodination of u-PA and a u-PA binding assay. Chemoinvasion was measured using the Boyden chamber invasion assay. u-PA induced proliferation of RA synoviocytes was blocked by RAL (p < 0.05) and antagonized by antibodies alone. The inhibitory effect of RAL was not additive with u-PA/u-PAR antagonism. RA synoviocytes treated with RAL showed, compared to basal, higher levels of PAI-1 (10.75 +/- 0.26 versus 5.5 +/- 0.1 microg/10(6) cells, respectively; p < 0.01), lower levels of u-PA (1.04 +/- 0.05 versus 3.1 +/- 0.4 ng/10(6) cells, respectively; p < 0.001), and lower levels of u-PAR (11.28 +/- 0.22 versus 23.6 +/- 0.1 ng/10(6) cells, respectively; p < 0.001). RAL also significantly inhibited u-PA-induced migration. Similar effects were also shown, at least partially, in controls. RAL exerts anti-proliferative and anti-invasive effects on synoviocytes, mainly modulating u-PAR and, to a lesser extent, u-PA and PAI-1 levels, and inhibiting cell migration and proliferation.
16494017 [The recent research situation of Euonymus alatus]. 2005 Dec The functions of Euonymus alatus in herbal canon, are removing blood stasis, restoring menstrual flow and killing worms, especially for gynecological diseases. The recently researches show E. alatus can depress blood sugar and blood lipid, resist hypersusceptibility, regulate immunity, and calcium abundant. It is effective for diabetes, hyperglycemia, chronic nephropathy, rheumatoid arthritis, urinary tract infection and prostate diseases, etc internal diseases, no matter singleness or together with other herbs.
16508943 Expression of platelet-derived growth factors C and D in the synovial membrane of patients 2006 Mar OBJECTIVE: To investigate the messenger RNA (mRNA) and protein expression of the recently discovered platelet-derived growth factor C (PDGF-C) and PDGF-D in the synovial membrane (SM) of patients with rheumatoid arthritis (RA) and osteoarthritis (OA) and to assess the localization and cellular source of these proteins in the SM and their functional influence on synovial fibroblasts. METHODS: Expression of mRNA for PDGFs A, B, C, and D as well as for PDGF receptor (PDGFR) alpha and beta chains in RA and OA SM samples was assessed by real-time reverse transcription-polymerase chain reaction. Protein levels of PDGF-C and PDGF-D were quantified by immunoblotting. Regional and cellular localization of PDGF-C and PDGF-D in the SM was investigated by double-staining immunohistochemistry. In addition, the influence of PDGF-D on the proliferation of synovial fibroblasts and their matrix metalloproteinase (MMP-1) mRNA expression were determined. RESULTS: The expression of mRNA for PDGFs A, B, and C and for PDGFR alpha and beta chains was comparable in RA and OA SM samples; in contrast, the expression of mRNA for PDGF-D was significantly higher in OA SM. PDGF-C protein was not differentially expressed in OA and RA. The expression of PDGF-D protein was significantly higher in RA SM (full-length and activated form). PDGF-C and PDGF-D were expressed throughout the SM (lining layer, diffuse infiltrates, and stroma) by both synovial fibroblasts and macrophages. In addition, PDGF-D increased the proliferation of synovial fibroblasts and the expression of mRNA for MMP-1. CONCLUSION: PDGF-C and PDGF-D are expressed by synovial fibroblasts and macrophages in RA and OA SMs. The levels of PDGF-D protein were significantly higher in RA SM. In addition, PDGF-D stimulated synovial fibroblast proliferation and expression of MMP-1. These findings may have pathogenetic implications for cellular transformation and matrix remodeling in the RA SM.
16203193 Non-steroidal anti-inflammatory drug (NSAID)-induced colonic strictures and perforation: a 2006 Apr Although non-steroidal anti-inflammatory drug-induced colopathy is well described, colonic perforations complicating non-steroidal anti-inflammatory drug intake are rare. We report a patient with rheumatoid arthritis who was on long-term diclofenac and presented with early colonic stricture formation and a caecal perforation, which to the best of our knowledge, has only been reported once before. It is important to suspect this diagnosis in patients on non-steroidal anti-inflammatory drug therapy who present with an acute abdomen.
16932663 Mechanisms of disease: atherosclerosis in autoimmune diseases. 2006 Feb Atherosclerosis is a pathologic process affecting blood vessels, which leads to the development of cardiovascular disease. The immune system is involved in atherogenesis and in the pathogenesis of atherosclerosis. Several autoimmune rheumatic conditions, including rheumatoid arthritis, systemic lupus erythematosus and antiphospholipid syndrome, are characterized by enhanced atherosclerosis and consequently higher cardiovascular morbidity and mortality rates. Enhanced atherosclerosis, in these diseases, can manifest as overt cardiovascular diseases, but could be detected at an earlier stage by identification of abnormal endothelial function and arterial intima-media thickening. Both classical and nonclassical risk factors are presumed to contribute to atherosclerosis progression in rheumatic diseases. As atherosclerosis can be considered to be an immune-mediated process, several experimental strategies exist for its immunomodulation, including induction of immune tolerance. In this article, we briefly review the contribution of autoimmune elements, such as autoreactive lymphocytes and autoantibodies to atherosclerosis and discuss the nature of atherosclerosis in autoimmune rheumatic diseases.
16710471 SOCS-3 negatively regulates innate and adaptive immune mechanisms in acute IL-1-dependent 2006 Jun RA is an autoimmune disease characterized by sustained imbalance between pro- and antiinflammatory immune mechanisms. The SOCS proteins are negative regulators of cytokine signaling, but to date there has been little information on their function in disease. The generation of Socs3(-/Delta vav) mice, which lack SOCS-3 in the hematopoietic and endothelial cell compartment, allowed us to explore the role of endogenous SOCS-3 during acute inflammatory arthritis. Joint inflammation in Socs3(-/Delta vav) mice was particularly severe and was characterized by increased numbers of neutrophils in the inflamed synovium, bone marrow, peripheral blood, and spleen. These features were most likely due to increased production of and enhanced responsiveness to G-CSF and IL-6 during arthritis in these mice. Local osteoclast generation and bone destruction were also dramatically increased in the absence of SOCS-3, as was macrophage activation. Finally, SOCS-3 was found to negatively regulate CD4+ T lymphocyte activation, including production of the pleiotropic cytokine IL-17. The absence of SOCS-3 therefore had dramatic effects in this disease model, with a broader impact on cellular responses than SOCS-1 deficiency. These findings provide direct in vivo evidence that endogenous SOCS-3 is a critical negative regulator of multiple cell types orchestrating inflammatory joint disease.
16273791 Laboratory monitoring of biologic therapies. 2005 Sep The purpose of this report is to provide suggested guidance concerning the monitoring of TNF blocker therapy. Since the completion of randomized trials, several new long-term safety concerns have arisen, involving mycobacterial and opportunistic infections, cytopenias, lymphoma, demyelinating disease, drug-induced lupus, congestive heart failure and hepatotoxicity. Since these serious events are rare, widespread post-marketing use and prolonged follow-up have been required to analyze their prevalence. Monitoring of TNF inhibitors is necessary to reassure physicians and patients of the continued efficacy and safety of these drugs. No published recommendations on monitoring are available. The clinician must weigh the potential clinical benefits of TNF inhibition against potential adverse effects. Patients should be evaluated carefully for the risk or presence of infection, tuberculosis and other serious adverse events by regular visits, careful clinical assessments, and an assiduous, high index of suspicion for these rare events. Tuberculin skin testing using PPD is recommended before starting treatment with any TNF inhibitor.
17014062 Rituximab for rheumatoid arthritis. 2006 Sep (1) Rituximab (RTX), a monoclonal antibody, selectively targets CD20+ B-cells that are implicated in the pathogenesis of rheumatoid arthritis (RA). (2) The use of RTX with methotrexate (MTX) results in statistically significant clinical improvements among RA patients who have an inadequate response to standard therapies, when compared to the use of MTX alone. (3) The optimal dose, duration of treatment or retreatment, long-term efficacy and safety, and placement of RTX in RA treatment algorithms need to be further investigated. (4) Health Canada has approved the combination of RTX with MTX for use in adult patients with moderate to severe active RA, who have had an inadequate response or intolerance to >1 tumour necrosis factor (TNF) inhibitor therapies.
15693704 Wild chamomile (Matricaria recutita L.) mouthwashes in methotrexate-induced oral mucositis 2005 Jan Oral mucositis is a known complication of methotrexate (MTX) therapy, but a single efficacious intervention or agent for prophylaxis or management of this side effect has not yet been identified. We report a case of MTX-induced oral mucositis in a patient with rheumatoid arthritis, who was successfully treated with Wild chamomile mouthwashes.
15934072 Interleukin-4 can be a key positive regulator of inflammatory arthritis. 2005 Jun OBJECTIVE: Development of arthritis in the K/BxN mouse model depends on the induction of high titers of antibodies against the enzyme glucose-6-phosphate isomerase (GPI), promoted by CD4(+) T cells expressing a GPI-specific transgenic T cell receptor (TCR). This study was undertaken to determine whether this strong autoantibody response depends on T cell differentiation to the Th1 or Th2 phenotype. METHODS: The roles of Th cell-biasing cytokines were investigated by introducing the interleukin-4 (IL-4) and IL-12-specific subunit p35 (IL-12p35)-knockout mutations into the K/BxN model and evaluating the impact of these deficiencies on disease. The IL-4-expressing cell types in K/BxN mice were revealed by crossing in a knockin alteration, which resulted in green fluorescent protein expression controlled by endogenous IL-4 gene-regulatory elements. Transfer experiments permitted the identification of the IL-4-producing cell type required for arthritis, and quantitative reverse transcriptase-polymerase chain reaction allowed for determination of the cytokine profile of K/BxN T cells. RESULTS: While IL-12p35 appeared dispensable for the development of arthritis, IL-4 was crucial for full development of disease. The GPI-reactive TCR of standard K/BxN mice induced the transcriptional activation of the IL-4 locus in CD4(+) T cells and eosinophils, and CD4(+) T cells were the obligatory source of IL-4 for disease. However, the cytokine profile of K/BxN T cells revealed that K/BxN arthritis is not a "pure" Th2 disease. CONCLUSION: The K/BxN model, although not a classic Th2 disease, depends critically on IL-4. The potential of IL-4 to promote inflammatory arthritis should be considered when proposing therapies for rheumatoid arthritis aimed at biasing T cells toward IL-4 production.
16861707 Increased expression of CD154 (CD40L) on stimulated T-cells from patients with psoriatic a 2007 Feb OBJECTIVES: CD40L is a costimulatory molecule and an early activation marker of T-lymphocytes. Based on the hypothesis that activated T-cells may play a role in the pathogenesis of psoriatic arthritis (PsA), we evaluated the level of CD40L expression on T-cells from patients with PsA. METHODS: We analysed 12 patients with PsA, six patients with rheumatoid arthritis (RA) and four healthy volunteers. T-cell surface expression of CD40L was evaluated using two-colour flow cytometry in (i) the resting state and (ii) following stimulation with phorbol myristate acetate/ionomycin, with or without ciclosporin (CsA)-mediated inhibition. RESULTS: Expression of CD40L was significantly increased on activated T-cells from patients with PsA, particularly those with active disease, when compared with normal individuals and patients with RA (mean percentages of CD3+ CD40L+ cells: 23.74, 11.59 and 9.57% for patients with active PsA, patients with RA and healthy volunteers, respectively). CsA-mediated inhibition of CD40L induction was equally effective in all study groups. CONCLUSION: CD40L is overexpressed on T-cells from patients with active PsA. This may indicate a role for CD40L in PsA pathogenesis. Larger-scale studies are warranted to address these issues.
17111929 [The role of regulatory T-cells in autoimmune rheumatic diseases]. 2006 Regulatory T-cells CD4+CD25+Foxp3, possessing suppressory activity, play the key role in the development of autoimmune diseases, maintenance of peripheral tolerance in transplantation immunity, and the prevention of a pathological immune response to intestinal microflora or microbial infection. A decrease in the total number of circulating CD4+CD25+ regulatory T-cells and their suppressive activity have been found in patients suffering from various autoimmune diseases, such as type 1 diabetes, multiple sclerosis, autoimmune hepatitis, psoriatic arthritis, juvenile idiopathic arthritis, and systemic lupus erythematosus (SLE). The authors of this study investigated the phenotypic characteristics of peripheral blood lymphocytes in 31 SLE patients and the effect of treatment on the content of CD4+CD25+ T-cells before and after pulse therapy with methylprednisolone and cyclophosphan. The total number of regulatory T-cells in the group of untreated patients was almost twice lower vs. the group of healthy donors. As a result of the therapy, the proportion of regulatory T-cells increased significantly, although it did not reach the values in the control group. The data from this research confirm the development of a defect of CD4+CD25+ T-cells at the active phase of SLE, and a possibility to partially correct this defect with an effective therapy.
16132613 The anti-angiogenic effect of sinomenine. 2005 Sinomenine is an alkaloid extracted from the Chinese medicinal plant, Sinomenium acutum, which has been utilized to treat rheumatoid arthritis (RA) in China for over 2000 years. Sinomenine has been shown to mediate a wide range of pharmacological actions which includes anti-inflammatory and anti-rheumatic effects. RA has been classified as a chronic immune-mediated disease that exhibits overlapping manifestation of inflammatory, abnormal cellular and hormonal immune responses with synovial hyperplasia. Since, angiogenesis is recognized to play a critical role in the development of RA and anti-angiogenic therapy has been proposed as a new therapeutic strategy for treatment of RA, we would like to see if sinomenine possesses anti-angiogenic property. In this study, sinomenine inhibited bFGF-induced proliferation of human umbilical vein endothelial cells (HUVEC) and arrested its cell cycle in G1 phase. Sinomenine disrupted tube formation of HUVEC on Matrigel and suppressed the chemotaxis of HUVEC. In addition, sinomenine reduced neovascularization in Matrigel plug assay as well as microvascular outgrowth in rat aorta ring sprouting assay. These results suggest that sinomenine inhibited bFGF-induced angiogenesis in vitro and in vivo. As the leukocytes-endothelial adhesive interactions also play an important role in inflammation, we found that sinomenine reduced the transmigration of granulocytic differentiated HL60 cells across IL-1beta activated HUVEC monolayer. Therefore, the inhibition of leukocytes migration across blood vessel walls and the anti-angiogenic effect of sinomenine may contribute towards its therapeutic mechanisms in alleviating the pathogenesis of RA.
16735693 Differential regulation of chemokine production by Fcgamma receptor engagement in human mo 2006 Aug CC chemokine ligand 1 (CCL1; I-309) is a CC chemokine that interacts with CC chemokine receptor 8, which is preferentially expressed in polarized T helper cell type 2 and Tc2 cells, in eosinophils, and in T regulatory cells. The present study, prompted by transcriptional profiling of human monocytes undergoing different forms of activation, was designed to characterize the production of CCL1 in monocytes compared with the production of other chemokines (CCL2, CCL22, and CCL18) differentially regulated by distinct activation signals. Lipopolysaccharide (LPS), interferon-gamma (IFN-gamma), interleukin (IL)-1beta, tumor necrosis factor alpha, IL-4, IL-13, IL-10, IL-6, IL-18, and combinations thereof did not induce CCL1 production in monocytes, and some of these signals stimulated production of reference chemokines. Induction of CCL1 in monocytes required engagement of Fc receptor for immunoglobulin G (FcgammaR)II and exposure to IL-1beta or LPS. This combination of stimuli results in a form of M2 (M2b, Type 2) macrophage activation. FcgammaR engagement also induced CCL22 and amplified its stimulation by IL-4. In contrast, FcgammaR stimulation inhibited the IL-10- and LPS-mediated induction of CCL18. IL-10, IL-4, and IFN-gamma inhibited induction of CCL1 by FcgammaR ligation and IL-1beta. CCL1 was present in synovial fluids and macrophages in juvenile idiopathic arthritis. Thus, regulation of CCL1 in human monocytes is unique, with an obligate requirement of FcgammaR engagement and costimulation by signals (IL-1beta and LPS), which use the myeloid differentiation primary-response protein 88 adaptor protein. Thus, CCL1 is a CC chemokine with a unique pattern of regulation associated with a distinct form of M2 (Type 2, M2b) monocyte activation, which participates in macrophage-dependent regulatory circuits of innate and adaptive immunity.
15995113 Range of motion of standard and high-flexion posterior stabilized total knee prostheses. A 2005 Jul BACKGROUND: The restoration of posterior femoral translation has been shown to be an important factor in enhancing knee flexion after total knee arthroplasty. The purpose of this study was to compare the ranges of motion associated with standard and high-flexion posterior stabilized total knee prostheses in patients managed with simultaneous bilateral total knee arthroplasty. METHODS: Fifty patients (mean age, sixty-eight years) received a standard fixed-bearing knee prosthesis in one knee and a high-flexion fixed-bearing knee prosthesis in the contralateral knee. Two patients were men, and forty-eight were women. At a mean of 2.1 years postoperatively, the patients were assessed clinically and radiographically with use of the knee-rating systems of the Knee Society and The Hospital for Special Surgery. RESULTS: The mean postoperative Hospital for Special Surgery knee score was 90 points for the knees treated with the standard fixed-bearing prosthesis and 89.4 points for those treated with the high-flexion prosthesis. At the time of the final follow-up, the knees with the standard prosthesis had a mean range of motion of 135.8 degrees (range, 105 degrees to 150 degrees ) and those with a high-flexion prosthesis had a mean range of motion of 138.6 degrees (range, 105 degrees to 150 degrees ) (p = 0.41). No knee had aseptic loosening, revision, or osteolysis. CONCLUSIONS: After a minimum duration of follow-up of two years, we found no significant differences between the groups with regard to range of motion or clinical and radiographic parameters, except for posterior femoral condylar offset.
16097922 Tumour necrosis factor inhibitors. 2005 Aug 15 The cytokine, tumour necrosis factor-alpha (TNF-alpha) plays a key role in the pathogenesis of many chronic inflammatory and rheumatic diseases, in particular, Crohn's disease, rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. Controlled trials have shown that the TNF inhibitors (etanercept, infliximab and adalimumab) significantly reduce symptoms and signs, improve function and quality of life, and reduce radiologically evident damage in patients with rheumatoid diseases. For reasons that are not entirely clear, etanercept does not work in Crohn's disease. Injection site and intravenous reactions and increased risk of infection (in particular, reactivation of tuberculosis) are associated with the use of these agents. Increased risk of lymphoproliferative disease, the development of lupus-like syndromes and demyelination, including optic neuritis and reactivation of multiple sclerosis, are under evaluation in long-term follow-up studies. The TNF inhibitors are expensive (about $18 000 per year), and in some patients need to be given continuously to maintain benefit, even in the presence of other immunosuppressive therapy.
15983635 [Pulmonary hypertension in autoimmune rheumatic diseases]. 2005 Apr OBJECTIVE: Pulmonary hypertension is a severe and rapidly progressive disease, particularly frequent in patients with rheumatic diseases. The aims of this study were the following: to determine the prevalence of pulmonary hypertension in Italian patients with autoimmune rheumatic diseases, and to evaluate if the presence of a rheumatic disease in general, or of a specific autoimmune rheumatic disease, is a risk factor for the development of pulmonary hypertension. PATIENTS AND METHODS: One hundred and thirteen Italian patients with connective tissue diseases (105 females, 8 males), aged 19 to 83 yrs, entered the study. Fifty-one had systemic sclerosis (SSc): 49 were females, 2 males, aged 34 to 83 yrs; 41 had limited cutaneous SSc, 8 diffuse cutaneous SSc, and 2 SSc sine scleroderma. Thirty-three patients had systemic lupus erythematosus (SLE): all but one were females, their age ranged from 19 to 82 yrs. Twenty-five had rheumatoid arthritis (RA): 21 females, 4 males, aged 26 to 45 yrs. Three females and one male, 51-77 yrs, had mixed connective tissue disease (MCTD). Systolic pulmonary arterial pressure (SPAP) was assessed by Doppler echocardiography. RESULTS: Twenty three patients had pulmonary hypertension, which was more frequent in MCTD than in SLE (75% vs 6.1%, p=0.0002) or in AR (20%, p=0.0313). Pulmonary hypertension was more frequent in SSc than in SLE (25.5% vs 6.1%, p=0.0028) and in limited than in diffuse SSc (21.6% vs 3.9%). SPAP was significantly related to age (r=0.35, p=0.0275), with patients with pulmonary hypertension older than patients with normal SPAP (66+/-13 vs 52+/-16 yrs, p=0.0003). CONCLUSIONS: These data show a significant association between pulmonary hypertension and autoimmune rheumatic diseases. Therefore, pulmonary hypertension assessment seems mandatory, at least in MCTD and SSc. However, more studies are needed to clarify the relationship between age and pulmonary hypertension and to verify whether the low prevalence of pulmonary hypertension we found in our SLE patients is related or not to their lower age.
16331755 Lipid profiles among US elderly with untreated rheumatoid arthritis--the Third National He 2005 Dec OBJECTIVE: Recent studies suggest that patients with active rheumatoid arthritis (RA) have adverse serum lipid profiles. We examined lipid profiles among individuals with RA in a national sample of persons aged 60 years and older. METHODS: Using data from 4862 participants (2379 men and 2483 women) aged 60 years and older in the Third National Health and Nutrition Examination Survey (1988-94), we examined lipid profiles among participants with RA who met the American College of Rheumatology (ACR) 1987 criteria and who were not taking glucocorticoids or disease modifying antirheumatic drugs (DMARD). RESULTS: Participants with RA had lower high density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I concentrations than those without RA. After adjusting for age and sex, the differences in HDL-C level between those with and those without RA were 2.5 mg/dl (95% CI 0.8 to 4.9) using > or = 3 of the ACR criteria (n of RA cases = 104) and 8.8 mg/dl (95% CI 3.2 to 14.3) using > or = 4 criteria (n of RA cases = 26). Adjusting for age, sex, race, education, smoking status, body mass index, alcohol consumption, physical activity, dietary factors, and other potential confounders attenuated the differences slightly. The multivariate difference in serum apolipoprotein A-I levels between those with and those without RA was 4.5 mg/dl (95% CI -0.8 to 9.8) using > or = 3 ACR criteria and 13.6 mg/dl (95% CI 3.2 to 24.1) using > or = 4 criteria. All individual RA disease activity measures tended to have inverse relations with HDL-C levels, but significant inverse associations were present only with the following variables: C-reactive protein [CRP; multivariate difference per 1 mg/dl of CRP, -1.3 mg/dl (95% CI -2.0 to -0.5)], presence of hand arthritis [-2.6 mg/dl (95% CI -5.0 to -0.2)], and positive rheumatoid factor [-3.4 mg/dl (95% CI -5.5 to -1.3)]. CONCLUSION: These national survey data indicate that RA not treated with DMARD or glucocorticoids is associated with adverse lipid profiles characterized by lower HDL-C and apolipoprotein A-I levels in persons aged > or = 60 years.