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ID PMID Title PublicationDate abstract
15930486 Inhibition of osteoporosis in autoimmune disease prone MRL/Mpj-Fas(lpr) mice by N-3 fatty 2005 Jun OBJECTIVE: Rheumatoid arthritis (RA) is a systemic autoimmune inflammatory disease involving the breakdown of cartilage and juxta-articular bone, which is often accompanied by decreased bone mineral density (BMD) and increased risk of fracture. Anti-inflammatory omega-3 fatty acids may prevent arthritis and bone loss in MRL/lpr mice model of arthritis and in humans. METHODS: In this study, the effect of long term feeding of 10% dietary n-3 (fish oil (FO)) and n-6 (corn oil (CO)) fatty acids begun at 6 weeks of age on bone mineral density (BMD) in different bone regions in an MRL/lpr female mouse model of RA was measured at 6, 9, and 12 months of age by dual energy x-ray absorptiometry (DEXA). After sacrificing the mice at 12 months of age, antioxidant enzyme activities were measured in spleen, mRNA for receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) was measured by RT-PCR in lymph nodes, and synovitis was measured in leg joints. RESULTS: At 6, 9 and 12 months of age, BMD was significantly higher (p < 0.05) in distal femur, proximal tibia, and lumbar spine of FO fed mice than those of CO fed mice. Spleen catalase (CAT) and superoxide dismutase (SOD) activities were also significantly higher (p < 0.01) in FO fed mice than in CO fed mice. Histology of knee joints revealed mild synovitis in CO fed mice, which was not present in FO fed mice. RT-PCR analysis of lymph nodes revealed decreased RANKL mRNA (p < 0.001) expression and enhanced OPG mRNA expression (p < 0.01) in FO fed mice compared to CO fed mice. CONCLUSIONS: These results suggest beneficial effects of long-term FO feeding in maintaining higher BMD and lower synovitis in this mouse model. These beneficial effects may be due, in part, to increased activity of antioxidant enzymes, decreased expression of RANKL, and increased expression of OPG in FO fed mice thereby altering the RANKL/OPG ratio. These significant beneficial effects on BMD suggest that FO may serve as an effective dietary supplement to prevent BMD loss in patients with RA.
15722972 Usefulness of the SCORE index as a predictor of osteoporosis in women with disabilities. 2005 Jan BACKGROUND: Osteoporosis is widely recognized as a common health problem among older women. It has also recently been identified as common in both pre- and postmenopausal women with disabilities. Although several clinical indices have been developed to identify nondisabled women likely to have low bone mineral density (BMD) when tested, studies that have tested the usefulness of these clinical indices have excluded women with disabilities. Thus, the usefulness of these indices in predicting low BMD and osteoporosis in women with disabilities is unknown. PURPOSE: This study examined the ability of one of these indices, the Simple Calculated Osteoporosis Risk Estimation (SCORE), to identify women with disabilities likely to have low BMD on screening. SAMPLE/DATA COLLECTION: Women with disabilities (N = 307) responded to the six-item SCORE index and underwent peripheral BMD screening. The sensitivity, specificity, and accuracy of the SCORE index in predicting BMD with the criterion of a T-score of
16557412 [NSAIDs and COX-2-inhibitors: current status]. 2006 May NSAIDs (non steroidal anti-inflammatory drugs) are a crucial component for the therapy of pain induced by inflammatory and degenerative joint diseases. Nevertheless their known therapeutic efficacy is contrasted by significant side effects. The recently developed selective COX-2-inhibitors appear to have a better gastrointestinal safety profile, especially relevant to patients with an increased risk for gastrointestinal ulcers and bleeding. However, this effect may similarly be reached by the combination of NSAIDs with proton pump inhibitors. Recent data relate to an elevated myocardial infarction rate in patients using COX-2-inhibitors. This risk may also occur in conventional NSAIDs. Therefore an individual risk calculation is necessary before COX-2-inhibitors or NSAIDs are used. Treatment should be performed with the lowest dosage for the shortest time possible. Combination therapy with salicylic acid seems to abolish the protective effect of COX-2-inhibitors in the GI-tract. Definite risk factors for the treatment with NSAIDs and COX-2-inhibitors have to be defined in further studies providing the best treatment schedule for an individual patient.
16736505 Functional assay of type I interferon in systemic lupus erythematosus plasma and associati 2006 Jun OBJECTIVE: Peripheral blood mononuclear cells (PBMCs) from patients with systemic lupus erythematosus (SLE) have increased expression of genes typically induced by type I interferon (IFN). However, it has been difficult to identify and quantify the factors responsible for activation of the IFN pathway in SLE. To characterize these mediators, we developed an assay that measures the functional effects of plasma or serum components on the gene expression of cultured target cells. METHODS: WISH epithelial cell line cells were cultured with medium, with recombinant IFNalpha, IFNbeta, or IFNgamma, or with 50% plasma from SLE patients (n = 73), rheumatoid arthritis (RA) patients (n = 19), or healthy donors (n = 30). Real-time quantitative polymerase chain reaction was used to determine WISH cell expression of IFN target genes, including PRKR, IFIT1, IFI44, MX1, and C1orf29 (preferentially induced by IFNalpha) and CXCL9 (Mig) (preferentially induced by IFNgamma). RESULTS: IFNalpha-regulated genes were induced by SLE plasma samples, but not by most of the RA or healthy control plasma samples. The activity in SLE plasma was inhibited >90% by anti-IFNalpha antibody, but not by anti-IFNbeta or anti-IFNgamma antibodies. The expression of each IFNalpha target gene induced by SLE plasma correlated with the expression of that gene studied ex vivo in PBMCs from the same patients and with the titer of anti-RNA binding protein (anti-RBP)-specific autoantibodies. Plasma activity paralleled PBMC expression of IFNalpha-inducible genes over time. CONCLUSION: IFNalpha in SLE plasma is a major stimulus of IFN target gene expression and is related to expression of those genes in PBMCs from SLE patients and to the titer of anti-RBP autoantibodies. These data provide additional support for the view that IFNalpha mediates immune system activation and dysregulation in SLE.
16778472 [Nonsteroidal anti-inflammatory agents--choice between disturbances of gastrointestinal tr 2006 Nonsteroidal anti-inflammatory agents are used more than 100 years. Most of them can cause undesirable effects on gastrointestinal tract: ulceration, bleeding and perforation of stomach and duodenum. Gastrointestinal toxicity is diminished when selective cyclooxygenase-2 inhibitors are used. However, recent clinical trials have showed that the use of cyclooxygenase-2 inhibitors increases the risk of cardiovascular event and cerebrovascular accident. According to the data such risk may be high using also nonselective nonsteroidal anti-inflammatory agents, however, it is lesser. Incidence rates of the cardiovascular events and cerebrovascular accidents increase due to activated thrombotic activity. Nonsteroidal anti-inflammatory agents are very useful in the management of rheumatic diseases and as pain relievers. Choosing appropriate nonsteroidal anti-inflammatory agent it is essential to consider the risk of gastrointestinal as well cardiovascular damage.
15917985 Acute renal failure due to mesangial proliferative glomerulonephritis in a pregnant woman 2006 Feb The most common form of renal involvement in Sjögren's syndrome (SS) is tubulointerstitial nephritis. Renal dysfunction is usually mild and subclinical. Glomerulonephritis (GMN) is rare in patients with SS. We report a 28-year-old multigravida patient with primary Sjögren's syndrome (pSS) and associated manifestations, who presented with acute renal failure in the 20th week of her fifth pregnancy. The complaints and clinical findings, positive Schirmer's test, findings of dry eye on ophthalmologic examination, and the salivary gland biopsy were compatible with SS. The patient exhibited no other clinical or laboratory findings indicative of other collagenous disease and/or rheumatoid arthritis. She refused renal biopsy, hesitating for fear of fetal loss; thus, based on the clinical and laboratory findings indicating rapidly progressive GMN and vasculitis, prednisolone, plasmapheresis, and one dose of cyclophosphamide were administered during the pregnancy. Hemodialysis five times weekly was performed. At the 28th week of gestation, she underwent a cesarean section due to early rupture of membranes and fetal distress. A healthy male boy was delivered. The renal biopsy performed 2 weeks after labor revealed mesangial proliferative glomerulonephritis. After the fourth cyclophosphamide treatment, her urinary output increased and she was discharged from the hemodialysis program. She remains in follow-up at our outpatient clinic free of hemodialysis for 4 months. This is the first report of mesangial proliferative GMN requiring dialysis in a pregnant pSS patient that has featured good maternal and fetal outcomes.
17121504 Total joint replacement surgery in a rural centre. 2006 Dec OBJECTIVE: To demonstrate that total joint replacement surgery can be safely and effectively performed in rural hospitals with acceptable outcomes. DESIGN: Case series. SETTING: A rural district hospital. PARTICIPANTS: PARTICIPANTS were 64 patients, 30 men and 34 women, who underwent total knee replacements (TKR); and 63 patients, 41 men and 22 women, who had total hip replacements (THR). MAIN OUTCOME MEASURES: Level of patient satisfaction following total joint replacement surgery, obtained by patient interview. Incidence of postoperative joint specific complications, for example infection, THR dislocation and manipulation under anaesthetic (MUA) of a TKR. RESULTS: None of the TKR or THR patients developed a deep wound infection. In this study 8.8% TKR patients had an MUA but all during a period of limited physiotherapy services; 5.8% THR patients suffered a dislocated prosthesis. Following TKR 95.3% patients reported to be 'happy' with the outcome of their surgery. Of the THR patients 97.0% declared they were 'happy' with their surgical outcome. CONCLUSIONS: There was a high level of patient satisfaction, low infection rate, acceptable levels of MUA for TKR and dislocation for THR following total joint replacement in our rural district hospital. The surgeons performed a medium volume of total joint replacements and an appropriate multidisciplinary team was in place. In such settings joint replacement surgery can be safely and successfully performed in rural centres to the benefit of rural patients, surgeons and GPs.
17294883 [System manifestations of primary biliary cirrhosis]. 2006 Primary biliary cirrhosis (PBC) is characterized by high frequency of systemic extrahepatic manifestations (EHM), which often precede the development of full clinical picture of PBC and play the leading part in the clinical course of the disease, sometimes determining its prognosis. The examination of 145 PBC patients (including two men) found a frequency of EHM of 72. 4%. The majority of EHM were caused by delayed-type hypersensitivity reactions, such as Sjogren syndrome, fibrosing alveolitis, autoimmune thyroiditis, tubulointerstitial nephritis, pulmonary granulomatosis/sarcoidosis, systemic scleroderma, rheumatoid arthritis, and ulcerative colitis; immunocomplex pathology including vasculites involving blood vessels of different caliber and localization and polyneuropathy was rarer. In 24.1% of PBC patients, system EHM manifestations were the first clinical signs of the disease. In 62.8% of patients with EHM their different combinations were registered. The most frequent one was a combination of Sjogren syndrome, fibrosing alveolitis, and tubulointerstitial nephritis, which was found in 16.2% of the patients. 6 7% of the patients had a combination of four EHM - Sjogren syndrome, fibrosing alveolitis, tubulointerstitial nephritis, and autoimmune thyroiditis. A long duration of PBC (more than five years from the debut), stage IV of the disease, and the presence of the rheumatoid factor in blood serum, were risk factors of the development of system PBC manifestations. In 20% of EHM patients their symptoms prevailed in the clinical picture, thus determining the severity of the condition. Three patients died of system EHM of PBC (systemic scleroderma, pulmonary granulomatosis). Thus, PBC diagnostics must be performed with taking into account system EHM found in this category of patients.
17110458 Specific antibodies to moesin, a membrane-cytoskeleton linker protein, are frequently dete 2007 Mar 15 To identify novel autoantibodies in acquired aplastic anemia (AA), we screened the sera of patients with AA possessing small populations of paroxysmal nocturnal hemoglobinuria (PNH)-type cells for the presence of antibodies (Abs) which recognize proteins derived from a leukemia cell line, UT-7. Immunoblotting using proteins derived from lysates or culture supernatants of UT-7 cells revealed the presence of IgG Abs specific to an 80-kDa protein. Peptide mass fingerprinting identified this 80-kDa protein as moesin. Enzyme-linked immunosorbent assay (ELISA) using recombinant moesin showed high titers of antimoesin Abs in 25 (37%) of 67 patients with AA. Moesin was secreted from several myeloid leukemia cell lines other than UT-7, such as OUN-1 and K562, as an exosomal protein. The presence of antimoesin Abs was significantly correlated with the presence of PNH-type cells and antidiazepam-binding inhibitor-related protein-1 (DRS-1) Abs. Patients with AA that did not show any of these 3 markers tended to respond poorly to immunosuppressive therapy. These findings suggest that a B-cell response to moesin, possibly derived from hematopoietic cells, frequently occurs in patients with AA and that detection of antimoesin Abs in combination with other markers may be useful in diagnosing immune pathophysiology in patients with AA.
16117603 Ginger--an herbal medicinal product with broad anti-inflammatory actions. 2005 Summer The anti-inflammatory properties of ginger have been known and valued for centuries. During the past 25 years, many laboratories have provided scientific support for the long-held belief that ginger contains constituents with antiinflammatory properties. The original discovery of ginger's inhibitory effects on prostaglandin biosynthesis in the early 1970s has been repeatedly confirmed. This discovery identified ginger as an herbal medicinal product that shares pharmacological properties with non-steroidal anti-inflammatory drugs. Ginger suppresses prostaglandin synthesis through inhibition of cyclooxygenase-1 and cyclooxygenase-2. An important extension of this early work was the observation that ginger also suppresses leukotriene biosynthesis by inhibiting 5-lipoxygenase. This pharmacological property distinguishes ginger from nonsteroidal anti-inflammatory drugs. This discovery preceded the observation that dual inhibitors of cyclooxygenase and 5-lipoxygenase may have a better therapeutic profile and have fewer side effects than non-steroidal anti-inflammatory drugs. The characterization of the pharmacological properties of ginger entered a new phase with the discovery that a ginger extract (EV.EXT.77) derived from Zingiber officinale (family Zingiberaceae) and Alpina galanga (family Zingiberaceae) inhibits the induction of several genes involved in the inflammatory response. These include genes encoding cytokines, chemokines, and the inducible enzyme cyclooxygenase-2. This discovery provided the first evidence that ginger modulates biochemical pathways activated in chronic inflammation. Identification of the molecular targets of individual ginger constituents provides an opportunity to optimize and standardize ginger products with respect to their effects on specific biomarkers of inflammation. Such preparations will be useful for studies in experimental animals and humans.
16600922 Cachexia: pathophysiology and clinical relevance. 2006 Apr Cachexia causes weight loss and increased mortality. It affects more than 5 million persons in the United States. Other causes of weight loss include anorexia, sarcopenia, and dehydration. The pathophysiology of cachexia is reviewed in this article. The major cause appears to be cytokine excess. Other potential mediators include testosterone and insulin-like growth factor I deficiency, excess myostatin, and excess glucocorticoids. Numerous diseases can result in cachexia, each by a slightly different mechanism. Both nutritional support and orexigenic agents play a role in the management of cachexia.
16324568 [Infectious complications associated with the use of tumor necrosis factor antagonist drug 2005 Nov Treatment with tumor necrosis factor antagonists (anti-TNF) is an innovative therapeutic approach that requires supervised administration by specialists in rheumatology and inflammatory diseases. Collaboration by infectious diseases consultants with expertise in these biological therapies is crucial to detect the development of one of the most frequent and fearsome associated adverse events: infections, particularly, tuberculosis. The tasks of these specialists include screening for tuberculosis prior to anti-TNF therapy, recommending prophylactic measures, detecting latent tuberculosis and avoiding its reactivation, and assessing potential risk and benefits before starting anti-TNF therapy. Moreover, close follow-up of on-treatment patients is mandatory to achieve early diagnosis and treatment of any infectious event caused by bacteria, fungi or mycobacteria.
16357735 Retrospective review of the clinical manifestations and outcomes in Puerto Ricans with idi 2005 Jun BACKGROUND: The idiopathic inflammatory myopathies (IIM) are a heterogeneous group of conditions characterized by chronic inflammation of muscles, resulting in skeletal muscle weakness. Racial differences are apparent in the clinical manifestations and outcome of IIM. No previous studies have been conducted to evaluate the clinical manifestations and outcome of Puerto Ricans with IIM. OBJECTIVE: The objective of this study was to describe demographic characteristics, clinical features, and functional outcome of Puerto Rican patients with IIM. METHODS: Medical records at a university medical center were reviewed retrospectively to collect data regarding demographic factors, initial presentation, diagnostic tests, serologic markers, treatment, and disease course. A Functional Grading Scale was administered to 40 of the patients with IIM to determine their functional status. RESULTS: Fifty patients with IIM were identified. Eight patients had polymyositis (PM), 23 patients had dermatomyositis (DM), 2 patients had DM/PM with coexistent malignancy, 12 patients had juvenile DM, and 5 patients had DM/PM with an associated other rheumatologic disease. At diagnosis, proximal muscle weakness was present in all patients, 15 (30%) had myalgias, 5 (10%) patients had dysphagia, and 87% had elevation of serum muscle enzymes. Visceral involvement was rare. Interstitial fibrosis was identified in only 2 patients (1 juvenile DM and 1 PM). Twenty-six patients (51%) achieved complete remission. The mean score for the Functional Grading Scale was 28.6 (maximum 30). The lowest scores were seen for patients with disease duration of less than 2 years. CONCLUSION: Puerto Ricans with IIM in this survey showed a low presence of visceral involvement, high remission rate, and low mortality.
17009243 Oncostatin M induces angiogenesis and cartilage degradation in rheumatoid arthritis synovi 2006 Oct OBJECTIVE: To investigate the role of oncostatin M (OSM) in cell adhesion, angiogenesis, and matrix degradation in rheumatoid arthritis (RA) synovial tissue and normal human cartilage. METHODS: Human dermal microvascular endothelial cell (HDMEC) and RA synovial fibroblast (RASF) proliferation and intercellular adhesion molecule 1 (ICAM-1) and vascular cell adhesion molecule 1 (VCAM-1) expression were assessed by a bromodeoxyuridine proliferation assay and flow cytometry. HDMEC tubule formation and migration were assessed by Matrigel culture and migration assay. Production of matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinases 1 (TIMP-1) in RA synovial explants, and proteoglycan/glycosaminoglycan (GAG) release, vascular endothelial growth factor (VEGF), and angiopoietin 2 production from RASF/normal cartilage cocultures were assessed by enzyme-linked immunosorbent assay and immunohistology. RESULTS: HDMEC/RASF proliferation was induced by OSM and interleukin-1beta (IL-1beta), alone and in combination. OSM enhanced cell surface expression of ICAM-1, but not VCAM-1, on endothelial cells and RASFs. OSM increased endothelial cell tubule formation and migration. In RA synovial explants, OSM induced production of MMP-1 and TIMP-1. When OSM was combined with IL-1beta, however, the MMP-1:TIMP-1 ratio was significantly increased. OSM potentiated IL-1beta-induced MMP-1 and MMP-13 expression in normal human cartilage/RASF cocultures, resulting in a significant increase in the MMP:TIMP ratio. In OSM/IL-1beta- stimulated cocultures, cartilage sections demonstrated significant proteoglycan depletion that was paralleled by a significant increase in GAG release in supernatants. Finally, compared with either cytokine alone, the combination of OSM and IL-1beta significantly induced VEGF production in RASF/cartilage cocultures. CONCLUSION: These data suggest that OSM promotes angiogenesis and endothelial cell migration and potentiates the effects of IL-1beta in promoting extracellular matrix turnover and human cartilage degradation. Furthermore, the induction of VEGF in cocultures supports the hypothesis of a link between angiogenesis and cartilage degradation.
16493080 Fibulin-4 is a target of autoimmunity predominantly in patients with osteoarthritis. 2006 Mar 1 Autoimmunity to chondrocyte-producing proteins has been reported in patients with osteoarthritis (OA) as well as in those with rheumatoid arthritis (RA). To answer whether or not OA-specific autoimmunity exist, we performed screening of chondrocyte-producing autoantigens by two-dimensional electrophoresis and Western blotting with each of 20 OA and 20 RA serum samples. We identified an apparently OA-specific autoantigen spot with a molecular mass of 52 kDa and a Isoelectric point of 4.1 as fibulin-4 by mass fingerprinting. By preparing recombinant proteins of fibulin-4, we determined prevalence of the autoantibodies to fibulin-4 in 92 patients with OA, 67 patients with RA, 40 patients with systemic lupus erythematosus, and 43 patients with systemic scleroderma. As a result, the IgG type anti-fibulin-4 autoantibodies were detected in 23.9% of sera from patients with OA, in 8.9% of sera from patients with RA, in 2.5% of sera from patients with systemic lupus erythematosus, and in 9.3% of sera from patients with systemic scleroderma. Furthermore, we immunized DBA/1J, ICR, BALB/c, and C57BL/6 mice with the recombinant fibulin-4 proteins to investigate arthritogenecity of fibulin-4. As a result, mild synovitis was detected in all of the four strains. In addition, we demonstrated expression of fibulin-4 in chondrocytes at both mRNA and protein levels in vivo and in vitro by RT-PCR, Western blotting, and immunohistochemistry. Taken together, fibulin-4, expressed in chondrocytes and recognized as an autoantigen mainly in OA rather than in RA, may play pathogenic roles in OA.
16888140 Anti-inflammatory activity of immunoglobulin G resulting from Fc sialylation. 2006 Aug 4 Immunoglobulin G (IgG) mediates pro- and anti-inflammatory activities through the engagement of its Fc fragment (Fc) with distinct Fcg receptors (FcgRs). One class of Fc-FcgR interactions generates pro-inflammatory effects of immune complexes and cytotoxic antibodies. In contrast, therapeutic intravenous gamma globulin and its Fc fragments are anti-inflammatory. We show here that these distinct properties of the IgG Fc result from differential sialylation of the Fc core polysaccharide. IgG acquires anti-inflammatory properties upon Fc sialylation, which is reduced upon the induction of an antigen-specific immune response. This differential sialylation may provide a switch from innate anti-inflammatory activity in the steady state to generating adaptive pro-inflammatory effects upon antigenic challenge.
16626426 Retinal nerve fibre layer thickness measurements in patients using chloroquine. 2006 Mar PURPOSE: Previous investigations have suggested that initial retinal damage from chloroquine toxicity occurs in ganglion cells, and other ocular tissues are affected only later on. The aim of this study was to evaluate retinal nerve fibre layer (RNFL) thickness measurements, as assessed by scanning laser polarimetry, in a group of patients under long-term treatment with chloroquine. METHODS: This case-control study included 34 patients using chloroquine diphosphate and 34 age-matched healthy subjects with no previous history of chloroquine intake. All subjects underwent RNFL assessment using the GDx -- Nerve Fibre Analyser (software v.2.0.01). One eye of each patient was randomly selected for statistical analysis. Peripapillary RNFL measurements were compared between the two groups. For patients using chloroquine, the correlation between RNFL measurements and chloroquine dosage was assessed. RESULTS: Mean +/- SD RNFL thickness for patients using chloroquine was 60.6 +/- 11.2 microm, 65.6 +/- 13.2 microm, 74.8 +/- 14.8 microm, 36.2 +/- 9.6 microm and 43.8 +/- 7.9 microm for global, superior, inferior, temporal and nasal regions, respectively. In the control group, the corresponding values were 72.1 +/- 12.7 microm, 79.9 +/- 14.8 microm, 88.3 +/- 14.0 microm, 44.2 +/- 12.8 microm and 49.7 +/- 11.9 microm. Mean RNFL thickness measurements from patients using chloroquine were significantly different from those in the control group in all regions (P < 0.05). Thinner RNFL thickness measurements were associated with higher daily dosages of chloroquine. CONCLUSION: Patients under long-term chloroquine treatment had significantly lower RNFL thickness measurements than healthy subjects, and the RNFL loss was correlated to chloroquine daily dosage.
15990993 The importance of alpha-fodrin antibodies in the diagnosis of Sjögren's syndrome. 2006 Feb OBJECTIVE: We wanted to determine the prevalence of IgA and IgG antibodies against alpha-fodrin in the patients with primary and secondary Sjögren's syndrome (SS) and also to compare with anti-Ro and anti-La antibodies in the diagnosis of SS. METHODS: We tested the prevalence of anti-alpha-fodrin IgA, IgG, anti-Ro, anti-La antibodies, anti-nuclear antibodies (ANA) and rheumatoid factor (RF) in naive patients with primary (n = 20) and secondary SS (n = 20) (Rheumatoid Arthritis [RA]+SS, n = 10; Systemic Lupus Erythematosus [SLE] + SS, n = 10), RA (n = 10), SLE (n = 10) and in healthy controls (n = 20). Salivary gland biopsies were performed in the patients with primary and secondary SS. RESULTS: In primary SS, anti-alpha-fodrin IgA, IgG, anti-Ro and anti-La antibodies were detected as 20, 10, 55 and 20% respectively. In RA + SS, anti-alpha-fodrin IgA was detected to be 10% and IgG was negative; however, anti-Ro antibodies and anti-La antibodies were found to be 40% and 20% respectively. In SLE + SS, anti-alpha-fodrin IgA was found to be 20% and IgG was found to be 10%, but anti-Ro and anti-La antibodies were found to be 90% and 20% respectively. Alpha-fodrin antibodies were not detected in RA, SLE and healthy controls. CONCLUSION: The detection of anti-alpha-fodrin antibodies by used ELISA does not give much contribution to the diagnosis of SS, and anti-Ro and anti-La are still useful serological markers in the diagnosis of SS.
16099671 Effects of the active metabolite of leflunomide, A77 1726, on cytokine release and the MAP 2005 Sep 7 Inflammatory cytokines or soluble factors are essential in the pathogenesis of rheumatoid arthritis (RA). Leflunomide is an effective disease modifying antirheumatic drug (DMARD) in RA. The objective of the present study was to evaluate for the first time the effects of A77 1726 on cytokine (interleukin (IL)-8, IL-10, IL-11 secretion and tumor necrosis factor-alpha soluble receptor I (sTNFRI)) shedding in human RA fibroblast-like synoviocytes (FLS). At 100 microM, we observed an increase in IL-10 secretion, a decrease in IL-11 release and no effect on sTNFRI shedding and IL-8 secretion in IL-1beta-stimulated human RA FLS. Furthermore, at this dose, our results also confirmed that A77 1726 decreased IL-6 and prostaglandin E2 (PGE2) synthesis while it increased IL-1 receptor antagonist secretion (IL-1Ra). The mitogen-activated protein kinases (MAPKs) represent an attractive target for RA because they can regulate cytokine expression. At 100 microM, the effect of A77 1726 on IL-10 and IL-11 secretion seemed to be associated with the status of p38 MAPK activation. Our results confirmed the immunoregulatory action of leflunomide in the cytokine network involved in RA pathogenesis. It could shift the balance from cytokine mediated inflammation to cytokine directed inhibition of the inflammatory process.
15807452 [Efficacy of colloid bismuth subcitrate (De-Nol) in gastropathies induced by nonsteroid an 2005 AIM: To evaluate efficiency of colloid bismuth subcitrate (CBS) in gastropathies induced by nonsteroid anti-inflammatory drugs (NSAID). MATERIAL AND METHODS: 45 patients with rheumatic diseases (RD) taking NSAID with gastric and/or duodenal up to 1 cm in size or multiple (more than 10) gastric mucosa erosions detected at esophagogastroduodenoscopy were randomized into two groups. Patients of group 1 (n = 30) received CBS (240 mg twice a day + amoxicillin 2 g/day and furozolidon 400 mg/day--subgroup 1a, n = 10 or CBS monotherapy in the same dose--subgroup 1b, n = 20). Patients of group 2 (n = 15) received ranitidine 150 mg twice a day. Older women, RA patients, patients with gastric ulcer prevailed. H. pylori was detected in 73.3 and 90% patients, respectively. Dispepsia and heartburn occurred in 90 and 93.3%, respectively. The efficacy was assessed after 4 weeks of therapy. RESULTS: Healing of ulcers and erosions were achieved in 22 of 26 patients of group 1 (84.6%) and in 7 of 14 (50%) of group 2 (p = 0.036, chi-square). After therapy dyspepsia persisted in 4 patients of group 1 and 9 patients of group 2. Side effects were in 3 patients on CBS. Untiulcer effect did not differ between the subgroups (88.8 and 82.4%, respectively) and was effective in 6 of 7 HP-negative patients (85.7%) and in 8 of 10 HP-positive patients (80%). CONCLUSION: De-Nol is effective in NSAID-induced gastropathies. Its action is not related with influence on HP.