Search for: rheumatoid arthritis methotrexate autoimmune disease biomarker gene expression GWAS HLA genes non-HLA genes
ID | PMID | Title | PublicationDate | abstract |
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26888573 | Atherosclerotic cardiovascular disease in patients with chronic inflammatory joint disorde | 2016 May 15 | Inflammatory joint disorders (IJD), including rheumatoid arthritis (RA), ankylosing spondylitis (ASp) and psoriatic arthritis (PsA), are prevalent conditions worldwide with a considerable burden on healthcare systems. IJD are associated with increased cardiovascular (CV) disease-related morbidity and mortality. In this review, we present an overview of the literature. Standardised mortality ratios are increased in IJD compared with the general population, that is, RA 1.3-2.3, ASp 1.6-1.9 and PsA 0.8-1.6. This premature mortality is mainly caused by atherosclerotic events. In RA, this CV risk is comparable to that in type 2 diabetes. Traditional CV risk factors are more often present and partially a consequence of changes in physical function related to the underlying IJD. Also, chronic systemic inflammation itself is an independent CV risk factor. Optimal control of disease activity with conventional synthetic, targeted synthetic and biological disease-modifying antirheumatic drugs decreases this excess risk. High-grade inflammation as well as anti-inflammatory treatment alter traditional CV risk factors, such as lipids. In view of the above-mentioned CV burden in patients with IJD, CV risk management is necessary. Presently, this CV risk management is still lacking in usual care. Patients, general practitioners, cardiologists, internists and rheumatologists need to be aware of the substantially increased CV risk in IJD and should make a combined effort to timely initiate CV risk management in accordance with prevailing guidelines together with optimal control of rheumatic disease activity. CV screening and treatment strategies need to be implemented in usual care. | |
27110949 | Association Between Serum Antibodies to Periodontal Bacteria and Rheumatoid Factor in the | 2016 Oct | OBJECTIVE: Alterations in the microbiome, including the periodontal microbiome, may be a risk factor for rheumatoid arthritis (RA). Most studies that have analyzed this association are relatively small, focus primarily on a single periodontal pathogen (Porphyromonas gingivalis), and are not population based. This study was undertaken to investigate the association between elevated serum levels of IgG antibodies to 19 periodontal species and the prevalence of rheumatoid factor (RF) in a large nationally representative sample of adults. METHODS: The Third National Health and Nutrition Examination Survey (NHANES-III) is a cross-sectional sample of the noninstitutionalized US population (n = 33,994). Our study population included all dentate participants who were 60 years and older, did not have RA as defined by a modified version of the American College of Rheumatology 1987 criteria, and had complete data for both serum IgG antibodies against periodontal bacteria and serum RF antibody titer (n = 2,461). RESULTS: Adjusted odds ratios (ORs) and 95% confidence intervals (95% CIs) summarizing the relationship between the 19 periodontal serum IgG antibodies and RF seropositivity ranged from 0.53 (95% CI 0.29-0.97) to 1.27 (95% CI 0.79-2.06), and 17 of the 19 observed ORs were <1.0. The ORs for RF seropositivity among participants with elevated Prevotella intermedia (0.53 [95% CI 0.29-0.97]) and Capnocytophaga ochracea (0.54 [0.31-0.95]) IgG levels were statistically significant. CONCLUSION: Our findings indicate that elevated levels of IgG antibodies to periodontal bacteria are mostly unassociated with RF seropositivity in the nationally representative NHANES-III. Elevated levels of antibodies to P intermedia and C ochracea are associated with lower odds of RF seropositivity. | |
28036132 | Diagnostic accuracy of salivary and serum-free light chain assays in primary Sjögren's sy | 2017 Jun | OBJECTIVE: To estimate levels of salivary and serum free light chains (FLCs) and explore its utility as a biomarker in primary Sjögren's syndrome (pSS). METHODS: Patients with pSS classified by American European Consensus group 2002 or American College of Rheumatology 2012 criteria between January 2015 and August 2015 were included. Healthy staff and non-first degree relatives of patients constituted controls. Serum and salivary FLCs were measured by immunoturbidometry using FREELITE(™) Human Kappa(κ) and Lambda(λ) Free Kit (Binding site, Birmingham, UK), on a Roche Modular P800. FLCs were compared between cases and controls using the Mann-Whitney U-test. The receiver operator characteristic curve was constructed to analyze the discriminating ability of salivary and serum kappa and lambda FLCs. RESULTS: Salivary and serum FLCs were assayed in 15 patients and 13 patients, respectively, and in 15 controls. Median age of cases and controls was 34 years. Salivary kappa and lambda FLCs were higher in pSS as compared to controls (P < 0.05 and P < 0.001, respectively). Serum kappa and lambda FLCs were also higher in pSS (both P < 0.05). Salivary lambda levels were higher in pSS with ocular signs; serum kappa and lambda levels were higher in those with ocular symptoms. A cut off of ≥ 1.1 mg/L for salivary lambda FLC had a sensitivity and specificity of 73.3% and 93.3%, respectively, for the diagnosis of pSS. Serum kappa FLC ≥ 30 mg/L had a sensitivity and specificity of 92.3% and 73.3%, respectively. CONCLUSION: Serum and salivary FLCs and in particular the latter, are potential biomarkers in pSS. Larger studies are required for validating the findings. | |
27179106 | Vitamin D treatment for connective tissue diseases: hope beyond the hype? | 2017 Feb | The prevalence of vitamin D deficiency is increased among patients with CTDs. The active form of vitamin D (calcitriol) is a potent regulator of the immune system and may suppress inflammatory responses. This has led to claims that vitamin D may be a safe treatment, or a treatment adjunct, to reduce systemic inflammation in this patient population. It is important to note, however, that there is insufficient evidence from robust clinical trials to support these novel uses for vitamin D. In this review we examine the potential role of vitamin D as a treatment adjunct for CTDs. We will discuss how vitamin D may modulate the immune response and review the current evidence for using vitamin D to treat CTDs and their associated co-morbidities. We conclude that while there is much excitement about vitamin D in this context, further well-designed trials are needed to demonstrate its efficacy in the treatment of patients with CTDs. | |
26962705 | What is the evidence for Sjögren's syndrome being triggered by viral infection? Subplot: | 2016 Jul | PURPOSE OF REVIEW: To clarify the involvement of viral infections in the pathogenesis of Sjögren's syndrome and to discuss whether viruses can be a trigger for the development of Sjögren's syndrome. RECENT FINDINGS: Although some viruses are candidate triggers of Sjögren's syndrome, we focus on human T lymphotropic virus type I (HTLV-I). Clinicoepidemiological studies show a relationship between HTLV-I and Sjögren's syndrome with a low frequency of salivary gland damage in magnetic resonance imaging, autoantibody production and ectopic germinal center in HTLV-I-associated myelopathy (HAM) patients with Sjögren's syndrome. Our recent study showed that HTLV-I has the potential to infect salivary gland epithelial cells (SGECs). After a coculture of HCT-5 (an HTLV-I-infected T-cell line derived from the cerebrospinal fluid) of an HAM patient and SGECs, we observed time-dependent increases in the levels of soluble intracellular adhesion molecule1, interferon gamma-induced protein 10 kDa and regulated on activation, normal T-cell expressed and secreted. In addition, SGECs themselves express these molecules along with the expression of HTLV-I proteins. SUMMARY: HTLV-I is involved in the pathogenesis of HTLV-I-seropositive patients with Sjögren's syndrome. By infecting CD4 T cells in vivo, HTLV-I induces specific clinicopathological conditions. In addition, HTLV-I-infected SGECs have the potential to augment the expression of molecules involved in cell adhesion, inflammation and migration. | |
25995032 | Decreased expression of thymic stromal lymphopoietin in salivary glands of patients with p | 2016 | OBJECTIVES: Thymic Stromal Lymphopoietin (TSLP) is a potent immunomodulatory cytokine involved in Th2- and Th17-mediated immune responses in different autoimmune diseases. TSLP expression in relation to disease activity was studied in salivary glands of primary Sjögren's syndrome (pSS) patients as compared to non-SS sicca (nSS) controls. METHODS: Tissue sections of minor salivary glands from pSS and nSS patients were stained with monoclonal antibodies against human TSLP, CD3, CD19 and cytokeratin high molecular weight (CK HMW) or stained for Alcian blue to detect mucus production. The number of TSLP-expressing cells was quantified and expression was correlated to local and systemic disease parameters. RESULTS: The number of TSLP-expressing cells was significantly lower in pSS patients than in nSS controls and correlated with a range of disease markers. In pSS patients, TSLP was expressed outside of lymphocytic infiltrates at sections that also encompassed high numbers of intact acinar cells. This difference was independent of tissue destruction. CONCLUSIONS: Reduced TSLP expression in pSS patients is associated with increased local and systemic inflammatory markers. Loss of TSLP expression may contribute to Th1/Th17-associated immunopathology in pSS, in line with previous studies demonstrating that TSLP promotes a protective Th2 milieu at mucosal sites. | |
26221616 | DC-Based Immunotherapy Combined with Low-Dose Methotrexate Effective in the Treatment of A | 2015 | We have previously demonstrated that semimature dendritic cell- (smDC-) based immunotherapy is effective for the treatment of collagen-induced arthritis (CIA) prior to disease onset. In the present study, we examined the efficacy of combination therapy with smDCs and methotrexate (MTX) in advanced CIA with a score of 2-3. Combination therapy with low-dose MTX and type II collagen- (CII-) pulsed smDCs (CII-smDCs) was more effective in inhibiting disease progression than high or low-dose MTX alone or a combination of high dose MTX and CII-smDCs. The effect of CII-smDCs alone was also comparable to the combination therapy. CD4(+)Foxp3(+) Treg populations and IL-10 secretion markedly increased, and CII-specific autoreactive T cells decreased in mice treated with CII-smDCs alone or in combination with MTX. Combination therapy reduced the secretion of interferon-γ (IFN-γ) and IL-17 with little influence on the IL-4 secretion in the mixed leukocyte reaction. These results imply that the combination therapy with low-dose MTX and smDCs is effective in controlling advanced CIA by enhancing Treg population and suppresses antigen-specific Th1/Th17 immunity, rather than initiating Th1 to Th2 immune deviation. Our findings provide a better understanding of the DC therapy in combination with MTX for the treatment of patients with rheumatoid arthritis (RA). | |
26725749 | Defective DNA methylation in salivary gland epithelial acini from patients with Sjögren's | 2016 Apr | The pathogenesis of primary Sjögren's syndrome (pSS) is complex, in part due to DNA methylation abnormalities. This study was undertaken to evaluate the importance of global DNA methylation ((5m)C) as determined in minor salivary glands (MSG) from well characterized pSS patients. Twenty-two pSS patients and ten controls were selected, and MSG were stained with anti-(5m)C, anti-(5m)C/anti-cytokeratin (KRT)19, or with anti-SSB/La antibodies (Ab). The DNA methylation status at the SSB gene promoter P1 and P1' was evaluated by methylation-sensitive restriction enzymes (MSRE) coupled with PCR. The effect of the DNA demethylating drug 5 azacytidine (5-Aza) was tested in the human salivary gland (HSG) cell line. In pSS, the reduction of global DNA methylation ((5m)C) was associated with lymphocyte infiltration, the emergence of (5m)C(low) and KRT19(high) acini, and the detection of circulating anti-SSB/La Ab, but not with disease activity (ESSDAI). Next, treating HSG cells with 5-Aza was effective in inducing SSB expression. Finally in pSS patients positive for anti-SSB/La Ab, we further observed DNA demethylation at the SSB gene promoter P1 with consequent SSB overexpression at both the transcriptional and protein levels in salivary gland epithelial cells. In conclusion, our results highlight the importance of DNA methylation in the pathophysiology of pSS and to the emergence of anti-SSB/La Ab. | |
26336930 | Low numbers of blood and salivary natural killer cells are associated with a better respon | 2015 Sep 4 | INTRODUCTION: In this study, we sought to address changes in blood lymphocyte subpopulations and labial salivary gland (LSG) inflammation after belimumab treatment in patients with primary Sjögren's syndrome (pSS) and to identify predictors of response to treatment. METHODS: Sequential blood lymphocyte subsets and LSG biopsies were analysed between week 0 (W0) and W28 in 15 patients with pSS treated with belimumab. Systemic response to treatment was defined as a decrease in the European League Against Rheumatism Sjögren's Syndrome Disease Activity Index score of ≥3 points at W28. RESULTS: After belimumab, we observed a decrease in blood B lymphocytes primarily involving CD27-negative/immunoglobulin D-positive naïve B cells (p=0.008). Lymphocytic sialadenitis (focus score >1) that was present in 12 patients (80.0 %) before belimumab treatment became negative in 5 of them after treatment (p=0.03). The median (interquartile range) LSG B-cell/T-cell ratio decreased from 0.58 (0.5-0.67) to 0.50 (0.5-0.5) (p=0.06). B-cell activating factor (BAFF) staining was detected in 11 (78.6 %) of 14 patients before belimumab treatment compared with 7 (50.0 %) of 14 after belimumab therapy (p=0.10). The median percentage of BAFF-positive cells in foci significantly decreased from 27.5 % (10-40) to 5 % (0-20) (p=0.03). A systemic response was achieved in six patients (40 %). The only predictor of response was the presence of a low number of natural killer (NK) cells, both in blood (8.5 % [7-10] vs 11 % [9-21]; p=0.04) and in LSG (20.6/mm(3) [20.0-21.4] vs 30.0/mm(3) [25.0-100.0], p=0.003). Serum BAFF levels did not influence response to treatment. CONCLUSIONS: Low blood and salivary NK cell numbers are associated with a better response to belimumab. This suggests that two distinct subsets of pSS may exist: one with a predominant type I interferon (IFN)-BAFF-B-cell axis, representing good responders to belimumab; and one with a predominant type II IFN-NK cell axis, representing non-responders. TRIAL REGISTRATION: ClinicalTrials.gov identifier: NCT01160666 . Registered 9 July 2010. | |
26970487 | Primary SjÓ§gren's syndrome: Clinical phenotypes, outcome and the development of biomarker | 2016 Jul | Primary SjÓ§gren's syndrome (pSS) is a complex autoimmune disease with distinct clinical phenotypes and variable outcomes. The systemic form of the disease is characterized by immune complex mediated manifestations and is complicated by lymphoma as a result of a polyclonal B cell hyperactivity that is evolving into B cell malignancy. In the past decades, well-established clinical and serological markers have been described in the literature to identify high-risk patients and to predict lymphoma development. However, specific biologic treatments have proven ineffective to control the disease. Significant research effort has been made to reveal the major underlying biological events in this subgroup and identify biomarkers for early diagnosis, prognosis and response to treatment. In this review, we summarize the current data for the proposed histological, molecular and genetic biomarkers. | |
26938585 | [Neuromyelitis optica spectrum disorders as initial presentation of Sjögren's syndrome: A | 2016 Feb 29 | Neuromyelitis Optica Spectrum Disorder (NMOSD) is a rare systemic autoimmune disease which is sometimes found in association with other autoimmune disorders including Sjogren's syndrome. Neurological manifestations occur in 20% to 25% of diagnosed cases of Sjögren's syndrome; however, less than 5% of patients with Sjögren's syndrome have neurological manifestations as the initial presenting feature of Sjögren's syndrome. We report the case of an elderly female with longitudinal myelitis as a presenting feature who had positive antibody to aquaporin-4 (NMO-IgG) and Sjögren's syndrome. | |
27988431 | Clinical utility of circulating anti-N-methyl-(d)-aspartate receptor subunits NR2A/B antib | 2017 Feb | BACKGROUND/PURPOSE: Neuropsychiatric (NP) events are found in patients with rheumatic diseases, commonly in systemic lupus erythematosus (SLE) and Sjögren's syndrome (SS). The standard nomenclature and case definitions for 19 NPSLE syndromes by the American College of Rheumatology (ACR) Committee on Research cover a wide range of NP events seen in both SLE and SS. Despite advances in the understanding of SLE and SS, NP syndromes continue to pose diagnostic challenges. Correct attribution of NP events is critical in determining the correct treatment and prognosis. Anti-N-methyl-(d)-aspartate receptor subunits NR2A/B (anti-NR2A/B) antibodies have been demonstrated in the sera of SLE and SS patients and have been associated with collective or specific NP syndromes, though not consistently. Interpretation of anti-NR2A/B antibody data in the medical literature is rendered difficult by small sample size of patient groups. By combining different studies to generate a pooled effect size, a meta-analysis can increase the power to detect differences in the presence or absence of NP syndromes. Hence, we set out to perform a meta-analysis to assess the association between anti-NR2A/B antibodies and NP syndromes in SLE and SS. METHODS: A literature search was conducted using PubMed and other databases from inception to June 2016. We abstracted data relating to anti-NR2A/B antibodies from the identified studies. The random effects model was used to calculate overall combined odds ratio (OD) with its corresponding 95% confidence interval (CI) to evaluate the relationship between anti-NR2A/B antibodies and NP syndromes in SLE and SS patients with and without NP events. We also included our own cohort of 57 SLE patients fulfilling the ACR 1997 revised classification criteria and 58 healthy controls (HCs). RESULTS: In total, 17 studies with data on anti-NR2A/B antibodies in 2212 SLE patients, 66 SS patients, 99 disease controls (DCs) (e.g. antiphospholipid syndrome, myasthenia gravis and autoimmune polyendocrine syndrome I) and 538 HCs were used in this analysis. Overall pooled prevalence of serum/plasma anti-NR2A/B antibodies was higher in SLE patients [24.6% (95% CI 18.5-32.0%)] and SS patients [19.7% (95% CI 11.8-31.0%)] compared to DCs [14.8% (95% CI 2.2-56.9)] and HCs [7.6% (95% CI 4.6-12.4%)] (p=0.001). There was a significantly greater proportion of SLE and SS patients with NP syndromes who demonstrated positivity for serum/plasma anti-NR2A/B antibody [pooled OR=1.607 (95% CI 1.041-2.479), p=0.032] as compared to SLE and SS patients without NP syndromes in 13 studies. Usable data for cerebrospinal fluid anti-NR2A/B antibodies were available in only 4 studies [pooled OR=0.831 (95% CI 0.365-1.888), p=0.658]. Among the 19 NP syndromes, serum/plasma anti-NR2A/B antibodies were not specifically associated with any NP syndrome, including cognitive dysfunction (p=0.259) and mood disorder (p=0.503). Meta-regression identified proportion of anti-double-stranded deoxyribonucleic acid antibody positivity (p=0.009) and SLE Disease Activity Index (p=0.028) as moderators for the heterogeneity of serum/plasma anti-NR2A/B antibodies. CONCLUSION: Circulating anti-NR2A/B antibody testing has a diagnostic value for NP syndromes in SLE and SS collectively. However, the evidence to date suggests that anti-NR2A/B antibody positivity cannot distinguish specific NP syndromes. | |
26807556 | Hyperviscosity in primary Sjögren's syndrome: clinical implications. | 2017 Jan | AIM: Increased serum viscosity is recognized in primary Sjögren's syndrome (pSS); however, a classic hyperviscosity syndrome (HVS) is rare. We compared the clinical and serological profile among three groups of pSS patients: (i) with HVS; (ii) with high serum viscosity (≥ 1.9 cP [centipoises]) but without HVS; and (iii) with normal viscosity (< 1.9 cP). METHODS: We identified four pSS patients with HVS and retrospectively assessed their clinical/serological features. We included as controls 62 pSS patients and registered their clinical features. We also measured the serum viscosity, C3, C4, immunoglobulins and evaluated the European League Against Rheumatism SS Disease Activity Index (ESSDAI) score at the last visit. We used χ(2) , Mann-Whitney U-tests and logistic regression analysis. RESULTS: Patients were predominantly female (95%), mean age 54 ± 14.2 years, median disease duration 9 years. All the HVS cases were diagnosed concomitantly with the onset of SS and had higher titers of immunoglobulin G (IgG), IgM, IgA and a higher prevalence of vasculitis, neutropenia, lymphopenia and splenomegaly. At the multivariate analysis, the variables vasculitis odds ratio (OR) 14.8 (95% CI 1.3-99, P = 0.02) and splenomegaly OR 25.3 (95% CI 1.68-380, P = 0.01) remained associated with HSV. Viscosity levels correlated with rheumatoid factor titers. Thirty (48.3%) patients had high viscosity but without HSV; this group had higher median ESSDAI scores and more vasculitis than patients with normal viscosity. CONCLUSION: High viscosity was present in almost half of the patients and was associated with vasculitis and higher activity scores. Conversely, HVS was infrequent and was associated with vasculitis and splenomegaly. It seems that both conditions have different physiopathological, clinical and treatment implications. | |
26658504 | Innate Immune Signaling Induces IL-7 Production, Early Inflammatory Responses, and Sjögre | 2015 Dec | PURPOSE: Innate immune signaling elicited by polyinosinic-polycytidylic acid (poly I:C) induces IL-7 production and early inflammatory responses in the salivary gland and accelerates the development of Sjögren's syndrome (SS)-like sialadenitis. Whether poly I:C can induce similar responses in the lacrimal gland (LAC) has not been characterized. In this study, we examined the early responses and pathologic changes of the LAC tissue in response to poly I:C treatment. METHODS: Poly I:C or recombinant human IL-7 was injected intraperitoneally into C57BL/6 mice, and the LAC was harvested at different time points. Expression of chemokines and cytokines in the LAC was measured by RT-PCR, immunofluorescence staining, and immunohistochemistry. Leukocytic infiltration and caspase-3 activation were analyzed by hematoxylin and eosin staining and immunohistochemistry. Serum antinuclear antibody levels were also determined. Tear secretion was measured by phenol red cotton threads. RESULTS: Administration of poly I:C induced IL-7 gene expression and protein production in the LAC. Poly I:C also induced the expression of CXCR3 ligands, monocyte chemoattractant protein-1, IL-23p19, and TNF-α in the LAC in an IL-7-dependent fashion. Similarly to poly I:C, administration of exogenous IL-7 also up-regulated these proinflammatory mediators. Furthermore, repeated administration of poly I:C to C57BL/6 mice over an 8-day period caused leukocytic infiltration and caspase-3 activation in the LAC, antinuclear antibody production, and impaired tear secretion. CONCLUSIONS: Poly I:C induces IL-7 production, early inflammatory responses, and characteristic pathologies of SS-like dacryoadenitis in non-autoimmune-prone C57BL/6 mice. These findings provide new evidence that viral infection-elicited innate immune signaling may be one of the early triggers of SS-like dacryoadenitis. | |
27833598 | Alteration of Fecal Microbiota Profiles in Juvenile Idiopathic Arthritis. Associations wit | 2016 | Alteration of gut microbiota is involved in several chronic inflammatory and autoimmune diseases, including rheumatoid arthritis, and gut microbial "pro-arthritogenic" profiles have been hypothesized. Intestinal inflammation may be involved in spondyloarthropathies and in a subset of patients affected by Juvenile Idiopathic Arthritis (JIA), the most common chronic rheumatic disease of childhood. We compared the fecal microbiota composition of JIA patients with healthy subjects (HS), evaluating differences in microbial profiles between sub-categories of JIA, such as enthesitis-related arthritis (JIA-ERA), in which inflammation of entheses occurs, and polyarticular JIA, non-enthesitis related arthritis (JIA-nERA). Through taxon-level analysis, we discovered alteration of fecal microbiota components that could be involved in subclinical gut inflammation, and promotion of joint inflammation. We observed abundance in Ruminococcaceae in both JIA categories, reduction in Clostridiaceae and Peptostreptococcaceae in JIA-ERA, and increase in Veillonellaceae in JIA-nERA, respectively, compared with HS. Among the more relevant genera, we found an increase in Clostridium cluster XIVb, involved in colitis and arthritis, in JIA-ERA patients compared with HS, and a trend of decrease in Faecalibacterium, known for anti-inflammatory properties, in JIA-nERA compared with JIA-ERA and HS. Differential abundant taxa identified JIA patients for the HLA-B27 allele, including Bilophila, Clostridium cluster XIVb, Oscillibacter, and Parvimonas. Prediction analysis of metabolic functions showed that JIA-ERA metagenome was differentially enriched in bacterial functions related to cell motility and chemotaxis, suggesting selection of potential virulence traits. We also discovered differential microbial profiles and intra-group variability among active disease and remission, suggesting instability of microbial ecosystem in autoimmune diseases with respect to healthy status. Similarly to other chronic autoimmune and inflammatory diseases, different microbial profiles, as observed among different JIA subgroups compared to HS, and potential functional acquisition related to migration, could promote inflammation and contribute to the disease pathogenesis. | |
26169749 | Optimized testing for C. trachomatis DNA in synovial fluid samples in clinical practice. | 2015 Nov | AIM: No standardized polymerase chain reaction (PCR) assay is available for detection of Chlamydia trachomatis (C. tr.) in synovial fluid (SF) for diagnostic use in clinical practice. This study tested the performance of two optimized molecular biology methods, to determine which is best suited for detecting C. tr. in SF clinical samples from patients with various rheumatologic diseases. METHODS: Two DNA extraction methods, i.e., (1) alkaline lysis and (2) QIAEX II Gel Extraction Kit® + cetyltrimethylammonium bromide (CTAB; Qiagen, Hilden, Germany), and C. tr.-omp1-152 bp PCR were tested in SF samples from a total of 329 patients with the following diagnoses: reactive arthritis (ReA; n = 10, 4 patients had posturethritic ReA), undifferentiated arthritis (UA; n = 66), rheumatoid arthritis (RA; n = 169), psoriatic arthritis (PSA; n = 12), and osteoarthritis (OA) n = 72. RESULTS: In SF samples, C. tr.-omp1-152 bp PCR in combination with alkaline lysis DNA extraction allowed detection of more C. tr.-positive samples: 3/10 (30%) ReA patients (all with posturethritic ReA) and 20/66 (38%) UA patients were positive, compared to the 0/10 (0%) patients with ReA and 1/66 (2%) with UA detected using the QIAEX II Gel Extraction Kit® + CTAB. Moreover, 2/12 (17%) SF samples from PSA patients tested positive with alkaline lysis. All samples from patients with OA and RA tested negative. CONCLUSION: Alkaline lysis in combination with C. tr.-omp1-152 bp PCR emerged as the most sensitive method for identification of C. tr. in clinical SF samples. | |
29933194 | Meta-analysis of the efficacy in treatment of primary sjögren's syndrome: Traditional Chi | 2016 Oct | OBJECTIVE: To compare the clinical efficacy of Traditional Chinese Medicine (TCM) to Western Medicine in the treatment of primary Sjögren's syndrome (pSS). METHODS: We collected randomized controlled trials of TCM vs Western Medicine for the treatment of pSS in Chinese and foreign databases. The study quality was evaluated as suggested in the Cochrane Handbook. The Meta-analysis was performed using Review Manager 5.0 statistical software. RESULTS: A total of 31 randomized controlled trials with 2137 cases were retrieved. The efficiencies of TCM and control treatments were 87.18% and 65.63% , respectively. The results of heterogeneity tests showed that the data were homogeneous (P = 0.83), thus a fixed effects model was used for analysis. The results revealed an odds ratio of 3.74 with a 95% confidence interval of 2.99-4.69. The overall effectiveness value was 11.48 (P < 0.000 01). These results suggest the efficacy of TCM therapy for pSS better than Western Medicine. CONCLUSION: Although our findings reveal that the TCM treatment of pSS had significant advantages over its counterpart, there were some flaws in the studies included. The findings warrant further investigation. | |
25916811 | ANCA-associated vasculitis in patients with primary Sjögren's syndrome: detailed analysis | 2015 Aug | OBJECTIVES: To describe the clinical presentation, management and prognosis of patients diagnosed with both primary Sjögren's syndrome (pSS) and anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). METHODS: French nation-wide survey completed by a systematic literature review. RESULTS: This work identified 7 new cases of coexisting pSS and AAV: 2 microscopic polyangiitis (MPA), 2 granulomatosis with polyangiitis (GPA), 2 anti-myeloperoxidase (MPO)-ANCA renal-limited AAV, and 1 eosinophilic granulomatosis with polyangiitis (EGPA). The systematic literature search identified 15 previously published cases. Among the 22 patients, 19 were females. Mean age at diagnosis of AAV was 63.9±9.8years. All individuals with available information experienced at least one extra-glandular manifestation attributable to pSS. p-ANCA with anti-MPO specificity were found in 76.2% (16/21), c-ANCA with anti-PR3 specificity in 14.3% (3/21) and isolated c-ANCA in 13.6% (3/22). Vasculitis involved kidneys (n=13), lungs (n=8), skin (n=6), peripheral nerves (n=5), central nervous system (n=2), small bowel (n=1), muscle (n=1), ear chondritis (n=1) and sinuses (n=1). The mean AAV follow-up was 73.5 (±120.0) months. While on treatment, disease remission occurred in 77.3% of cases, and one death was reported in the first 6months after diagnosis. CONCLUSION: This work shows that AAV may occur in patients with pSS. These are most commonly p-ANCA associated vasculitis with anti-MPO specificity. AAV may reveal an underlying pSS or arise during its evolution, but did not precede pSS in any of these cases. AAV occurrence appears to be correlated with extra-glandular manifestations of pSS. | |
27603335 | Occasional detection of thymic epithelial tumor 4 years after diagnosis of adult onset Sti | 2016 Sep | BACKGROUND: Thymoma is a T cell neoplasm arising from the thymic epithelium that due to its immunological role, frequently undercover derangements of immunity such a tumors and autoimmune diseases. METHODS: Herein, we report, to the best of our knowledge, the first description of an association between thymoma and adult onset Still disease (AOSD) in a 47-year-old man. The first one was occasionally detected 4 years later the diagnosis of AOSD, and surgically removed via right lateral thoracotomy. Histology confirmed an encapsulated thymic tumor (type AB sec. WHO-classification). RESULTS: The AOSD was particularly resistant to the therapy, requiring a combination of immunosuppressant followed by anti-IL1R, that was the only steroids-sparing treatment capable to induce and maintain the remission. The differential diagnosis was particularly challenging because of the severe myasthenic-like symptoms that, with normal laboratory tests, were initially misinterpreted as fibromyalgia. The pathogenic link of this association could be a thymus escape of autoreactive T lymphocytes causing autoimmunity. CONCLUSION: Clinicians should be always include the possibility of a thymoma in the differential diagnosis of an unusual new onset of weakness and normal laboratories data, in particular once autoimmune disease is present in the medical history. | |
27092358 | Challenges in implant-supported dental treatment in patients with Sjogren's syndrome: A ca | 2016 | Sjogren's syndrome (SS) is a systemic autoimmune disease that has several oral manifestations, with reduced salivary flow being the most prevalent. As a result of the dry mouth and irritated oral tissues, dental treatment may be challenging. In particular, a patient's satisfaction with removable prosthesis may be limited. This case report and the literature review discuss the feasibility of implant-supported dental prostheses. The clinical and functional advantages provided by implant prostheses might outweigh the slightly lower overall implant success rate in SS patients. The impacts of SS on dental treatment are summarized in this review. |