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ID PMID Title PublicationDate abstract
23990836 Radiation protection following nuclear power accidents: a survey of putative mechanisms in 2012 There are several animal experiments showing that high doses of ionizing radiation lead to strongly enhanced leakage of taurine from damaged cells into the extracellular fluid, followed by enhanced urinary excretion. This radiation-induced taurine depletion can itself have various harmful effects (as will also be the case when taurine depletion is due to other causes, such as alcohol abuse or cancer therapy with cytotoxic drugs), but taurine supplementation has been shown to have radioprotective effects apparently going beyond what might be expected just as a consequence of correcting the harmful consequences of taurine deficiency per se. The mechanisms accounting for the radioprotective effects of taurine are, however, very incompletely understood. In this article an attempt is made to survey various mechanisms that potentially might be involved as parts of the explanation for the overall beneficial effect of high levels of taurine that has been found in experiments with animals or isolated cells exposed to high doses of ionizing radiation. It is proposed that taurine may have radioprotective effects by a combination of several mechanisms: (1) during the exposure to ionizing radiation by functioning as an antioxidant, but perhaps more because it counteracts the prooxidant catalytic effect of iron rather than functioning as an important scavenger of harmful molecules itself, (2) after the ionizing radiation exposure by helping to reduce the intensity of the post-traumatic inflammatory response, and thus reducing the extent of tissue damage that develops because of severe inflammation rather than as a direct effect of the ionizing radiation per se, (3) by functioning as a growth factor helping to enhance the growth rate of leukocytes and leukocyte progenitor cells and perhaps also of other rapidly proliferating cell types, such as enterocyte progenitor cells, which may be important for immunological recovery and perhaps also for rapid repair of various damaged tissues, especially in the intestines, and (4) by functioning as an antifibrogenic agent. A detailed discussion is given of possible mechanisms involved both in the antioxidant effects of taurine, in its anti-inflammatory effects and in its role as a growth factor for leukocytes and nerve cells, which might be closely related to its role as an osmolyte important for cellular volume regulation because of the close connection between cell volume regulation and the regulation of protein synthesis as well as cellular protein degradation. While taurine supplementation alone would be expected to exert a therapeutic effect far better than negligible in patients that have been exposed to high doses of ionizing radiation, it may on theoretical grounds be expected that much better results may be obtained by using taurine as part of a multifactorial treatment strategy, where it may interact synergistically with several other nutrients, hormones or other drugs for optimizing antioxidant protection and minimizing harmful posttraumatic inflammatory reactions, while using other nutrients to optimize DNA and tissue repair processes, and using a combination of good diet, immunostimulatory hormones and perhaps other nontoxic immunostimulants (such as beta-glucans) for optimizing the recovery of antiviral and antibacterial immune functions. Similar multifactorial treatment strategies may presumably be helpful in several other disease situations (including severe infectious diseases and severe asthma) as well as for treatment of acute intoxications or acute injuries (both mechanical ones and severe burns) where severely enhanced oxidative and/or nitrative stress and/or too much secretion of vasodilatory neuropeptides from C-fibres are important parts of the pathogenetic mechanisms that may lead to the death of the patient. Some case histories (with discussion of some of those mechanisms that may have been responsible for the observed therapeutic outcome) are given for illustration of the likely validity of these concepts and their relevance both for treatment of severe infections and non-infectious inflammatory diseases such as asthma and rheumatoid arthritis.
19926120 Receptor Activator for Nuclear Factor kappa B Ligand (RANKL) as an osteoimmune key regulat 2011 Feb The strength and integrity of the human skeleton depends on a delicate equilibrium between bone resorption and bone formation. Bone resorption is an elementary cellular activity in the modelling of the skeleton during growth and development. Later in life a most important physiological process in the skeleton is bone remodelling, which is locally initiated by resorption. During remodelling bone resorption is coupled to new bone formation that ensures renewal of bone with only minor local and temporary bone loss. Cells responsible for bone resorption and subsequent bone formation are the osteoclasts and osteoblasts, respectively. The osteoclast is derived from the pluripotent hematopoietic stem cell, which gives rise to a myeloid stem cell that can further differentiate into megakaryocytes, granulocytes, monocytes/macrophages and osteoclasts. The respective bone resorbing and forming actions of osteoclasts and osteoblasts are finely coupled, so that bone mass remains remarkably stable in a healthy adult. Imbalance between osteoclast and osteoblast activities can arise from a wide variety of hormonal changes or perturbations of inflammatory and growth factors resulting in postmenopausal osteoporosis, Paget's disease, lytic bone metastases, or rheumatoid arthritis, leading to increased bone resorption and crippling bone damage. In view of the critical role of osteoclasts in diverse pathology, there has been immense effort aimed at understanding the biology of this unique cell. The present review is focused on the current knowledge of the mechanisms that regulate the functional links between bone turnover and the immune system helping us to understand the main factors that lead to bone loss observed in osteoporosis, cancer and in rheumatoid arthritis. The aim of this review paper is to consider the key molecular interactions involved in the formation of osteoclast cells in normal and pathological conditions.
23075162 Mid- term results of stryker® scorpio plus mobile bearing total knee arthroplasty. 2012 Oct 18 BACKGROUND: The mobile bearing knee system was introduced to lessen contact stress on the articular bearing surface and reduce polyethylene wear. The purpose of the current study was to investigate the mid-term results of patients undergoing total knee arthroplasties (TKAs) using Scorpio Plus Mobile Bearing Knee System (Stryker, Mahwah, NJ), and compare the outcomes between patients with osteoarthritis and osteonecrosis (OA·ON group) and patients with rheumatoid arthritis (RA group). METHODS: Eight males and 58 females were followed up for a period of 4.4- 7.6 years from June 1, 2003 to December 31, 2005. There were 53 knees with osteoarthritis, 17 knees with rheumatoid arthritis, and 6 knees with osteonecrosis. Clinical and radiographic follow- up was done using The Japanese Orthopedic Association knee rating score (JOA score) and Knee Society Total Knee Arthroplasty Roentgenographic Evaluation and Scoring System. RESULTS: With regard to the JOA score, there was significant improvement in both groups. The postoperative range of motion was between 0.8°and 116.8° in OA·ON group, and between 0.0° and 113.7° in RA group. There were no significant differences with the radiographic evaluation between two groups. Spontaneous dislocation of a polyethylene insert occurred in one patient, and deep infection was occurred in one patient. CONCLUSION: There was significant improvement with regard to the clinical and radiographic results of patients undergoing TKAs using the model. The risk of polyethylene insert dislocation related to the mobile bearing TKA is a cause for concern.
23198006 Anti-Tumor Necrosis Factor-α Induced Systemic Lupus Erythematosus(). 2012 Anti-tumor necrosis factor-alpha induced lupus (ATIL) represents a major diagnostic and therapeutic challenge. Most cases of ATIL are caused by infliximab, followed by etanercept and adalimumab. Symptoms can range from common, mild cutaneous lesions to rare, serious pleural or pericardial effusions, deep venous thrombosis, life-threatening pneumonitis, and neuritis. Constitutional symptoms often present in association with positive autoantibody serology. Diagnosis can be considered if there is a temporal relationship between symptoms and anti-tumor necrosis factor-α (TNF- α) therapy and at least one serologic and one non-serologic American College of Rheumatology criteria. Since it is contraindicated to use anti-TNF-α drugs in patients with systemic lupus erythematosus, it is recommended to perform a thorough immunological screening in any patient with polyarthritis to assure accurate diagnosis. In addition, prior to anti- TNF therapy, baseline immunological investigations (including antinuclear antibodies) should be performed, and there should be close follow up to assess the development of lupus manifestations. The main approach in the treatment of ATIL is withdrawal of the offending drug. Traditional therapy with corticosteroids and immunosuppressive agents may be required to achieve full resolution of lupus symptoms. In this review, we discuss the pathogenesis, clinical manifestations, and management of ATIL.
22751606 The inhibitor of costimulation of T cells: abatacept. 2012 Jul OBJECTIVE: T cell costimulation is a key point in the regulation of immune tolerance, immune response, and autoimmunity. T cell activation does not take place upon the simple engagement of T cell receptor; a second signal is needed to fully stimulate T cells. There are a variety of molecules that can act as costimulators, and among those CD28/CD80 signaling plays a crucial role in modulating T cell response. Cytotoxic T lymphocyte antigen-4, CD152 (CTLA4) is a physiologic antagonist of CD28, and abatacept, a synthetic analog of CTLA4, has recently been approved to treat rheumatoid arthritis. An abnormal T cell activation is also believed to sustain psoriatic disease both at skin and joint sites. We aimed to evaluate the rationale of blocking CD28/CD80 signaling and the possible use of abatacept for treating psoriatic arthritis (PsA). METHODS: We reviewed the role of CD28/CD80 signaling in promoting T cell inflammation in psoriasis and the effects of CTLA4 modulation in experimental models of psoriasis and in humans. RESULTS: CD28/CD80 seems to be crucial in stimulating T cell activation and inflammation in psoriasis, and its inhibition by CTLA4 analogs or by anti-CD28 blocking antibodies is effective against psoriasis. Few data are available on abatacept, which seems to be valuable for the treatment of PsA but less useful in the therapy of skin psoriasis. CONCLUSION: Although the CD28 molecule is crucial in activating T cells and inflammation in psoriasis, data on the efficacy of abatacept in the treatment of PsA are still not conclusive.
25386292 Infliximab-induced intertriginous psoriasis in patient with Crohn's disease. 2011 Oct 5 Tumor necrosis factor-α (TNFα) inhibition is an effective treatment of moderate-to-severe psoriasis and other diseases (rheumatoid arthritis, ankylosing spondylitis, psoriasis or Crohn's disease). We report a case of a 32-years-old patient affected by Crohn's disease since the age of 25 who started infliximab infusion after four years of treatment with prednisone and azathioprine per os without improvement. After the fifth infusion of infliximab, he developed a form of intertriginous psoriasis which was approached with topical steroid cream. The patient never presented psoriasis in the past. New onset of psoriasis in patients without history for skin diseases (as in our case) is a quite uncommon complication of TNFα inhibitor therapy. The increased production of IFNα during TNFα inhibitor therapy is a possible pathophysiologic explanation for this paradoxical effect of the anti-TNFα.
25182056 Dysfunctional Immune-Mediated Inflammation in Rheumatoid Arthritis Dictates that Developme 2011 A skewed repertoire of pro-inflammatory cytokines produced by the Th1 subset, one of the hallmarks of rheumatoid arthritis (RA), is characterized by an overabundance of pro-inflammatory cytokines. Tumor necrosis factor-α, interleukin- 1 (IL-1), IL-6, IL-7, IL-8, IL-21, IL-12/IL-23, IL-15, IL-17, IL-18, IL-32, and interferon-γ are primarily responsible for immune-mediated inflammation of RA by activating Janus kinases (JAK) -1, -2, -3, p38 kinase, C-Jun-Nterminal kinase, extracellular signal-regulated kinase 1/2 and the phosphatidylinosotide-3-kinase/Akt/mTor pathways. Activation of these signaling pathways results in up-regulation of pro-inflammatory cytokines, cyclooxygenase-2, matrix metalloproteinases, pro-angiogenesis proteins and anti-apoptosis proteins, the latter resulting in abnormal survival of activated T- and B-cells. Further, IL-17 also regulates the differentiation of CD4+ T-helper cells by inducing a Th17 T-cell subset, and a subpopulation of T-regulatory (Treg) cells. Although Treg cells are sufficiently abundant in RA synovial fluid, they fail to induce immune tolerance suggesting a functional deficiency likely coupled to putative protein kinase signaling abnormalities. The results of in vitro and studies in animal models of arthritis have indicated that inhibiting individual signaling pathways can blunt the synthesis of several of the pro-inflammatory biomarkers characteristic of human RA pathology. However, RA clinical trials indicated that small molecule inhibitors of JAK-1, -2-, 3 and/or p38 kinase while exhibiting acceptable safety and tolerability profiles have only marginal and transient clinical effectiveness. These results suggested that future RA clinical studies using these or other kinase inhibitors will have to consider strategies designed to simultaneously inhibit multiple kinase pathways.
21424891 [Erythema elevatum et diutinum]. 2011 Apr Erythema elevatum et diutinum (EED) is a rare, chronic, cutaneous, leukocytoclastic vasculitis. It is characterized by symmetric, plaques, papules and nodules occurring preferentially on the extensor aspects of the arms. An association with chronic infections, neoplasms, especially myeloproliferative diseases and paraproteinemia, as well as autoimmune disorders (rheumatoid arthritis, Crohn disease) has been described. An 83-year-old woman with EED presented with symmetric, skin colored, firm nodules on the extensor surfaces of her fingers for two years. This case report summarizes the central clinical aspects and differential diagnosis of EED as well as its therapeutic options.
23141717 The relationship between peripheral arthritis and anti-cyclic citrullinated peptide antibo 2013 Jul OBJECTIVES: Although ankylosing spondylitis (AS) primarily affects the axial skeleton, peripheral arthritis occurs in up to 35% of cases. Anti-cyclic citrullinated peptide (anti-CCP) antibodies are highly specific for rheumatoid arthritis, whereas their role in AS remains unclear. In this study we aimed to assess the prevalence of anti-CCP antibodies in AS patients with peripheral arthritis and their clinical association with peripheral arthritis. METHODS: We retrospectively selected for this study 625 AS patients who fulfilled the modified New York criteria. The patients were divided into those with and those without peripheral arthritis on smoking history, the basis of symptoms, physical examination and medical records. The presence of anti-CCP antibodies was investigated in all the patients. RESULTS: Anti-CCP antibodies were found in 4% (25/625) of the patients, and peripheral arthritis was diagnosed in 37.4% (234/625) of the patients. In multiple logistic regression, peripheral arthritis was significantly associated with female gender (P = 0.001) and the presence of anti-CCP antibodies (P = 0.001), especially with the presence of titers of anti-CCP antibodies over three times the normal upper limit of the laboratory and assay. CONCLUSIONS: Anti-CCP antibodies are occasionally present in AS, and their presence may be helpful as a serum marker for predicting peripheral arthritis.
22703581 Acquired leptin resistance by high-fat feeding reduces inflammation from collagen antibody 2012 Sep OBJECTIVES: Rheumatoid arthritis (RA) patients with high body mass index (BMI) show lower mortality than thinner patients, indicating a paradoxical effect of body mass on mortality in RA. We considered that leptin might play some part in this mechanism. Leptin regulates not only body weight, but also inflammatory processes. Furthermore, hyperleptinemia decreases sensitivity to leptin (leptin resistance). This study examined whether high-fat diet-induced hyperleptinemic obese mice with acquired leptin resistance show reduced inflammation induced by collagen antibody-induced arthritis (CAIA). METHODS: Diet therapies were induced in mice by exposure to 50% fat to obesity for 6 weeks. We examined serum leptin concentrations and leptin responses after 6 weeks and induced CAIA. Leptin effects were examined by intraperitoneal (IP) or intracerebroventricular (ICV) leptin administration after CAIA. Hindpaw swelling was monitored daily. Histopathological features were also determined at sacrifice. RESULTS: Serum leptin concentrations were approximately 5-fold higher than in normal mice. IP leptin did not inhibit food intake, but ICV leptin did. Obese mice thus acquired peripheral leptin resistance. Arthritis was reduced approximately 30% compared with normal controls and was not exacerbated by IP leptin injection, but ICV leptin injection exacerbated arthritis to levels equal to normal controls. Histopathological assessment showed that cartilage damage was reduced by 76% compared to normal controls. CONCLUSIONS: High-fat diet-induced obese mice acquired peripheral leptin resistance reducing the development of CAIA. Leptin sensitivity was associated with severity of arthritis. These results suggest that RA patients with high BMI who acquire leptin resistance may show reduced inflammation. However, the real function of leptin in the immune system remains partly unclear.
21936801 Free radicals and redox signalling in T-cells during chronic inflammation and ageing. 2011 Oct During chronic inflammation and ageing, the increase in oxidative stress in both intracellular and extracellular compartments is likely to influence local cell functions. Redox changes alter the T-cell proteome in a quantitative and qualitative manner, and post-translational modifications to surface and cytoplasmic proteins by increased reactive species can influence T-cell function. Previously, we have shown that RA (rheumatoid arthritis) T-cells exhibit reduced ROS (reactive oxygen species) production in response to extracellular stimulation compared with age-matched controls, and basal ROS levels [measured as DCF (2',7'-dichlorofluorescein) fluorescence] are lower in RA T-cells. In contrast, exposing T-cells in vitro to different extracellular redox environments modulates intracellular signalling and enhances cytokine secretion. Together, these data suggest that a complex relationship exists between intra- and extra-cellular redox compartments which contribute to the T-cell phenotype.
22710496 Dry eyes and migraines: is there really a correlation? 2012 Dec PURPOSE: The purpose of this study was to evaluate the tear film functions and clinical symptoms of patients with migraines. METHODS: This observational comparative study consisted of 33 migraine (26 women and 7 men) patients referred from neurology clinics and 33 (22 women and 11 men) control subjects referred from ophthalmology outpatient clinics. The control subjects had neither systemic nor ocular disease nor any type of headache. All 66 patients underwent a complete ophthalmic examination and diagnostic tests for dry eye, including tear break-up time, Schirmer test with topical anesthesia, lissamine green staining, and an ocular surface disease score. Patients with migraine were classified as migraine with an aura, migraine without an aura, and basilar migraine; a pain score from 1 to 4 was determined for each patient, based on the American Headache Society's Migraine Disability Assessment Test. RESULTS: Of the 33 patients who participated in the migraine group, 17 (51%) suffered from migraine with aura, 11 (33%) suffered from migraine without aura, and 5 (15%) suffered from basilar migraine. Significant differences in dry eye scores were found between the patients with migraine and the control subjects. In the migraine group, the mean tear break-up time was 7.75±2.37 seconds, whereas in the control group it was 9.15±1.93 seconds. For the Schirmer test, the migraine group had a mean value of 12.09±4.95 mm/5 minutes, whereas the control group had a mean value of 14.90±4.26 mm/5 minutes. Testing with lissamine green staining resulted in a mean value of 1.00±0.16 in the migraine group and 0.30±0.46 in the control group. In the migraine group, the mean for the ocular surface disease index scoring was 36.27±17.54. In the control group, it was 28.42±9.0. A significant difference (P<0.05) was found in the dry eye syndrome testing results between the 2 groups in this study. CONCLUSIONS: An increased frequency of dry eye disease was found to occur in patients with migraine, which might suggest that migraine headaches are related to dry eye disease. Some migraine attacks may be aggravated in the presence of dry eye syndrome.
22490758 [The efficacy and safety of low-dose rituximab in treatment of primary Sjögren's syndrome 2012 Jan OBJECTIVE: To investigate the clinical efficacy and safety of low-dose rituximab (RTX) for patients in primary Sjögren's syndrome (pSS) with thrombocytopenia. METHODS: Four pSS patients, 2 with refractory thrombocytopenia and 2 with glucocorticoid-dependent thrombocytopenia, were treated with rituximab at 100 mg, intravenous, weekly for a total of two cycles, together with prednisone 1 - 2 mg×kg(-1)×d(-1), and the counts of platelets and B-cells were evaluated. RESULTS: Efficacy of treatment was observed in all patients. The counts of platelets, at (3 - 39) × 10(9)/L baseline, increased in 1 - 2 weeks, and went up to (107 - 241) × 10(9)/L in 3 - 8 weeks. Sustained remission had been achieved for 27 - 52 weeks. The doses of prednisone were tappered to 3.75 - 7.50 mg/day in 12 weeks. One patient who relapsed at the 27th week (platelet count 47 × 10(9)/L), was retreated with 100 mg of RTX and still had good efficacy. The counts of B-cells reduced to (0.007 - 0.010) × 10(9)/L, but they did not achieved the depletion. There were no severe adverse events during RTX therapy. CONCLUSIONS: Our study has shown good efficacy and tolerability of low-dose RTX for pSS with thrombocytopenia. Low-dose RTX allows for reduction in corticosteroid doses and B-cells, while large-scale randomized double-blind controlled trials are needed to confirm the results.
20882668 Efficacy and safety of an intraoral electrostimulation device for xerostomia relief: a mul 2011 Jan OBJECTIVE: To evaluate the efficacy and safety of an intraoral electrostimulation device, consisting of stimulating electrodes, an electronic circuit, and a power source, in treating xerostomia. The device delivers electrostimulation through the oral mucosa to the lingual nerve in order to enhance the salivary reflex. METHODS: The device was tested on a sample of patients with xerostomia due to Sjögren's syndrome and other sicca conditions in a 2-stage prospective, randomized, multicenter trial. Stage I was a double-blind, crossover stage designed to compare the effects of the electrically active device with the sham device, each used for 1 month, and stage II was a 3-month open-label stage designed to assess the long-term effects of the active device. Improvement in xerostomia severity from baseline was the primary outcome measure. RESULTS: A total of 114 patients were randomized. In stage I, the active device performed better than the sham device for patient-reported xerostomia severity (P<0.002), xerostomia frequency (P<0.05), quality of life impairment (P<0.01), and swallowing difficulty (P<0.02). At the end of stage II, statistically significant improvements were verified for patient-reported xerostomia severity (P<0.0001), xerostomia frequency (P<0.0001), oral discomfort (P<0.001), speech difficulty (P<0.02), sleeping difficulty (P<0.001), and resting salivary flow rate (P<0.01). CONCLUSION: Our findings indicate that daily use of the device alleviated oral dryness, discomfort, and some complications of xerostomia, such as speech and sleeping difficulties, and increased salivary output. The results show a cumulative positive effect of the device over the period of the study, from baseline to the end of the trial.
20693261 United Kingdom Primary Sjogren's Syndrome Registry--a united effort to tackle an orphan rh 2011 Jan Primary SS (pSS) is a multi-system autoimmune disease with a prevalence and health economic impact that are comparable with RA. However, pSS research has been relatively poorly supported. The creation of a large cohort of clinically well-characterized pSS patients will provide a catalyst and valuable resources to promote high-quality pSS research. In this review, we will describe the creation of such a cohort and the associated research biobank that is currently being established in the UK--entitled United Kingdom Primary Sjögren's Syndrome Registry (UKPSSR). We will discuss the strengths and weaknesses of the design of the registry and highlight the key challenges in the establishment of the registry and the strategies that we employ to overcome these barriers. Finally, we will consider the future development of the UKPSSR including utilization and maintenance of the cohort.
22768996 Analysis of adipose tissues and stromal vascular cells in a murine arthritis model. 2012 Dec PURPOSE: Changes in body composition in rheumatoid arthritis (RA), including a reduction in skeletal muscle mass and the accumulation of visceral fat, have been identified, and the interaction between immune abnormality and metabolic disorders has received much attention. The effect of a high-fat (HF) diet and the role of adipose tissue in an arthritis model were investigated. METHODS: The effect of an HF diet on the histopathology of joints in murine type II collagen-induced arthritis (CIA) was evaluated. The morphology and adipokine production of adipose tissues were analyzed, and macrophages in the stromal vascular fraction (SVF) were counted by flow cytometry. Serum adipokine levels were measured by ELISA. RESULTS: Significant exacerbation of joint destruction and aggravated pathological conditions were observed in CIA mice that were fed an HF diet. However, the boundary length of adipose tissue tended to decrease and the levels of adipokines (leptin and adiponectin) were lowered by the induction of arthritis. In HF/CIA mice, nevertheless, the production of MCP-1 in adipose tissues and the accumulation of macrophages in the SVF were significantly higher than CON/CIA group. The serum leptin/adiponectin (L/A) ratio was positively correlated with the number of macrophages in the SVF and MCP-1 production by adipose tissue, particularly in the CIA group. CONCLUSION: Functional alterations of adipose tissues could be originated from HF diet during developing arthritis. An abnormal activation of macrophages and an increased production of MCP-1 in adipose tissues might be both involved in joint destruction and inflammation.
22516996 [Screening for serum specific biomarkers in patients with primary Sjögren's syndrome and 2012 Apr 18 OBJECTIVE: To detect the serum protein biomarkers and establish a diagnostic model for primary Sjögren's syndrome (pSS) with interstitial lung disease (ILD). METHODS: Serum samples from 69 patients with pSS were prepared with WCX magnetic beads, and analyzed on PBS II-C mass spectrometer reader. Biomarker Wizard software was used to detect protein peaks and potential difference between the patients with pSS-ILD and with non-ILD. The model was developed by Biomarker Patterns software. RESULTS: Totally 7 discriminative mass-to-charge (m/z) ratios were identified to be related with pSS-ILD (P<0.05). Among these, the m/z peaks at 3 778.3, 3 318.3 and 2 236.6 were used to construct a diagnostic model. The sensitivity and specificity of the model were 93.1% and 87.5%, respectively. In a testing set, the sensitivity and specificity of the model were 84.0% and 85.7%, respectively. CONCLUSION: The potential protein biomarkers for pSS-ILD are discovered in the serum by MALDI-TOF-MS combined with WCX magnetic beads. The diagnostic pattern combining 3 778.3, 3 318.3 and 2 236.6 m/z protein peaks can discriminate pSS-ILD and non-ILD.
22679320 Primary Sjogren's syndrome with tuberculous arthritis of left knee. 2011 Sep 28 A 56-year-old woman presented with recurrent pain and swelling of left knee, Raynaud's phenomenon and dry mouth. She was initially diagnosed with primary Sjögren's syndrome and was put on prednisone, which substantially relieved her complaints. But 8 months later, pain and swelling of left knee recurred with spiking fever, chills and shortness of breath. Escalation of prednisone did not improve the pain and swelling of left knee. CT of chest revealed pulmonary interstitial changes with coexisting infection. MRI of left knee was highly consistent with tuberculous arthritis, which was further confirmed by positive blood culture of Mycobacterium tuberculosis and acid-fast stain of synovial fluid.
23043711 Atrial electromechanical delay and diastolic dysfunction in primary Sjögren syndrome. 2012 Oct 6 PURPOSE: In this study we aimed to investigate myocardial function and atrial electromechanical properties by conventional and tissue doppler echocardiography in patients with primary Sjögren syndrome. METHODS: Forty patients with Sjögren syndrome (SS) and 25 age- and sex-matched healthy volunteers were enrolled in the study. Using transthoracic echocardiography, myocardial performance index and atrial electromechanical properties were measured. RESULTS: Basal characteristics were similar between two groups. Myocardial performance index values were disturbed in patients with Sjögren syndrome (0.41 vs. 0.32, p < 0.01). There was significant intraatrial (16.4±6.4, 5.0±4.5, p < 0.01) and interatrial (30.6±10.1, 15.4±5.9, p < 0.01) electromechanical delay in this patient group. CONCLUSION: Myocardial function is disturbed and there is significant atrial electromechanical delay in patients with primary SS. This study is the first to show altered myocardial function and atrial electromechanical properties in primary SS.
22562982 Autonomic symptoms are common and are associated with overall symptom burden and disease a 2012 Dec OBJECTIVES: To determine the prevalence of autonomic dysfunction (dysautonomia) among patients with primary Sjögren's syndrome (PSS) and the relationships between dysautonomia and other clinical features of PSS. METHODS: Multicentre, prospective, cross-sectional study of a UK cohort of 317 patients with clinically well-characterised PSS. Symptoms of autonomic dysfunction were assessed using a validated instrument, the Composite Autonomic Symptom Scale (COMPASS). The data were compared with an age- and sex-matched cohort of 317 community controls. The relationships between symptoms of dysautonomia and various clinical features of PSS were analysed using regression analysis. RESULTS: COMPASS scores were significantly higher in patients with PSS than in age- and sex-matched community controls (median (IQR) 35.5 (20.9-46.0) vs 14.8 (4.4-30.2), p<0.0001). Nearly 55% of patients (vs 20% of community controls, p<0.0001) had a COMPASS score >32.5, a cut-off value indicative of autonomic dysfunction. Furthermore, the COMPASS total score correlated independently with EULAR Sjögren's Syndrome Patient Reported Index (a composite measure of the overall burden of symptoms experienced by patients with PSS) (β=0.38, p<0.001) and disease activity measured using the EULAR Sjögren's Syndrome Disease Activity Index (β=0.13, p<0.009). CONCLUSIONS: Autonomic symptoms are common among patients with PSS and may contribute to the overall burden of symptoms and link with systemic disease activity.