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ID PMID Title PublicationDate abstract
29382694 Sickness absence due to different musculoskeletal diagnoses by occupational class: a regis 2018 Apr OBJECTIVES: Those in lower occupational classes have an increased risk of sickness absence due to musculoskeletal diseases (MSDs), but studies examining the associations simultaneously across specified diagnostic groups within MSDs are lacking. We examined occupational class differences in the occurrence and length of long-term sickness absence due to different musculoskeletal diagnoses. METHODS: A 70% random sample of employed Finns aged 25-64 years old at the end of 2013 was linked to data on sickness absence of over 10 working days obtained from The Social Insurance Institution of Finland and occupational class from Statistics Finland. Sickness absences due to MSDs initiated in 2014 were followed until the end of each episode for female (n=675 636) and male (n=604 715) upper non-manuals, lower non-manuals and manual workers. Negative binomial hurdle models were used to analyse the associations. RESULTS: Within the studied MSDs, the most common causes of absence were back disorders, particularly back pain, and shoulder disorders. Osteoarthritis, disc disorders and rheumatoid arthritis induced the longest episodes of absence. Clear hierarchical class differences were found throughout, but the magnitude of the differences varied across the diagnostic causes. The largest class differences in the occurrence were detected in shoulder disorders and back pain. The class differences in length were greatest in rheumatoid arthritis, disc disorders and, among men, also in hip osteoarthritis. CONCLUSIONS: Hierarchical occupational class differences were found across different MSDs, with large differences in back and shoulder disorders. Occupational class and diagnosis should be considered when attempting to reduce sickness absence due to MSDs.
30310087 Interplay between P. gingivalis, F. nucleatum and A. actinomycetemcomitans in murine alveo 2018 Oct 11 Increasing evidence supports the association of periodontitis with rheumatoid arthritis. Even though a prominent role has been postulated for Porphyromonas gingivalis, many bacterial species contribute to the pathogenesis of periodontal disease. We therefore investigated the impact of Porphyromonas gingivalis as well as other major pathobionts on the development of both, periodontitis and arthritis in the mouse. Pathobionts used - either alone or in combination - were Porphyromonas gingivalis, Fusobacterium nucleatum and Aggregatibacter actinomycetemcomintans. Periodontitis was induced via oral gavage in SKG, DBA/1 and F1 (DBA/1 × B10.Q) mice and collagen-induced arthritis was provoked via immunization and boost with bovine collagen type II. Alveolar bone loss was quantified via micro computed tomography, arthritis was evaluated macroscopically and histologically and serum antibodies were assessed. Among the strains tested, only F1 mice were susceptible to P. gingivalis induced periodontitis and showed significant alveolar bone loss. Bone loss was paralleled by antibody titers against P. gingivalis. Of note, mice inoculated with the mix of all three pathobionts showed less alveolar bone loss than mice inoculated with P. gingivalis alone. However, oral inoculation with either F. nucleatum or A. actinomycetemcomintans alone accelerated subsequent arthritis onset and progression. This is the first report of a triple oral inoculation of pathobionts combined with collagen-induced arthritis in the mouse. In this interplay and this particular genetic setting, F. nucleatum and A. actinomycetemcomitans exerted a protective impact on P. gingivalis induced alveolar bone loss. By themselves they did not induce periodontitis yet accelerated arthritis onset and progression.
30476367 The Safety Profile of Tumor Necrosis Factor Inhibitors in Ankylosing Spondylitis: Are TNF 2019 Apr Tumor necrosis factor (TNF) inhibitors significantly improved the treatment options for patients with ankylosing spondylitis. Unfortunately, currently, there is no strategy for sustaining remission of the disease with TNF inhibitors; after discontinuation, a high percentage of patients experience flares in a short time. Therefore, up-to-date, long-term use of TNF inhibitors in patients with ankylosing spondylitis remains necessary. For this reason, the issue of the long-term safety of TNF inhibitors in patients with ankylosing spondylitis raises concerns. Although TNF inhibitors are well established in ankylosing spondylitis treatment, the majority of studies on TNF inhibitors' safety have been performed in patients with rheumatoid arthritis. Until recently, there were very few studies of TNF inhibitors' safety in ankylosing spondylitis. Meanwhile, TNF inhibitors appear to have different safety profiles in ankylosing spondylitis and rheumatoid arthritis. In this review, we describe available data on the occurrence of adverse events associated with TNF inhibitor treatment in ankylosing spondylitis, including serious adverse events, infections, serious infections, tuberculosis, opportunistic infections, hepatitis B reactivation, malignancies, laboratory test abnormalities, autoimmune diseases, paradoxical adverse events, and heart failure.
29992394 Ultrasonographic findings in a patient with reactive arthritis induced by intravesical BCG 2019 Jan Intravesical bacillus Calmette-Guerin (BCG) therapy is an effective and safe immunotherapy for superficial bladder cancer. However, reactive arthritis (ReA) is reported as an adverse event in about 0.5-1% of patients receiving intravesical BCG therapy. ReA is known as a kind of spondyloarthritis, the main pathological finding of which is enthesitis. Here we report a patient with ReA induced by intravesical BCG therapy for bladder cancer, in whom the diagnosis of ReA was supported by ultrasonographic findings of enthesitis and synovitis. A 69-year-old male was diagnosed with carcinoma in situ of the bladder and treated with intravesical BCG therapy. After the third intravesical BCG injection, pain and swelling appeared in both wrists. Ultrasonographic examination revealed not only intra-articular synovitis in the bilateral wrist joint, wrist flexor tenosynovitis, and wrist extensor tenosynovitis, but also enthesitis of the flexor carpi radialis tendon (FCR). The severe enthesitis of the FCR in both wrists was considered to be an important finding that supported the diagnosis in this patient. Thus, we diagnosed this case as ReA induced by intravesical BCG therapy. In clinical practice, ReA is often difficult to distinguish from seronegative rheumatoid arthritis and other rheumatic diseases. Ultrasonographic findings of enthesitis may support a definitive diagnosis for these patients.
30017519 Anti-TNF modulation reduces myocardial inflammation and improves cardiovascular function i 2018 Nov 1 BACKGROUND: Rheumatoid arthritis (RA), ankylosing spondylitis (AS) and psoriatic arthritis (PsA) are common disorders associated with increased rates of cardiovascular disease (CVD), but the contribution of cytokine-induced inflammation to impaired cardiovascular function in these conditions remains poorly understood. OBJECTIVES: We assessed the effect of anti-TNF therapy on myocardial and vascular function, myocardial tissue characteristics and perfusion in inflammatory arthropathy and systemic rheumatic disease (IASRD) patients, using cardiovascular magnetic resonance (CMR). METHODS: 20 RA patients, 7 AS patients, 5 PsA patients without previously known CVD scheduled to commence anti-TNF therapy and 8 RA patients on standard disease modifying antirheumatic drugs underwent CMR at 1.5 T, including cine, tagging, pulse wave velocity (PWV), T2-weighted, native and postcontrast T1 mapping, ECV quantification, rest and stress perfusion and late gadolinium enhancement (LGE) imaging. RESULTS: Following anti-TNF therapy, there was significant reversal of baseline subclinical cardiovascular dysfunction, as evidenced by improvement in peak systolic circumferential strain (p < 0.001), peak diastolic circumferential strain rate (p < 0.001), and total aortic PWV, (p < 0.001). This was accompanied by a reduction in myocardial inflammation, as assessed by T2-weighted imaging (p = 0.005), native T1 mapping (p = 0.009) and ECV quantification (p = 0.001), as well as in serum inflammatory markers like CRP (p < 0.001) and ESR (p < 0.001), and clinical measures of disease activity (DAS28-CRP, p = 0.001; BASDAI, p < 0.001). A trend towards improvement in myocardial perfusion was observed (p = 0.07). Focal myocardial fibrosis, as detected by LGE CMR was not altered by anti-TNF therapy (p = 0.92). CONCLUSIONS: Anti-TNF therapy reduces subclinical myocardial inflammation and improves cardiovascular function in RA, AS and PsA. CMR may be used to track disease progression and response to therapy. Future CMR-based studies to demonstrate effect of anti-TNF therapy modulation of vascular structure and function on hard clinical events and outcomes would be useful.
29764383 An automated algorithm for the detection of cortical interruptions and its underlying loss 2018 May 15 BACKGROUND: We developed a semi-automated algorithm that detects cortical interruptions in finger joints using high-resolution peripheral quantitative computed tomography (HR-pQCT), and extended it with trabecular void volume measurement. In this study we tested the reproducibility of the algorithm using scan/re-scan data. METHODS: Second and third metacarpophalangeal joints of 21 subjects (mean age 49 (SD 11) years, 17 early rheumatoid arthritis and 4 undifferentiated arthritis, all diagnosed < 1 year ago) were imaged twice by HR-pQCT on the same day with repositioning between scans. The images were analyzed twice by one operator (OP1) and once by an additional operator (OP2), who independently corrected the bone contours when necessary. The number, surface and volume of interruptions per joint were obtained. Intra- and inter-operator reliability and intra-operator reproducibility were determined by intra-class correlation coefficients (ICC). Intra-operator reproducibility errors were determined as the least significant change (LSC(SD)). RESULTS: Per joint, the mean number of interruptions was 3.1 (SD 3.6), mean interruption surface 4.2 (SD 7.2) mm(2), and mean interruption volume 3.5 (SD 10.6) mm(3) for OP1. Intra- and inter-operator reliability was excellent for the cortical interruption parameters (ICC ≥0.91), except good for the inter-operator reliability of the interruption surface (ICC = 0.70). The LSC(SD) per joint was 4.2 for the number of interruptions, 5.8 mm(2) for interruption surface, and 3.2 mm(3) for interruption volume. CONCLUSIONS: The algorithm was highly reproducible in the detection of cortical interruptions and their volume. Based on the LSC findings, the potential value of this algorithm for monitoring structural damage in the joints in early arthritis patients needs to be tested in clinical studies.
30374145 Complex Role of Capsaicin-Sensitive Afferents in the Collagen Antibody-Induced Autoimmune 2018 Oct 29 Capsaicin-sensitive afferents have complex regulatory functions in the joints orchestrated via neuropeptides. This study aimed to determine their role in the collagen-antibody induced rheumatoid arthritis model. Capsaicin-sensitive nerves were defunctionalized by the capsaicin receptor agonist resiniferatoxin in C57Bl/6 mice. Arthritis was induced by the ArithroMab antibody cocktail and adjuvant. Arthritis was monitored by measuring body weight, joint edema by plethysmometry, arthritis severity by clinical scoring, mechanonociceptive threshold by plantar esthesiometry, thermonociceptive threshold by hot plate, cold tolerance by paw withdrawal latency from 0 °C water. Grasping ability was determined by the wire-grid grip test. Bone structure was evaluated by in vivo micro-CT and histology. Arthritic animals developed a modest joint edema, mechanical and cold hyperalgesia, weight loss, and a diminished grasping function, while thermal hyperalgesia is absent in the model. Desensitised mice displayed reduced arthritis severity, edema, and mechanical hyperalgesia, however, cold hyperalgesia was significantly greater in this group. Arthritic controls displayed a transient decrease of bone volume and an increased porosity, while bone density and trabecularity increased in desensitised mice. The activation of capsaicin-sensitive afferents increases joint inflammation and mechanical hyperalgesia, but decreases cold allodynia. It also affects inflammatory bone structural changes by promoting bone resorption.
29149703 Quercetin attenuates collagen-induced arthritis by restoration of Th17/Treg balance and ac 2018 Jan Quercetin (QU) has been shown obvious anti-arthritic property in pre-clinical studies or clinical studies. Howbeit, the underlying mechanism of it is still not revealed distinctly and should be gotten further insight into. QU at a dosage of 150 mg/kg was administered orally in collagen-induced arthritis rats and then the clinical symptoms were monitored. The protein levels of Th17/Treg-related cytokines were determined by ELISA, and the mRNA levels of cytokines and transcription factors associated with the Th17 and Treg phenotypes were evaluated by real-time PCR, the proportions of Th17 and Treg cells were assessed by flow cytometry. The results showed that QU administration yielded an obvious mitigation of arthritic manifestations including high arthritic scores and paw edema, which was accompanied with decrement of Th17-related cytokines (IL-17A and IL-21) and increment of Treg-related cytokines (IL-10 and TGF-β). QU decreased the percentage of Th17 cells, while increased the percentage of Treg cells. In addition, the activation of NLRP3 inflammasome which plays a crucial role in the development of RA was determined and found that the protein expressions of NLRP3, Caspase-1 and IL-1β were diminished by QU significantly. Moreover, the protein levels of inflammatory mediators which were recognized as chief culprits in inflammatory reaction were assayed. The contents of inflammatory mediators inclusive of TNF-α, IL-1β, IL-6, PGE2, COX-2 and iNOS were down-regulated markedly by QU. But the inhibitory effect of QU on inflammatory mediators was nearly abolished by Heme Oxygenase 1 (HO-1) siRNA. Taken together, QU attenuates CIA via modulating the Th17/Treg balance, inhibiting NLRP3 inflammasome activation as well as activating HO-1-mediated anti-inflammatory response.
29992179 Effect of a cathepsin K inhibitor on arthritis and bone mineral density in ovariectomized 2018 Dec OBJECTIVES: Cathepsin K is expressed by osteoclasts and synovial fibroblasts and degrades key components of bone and cartilage. Inhibition of cathepsin K protease activity may be beneficial for the prevention of bone erosion and cartilage degradation in rheumatoid arthritis (RA). The collagen-induced arthritis (CIA) rat model is well established for studying the pathology and treatment of RA. We investigated the effect of ONO-KK1-300-01, a cathepsin K inhibitor (CKI), on arthritis and bone mineral density (BMD) in rats with CIA. METHODS: Seven-month-old female Sprague Dawley rats were divided into 5 groups: rats without CIA (CNT); CIA rats that underwent ovariectomy (OVX) and were treated with CKI; CIA rats that underwent OVX and were treated with vehicle (Veh); CIA rats that underwent sham surgery and were treated with CKI; and CIA rats that underwent sham surgery and were treated with Veh. CKI was orally administered at a dose of 15 mg/kg, thus initiating collagen sensitization, until death at 4 weeks. We evaluated hind paw thickness and the arthritis score every week until death. Radiographs of the resected left foot were obtained with a soft X-ray apparatus. Destruction of bone and cartilage was classified and scored as previously described by Engelhardt et al. BMD was measured by bone densitometry at the halfway point between the distal metaphysis and the diaphysis of the resected right femur. We also performed histomorphometry of the proximal left tibia, histological evaluation of arthritis, and a bone strength test. RESULTS: CKI administration significantly reduced hind paw thickness and the arthritis score, and prevented a decrease in BMD. The radiographic score was significantly lower in the CKI group than in the Veh group. In the histomorphometric analysis, bone-resorption parameters were significantly lower in the CKI groups than in the Veh groups. CKI significantly inhibited synovial proliferation in the CIA rats. In the bone strength test, the ultimate stress was significantly higher in the CKI groups than in the Veh groups. CONCLUSION: Our findings indicate that cathepsin K inhibitors may inhibit systemic and local bone loss, ameliorate arthritis, and attenuate the decrease of bone strength in an animal model of arthritis.
30282444 Histopathology of the skin in rheumatic diseases. 2018 Oct 3 Rheumatological systemic autoimmune diseases, such as connective tissue diseases, rheumatoid arthritis or spondyloarthritis, are characterized by the presence of joint involvement associated with extra-articular manifestations. Among them, cutaneous diseases are often the most relevant and representative clinical manifestation, as in psoriatic arthritis, scleroderma or systemic lupus erythematosus. In this context, it is useful for rheumatologists to understand better skin diseases and their histopathological features. Evaluation of skin biopsy specimens can be helpful not only to confirm the diagnosis in both classic and clinically atypical variants, but also to improve further our knowledge of the pathogenetic mechanisms and the close link between skin and articular diseases. In this review, we discuss the clinical features, diagnostic evaluation and the histopathological features of skin manifestation of the most relevant rheumatological autoimmune diseases.
29624870 Characteristics and risk factors of pulmonary arterial hypertension in patients with prima 2018 May AIM: To describe baseline characteristics of patients with primary Sjögren's syndrome (pSS) with right heart catheterization (RHC)-confirmed pulmonary arterial hypertension (PAH) and explore risk factors for PAH in pSS. METHODS: This case-control study included consecutive patients hospitalized with pSS-PAH from 2007 to 2015, and pSS patients without PAH (in a 4 : 1 ratio) as controls. All patients fulfilled the 2002 American-European Consensus Group classification criteria for pSS-PAH was defined according to RHC-based European Society of Cardiology/European Respiratory Society guidelines. Associated variables were analyzed by univariate binary logistic regression to identify possible risk factors for PAH. RESULTS: Twenty-nine patients with RHC-confirmed pSS-PAH were included (mean age at onset, 38.4 ± 8.3 years; mean pSS duration, 54.6 months). PAH was the initial manifestation of pSS in 12 patients (41.4%), and shortness of breath was the most common symptom (29/29, 100%). Mean pulmonary arterial pressure was 51.8 ± 10.0 mmHg, mean cardiac index was 2.3 ± 0.8 L/min/m(2) , and mean pulmonary vascular resistance was 13.0 ± 6.0 Wood units in this group. Treatments included immunosuppressive agents (93.1%) and PAH-targeted therapies (86.2%). We identified four independent risk factors for PAH in pSS: Raynaud's phenomenon (odds ratio [OR] = 9.660, P = 0.000), rheumatoid factor ≥ 200 U/mL (OR = 6.691, P = 0.001), hepatic injury (OR = 3.284, P = 0.008) and pericardial effusion (OR = 3.279, P = 0.016). CONCLUSIONS: PAH can be the first manifestation of pSS. The pSS patients with Raynaud's phenomenon, high-titer rheumatoid factor, hepatic injury or pericardial effusion should be screened for PAH.
29465360 Serum soluble interleukin-2 receptor is a useful biomarker for disease activity but not fo 2018 May OBJECTIVES: To identify biomarkers for disease activity in IgG4-related disease (IgG4-RD) and primary Sjögren's syndrome (pSS). METHODS: Forty-three consecutive treatment-naïve patients with IgG4-RD, 62 patients with pSS, and 5 patients with sicca syndrome were enrolled. IgG4-RD and pSS disease activity was assessed based on the IgG4-RD responder index (IgG4-RD RI) and EULAR Sjögren's Syndrome Disease Activity Index (ES- SDAI), respectively. The associations of biomarkers with disease activity were examined. RESULTS: Comparison of the three dis- eases identified the serum levels of IgG, IgG4, IgG4/IgG ratio, IgE, and soluble interleukin-2 receptor (sIL-2R) for IgG4-RD and the serum levels of IgM and sIL-2R and lymphocyte counts for pSS as potential biomarkers of disease activity. Among these, serum sIL-2R levels correlate with baseline IgG4-RD RI scores and the number of affected organs in IgG4-RD (ρ=0.74, p<0.0001 and ρ=0.75, p<0.0001, respectively). Serum sIL-2R levels also correlate with ESSDAI scores and the number of af- fected organs in pSS (ρ=0.67, p<0.0001 and ρ=0.41, p<0.0001, respectively). Receiver operating characteristic curve analysis suggested serum sIL-2R levels as an efficient biomarker to distinguish the presence of extra-dacryosialadenitis involvements in IgG4-RD with a cut-off value of 424 U/mL (AUC=0.93, p<0.0001), and in pSS with 452 U/mL (AUC=0.89, p<0.0001). Serum sIL-2R levels decreased significantly after treatment in patients with IgG4-RD and pSS. CONCLUSIONS: Serum sIL-2R levels are a potentially valuable biomarker for evaluating disease activity and treatment response in IgG4-RD and pSS.
30591891 Evaluation of the anti-arthritic activity of Cinnamomum cassia bark extract in experimenta 2018 Dec BACKGROUND: Cinnamomum cassia iswidely used as a traditional medicinal plant for the treatment of rheumatoid arthritis. OBJECTIVE: The present study aimed to assess the anti-arthritic activity of C. cassia bark hydroalcoholic extract (CCHE) in different arthritic animal models. METHODS: In formaldehyde model, sub-plantar administration of 0.1 ml of formaldehyde (2% v/v) into the right hind paws of Wistar albino rats on days 0 and 3. The rats were divided into six groups as follows: normal control, disease control, indomethacin group (3 mg/kg, p.o.) and three groups, treated with 50, 100 and 200 mg/kg CCHE (p.o.). Joint diameter was measured, and ankle joints were collected for MDA and GSH measurements. In complete Freund's adjuvant (CFA)-induced arthritis model, CFA was injected into the sub-plantar surface of the right hind paw in rats. Joint diameter was measured, and serum TNF-α and IL-1β were measured. Histopathological and immunohistochemical analyses were also performed. RESULTS: CCHE treatment significantly (p < 0.01) reduced MDA levels and joint swelling in a concentration-dependent manner in rats with formaldehyde-induced arthritis, in which GSH levels were elevated (p < 0.01). In rats with CFA-induced arthritis, CCHE treatment significantly reduced joint swelling as well as IL-1β and TNF-α levels (p < 0.01). TNF-α receptor expression was decreased in rats treated with indomethacin or CCHE. CONCLUSION: Based on these findings, it can be concluded that C. cassia possesses anti-arthritic properties.
29356963 Pathologic conditions of hard tissue: role of osteoclasts in osteolytic lesion. 2018 Apr Hard tissue homeostasis is regulated by the balance between bone formation by osteoblasts and bone resorption by osteoclasts. This physiologic process allows adaptation to mechanical loading and calcium homeostasis. Under pathologic conditions, however, this process is ill-balanced resulting in either over-resorption or over-formation of hard tissue. Local over-resorption by osteoclasts is typically observed in osteolytic metastases of malignancies, autoimmune arthritis, and giant cell tumor of bone (GCTB). In tumor-related local osteolysis, tumor-derived osteoclast-activating factors induce bone resorption not by directly acting on osteoclasts but by indirectly upregulating receptor activator of NFκB ligand (RANKL) on osteoblastic cells. Similarly, synovial tissue in the autoimmune arthritis model does overexpress RANKL and contains numerous osteoclast precursors, and like a landing craft, when it comes in contact with eroded bone surfaces, osteoclast precursors are immediately polarized to become mature osteoclasts, inducing rapidly progressive bone destruction at a late stage of the disease. GCTB, on the other hand, is a common primary bone tumor, usually arising at the metaphysis of the long bone in young adults. After the discovery of RANKL, the concept of GCTB as a tumor of RANKL-expressing stromal cells was established, and comprehensive exosome studies finally disclosed the causative single-point mutation at histone H3.3 (H3F3A) in stromal cells. Thus, osteolytic lesions under various pathological conditions are ultimately attributable to the overexpression of RANKL, which opens up a common, practical and useful therapeutic target for diverse osteolytic conditions.
29901091 Suppressive effects of Wang‑Bi Tablet on adjuvant‑induced arthritis in rats via NF‑Π2018 Sep Rheumatoid arthritis (RA) severely affects the quality life of patients due to its high association with disability. Traditional Chinese medicines have been reported to exert notable therapeutic effects on RA. The Chinese medicinal prescription Wang‑Bi Tablet (WB) has been successfully used to clinically treat RA for many years; however, its pharmacological mechanism of action is largely unclear. In the present study, adjuvant‑induced arthritis (AIA) rats were used to evaluate the anti‑inflammatory effects of WB and western blotting was used to explore the molecular mechanisms. The experimental results demonstrated that WB treatment significantly reduced arthritis score and hind‑paw volume. Furthermore, synovial hyperplasia, inflammatory cell infiltration and joint destruction were ameliorated by WB. The expression levels of the proinflammatory cytokines interleukin (IL)‑1β, tumor necrosis factor‑α and IL‑6, were reduced in the joints of WB‑treated rats. Western blotting revealed that WB could also inhibit excessive activation of nuclear factor (NF)‑κB and Janus kinase (JAK)‑signal transducer and activator of transcription 3 (STAT3) signaling pathways. These results indicated that the therapeutic effects of WB on AIA may be accomplished through inhibition of the NF‑κB and JAK‑STAT3 signaling pathways. These findings provide experimental evidence to support WB as a therapeutic agent for the treatment of patients with RA.
31497769 Serum/Synovial Fluid Urate Ratio as an Indicator for Distinguishing Gouty Arthritis From O 2019 Jun OBJECTIVES: This study aims to compare the serum/synovial fluid (SF) urate ratio of gouty arthritis and other arthritides and investigate whether this ratio may be an indicator for distinguishing gouty arthritis from other arthritides. PATIENTS AND METHODS: Paired serum and SF samples from 70 patients (38 males, 32 females; mean age 57.9 years; range, 27.5 to 78.4 years) comprised of 20 patients with gout, 20 patients with rheumatoid arthritis and 30 patients with osteoarthritis were collected simultaneously for urate measurement. Patient data were recorded including demographic data (age, sex), body mass index, estimated glomerular filtration rate, comorbidities (diabetes, hypertension and dyslipidemia), disease duration (from the first symptoms), pain duration before arthrocentesis at this time, presence of tophi or not, serum albumin, erythrocyte sedimentation rate, C-reactive protein and SF white blood cell count. RESULTS: Gout patients had highest levels of urate in both serum and SF among the three groups (p<0.001). The serum/SF urate ratio of gout patients was significantly lower among the three groups (p<0.001). Receiver-operating characteristic curve analysis demonstrated that serum/SF urate ratio can predict the extent of gouty arthritis (the value of area under the curve was 0.867, p<0.001). CONCLUSION: Serum/SF urate ratio may be an indicator for distinguishing gouty arthritis from other arthritides.
28946518 Comparison of 25-hidroksi Vitamin D serum concentrations in patients with psoriasis and ps 2018 Feb 6 BACKGROUND AND OBJECTIVE: Rheumatoid arthritis (RA), insulin-dependent diabetes mellitus (IDDM), inflammatory bowel disease, systemic lupus erythematosus (SLE) and multiple sclerosis (MS) are some of the autoimmune diseases related to the decreases in Vitamin D levels. The same immunological properties as psoriasis, such as Th1/Th2 dysregulation, are seen in all of them. This study aims to compare 25-hidroksi Vitamin D (25-OHD) serum concentrations in patients with psoriasis and psoriatic arthritis. METHODS: This study includes 91 outpatients; 48 of these patients were chosen randomly among the psoriasis (PS) patients from the dermatology department of the researchers' hospital. Forty-three of them were chosen among the psoriatic arthritis (PsA) patients matching the age and gender criteria from the rheumatology department of the researchers' hospital. In this study, 25-OHD serum concentrations among the psoriasis and psoriatic arthritis patients were compared. RESULT: There are more patients in the PsA group with 25-OHD levels lower than 20 ng/ml; however, this finding is insufficient to obtain statistical significance (p= 0.09). PsA and psoriasis groups had similar numbers of patients with 25-OHD levels ranging from 20 to 30 mg/mL and those higher than 30 mg/mL (p> 0.05). CONCLUSION: The literature does not show significant differences between the PS and PsA groups in terms of serum 25-OHD levels and a prevalence of Vitamin D deficiency. Besides, PASI scores were higher in the PS group. CRP values in the PsA group were higher than in the PS group. There was a poor negative correlation between CRP and serum 25-OHD levels in the PsA group. This correlation was not found in the PS group.
28748366 Clinical Features of Psoriatic Arthritis: a Comprehensive Review of Unmet Clinical Needs. 2018 Dec Psoriatic arthritis (PsA) is a form of inflammatory arthritis (IA) affecting approximately 0.25% of the population. It is a heterogeneous disorder associated with joint damage, disability, disfiguring skin disease and in severe cases, premature mortality. Inherently irreversible and frequently progressive, the process of joint damage begins at, or before, the clinical onset of disease. Early recognition and intervention is thus crucial to patient outcome. At disease onset, however, PsA often resembles other forms of arthritis-especially rheumatoid arthritis (RA). Despite the similarities between PsA and RA, their distinctive pathologies require different treatments. For example, drugs that are effective in RA may not be effective in PsA and can even cause adverse effects. Since there is no currently validated test for PsA, the diagnosis is often missed or delayed and this has functional consequences for the patient. In the context of PsA and RA, making an accurate diagnosis is not the only challenge faced by rheumatologists. Choosing an effective and safe medication to manage the disease is another significant challenge and currently approximately 40% achieve meaningful responses such as minimal disease activity status. For the patient, several months may be lost as a result of trial and error testing-meanwhile, irreversible joint damage may occur. Clearly, more effective clinical tests are urgently needed to improve personalised patient care in PsA. Specifically, there is need to develop minimally invasive tests predictive of diagnosis, response to treatment and radiographic progression. In this review, we examined the biomarker development process, highlighted the importance of qualifying unmet clinical needs and emphasised the challenges that impede biomarker studies. We have compiled a comprehensive list of potentially clinically relevant biomarkers in PsA and provided a summary of proteomic technologies that might usefully support additional biomarker research in PsA.
30104220 Acute hyperviscosity: syndromes and management. 2018 Sep 27 Plasma hyperviscosity is a rare complication of both monoclonal and polyclonal disorders associated with elevation of immunoglobulins. Asymptomatic patients with an elevation in the serum viscosity do not require plasma exchange, and the majority will have other indications for therapeutic intervention. For patients with hemorrhagic or central nervous system manifestations, plasma exchange is the therapy of choice and is relatively safe. Viscosity measurements are not required to initiate therapy if the index of suspicion is high and the clinical presentation is typical. However, patients should have a sample sent for confirmation of the diagnosis. Whole-blood hyperviscosity is seen in patients with extreme elevation of the red cell and white cell count. Phlebotomy of patients with primary and secondary elevation of the red cell count is a well-established therapy.
29981359 Disruption of endothelial barrier function is linked with hyposecretion and lymphocytic in 2018 Oct Sjögren's syndrome (SS) is an inflammatory autoimmune disease that causes hyposecretion in salivary glands. Endothelial tight junctions (TJs) play crucial roles in salivation and barrier function of blood vessels. However, whether the alteration of endothelial TJs were involved in pathogenesis of SS was still unknown. Here, the ultrastructure and function of endothelial TJs in submandibular glands (SMGs) were detected by transmission electron microscopy and in vivo paracellular permeability assay in different aged NOD mouse model for SS. CFSE-labeled lymphocytes were injected into tail vein to trace the infiltration, while claudin-5 expression and distribution were detected by immunofluorescence, qRT-PCR, and western blot. Results showed that the stimulated salivary flow rate was gradually decreased and lymphocytic infiltration was found as age increased in 12- and 21-week-old NOD mice, but not 7-week-old NOD mice. Blood vessels were dilated, while endothelial TJ width and paracellular tracer transport were increased in 12-week-old NOD mice. Moreover, the injected CFSE-labeled lymphocytes were observed in SMGs of 12-week-old NOD mice. Claudin-5 level was increased and relocalized from the apical portion of neighboring endothelial cells to lateral membranes and cytoplasm in 12-week-old NOD mice. Additionally, the alteration of claudin-5 expression and distribution was further confirmed in labial salivary glands and bilateral parotid glands from SS patients. In cultured human microvessel endothelial cell line (HMEC-1), IFN-γ stimulation significantly increased claudin-5 expression. Taken together, we identified that the endothelial TJ barrier was disrupted and contributed to the development of salivary hyposecretion and lymphocytic infiltration in SS.