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ID PMID Title PublicationDate abstract
29880622 Cerebellar degeneration in primary Sjӧgren syndrome. 2018 Jun 6 Neurological manifestations are reported as a consequence of primary Sjӧgren syndrome (PSS). Any part of the brain and peripheral nervous system can be involved in PSS. However, cerebellar degeneration and atrophy associated with PSS have been rarely reported. Our report describes a 22-year-old woman who presented with cerebellar ataxia, arthritis and arthralgia. Evaluation of her symptoms, autoantibodies and salivary gland pathology was in favour of the diagnosis of Sjögren syndrome. Also, her brain MRI revealed cerebellar degeneration. There are only four patients reported to be affected by cerebellar atrophy associated with PSS. Administration of high doses of methylprednisolone and cyclophosphamide leads to substantial improvement in the cerebellar symptoms of this case. In addition, after 2 months of follow-up, the patient's ataxia recovered significantly. It could be concluded that in addition to neurological degenerative disorders, in some cases cerebellar atrophy could also be associated with autoimmune conditions such as PSS.
30156545 Discrepancy between subjective symptoms, objective measures and disease activity indexes: 2018 May Mucosal dryness is a key clinical feature in primary Sjögren's syndrome (pSS) and its assessment relies on both objective measurement of residual secretion and subjective symptoms reported by patients. However, while the objective assessment and grading of glandular dysfunction can be easily performed, the spectrum of clinical symptoms encompassed by the terms 'dry eye' and 'dry mouth' is wide and heterogeneous. Therefore, patient reported outcomes (PROs) for dryness in pSS poorly correlate with the amount of glandular secretion. In addition, subjective dryness is not correlated with the severity of systemic disease and severely affects the patient quality of life even in presence of active extraglandular manifestations. The purpose of this review article is to provide an overview of glandular dysfunction in pSS as well as the impact of discrepancy between objective assessment, subjective symptom and extraglandular disease activity on disease management.
29484197 Feasibility and assessment of outcome measures for yoga as self-care for minorities with a 2018 BACKGROUND: While there is a growing interest in the therapeutic benefits of yoga, minority populations with arthritis tend to be under-represented in the research. Additionally, there is an absence of guidance in the literature regarding the use of multicultural teams and sociocultural health beliefs, when designing yoga studies for a racially diverse population with arthritis. This pilot study examined the feasibility of offering yoga as a self-care modality to an urban, bilingual, minority population with osteoarthritis (OA) or rheumatoid arthritis (RA), in the Washington, DC area. METHODS: The primary objective of the study was to assess the feasibility of offering an 8-week, bilingual yoga intervention adapted for arthritis to a convenience sample of primarily Hispanic and Black/African-American adults. A racially diverse interdisciplinary research team was assembled to design a study to facilitate recruitment and retention. The second objective identified outcome measures to operationalize potential facilitators and barriers to self-care and self-efficacy. The third objective determined the feasibility of using computer-assisted self-interview (CASI) for data collection. RESULTS: Enrolled participants (n = 30) were mostly female (93%), Spanish speaking (69%), and diagnosed with RA (88.5%). Feasibility was evaluated using practicality, acceptability, adaptation, and expansion of an arthritis-adapted yoga intervention, modified for this population. Recruitment (51%) and participation (60%) rates were similar to previous research and clinical experience with the study population. Of those enrolled, 18 started the intervention. For adherence, 12 out of 18 (67%) participants completed the intervention. All (100%), who completed the intervention, continued to practice yoga 3 months after completing the study. Using nonparametric tests, selected outcome measures showed a measurable change post-intervention suggesting appropriate use in future studies. An in-person computerized questionnaire was determined to be a feasible method of data collection. CONCLUSIONS: Findings from this pilot study confirm the feasibility of offering yoga to this racially/ethnically diverse population with arthritis. This article provides recruitment/retention rates, outcome measures with error rates, and data collection recommendations for a previously under-represented population. Suggestions include allocating resources for translation and using a multicultural design to facilitate recruitment and retention. TRIAL REGISTRATION: ClinicalTrials.gov, NCT01617421.
32289062 Novel nano therapeutic materials for the effective treatment of rheumatoid arthritis-recen 2018 Dec Rheumatoid arthritis (RA) is the most common complex multifactorial joint related autoimmune inflammatory disease with unknown etiology accomplished with increased cardiovascular risks. RA is characterized by the clinical findings of synovial inflammation, autoantibody production, and cartilage/bone destruction, cardiovascular, pulmonary and skeletal disorders. Pro-inflammatory cytokines such as IL-1, IL-6, IL-8, and IL-10 were responsible for the induction of inflammation in RA patients. Drawbacks such as poor efficacy, higher doses, frequent administration, low responsiveness, and higher cost and serious side effects were associated with the conventional dosage forms for RA treatment. Nanomedicines were recently gaining more interest towards the treatment of RA, and researchers were also focusing towards the development of various anti-inflammatory drug loaded nanoformulations with an aid to both actively/passively targeting the inflamed site to afford an effective treatment regimen for RA. Alterations in the surface area and nanoscale size of the nanoformulations elicit beneficial physical and chemical properties for better pharmacological activities. These drug loaded nanoformulations may enhances the solubility of poorly water soluble drugs, improves the bioavailability, affords targetability and may improve the therapeutic activity. In this regimen, the present review focus towards the novel nanoparticulate formulations (nanoparticles, nanoemulsions, solid lipid nanoparticles, nanomicelles, and nanocapsules) utilized for the treatment of RA. The recent advancements such as siRNA, peptide and targeted based nanoparticulate systems for RA treatment were also discussed. Special emphasis was provided regarding the pathophysiology, prevalence and symptoms towards the development of RA.
29652832 Sympathetic Nerve Hyperactivity in the Spleen: Causal for Nonpathogenic-Driven Chronic Imm 2018 Apr 13 Immune-Mediated Inflammatory Diseases (IMIDs) is a descriptive term coined for an eclectic group of diseases or conditions that share common inflammatory pathways, and for which there is no definitive etiology. IMIDs affect the elderly most severely, with many older individuals having two or more IMIDs. These diseases include, but are not limited to, type-1 diabetes, obesity, hypertension, chronic pulmonary disease, coronary heart disease, inflammatory bowel disease, and autoimmunity, such as rheumatoid arthritis (RA), Sjőgren's syndrome, systemic lupus erythematosus, psoriasis, psoriatic arthritis, and multiple sclerosis. These diseases are ostensibly unrelated mechanistically, but increase in frequency with age and share chronic systemic inflammation, implicating major roles for the spleen. Chronic systemic and regional inflammation underlies the disease manifestations of IMIDs. Regional inflammation and immune dysfunction promotes targeted end organ tissue damage, whereas systemic inflammation increases morbidity and mortality by affecting multiple organ systems. Chronic inflammation and skewed dysregulated cell-mediated immune responses drive many of these age-related medical disorders. IMIDs are commonly autoimmune-mediated or suspected to be autoimmune diseases. Another shared feature is dysregulation of the autonomic nervous system and hypothalamic pituitary adrenal (HPA) axis. Here, we focus on dysautonomia. In many IMIDs, dysautonomia manifests as an imbalance in activity/reactivity of the sympathetic and parasympathetic divisions of the autonomic nervous system (ANS). These major autonomic pathways are essential for allostasis of the immune system, and regulating inflammatory processes and innate and adaptive immunity. Pathology in ANS is a hallmark and causal feature of all IMIDs. Chronic systemic inflammation comorbid with stress pathway dysregulation implicate neural-immune cross-talk in the etiology and pathophysiology of IMIDs. Using a rodent model of inflammatory arthritis as an IMID model, we report disease-specific maladaptive changes in β₂-adrenergic receptor (AR) signaling from protein kinase A (PKA) to mitogen activated protein kinase (MAPK) pathways in the spleen. Beta₂-AR signal "shutdown" in the spleen and switching from PKA to G-coupled protein receptor kinase (GRK) pathways in lymph node cells drives inflammation and disease advancement. Based on these findings and the existing literature in other IMIDs, we present and discuss relevant literature that support the hypothesis that unresolvable immune stimulation from chronic inflammation leads to a maladaptive disease-inducing and perpetuating sympathetic response in an attempt to maintain allostasis. Since the role of sympathetic dysfunction in IMIDs is best studied in RA and rodent models of RA, this IMID is the primary one used to evaluate data relevant to our hypothesis. Here, we review the relevant literature and discuss sympathetic dysfunction as a significant contributor to the pathophysiology of IMIDs, and then discuss a novel target for treatment. Based on our findings in inflammatory arthritis and our understanding of common inflammatory process that are used by the immune system across all IMIDs, novel strategies to restore SNS homeostasis are expected to provide safe, cost-effective approaches to treat IMIDs, lower comorbidities, and increase longevity.
29970960 Relationship between beliefs about medicines, adherence to treatment, and disease activity 2018 OBJECTIVE: In patients with rheumatoid arthritis (RA), nonadherence to treatment is often related to patients' beliefs and concerns regarding their medication. This study aimed to analyze the correlations regarding patients' medication beliefs, medication adherence, and objective measures of disease activity and safety in patients with RA established on subcutaneous (SC) anti-tumor necrosis factor α (TNFα) therapy. METHODS: This Phase IV, noninterventional, non-drug-specific study enrolled patients with RA being treated with stable-dose SC anti-TNFα (adalimumab, etanercept, golimumab, and certolizumab pegol). At initial visit and 6 and 12 months later, patients completed the Beliefs about Medicines Questionnaire-Specific section, assessing perceptions of personal need for anti-TNFα therapy (anti-TNFα-Necessity) and concerns (anti-TNFα-Concerns), Medication Adherence Rating Scale (MARS), mean Disease Activity Score in 28 joints (DAS28), and other scales. Longitudinal data were analyzed by linear mixed models. RESULTS: A total of 460 patients were included. At initial visit, anti-TNFα-Necessity beliefs were high (mean ± SD: 4.3 ± 0.55) vs anti-TNFα-Concerns (2.8 ± 0.78). Medication adherence (MARS) was high (4.8 ± 0.39). All scores remained stable over the 1-year follow-up period. Anti-TNFα-Necessity beliefs and anti-TNFα-Concerns were not related to each other, but strongly correlated with medication adherence. While concerns worsened with disease activity, clinical status, and low quality of life, necessity beliefs remained unaffected. CONCLUSION: In patients with RA established on stable-dose SC anti-TNFα, anti-TNFα-Necessity beliefs persistently outweighed anti-TNFα-Concerns, but both correlated with adherence. These findings may be of use in subsequent studies looking to predict adherence in patients starting treatment with SC anti-TNFα.
30274625 Secondary, AA, Amyloidosis. 2018 Nov Secondary, AA, amyloidosis is a rare systemic complication that can develop in any long-term inflammatory disorder, and is characterized by the extracellular deposition of fibrils derived from serum amyloid A (SAA) protein. SAA is an acute-phase reactant synthetized largely by hepatocytes under the transcriptional regulation of proinflammatory cytokines. The kidney is the major involved organ with proteinuria as first clinical manifestation; renal biopsy is the commonest diagnostic investigation. Targeted anti-inflammatory treatment promotes normalization of circulating SAA levels preventing amyloid deposition and renal damage. Novel therapies aimed at promoting clearance of existing amyloid deposits soon may be an effective treatment approach.
30405932 A Case of Multiple Myeloma Misdiagnosed as Seronegative Rheumatoid Arthritis and Review of 2018 Multiple myeloma (MM) is a malignant plasma cell proliferation producing large numbers of monoclonal immunoglobulins. Typical MM symptoms include anemia, renal failure, hypercalcemia, and bone pain. Atypical symptoms have rarely been reported in the literature. We report a case of a 58-year-old male who presented with symmetrical inflammatory polyarthritis and was misdiagnosed with seronegative rheumatoid arthritis (RA). After failing many RA treatments and with further workup, the diagnosis of MM was made. This rare manifestation of MM carries a diagnostic challenge and causes a significant delay in treating such patients. Here, we report this unusual initial presentation with review of several cases in the English literature describing similar presentations.
29783736 Revisiting CD28 Superagonist TGN1412 as Potential Therapeutic for Pediatric B Cell Leukemi 2018 May 19 Pediatric acute lymphoblastic leukemia (ALL) represents the most common pediatric cancer diagnosis, with numbers rising gradually every year. This paper proposes a novel therapeutic agent for pediatric ALL on the basis of a failed clinical drug trial in 2006. TGN1412 was a promising therapeutic agent that yielded outstanding results in both in vitro studies and animal trials. It is a CD28 superagonist monoclonal antibody that activates T regulatory (T(Reg)) cells in the absence of costimulation of the T cell receptor (TCR) by an antigen-presenting cell. This drug was intended as a solution to T cell deficient diseases such as B cell leukemia and autoimmune diseases such as rheumatoid arthritis. When phase I clinical trials were conducted, all volunteers that received the drug experienced severe cytokine release syndrome (CRS) and faced multiple-organ failure within hours. TGN1412 was reassessed and re-entered clinical trials as a therapeutic for rheumatoid arthritis. A new assay was developed to better quantify T cell response, and volunteers in this trial experienced no pro-inflammatory cytokine release. This essay analyzes how misinformation contributed to the failure of TGN1412 in clinical trials and how revisiting this therapeutic could yield a novel treatment for pediatric B cell leukemia.
29044530 Gingival tissue, an extrasynovial source of malondialdehyde-acetaldehyde adducts, citrulli 2018 Feb BACKGROUND AND OBJECTIVE: Postranslational modification of proteins can lead to the production of autoantibodies and loss of immune tolerance. This process has been hypothesised to be a critical factor in the pathogenesis of rheumatoid arthritis. The objective of this study was to demonstrate that inflamed human gingival tissue provides an extrasynovial source of malondialdehyde-acetaldehyde adducts, citrullinated and carbamylated proteins all of which are considered to be linked to the development of rheumatoid arthritis. Identification of such modified proteins in inflamed gingiva may explain, in part, how inflammation of the periodontal tissues may influence the development of rheumatoid arthritis. MATERIAL AND METHODS: Gingival biopsies of healthy, mild and moderate periodontitis were triple stained with antibodies against malondialdehyde-acetaldehyde adducts, citrullinated and carbamylated proteins. RESULTS: Assessment of healthy gingival tissue revealed negligible staining for carbamylated, malondialdehyde-acetaldehyde (MAA), or citrullinated proteins. Mild periodontitis was positive for all three modifications. Furthermore, there was an increase in staining intensity for carbamylated, citrullinated and MAA-modified proteins in moderate periodontitis. Negative staining results were observed for the isotype controls. CONCLUSION: This study provides evidence for the presence of citrullinated, carbamylated and MAA adduct modified proteins in inflamed periodontal tissues. The potential for these proteins to play a role in autoimmunity in a multi-system inflammatory syndromic disease model now needs to be determined.
29690863 IL-20 bone diseases involvement and therapeutic target potential. 2018 Apr 24 BACKGROUND: Millions of people around the world suffer from bone disorders, likes osteoporosis, rheumatoid arthritis (RA), and cancer-induced osteolysis. In general, the bone remodeling balance is determined by osteoclasts and osteoblasts, respectively responsible for bone resorption and bone formation. Excessive inflammation disturbs the activities of these two kinds of cells, typically resulting in the bone loss. MAIN BODY: IL-20 is emerging as a potent angiogenic, chemotactic, and proinflammatory cytokine related to several chronic inflammatory disorders likes psoriasis, atherosclerosis, cancer, liver fibrosis, and RA. IL-20 has an important role in the regulation of osteoclastogenesis and osteoblastogenesis and is upregulated in several bone-related diseases. The anti-IL-20 monoclonal antibody treatment has a therapeutic potential in several experimental disease models including ovariectomy-induced osteoporosis, cancer-induced osteolysis, and bone fracture. CONCLUSION: This review article provides an overview describing the IL-20's biological functions in the common bone disorders and thus providing a novel therapeutic strategy in the future.
29663334 The rheumatic disease-associated FAM167A-BLK locus encodes DIORA-1, a novel disordered pro 2018 Aug Triggering of autoimmunity that leads to rheumatic disease has been suggested to depend upon gene-environment interactions occurring in epithelial barriers and associated immune cells. Genetic studies have identified associations of the FAM167A-BLK locus with rheumatoid arthritis, systemic lupus erythematosus (SLE) and Sjögren's syndrome. While BLK (B lymphocyte kinase) has a well-established role in B cells, family with sequence similarity to 167 member A (FAM167A) and its gene family remain uncharacterized. To begin to understand the role of FAM167A in rheumatic disease pathogenesis, we explored this gene family and cloned and investigated the gene products. Expression of quantitative trait locus analysis was performed in immune cells. FAM167A and FAM167B were cloned from human peripheral blood mononuclear cells (PBMC). Gene conservation and protein properties were analysed by online tools, mRNA expression measured in mouse organs by quantitative polymerase chain reaction (qPCR) and protein expression investigated in human tissues by immunohistochemistry. We found that autoimmune risk genotypes within the FAM167A-BLK locus lead to increased expression of FAM167A. The FAM167 gene family includes two members, FAM167A and FAM167B, which are not homologous to any other annotated gene but are evolutionarily conserved. The encoded proteins, which we denote 'disordered autoimmunity' (DIORA)-1 and DIORA-2, respectively, are characterized by a high content of intrinsic disorder. Notably, DIORA-1 has its highest expression in the lung, detectable in both bronchial epithelium and alveolar macrophages with an endosomal localization pattern. In summary, the FAM167A gene is associated with several rheumatic diseases and encodes a novel disordered protein, DIORA-1, which is expressed highly in the lung, consistent with a potential role in disease pathogenesis.
29562298 The subgingival microbiome in patients with established rheumatoid arthritis. 2018 Jul 1 OBJECTIVES: To profile and compare the subgingival microbiome of RA patients with OA controls. METHODS: RA (n = 260) and OA (n = 296) patients underwent full-mouth examination and subgingival samples were collected. Bacterial DNA was profiled using 16 S rRNA Illumina sequencing. Following data filtering and normalization, hierarchical clustering analysis was used to group samples. Multivariable regression was used to examine associations of patient factors with membership in the two largest clusters. Differential abundance between RA and OA was examined using voom method and linear modelling with empirical Bayes moderation (Linear Models for Microarray Analysis, limma), accounting for the effects of periodontitis, race, marital status and smoking. RESULTS: Alpha diversity indices were similar in RA and OA after accounting for periodontitis. After filtering, 286 taxa were available for analysis. Samples grouped into one of seven clusters with membership sizes of 324, 223, 3, 2, 2, 1 and 1 patients, respectively. RA-OA status was not associated with cluster membership. Factors associated with cluster 1 (vs 2) membership included periodontitis, smoking, marital status and Caucasian race. Accounting for periodontitis, 10 taxa (3.5% of those examined) were in lower abundance in RA than OA. There were no associations between lower abundance taxa or other select taxa examined with RA autoantibody concentrations. CONCLUSION: Leveraging data from a large case-control study and accounting for multiple factors known to influence oral health status, results from this study failed to identify a subgingival microbial fingerprint that could reliably discriminate RA from OA patients.
29556418 Identification of sarilumab pharmacodynamic and predictive markers in patients with inadeq 2018 INTRODUCTION: Interleukin-6 (IL-6) orchestrates formation of an inflammatory pannus, leading to joint damage in rheumatoid arthritis (RA). Sarilumab is a human monoclonal antibody blocking the IL-6Rα. In TARGET (NCT01709578), a phase 3 study in adults with moderate-to-severe RA and inadequate response or intolerance to tumour necrosis factor inhibitors, subcutaneous sarilumab 200 mg or 150 mg every 2 weeks (q2w) plus conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) significantly reduced disease activity versus placebo plus csDMARDs. METHODS: Circulating levels of biomarkers associated with synovial inflammation (matrix metalloproteinase 3 (MMP-3), collagen type I MMP-cleaved fragment (C1M), collagen type III MMP-cleaved fragment (C3M)), myeloid (soluble intercellular adhesion molecule 1 (sICAM-1), IL-8 and calprotectin) and lymphoid activation (chemokine, CXC motif, ligand 13 (CXCL13), CXCL10, B cell-activating factor) and bone remodelling (receptor activator of nuclear factor-κB ligand (RANKL), osteoprotegerin and osteocalcin) were evaluated in patients from a TARGET substudy. RESULTS: Sarilumab significantly decreased C1M, C3M, CXCL13, MMP-3 and total RANKL levels at week 24 versus placebo; some markers were significantly suppressed at week 2 and normalised to levels in healthy controls. Levels of sICAM-1 were predictive of disease activity score by C-reactive protein and clinical disease activity index low disease activity (LDA) response in the sarilumab 200 mg q2w group at week 12. A trend was observed in which patients with lower sICAM-1 levels at baseline had better response compared with patients with higher sICAM-1. CONCLUSIONS: Sarilumab plus csDMARDs decreased circulating biomarkers of synovial inflammation and bone resorption; sICAM-1 was predictive of achieving LDA with sarilumab. TRIAL REGISTRATION NUMBER: NCT01709578; Post-results.
29197963 Synthesis and biological evaluation of imidazo[1,2-[Formula: see text]]pyridazines as inhi 2018 Aug Tumor necrosis factor-alpha (TNF-[Formula: see text] is an important pro-inflammatory cytokine responsible for a diverse range of inflammatory diseases including rheumatoid arthritis. In the present manuscript, our medicinal chemistry efforts on the design, synthesis and TNF-[Formula: see text] evaluation of a series of 3, 6-disubstituted imidazo[1,2-b]pyridazine is described. The best compounds were 3-pyridyl and (4-(methylsulfonyl)phenyl) analogs 8q and 8w, showing inhibition of TNF-[Formula: see text] production with IC[Formula: see text]values of 0.9 and 0.4 [Formula: see text]M, respectively. The identified leads have potential for further development for treatment of inflammatory diseases.
29877270 The Spontaneous Regression of Grade 3 Methotrexate-related Lymphomatoid Granulomatosis: A 2018 Nov 1 Lymphomatoid granulomatosis (LYG) is a rare lung disorder diagnosed by radiological imaging of multiple pulmonary nodules and occasionally induced by methotrexate (MTX) use. To date, the treatment of LYG has not been standardized. We herein report the case of a patient with grade 3 MTX-related LYG who presented a bulky lung mass. Importantly, the disease condition only improved after the discontinuation of MTX and remained stable for more than 1 year. Chest physicians should be aware that LYG can develop as a single lung mass and spontaneously regress, even without aggressive chemotherapy, following the cessation of MTX.
29862158 Severe bacterial sepsis results in delayed diagnosis of tuberculous lymphadenitis in a rhe 2018 May Although tumor necrosis factor (TNF)-α inhibitors are effective in patients with rheumatoid arthritis (RA), an increased risk of infections often becomes a serious problem. It is well known that TNF-α inhibitors increase the risk of tuberculosis, but extrapulmonary tuberculosis often induced by them is difficult to diagnose using routine imaging examinations. We described a case of delayed diagnosis of a tuberculous lymphadenitis in a patient with RA treated with TNF-α inhibitor because of the complications of severe bacterial sepsis. In this case, rescreening with the interferon-γ release assay and excisional biopsy were useful in confirming the diagnosis of extrapulmonary tuberculosis. In the case we presented, she had other risk factors, that is, advanced age at the start of anti- TNF-α treatment or concomitant use of corticosteroid, might contribute to the development of complex infections. We should keep in mind that careful follow-up and appropriate examinations are necessary in caring for patients administering immunosuppressive treatments including anti- TNF-α drugs.
30042945 Endothelial Progenitor Cells: New Targets for Therapeutics for Inflammatory Conditions Wit 2018 Over the past decade, we have witnessed an exponential growth of interest into the role of endothelial progenitor cells (EPCs) in cardiovascular disease. While the major thinking revolves around EPC angiogenic repair properties, we have used a hypothesis-driven approach to discover disease-related defects in their characteristics and based on these findings, have identified opportunities for functional enhancement, which offer an exciting avenue for translation into clinical intervention. In this review, we focus on two groups; circulating myeloid angiogenic cells (MACs) and late outgrowth endothelial colony forming cells (ECFCs), and will discuss the unique properties and defects of each population, as new insights have been gained into the potential function of each sub-type using current techniques and multiomic technology. We will discuss their role in inflammatory disorders and alterations in mitochondrial function. In addition, we share key insights into the glycocalyx, and propose this network of membrane-bound proteoglycans and glycoproteins, covering the endothelium warrants further investigation in order to clarify its significance in ECFC regulation of vascularization and angiogenesis and ultimately for potential translational therapeutic aspects.
29116386 Clinical and ultrasonographic enthesopathy in inflammatory rheumatic diseases : Is MASEI o 2018 Oct AIM: We aimed at investigating the ultrasonographic (US) and clinical prevalence of enthesopathy in patients with rheumatoid arthritis (RA), and axial spondyloarthropathy (SpA), as well as the correlation between this condition and disease activity, along with the quality of life. METHODS: Included in the study were 30 axial SpA, 21 patients with RA, and 25 healthy cases. Bath Anklylosing Spondylitis Disease Activity Index (BASDAI), Ankylosing Spondylitis Quality of Life (ASQoL), Disease activity index  28 (DAS28), and Health Assessment Questionnaire (HAQ) were used for clinical evaluation, and enthesal pain was evaluated by VAS, whereas enthesitis US evaluation was performed by using the MAdrid Sonographic Enthesitis Index (MASEI). A total of 152 knees, ankles, and elbow regions of all patients and controls were examined by US. RESULTS: Total scores of physical examination of enthesitis were 1.97 ± 2.68 in axial SpA, 2.43 ± 1.80 in RA, and 0.23 ± 0.12 in the control groups. No statistically significant difference was identified in the enthesitis examination between axial SpA and RA groups (p = 0.123). According to the MASEI, no significant difference was observed in quadriceps tendon enthesitis or in distal patellar ligament enthesitis between axial SpA and RA groups (MASEI 3, 4, 5: p = 0.993, p = 0.124, p = 0.652). Aside from those points, axial SpA patients had statistically higher enthesitis scores at all MASEI enthesitis points (p < 0.05). In the axial SpA group, a significant and positive correlation was identified between BASDAI scores and total scores of enthesitis physical examination and MASEI total scores (r = 0.739, p = 0.0001, r = 0.516, p = 0.002). A moderately significant correlation was identified between ASQoL total scores and MASEI total scores (r = 0.466, p = 0.006), but not between the HAQ total scores and MASEI total scores (r = 0.213, p = 0.065). CONCLUSIONS: Compared to RA, US and clinical examination of enthesitis in patients with axial SpA should focus on the calcaneal enthesitis region. In axial SpA, ultrasonographic enthesitis is associated with impaired quality of life.
30224931 Investigation of Lake Hévíz Mineral Water Balneotherapy and Hévíz Mud Treatment in Mur 2018 Arthritic diseases are the most frequent causes of chronic pain and disability. Rheumatoid arthritis (RA) is an autoimmune disease characterized by synovial inflammation and progressive structural joint damage. Osteoarthritis is a degenerative process of the articular cartilage associated with hypertrophic changes in the bone. The aim of the present study was to investigate the anti-inflammatory and analgesic effects of Hévíz thermal water and mud in monosodium iodoacetate- (MIA-) (25 mg/ml, 20 μl i.a.) induced osteoarthritis and Complete Freund's adjuvant- (CFA-) (1 mg/ml, 50-50 μl s.c) induced rheumatoid arthritis murine models. The mechanonociceptive threshold of female NMRI mice (n=6- 8 mice/ group) was measured by aesthesiometry, and paw volume was monitored with plethysmometry, knee joint diameter with digital micrometer, and dynamic weight bearing on the hind limbs with a Bioseb instrument. Periarticular bone destruction was assessed by SkyScan 1176 in vivo micro-CT. Inflammatory cytokines were detected by ELISA in plasma samples. Treatments (30 min, every working day) with tap water, sand, and a combined therapy of tap water and sand served as controls. Hévíz medicinal water and combined treatment with water and mud significantly decreased the mechanical hyperalgesia and knee oedema in MIA-induced osteoarthritis model. However, balneotherapy did not influence mechanical hyperalgesia, weight bearing, or oedema formation induced by CFA. Neither medicinal water nor mud treatment ameliorated deep structural damage of the bones or the joints in the animal models. On the basis of the present findings, we conclude that balneotherapy is an effective complementary treatment to reduce the pain sensation and swelling in degenerative joint diseases such as osteoarthritis. Our experimental data are in agreement with the previous human studies that also confirmed antinociceptive and anti-inflammatory effects of thermal water and Hévíz mud treatments.