scholarly journals From Rheumatoid Factor to Anti-Citrullinated Protein Antibodies and Anti-Carbamylated Protein Antibodies for Diagnosis and Prognosis Prediction in Patients with Rheumatoid Arthritis

2021 ◽  
Vol 22 (2) ◽  
pp. 686
Author(s):  
Chao-Yi Wu ◽  
Huang-Yu Yang ◽  
Shue-Fen Luo ◽  
Jenn-Haung Lai
Keyword(s):  
Rheumatoid Arthritis ◽  
Treatment Options ◽  
Clinical Manifestations ◽  
Bone Destruction ◽  
Response To Therapy ◽  
Current Evidence ◽  
Prognosis Prediction ◽  
Diagnosis And Prognosis ◽  
Systemic Inflammatory Disease ◽  
Citrullinated Protein

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease mainly involving synovial inflammation and articular bone destruction. RA is a heterogeneous disease with diverse clinical presentations, prognoses and therapeutic responses. Following the first discovery of rheumatoid factors (RFs) 80 years ago, the identification of both anti-citrullinated protein antibodies (ACPAs) and anti-carbamylated protein antibodies (anti-CarP Abs) has greatly facilitated approaches toward RA, especially in the fields of early diagnosis and prognosis prediction of the disease. Although these antibodies share many common features and can function synergistically to promote disease progression, they differ mechanistically and have unique clinical relevance. Specifically, these three RA associating auto-antibodies (autoAbs) all precede the development of RA by years. However, while the current evidence suggests a synergic effect of RF and ACPA in predicting the development of RA and an erosive phenotype, controversies exist regarding the additive value of anti-CarP Abs. In the present review, we critically summarize the characteristics of these autoantibodies and focus on their distinct clinical applications in the early identification, clinical manifestations and prognosis prediction of RA. With the advancement of treatment options in the era of biologics, we also discuss the relevance of these autoantibodies in association with RA patient response to therapy.

scholarly journals Rheumatoid Arthritis and the Cervical Spine: A Review on the Role of Surgery

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
John L. Gillick ◽  
John Wainwright ◽  
Kaushik Das
Keyword(s):  
Rheumatoid Arthritis ◽  
Cervical Spine ◽  
Treatment Options ◽  
Surgical Techniques ◽  
Clinical Manifestations ◽  
Atlantoaxial Instability ◽  
Disease Modifying Antirheumatic Drugs ◽  
Systemic Inflammatory Disease ◽  
Neurologically Intact

Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease affecting a significant percentage of the population. The cervical spine is often affected in this disease and can present in the form of atlantoaxial instability (AAI), cranial settling (CS), or subaxial subluxation (SAS). Patients may present with symptoms and disability secondary to these entities but may also be neurologically intact. Cervical spine involvement in RA can pose a challenge to the clinician and the appropriate role of surgical intervention is controversial. The aim of this paper is to describe the pathology, pathophysiology, clinical manifestations, and diagnostic evaluation of rheumatoid arthritis in the cervical spine in order to provide a better understanding of the indications and options for surgery. Both the medical and surgical treatment options for RA have improved, so has the prognosis of the cervical spine disease. With the advent of disease modifying antirheumatic drugs (DMARDs), fewer patients are presenting with cervical spine manifestations of RA; however, those that do, now have improved surgical techniques available to them. We hope that, by reading this paper, the clinician is able to better evaluate patients with RA in the cervical spine and determine in which patients surgery is indicated.

scholarly journals P09.05 177Lu-DOTATATE therapy in progressive meningioma

2019 ◽  
Vol 21 (Supplement_3) ◽  
pp. iii39-iii39
Author(s):  
M Müther ◽  
W Roll ◽  
B Zinnhardt ◽  
M Schäfers ◽  
K Rahbar ◽  
...  
Keyword(s):  
Stable Disease ◽  
Treatment Options ◽  
Somatostatin Receptor ◽  
Therapy Response ◽  
Response To Therapy ◽  
Current Evidence ◽  
Promising Alternative ◽  
Multifocal Disease ◽  
Post Therapy

Abstract BACKGROUND Progressive meningioma is a challenging condition with a decreasing number of treatment options over the course of disease. Neurovascular involvement and multifocal disease often complicate surgical management. In addition, repeated radiotherapy carriers a risk of side effects. In somatostatin receptor expressing meningioma, peptide receptor radiotherapy (PPRT) with 177Lu-DOTATATE poses a promising alternative. However, current evidence is scarce. Hereby we present our single center experience of (PPRT) with 177Lu-DOTATATE in progressive meningioma. METHODS Eight patients (median age: 71 years; range 56–77) with progressive meningioma underwent PRRT using 177Lu-DOTATATE were included in this retrospective analysis. Response to therapy was assessed by interim and post-therapy 68Ga-DOTATATE-PET-CT and MRI. 177Lu-DOTATATE scintigraphies 48h p.i. were evaluated according to Krenning scale. Additionally, clinical outcome and follow up imaging were analyzed for progression free interval times. RESULTS Eight patients were included: Six patients with grade II and two patients with grade I meningiomas, according to the 2016 WHO classification. Six of eight patients harbored multifocal disease. One patients suffered systemic metastatic disease. Patients received a median of three cycles (range: 1 - 5) of PRRT with 177Lu-DOTATATE (mean injected dose 7.1 GBq) between 1/2015 and 1/2019. Tumor uptake in 48h p.i. 177Lu-Scintigraphies was heterogeneous (Krenning scale; median: 3; range: 1–4). Post-therapy imaging scheduled eight weeks after completion of therapy showed progressive disease in five patients, three patients had stable disease. Median follow-up post therapy response evaluation was 24 months in patients with stable disease. Median time to progression was 10 months. CONCLUSION In this cohort of eight progressive meningioma patients 177Lu-DOTATATE therapy showed heterogeneous efficacy.

scholarly journals The Results of Fetal Chondrocytes Transplantation in Patients with Rheumatoid Arthritis

2014 ◽  
Vol 3 ◽  
Author(s):  
Natalya Krivoruchko ◽  
Saltanat Tuganbekova ◽  
Gulnar Rakhimbekova ◽  
Karlygash Kuzembaeva ◽  
Lina Zaripova
Keyword(s):  
Rheumatoid Arthritis ◽  
Morphological Changes ◽  
Control Cell ◽  
Clinical Manifestations ◽  
Bone Destruction ◽  
Human Embryos ◽  
Control Group ◽  
X Ray ◽  
Donor Cells

Introduction. Nowadays anti-inflammatory and immunosuppressive therapy has significantly improved the quality of life and prognosis of rheumatoid arthritis (RA). Nevertheless, there are still many patients with progressive rheumatoid inflammation, resulting in the destruction of joints. Cell therapy seems like a promising direction in rheumatology. The aim of our research was to evaluate the efficacy of fetal chondrocyte transplantation in patients with RA.Methods. We examined 60 patients with rheumatoid arthritis (I - III stages) between 20 and 63 years of age. They were divided into 2 groups: the first group underwent the fetal chondrocytes transplantation (n = 40), and the second was a control group who got conservative therapy (n = 20). Donor cells were taken from the chondrogenic layer of the humerus or femur heads and hip condyles of human embryos in gestation for 17-20 weeks. A suspension of fetal chondrocytes injected into affected areas of the articular surfaces under X-ray control. Cell viability was determined before the injection. Efficacy of the therapy was assessed by clinical, instrumental, and laboratory tests. This clinical trial was allowed by The Ministry of Public Health and Ethics Committee. All of our patients gave informed consent for the fetal chondrocytes transplantation.Results. Evaluation of the clinical manifestations of RA in the first group of patients showed 3.7 times decrease in pain and 1.6 times relief of synovitis. Complete reduction of contracture was observed in 82% of patients in the first group. Morphometric changes in X-ray demonstrated inhibition of the destruction in articular cartilage and surfaces of bones after transplantation of fetal chondrocytes. The dynamics of morphological changes in synovium showed 2.5 times reduction of the inflammatory reaction. Transplantation of fetal chondrocytes led to a significant reduction in ESR, CRP, fibrinogen , γ-globulin after a period of 12 months (p < 0.03). Furthermore, patients in the second group had 2.7 times higher risk of ankylosis compared to the first group. We did not observe any complications of fetal chondrocytes transplantation.Conclusions. Application of fetal chondrocytes therapy had the desired clinical effect, which was confirmed by reduction of the RA activity and decrease of cartilage and bone destruction. 

scholarly journals Pathogenesis of rheumatoid arthritis

2014 ◽  
Vol 1 (1) ◽  
pp. 8-11
Author(s):  
Bilal Bengana ◽  
◽  
Samy Slimani ◽  
Bachir Hachemi ◽  
◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Interleukin 1 ◽  
Bone Destruction ◽  
Joint Inflammation ◽  
Transforming Growth Factor Β ◽  
High Serum ◽  
Autoimmune Reaction ◽  
Systemic Inflammatory Disease

Rheumatoid arthritis is a chronic systemic inflammatory disease of unknown cause. An external trigger (eg, cigarette smoking, infection, or trauma) that triggers an autoimmune reaction, leading to synovial hypertrophy and chronic joint inflammation along with the potential for extra-articular manifestations, is theorized to occur in genetically susceptible individuals. Several genes are implicated including class II major histocompatibility complex genes, PTPN22, and C5-TRAF1. Adaptive and innate immune responses in the synovium have been implicated in the pathogenesis of RA. Evidence of autoimmunity, including high serum levels of autoantibodies such as rheumatoid factors and anticitrullinated peptide antibodies, can be present for many years before the onset of clinical arthritis. Although inciting factors have yet to be identified, the presence and activity of a number of proinflammatory chemokines and cytokines have established roles in disease pathogenesis. The activation and infiltration of T cells and macrophages in the synovium result in the production of interleukin-1, -2, -6, -8, -10, -17; tumor necrosis factor-α (TNF-α); platelet-derived growth factor; insulin-like growth factor; and transforming growth factor β (TGF β). These effector molecules are implicated in synovial tissue inflammation and proliferation, cartilage and bone destruction, and systemic effects.

scholarly journals Surgical management of aneurysmal bone cysts of the spine

2003 ◽  
Vol 15 (5) ◽  
pp. 1-7 ◽  
Author(s):  
James K. Liu ◽  
Douglas L. Brockmeyer ◽  
Andrew T. Dailey ◽  
Meic H. Schmidt
Keyword(s):  
Treatment Options ◽  
Clinical Manifestations ◽  
Treatment Strategies ◽  
Bone Destruction ◽  
Unknown Origin ◽  
Neurological Deficits ◽  
Bone Cysts ◽  
Complete Excision ◽  
Aneurysmal Bone Cysts ◽  
Special Factors

Object Aneurysmal bone cysts of the spine are benign, highly vascular osseous lesions of unknown origin that may present difficult diagnostic and therapeutic challenges. They are expansile lesions containing thin-walled, blood-filled cystic cavities that cause bone destruction and sometimes spinal deformity and neurological compromise. The treatment of aneurysmal bone cysts of the spine remains controversial according to the literature. In this review, the authors discuss the clinical manifestations, pathophysiological features, neuroimaging characteristics, and treatment strategies for these lesions. Methods Treatment options include simple curettage with bone grafting, complete excision, embolization, and radiation therapy. Reconstruction and stabilization of the spine may be warranted if deformity and instability are present. Special factors need to be considered in the management of these lesions. Conclusions Complete excision of aneurysmal bone cysts offers the best chance of cure and spinal decompression if neurological deficits are present.

scholarly journals A Case of Sporadic Blau Syndrome with an Uncommon Clinical Course

2018 ◽  
Vol 2018 ◽  
pp. 1-5 ◽  
Author(s):  
Miyoko Imayoshi ◽  
Yoshiyasu Ogata ◽  
Shuichi Yamamoto
Keyword(s):  
Clinical Course ◽  
Clinical Manifestations ◽  
Gene Mutations ◽  
Bone Destruction ◽  
Joint Space ◽  
Infliximab Treatment ◽  
Blau Syndrome ◽  
Case Presentation ◽  
Systemic Inflammatory Disease ◽  
Systemic Onset

Background. Sporadic Blau syndrome (SBS), a rare systemic inflammatory disease in children, is associated with NOD2 gene mutations. SBS is often misdiagnosed as juvenile idiopathic arthritis (JIA) because of their similar clinical manifestations. Herein, we present a case of SBS with an uncommon clinical course. Case Presentation. An 11-year-old girl with recurrent right ankle swelling for 4 years was referred to our hospital. One month before admission, she developed an intermittent high fever. She was diagnosed with systemic-onset JIA on the basis of physical and blood examination results. She was treated with ibuprofen, prednisolone, and methotrexate for 5 years. During this period, her joint lesion showed neither bone destruction nor joint space narrowing on radiography, which are characteristics of JIA. Twelve months after the termination of methotrexate treatment, she presented with bilateral panuveitis. A missense mutation, p.(R587C), was detected in her NOD2 gene, and she was diagnosed with SBS. Then, infliximab treatment was started, and her visual acuity recovered. Conclusion. SBS may sometimes be misdiagnosed as JIA. A joint lesion without bone destruction might be a key feature to distinguish SBS from JIA. Analysis of the NOD2 gene is recommended in such cases.

scholarly journals Bridging Insights From Lymph Node and Synovium Studies in Early Rheumatoid Arthritis

2022 ◽  
Vol 8 ◽  
Author(s):  
Aoife M. O'Byrne ◽  
Tineke A. de Jong ◽  
Lisa G. M. van Baarsen
Keyword(s):  
Rheumatoid Arthritis ◽  
Lymph Node ◽  
Lymph Nodes ◽  
Stromal Cells ◽  
Clinical Manifestations ◽  
Bone Destruction ◽  
Peripheral Tolerance ◽  
Unknown Etiology ◽  
Synovial Joint ◽  
Innovative Drug

Rheumatoid arthritis (RA) is a chronic autoimmune disease of unknown etiology characterized by inflammation of the peripheral synovial joints leading to pannus formation and bone destruction. Rheumatoid Factor (RF) and anti-citrullinated protein antibodies (ACPA) are present years before clinical manifestations and are indicative of a break in tolerance that precedes chronic inflammation. The majority of studies investigating disease pathogenesis focus on the synovial joint as target site of inflammation while few studies explore the initial break in peripheral tolerance which occurs within secondary lymphoid organs such as lymph nodes. If explored during the earliest phases of RA, lymph node research may provide innovative drug targets for disease modulation or prevention. RA research largely centers on the role and origin of lymphocytes, such as pro-inflammatory T cells and macrophages that infiltrate the joint, as well as growing efforts to determine the role of stromal cells within the synovium. It is therefore important to explore these cell types also within the lymph node as a number of mouse studies suggest a prominent immunomodulatory role for lymph node stromal cells. Synovium and proximal peripheral lymph nodes should be investigated in conjunction with one another to gain understanding of the immunological processes driving RA progression from systemic autoimmunity toward synovial inflammation. This perspective seeks to provide an overview of current literature concerning the immunological changes present within lymph nodes and synovium during early RA. It will also propose areas that warrant further exploration with the aim to uncover novel targets to prevent disease progression.

scholarly journals Epigenetic Regulation Mediated by miRNA in the Susceptibility and Pathogenesis of Rheumatoid Arthritis

2020 ◽  
Author(s):  
Shicheng Guo ◽  
Cen Chang ◽  
Lingxia Xu ◽  
Runrun Zhang ◽  
Yehua Jin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Therapeutic Intervention ◽  
Target Genes ◽  
Cell Types ◽  
Micro Rna ◽  
Current Evidence ◽  
Diagnosis And Prognosis ◽  
Transcriptome Regulation ◽  
Therapy Target ◽  
Different Cell Types

micro-RNA (miRNA) has been demonstrated to play important roles in the transcriptome regulation and disease development including cancer and autoimmune disease such as rheumatoid arthritis. However, a comprehensive map on how the mRNAs regulate transcripts, pathways, immune system differentiation and interaction with terminal cells like T-cells, fibroblast-like synoviocytes (FLS), osteoblast and osteoclast still unknown. In this review, we have provided a thorough summary on the roles of miRNAs in the susceptibility, pathogenesis, diagnosis, therapeutic intervention and prognosis. Numerous miRNAs were found abnormally expressed in rheumatoid arthritis relevant cells and regulated the target genes and pathways like NF-&kappa;B, Fas-FasL, JAK-STAT, IRE1-RIDD, mTOR pathway. In addition, miRNA act as gene expression regulators affect the T-cell differentiate to different cell types including Th17 and T-reg cells which provide promising gene therapy target to regulate immune systems in rheumatoid arthritis. We also summarized interesting diagnosis and prognosis roles of blood and cell-free based miRNAs which provided novel opportunity to work together with rheumatoid factors (RF), anti-CCP to provide accurate diagnosis and prognosis especially for seronegative patients. Furthermore, functional genetic variants in miRNA-499 and miRNA-146a explained part of missing susceptibility of rheumatoid arthritis. Finally, miRNAs were showed as promising biomarker to indicate the DMRDS and immunotherapy efficiency, drug response and resistance. What&rsquo;s more, autotherapeutic effect of miRNA intervention provided promising to develop miRNA based rheumatoid arthritis drugs. Overall, current evidence supports miRNAs as the interesting targets to better understand the pathogenetic mechanism and therapeutic intervention of rheumatoid arthritis.

scholarly journals Epigenetic Regulation Mediated by microRNAs in the Susceptibility and Pathogenesis of Rheumatoid Arthritis

2020 ◽  
Author(s):  
Shicheng Guo ◽  
Cen Chang ◽  
Lingxia Xu ◽  
Runrun Zhang ◽  
Yehua Jin ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Immune System ◽  
Target Genes ◽  
Cell Types ◽  
Therapeutic Interventions ◽  
Current Evidence ◽  
The Novel ◽  
Diagnosis And Prognosis ◽  
Therapy Targets ◽  
System Differentiation

MicroRNAs (miRNAs) play crucial roles in the regulation of the transcriptome and development of diseases including cancer and autoimmune diseases, such as rheumatoid arthritis (RA). Currently, a comprehensive map, illustrating how miRNAs regulate transcripts, pathways, immune system differentiation, and their interaction with terminal cells, such as T cells, fibroblast-like synoviocytes (FLS), osteoblasts, and osteoclasts, is still missing. In this review, we provide a thorough summary of the roles of miRNAs in the susceptibility to pathogenesis, diagnosis, therapeutic intervention, and prognosis of RA. Numerous miRNAs are abnormally expressed in cells involved in RA, and regulate target genes and pathways including the NF-&kappa;B, Fas-FasL, JAK-STAT, IRE1-RIDD, and mTOR pathways. By regulating gene expression, miRNAs affect T cell differentiation to diverse cell types, including Th17 and T-reg cells, and thus constitute promising gene therapy targets to modulate the immune system in RA. We summarize the diagnostic and prognostic potential of blood-circulating and cell-free miRNAs, highlighting the novel opportunities to combine these with rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) to provide accurate diagnosis and prognosis, especially for seronegative patients. Furthermore, we outline how functional genetic variants of miR-499 and miR-146a partly explain the unmet susceptibility to RA. Additionally, we review the evidence implicating miRNAs as promising biomarkers of efficiency, response, and resistance to disease-modifying anti-rheumatic drugs (DMRDs) and immunotherapy. Finally, we discuss the autotherapeutic effect of miRNA intervention as a step toward the development of miRNA-based anti-RA drugs. Collectively, the current evidence supports miRNAs as interesting targets to better understand the pathogenetic mechanisms of RA and design more efficient therapeutic interventions.

scholarly journals Dietary Habits and Nutrition in Rheumatoid Arthritis: Can Diet Influence Disease Development and Clinical Manifestations?

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1456 ◽  
Author(s):  
Chiara Gioia ◽  
Bruno Lucchino ◽  
Maria Grazia Tarsitano ◽  
Cristina Iannuccelli ◽  
Manuela Di Franco
Keyword(s):  
Rheumatoid Arthritis ◽  
Dietary Habits ◽  
Disease Risk ◽  
Harmful Effect ◽  
Antioxidant Properties ◽  
Clinical Manifestations ◽  
Bone Destruction ◽  
Systemic Autoimmune Disease ◽  
Joint Involvement ◽  
Protective Effects

Rheumatoid arthritis (RA) is a systemic, autoimmune disease characterized by joint involvement, with progressive cartilage and bone destruction. Genetic and environmental factors determine RA susceptibility. In recent years, an increasing number of studies suggested that diet has a central role in disease risk and progression. Several nutrients, such as polyunsaturated fatty acids, present anti-inflammatory and antioxidant properties, featuring a protective role for RA development, while others such as red meat and salt have a harmful effect. Gut microbiota alteration and body composition modifications are indirect mechanisms of how diet influences RA onset and progression. Possible protective effects of some dietary patterns and supplements, such as the Mediterranean Diet (MD), vitamin D and probiotics, could be a possible future adjunctive therapy to standard RA treatment. Therefore, a healthy lifestyle and nutrition have to be encouraged in patients with RA.

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