Induction of inflammatory arthropathy resembling rheumatoid arthritis in mice transgenic for HTLV-I

Y. Iwakura; M. Tosu; E. Yoshida; M. Takiguchi; K. Sato; I. Kitajima; K. Nishioka; K. Yamamoto; T. Takeda; M. Hatanaka; a. et

doi:10.1126/science.1887217

Development of Chronic Inflammatory Arthropathy Resembling Rheumatoid Arthritis in Interleukin 1 Receptor Antagonist–Deficient Mice

Journal of Experimental Medicine ◽

10.1084/jem.191.2.313 ◽

2000 ◽

Vol 191 (2) ◽

pp. 313-320 ◽

Cited By ~ 504

Author(s):

Reiko Horai ◽

Shinobu Saijo ◽

Hidetoshi Tanioka ◽

Susumu Nakae ◽

Katsuko Sudo ◽

...

Keyword(s):

Rheumatoid Arthritis ◽

Receptor Antagonist ◽

Interleukin 1 ◽

Type Ii Collagen ◽

Cytokine Network ◽

Gene Deficiency ◽

Double Stranded Dna ◽

Inflammatory Arthropathy ◽

Factor Α ◽

Deficient Mice

Interleukin (IL)-1 is a proinflammatory cytokine that plays important roles in inflammation, host defense, and the neuro-immuno-endocrine network. IL-1 receptor antagonist (ra) is an endogenous inhibitor of IL-1 and is supposed to regulate IL-1 activity. However, its pathophysiological roles in a body remain largely unknown. To elucidate the roles of IL-1ra, IL-1ra–deficient mice were produced by gene targeting, and pathology was analyzed on different genetic backgrounds. We found that all of the mice on a BALB/cA background, but not those on a C57BL/6J background, spontaneously developed chronic inflammatory polyarthropathy. Histopathology showed marked synovial and periarticular inflammation, with articular erosion caused by invasion of granulation tissues closely resembling that of rheumatoid arthritis in humans. Moreover, elevated levels of antibodies against immunoglobulins, type II collagen, and double-stranded DNA were detected in these mice, suggesting development of autoimmunity. Proinflammatory cytokines such as IL-1β, IL-6, and tumor necrosis factor α were overexpressed in the joints, indicating regulatory roles of IL-1ra in the cytokine network. We thus show that IL-1ra gene deficiency causes autoimmunity and joint-specific inflammation and suggest that IL-1ra is important in maintaining homeostasis of the immune system. Possible involvement of IL-1ra gene deficiency in RA will be discussed.

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Osteoarthritis, osteoarthrosis and osteoarthropathy: What is the difference?

Srpski medicinski casopis Lekarske komore ◽

10.5937/smclk2101015j ◽

2021 ◽

Vol 2 (1) ◽

pp. 25-32

Author(s):

Danilo Jeremić ◽

Boris Gluščević ◽

Stanislav Rajković ◽

Želimir Jovanović ◽

Branislav Krivokapić

Keyword(s):

Rheumatoid Arthritis ◽

Clinical Presentation ◽

Joint Disease ◽

Joint Diseases ◽

Significant Progress ◽

Inflammatory Joint Diseases ◽

The Past ◽

Inflammatory Arthropathy ◽

The Difference ◽

Made In

Osteoarthritis, osteoarthrosis, and osteoarthropathy are diseases that doctors encounter daily in their practice. The use of all three terms is customary, often without a clear justification as to why a particular term is used for a particular case. In the past several decades, doctors mainly differentiated among these diseases based on clinical presentation and radiography. In the past several years, however, significant progress has been made in the field of biochemical, immunological, and cytohistological research, which has provided explanations for the pathogenesis of these conditions, enabled defining differences amongst them and facilitated the use of appropriate terms for each one of these diseases. The term arthritis (osteoarthritis) should be used exclusively for primarily inflammatory joint diseases-rheumatoid arthritis, juvenile arthritis, reactive arthritis (Reiter's syndrome). If the etiology is infectious, this must also be emphasized-septic (purulent) arthritis, tuberculous arthritis. Arthrosis (osteoarthrosis) relates to changes in the joints occurring due to pathological processes within the joint itself, but which, in their basis, are not inflammatory. Arthropathy is a term for joint disease stemming from another diseased organ or system of organs.

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POS0047 OUTCOMES IN INFLAMMATORY ARTHROPATHY PATIENTS HOSPITALIZED FOR COVID-19

Annals of the Rheumatic Diseases ◽

10.1136/annrheumdis-2021-eular.482 ◽

2021 ◽

Vol 80 (Suppl 1) ◽

pp. 228.2-229

Author(s):

T. Collins ◽

V. Patel ◽

A. Babajanians ◽

S. Kubomoto

Keyword(s):

Rheumatoid Arthritis ◽

Length Of Stay ◽

Odds Ratio ◽

Inflammatory Markers ◽

Composite Endpoint ◽

P Value ◽

Invasive Ventilation ◽

Icu Admission ◽

Inflammatory Arthropathy ◽

Comorbidity Index

Background:Covid 19 is a new and rapidly spreading corona virus which has reached pandemic proportions. As of 5/22/20 there are 5.08 million confirmed cases and 332,000 deaths worldwide. Primary manifestations are respiratory, with a subset developing severe hypoxic respiratory failure. Several risk factors predispose patients to worse outcomes including age, obesity, hypertension, chronic kidney disease, COPD, asthma, CHF, and diabetes. This is a retrospective cohort analysis of patients with Rheumatoid arthritis, Ankylosing spondylitis, or Psoriatic arthritis who were hospitalized for COVID-19 infection across 165 HCA hospitals from 1/1/2020 to 5/30/2020. We compared endpoints and calculated odds of ICU admission, invasive ventilation, mortality compared to control as well as length of stay and discharge location.Objectives:Our objectives include measuring the outcome of Patients in two arms, the first being those with Rheumatoid arthritis, Ankylosing spondylitis, and Psoriatic arthritis who are infected with COVID 19 to an age matched and comorbidity matched arm (using the Charlson comorbidity index) for the composite endpoint of ICU admission, invasive ventilation, and death. We believe the inflammatory arthropathy arm will have a worse composite endpoint then the control arm. we will also attempt to calculate a hazard ratio of this arm vs the control to the composite endpoint. We will also examine the length of stay as well as inflammatory markers mentioned in between the two arms. We suspect initial inflammatory markers will be lower in the inflammatory arthropathy arm, particularly CRP and LDH, due to chronic immune modulating medication and these markers will not correlate as closely with severe illness represented by the composite endpoint as in the control arm.Methods:We analyzed 86,217 patients admitted with COVID-19 comparing 751 patients who had inflammatory arthropathy to patients who did not. T tests were used for parametric outcome and chi square tests for non-parametric outcomes. Multivariate analysis included potential confounders such as age, and comorbidities such as diabetes, heart disease, etc.Results:The odds ratio for mortality in the arthropathy arm was 1.37 with a confidence interval of 1.09 to 1.71 with a p value of 0.006. The odds ratio for ventilation was 1.35 with CI of 1.09 to 1.67 and p value of 0.006. The odds ratio of ICU admission was 1.46 with CI of 1.24 to 1.72 and P value of 0.000. The average length of stay of the arthropathy arm was 8.51 days +/- 10.02 vs 4.59 days +/- 8.26 of the control, p < 0.001. The discharge disposition of the arthropathy arm vs control group is as follows, 13.32% died inpatient vs 5.87% in the control, 56.72% were discharged home vs 77.19%, 6.79% went to hospice care vs 3.10%, 4.79% remained inpatient at the end of the study interval vs 3.45%, 17.18% were discharged to rehab vs 8.43%, and other discharges not included in the above groupings were 1.2% vs 1.96%, p<0.001. 31.29% of the arthropathy group required ICU admission vs 16.32% and 13.98% required ventilation vs 6.9%, p <0.001. The average age was higher in the arthropathy arm vs control at 66.56 years old vs 51.53, p <0.001. Charlson comorbidity index was also higher in the arthropathy arm at 2.72 vs 0.96, p <0.001.Conclusion:This is a large analysis of inflammatory arthropathy patients hospitalized with COVID-19. While the arthropathy group was older, and had more co-morbidities, when adjusting for potential confounders, inflammatory arthropathy patients had a higher risk of death and mechanical ventilation, as well as longer length of stay.Disclosure of Interests:None declared.

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DPP-4 inhibitor (sitagliptin)-induced seronegative rheumatoid arthritis

BMJ Case Reports ◽

10.1136/bcr-2018-228981 ◽

2019 ◽

Vol 12 (8) ◽

pp. e228981 ◽

Cited By ~ 4

Author(s):

Simonette Padron ◽

Everett Rogers ◽

Michelle Demory Beckler ◽

Marc Kesselman

Keyword(s):

Rheumatoid Arthritis ◽

Classification Criteria ◽

Predisposing Factor ◽

Dipeptidyl Peptidase 4 ◽

American College Of Rheumatology ◽

European League Against Rheumatism ◽

Dipeptidyl Peptidase 4 Inhibitor ◽

Inflammatory Arthropathy ◽

European League

Sitagliptin is a dipeptidyl peptidase-4 inhibitor commonly used in the treatment of type 2 diabetes mellitus for glycaemic control. Concerns have arisen regarding adverse events caused by this drug, particularly concerning arthralgias. Here, we report on a 56-year-old man being treated with sitagliptin who developed inflammatory arthritis after taking the drug for 6 months. The patient presented with pain, swelling and erythema in multiple joints and was eventually diagnosed with seronegative rheumatoid arthritis (RA) under the 2010 American College of Rheumatology/European League Against Rheumatism classification criteria. His symptoms continued for several months after stopping sitagliptin and eventually went into remission after a tapered course of steroids, hydroxychloroquine and methotrexate. Furthermore, the patient is HLA-DRB3 positive, a genetic marker that is still being investigated for its role in the pathogenesis of RA and that may have been a predisposing factor in the development of this patient’s inflammatory arthropathy.

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THE MANAGEMENT OF AMAVATA (RHEUMATOID ARTHRITIS) WITH VATARI GUGGULU AND BRIHAT SIMHANADA GUGGULU

November 2020 - International Ayurvedic Medical Journal ◽

10.46607/iamj0209022021 ◽

2021 ◽

Vol 9 (2) ◽

pp. 335-342

Author(s):

Praveen Kumar ◽

Sriram Chandra Mishra ◽

Vandana Gupta

Keyword(s):

Rheumatoid Arthritis ◽

Clinical Research ◽

Therapeutic Approach ◽

Severe Pain ◽

Clinical Entity ◽

Moderate Improvement ◽

Mild Improvement ◽

Pathogenic Factors ◽

Inflammatory Arthropathy ◽

Principles Of Treatment

The detail knowledge on Amavata was first explained by Madhavakar, whereas Chakrapani Dutta first gave knowledge about principle and management of the disease. Amavata is a clinical entity very much similar to the chronic but active inflammatory arthropathy, the Rheumatoid arthritis. Till now, the etio-pathogenesis of Rheumatoid arthritis is not known precisely but among the hypothesis, entero-pathy along with autoimmune have important role regarding this disease. In Amavata, due to impaired functioning of 'Kayagni' the anna-rasa undergoes fermentation resulted formation of ama (biotoxin) which combines with vitiated Vata (biophysical force for movement) to form Amavata.(1) So, two important entities one is toxin and other is movement, when comes together kha vaigunya concept the disease formed which is worst one. That’s why swelling, severe pain, and restricted movements are the main features of Amavata. Severe pain, difficulty in movements, and swelling on the joints along with fever etc makes the patient’s life miserable. Although Ama and Vata are chiefly pathogenic factors, Kapha and Pitta are also invariably involved in its pathogenesis (Samprapti). The therapeutic approach should be on Vata dosha, Kapha dosha and correction of Amadosha and of Agni viz. Pitta. The line of treatment for amavata also includes langhanam, swedanam, tiktam, deepana, katu drugs and sodhana treatment like virechana, basti etc. The shamana drugs which are having Vatashamaka, Amapachaka, Ama Shoshaka, and Deepniya properties can be used in the treatment of this disease. Vatari Guggulu and Brihat simhanada guggulu carries indication for Amavata according to Bhaisajya Ratnavali. The compositions in it are approachable lieu of principles of treatment of Amavata. The clinical research shows that in TG I, 7 (46.67%) patients were got Moderate im-provement while 8 (53.33%) patients were got Mild improvement. In TG II 10 (66.67%) patients were get Moderate improvement while 5 (33.33%) patients were got Mild improvement.

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