Rheumatoid Arthritis

Rheumatoid arthritis (RA) is an autoimmune disease in which the body’s immune system attacks its own tissue. It is a chronic disorder that increases in prevalence with advancing age, but it can begin at any age. Symptoms include pain, swelling, and stiffness of the joints. When untreated, joint damage and deformities can eventually lead to difficulty moving the hands, wrists, knees, and/or hips. RA is considered a systemic disease because it can also involve more than just joints—potentially damaging skin, blood vessels, lungs, eyes, and/or the heart.

Prescription treatments include anti-inflammatory medications, disease-modifying anti-rheumatic drugs (DMARDs), Janus kinase (JAK) inhibitors. Physical therapy and low impact exercises are recommended as well.

Frequently Asked Questions

  • What causes rheumatoid arthritis?

    Rheumatoid arthritis is caused by inflammation and immune-mediated damage to the body’s tissue. These effects are produced by immune cells that mistakenly attack joints, and sometimes other organs of the body as well. Several underlying risk factors increase a person’s predisposition to RA, including having other immune diseases, a family history of RA, smoking, obesity, and stress.

  • Is rheumatoid arthritis an autoimmune disease?

    RA is considered an autoimmune disease. It is characterized by inflammation and tissue damage that is caused by the body’s own immune system working against itself. Excess immune cells and immune proteins chronically flood the joints and other tissue, attacking these structures as they would combat an infectious organism. There isn’t a clear trigger for the immune system overactivity.

  • Is rheumatoid arthritis hereditary?

    There is a hereditary component to RA, and you may be more prone to developing the disorder if you have a family history of RA or other autoimmune conditions. Certain inherited abnormalities in the genes that direct the immune system have been identified in association with RA. And genetic changes tend to be more commonly identified among people who develop RA at a young age.

  • How is rheumatoid arthritis diagnosed?

    RA diagnosis relies on a combination of symptoms, clinical exam, and diagnostic tests. The physical exam shows joint tenderness and swelling. Joint inflammation and degeneration may be seen on imaging tests. Inflammatory markers, including erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP), may be elevated in the blood. The 2010 RA Classification Criteria, a point-based system, may be used to aid in the diagnosis of RA.

  • What is the difference between osteoarthritis and rheumatoid arthritis?

    Both conditions involve joint pain, and degeneration. Osteoarthritis is caused by wear and tear, and RA by immune system dysfunction. Osteoarthritis affects injured or overused joints and doesn’t involve other organs. RA affects multiple joints, and is a result of systemic disease. Prescription disease-modifying agents are a cornerstone of RA treatment, and exercise is central to osteoarthritis treatment. They don’t cause each other, but osteoarthritis and RA can coexist.

  • What are the first signs of rheumatoid arthritis?

    You may have joint stiffness, swelling, and tenderness with RA. The symptoms tend to be more noticeable in the morning, especially early in the disease course. And you can also have fatigue and fever. Because the early symptoms can be somewhat vague, RA can seem similar to other conditions like lupus and Lyme disease. Late signs include severe pain, joint deformity, and limited mobility.

Key Terms

Page Sources
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  1. Centers for Disease Control and Prevention. Rheumatoid arthritis (RA). Updated July 27, 2020.

  2. National Institute of Arthritis and Musculoskeletal and Skin Diseases. Rheumatoid arthritis. Updated September 2019.

  3. American College of Rheumatology. Rheumatoid arthritis. Updated March 2019.

  4. Fatima Rizvi ST, Arif A, Azhar A. TNF gene promoter region polymorphisms and association with young-onset rheumatoid arthritis. Pak J Pharm Sci. 2019 Sep;32(5(Supplementary)):2295-2297. PMID: 31894057.

  5. Mjaavatten MD, Bykerk VP. Early rheumatoid arthritis: the performance of the 2010 ACR/EULAR criteria for diagnosing RA. Best Pract Res Clin Rheumatol. 2013 Aug;27(4):451-66. doi: 10.1016/j.berh.2013.09.001

  6. Cho J, Pyo JY, Fadriquela A, Uh Y, Lee JH. Comparison of the analytical and clinical performances of four anti-cyclic citrullinated peptide antibody assays for diagnosing rheumatoid arthritis. Clin Rheumatol. 2020 Sep 23. doi: 10.1007/s10067-020-05412-w

  7. American College of Rheumatology. Rheumatoid arthritis. Updated March 2019

  8. Jacob H, Curtis AM, Kearney CJ. Therapeutics on the clock: circadian medicine in the treatment of chronic inflammatory diseases. Biochem Pharmacol. 2020 Sep 30:114254. doi:10.1016/j.bcp.2020.114254

  9. Nehring SM, Goyal A, Bansal P, Patel BC. C reactive protein (CRP). 2020 Jun 5. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan–.

  10. Alves F, Gonçalo M. Suspected inflammatory rheumatic diseases in patients presenting with skin rashes. Best Pract Res Clin Rheumatol. 2019 Aug;33(4):101440. doi:10.1016/j.berh.2019.101440

  11. Lipina M, Makarov M, Mukhanov V, Karpashevich A, Maglevaniy S, Amirdjапоvа V, Archipov S. Arthroscopic synovectomy of the knee joint for rheumatoid arthritis. Int Orthop. 2019 Aug;43(8):1859-1863. doi:10.1007/s00264-018-4160-z

  12. Amini A, Yahyanezhad S, Velez E, Gholamrezanezhad A, Fotoohi M, Jafari E, Assadi M. Prospective evaluation of phosphorus-32 radiation synovectomy in patients with severe and chronic rheumatoid arthritis unresponsive to conventional medical treatment. Nucl Med Commun. 2020 Jan;41(1):65-72. doi:10.1097/MNM.0000000000001116

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