Rheumatoid Arthritis

Rheumatoid arthritis (RA) is a chronic, systemic autoimmune disease in which the immune system attacks the body’s own tissues, particularly the lining of joints. It causes pain, swelling, stiffness, and reduced joint function. Persistent inflammation can damage cartilage, bone, and surrounding tissues, while disease outside the joints can affect the lungs, heart, eyes, skin, and other organs. (niams.nih.gov)

Occurrence and risk factors

The World Health Organization estimated that 18 million people worldwide were living with rheumatoid arthritis in 2019. Approximately 70% were women, and 55% were older than 55 years. These figures describe the population living with the disease, rather than the age at which symptoms first appeared. (who.int)

RA can develop across a broad age range, although its occurrence increases with age. Recognized risk factors include female sex, family history, and smoking. Genetic susceptibility contributes to risk, but possessing associated genetic variants does not mean that a person will develop the disease. Its precise initiating cause remains unknown. (niams.nih.gov)

Disease process

The principal site of joint inflammation is the synovium, the tissue lining the inner surface of the joint capsule. Immune activity causes this lining to become inflamed and thickened. Continued inflammation can destroy cartilage and bone and impair the tendons, ligaments, and muscles that stabilize the joint. The resulting structural changes may produce deformity and loss of function. Immune abnormalities can begin before recognizable joint symptoms appear. (niams.nih.gov)

This process differs from osteoarthritis, another common cause of joint pain and stiffness. Although symptoms overlap, RA is an autoimmune inflammatory disease, and its diagnosis cannot be established from pain or stiffness alone. (nhs.uk)

Symptoms and complications

RA commonly affects the small joints of the hands and feet and the wrists. Involvement is often symmetrical, affecting corresponding joints on both sides of the body, but symmetry is not universal. Typical symptoms include:

Joint pain, tenderness, swelling, and warmth.
Stiffness after inactivity, especially in the morning, often lasting longer than 30 minutes.
Difficulty gripping objects or performing everyday tasks.
Fatigue, reduced appetite, and sometimes fever or weight loss.

Symptoms may develop gradually or more rapidly, and periods of worsening activity are called flares. (nhs.uk)

Complications include permanent joint damage, tendon rupture, and joint deformity. Disease beyond the joints may cause lung inflammation or scarring, inflammation around the heart, eye inflammation, and inflammation of blood vessels. RA is also associated with an increased risk of cardiovascular disease, including heart attack and stroke. These complications do not occur in every affected person. (nhs.uk)

Diagnosis

Diagnosis combines the history of symptoms, physical examination, laboratory findings, and imaging. No single test definitively establishes or excludes RA, and early disease may be difficult to distinguish from other joint disorders. (nhs.uk)

Blood tests commonly include:

Rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) antibodies: immune markers that can support the diagnosis. Positive results are not sufficient by themselves, and some people with RA have negative results.
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP): measures used to assess inflammation.
Complete blood count: useful for identifying anemia and assessing general health. (nhs.uk)

X-rays assess structural damage, although they may appear normal early in the disease. Ultrasound and magnetic resonance imaging can help assess inflammation and damage. (niams.nih.gov)

Treatment and monitoring

Treatment aims to suppress inflammation, preserve function, and prevent further damage. A treat-to-target approach uses repeated assessments of disease activity to guide treatment toward remission or low disease activity. Remission describes a state of minimal or absent disease activity, not a proven permanent cure. (pmc.ncbi.nlm.nih.gov)

Disease-modifying antirheumatic drugs (DMARDs) alter the course of the disease. Conventional drugs include methotrexate, leflunomide, sulfasalazine, and hydroxychloroquine. Biological treatments target particular immune pathways; targeted synthetic drugs include Janus kinase (JAK) inhibitors. Nonsteroidal anti-inflammatory drugs can relieve pain and inflammation but do not prevent disease progression. Corticosteroids can provide rapid symptom control, but prolonged use has important adverse effects. (nhs.uk)

Treatment requires monitoring for effectiveness and adverse effects. Some medicines increase susceptibility to infection. In the United States, certain JAK inhibitors carry boxed warnings concerning serious cardiovascular events, cancer, blood clots, and death. The pivotal comparative safety trial involved people with RA aged 50 or older who had at least one cardiovascular risk factor. (niams.nih.gov)

Rehabilitation, physical therapy, occupational therapy, and assistive devices address mobility and everyday function. Surgery, including joint repair or replacement, may be used for established damage or persistent functional limitation. Existing structural damage is generally irreversible, even when treatment controls active inflammation; consequently, symptom control and preservation of joint structure are distinct treatment outcomes. (niams.nih.gov)

Occurrence and risk factors

Disease process

Symptoms and complications

Diagnosis

Treatment and monitoring

References