Rheumatoid Arthritis

Introduction

Rheumatoid arthritis is an autoimmune disease that causes chronic, erosive joint damage along with extra-articular manifestations – meaning other non-joint issues.

In terms of causes, its pathogenesis is multifactorial, with genetic, environmental, and immunologic factors – in fact, we think many pathways can lead to autoreactivity.

As a summary, the most important genetic risk factor is having the gene HLA-DR4 which encodes for a type of MHC class II protein.

Pathophysiologically, it probably starts with a trigger at mucosal surfaces, such as cigarette smoke irritating the lungs. This can result in peptide residues getting converted from arginine into citrulline. These modified proteins are picked up by antigen-presenting cells, shown to overzealous lymphocytes, which ultimately perpetuate an immune response including the production of anti-citrullinated protein antibodies.

In the synovium of joints, these can stick together to form immune complexes, which induces local inflammation.

In conjunction with clinical assessment, investigations can aid diagnosis.

In terms of blood tests, CRP and ESR are usually high.

We have two main serological markers for RA: Rheumatoid factor and Anti-citrullinated peptide antibodies (aka Anti-CCP).

RF has historically been taught as the sensitive but non-specific test while anti-ccp is often thought to be the specific test.

My vibe from UpToDate is that RF has a super variable sensitivity and positive predictive value, and has less utility than I previously thought. Meanwhile, it stands true that anti-CCP is specific at 96%/

Radiologic studies should be done to assess all joints affected – plus a minimum of baseline plain xrays of the hands and feet. Its hallmarks on xray include marginal erosions which are well-defined areas of bone loss at the edges of joints.

There are four tenants of RA management.

Lifestyle Management. Encourage regular exercise, a good diet, and alcohol and smoking cessation
Induce clinical remission as early as possible. This is defined as symptom relief, normalisation of inflammatory markers, and absence of joint swelling. This is often done with conventional antirheumatic drugs like Methotrexate. Corticosteroids are often initially combined with this during induction.
Maintaining clinical remission. When disease control has been achieved, the DMARD may be continued at a reduced dose.
Monitoring for complications. Atlanto-axial involvement requires a special mention - cervical spine instability from joint erosion is a known sequalae and can have catastrophic consequences – it needs urgent attention.

Clinical features include articular and non-articular findings.

It usually causes a symmetrical polyarticular arthritis with a gradual onset affecting the hand’s metacarpophalangeal joints and proximal interphalangeal joints

Classic exam findings include a swan neck deformity, Boutonniere's deformity, Ulnar deviation, and rheumatoid nodules.

Common non-articular features include weight loss, depression, and fatigue. Interstitial lung disease, coronary artery disease, and other forms of organ damage can also subsequent.

Anti-CCP is the more specific serology test because they both have Ps

When the ESR’s prolonged and late, methotrexate cant wait (this is a reminder to induce remission ASAP)

A pain in the neck needs an urgent health check (as C spine instability is an emergency)