Rheumatoid Arthritis

Introduction and Facts

Rheumatoid arthritis (RA) is a systemic autoimmune disease (Symmons, 2006). RA is a multisystem disorder whose etiology is unknown and is characterized by synovitis destruction (Helmick, 2008). This disease is the most common systemic inflammation characterized by symmetrical joint involvement (Dipiro, 2008). RA is an autoimmune disorder that causes chronic joint inflammation and affects more than five joints (polyarthritis) (Pradana, 2012).

Pathophysiology

RA is a systemic autoimmune disease that attacks the joints. Autoimmune reactions occur in synovial tissue. Joint damage begins from the proliferation of macrophages and synovial fibroblasts. Lymphocytes infiltrate the perivascular area, and endothelial cells proliferate, and neovascularization occurs. The blood vessels in the involved joint are occluded by small clots or inflammatory cells. Pannus is formed due to irregular growth of inflamed synovial tissue. Pannus then invades and damages joint cartilage and bone. The immunologic response involves the role of cytokines, interleukins, proteinases, and growth factors—this response results in joint destruction and systemic complications (Surjana, 2009). T cells and B cells are specific immunological responses. T cells are part of the cellular-specific immunological system in Th1, Th2, Th17, Treg, Tdth, CTL/Tc, NKT. Cytokines and B cells are humoral-specific immunological responses, B cells are IgG, IgA, IgM, IgE, IgD (Baratwidjaja, 2012). The role of T cells in RA is initiated by the interaction between T cell receptors with shared epitopes of the major histocompatibility complex class II (MHCII-SE) and peptides on antigen-presenting cells (APCs) in the synovium or systemic. And the role of B cells in the immunopathology of RA is not known with certainty (Suarjana, 2009).

Clinical Symptoms and Complications

Rheumatoid arthritis (RA) can be found in all joints and tendon sheaths but is most common in the hands. RA can also affect the joints of the elbows, feet, ankles, and knees. Synovial joints, tendon sheaths, and bursa thicken due to inflammation followed by bone erosion and destruction of bone around the joint (Syamsuhidajat, 2010). There are three stages in RA, namely (Nasution, 2011):

a. Synovitis stage. Arthritis in RA is caused by synovitis, inflammation of the synovial membrane that covers the joint. The joints involved are generally symmetrical, although they may initially be asymmetrical. This synovitis causes erosion of the joint surface resulting in deformity and loss of function (Nasution, 2011). The wrist joints are almost always involved, including the proximal interphalangeal and metacarpophalangeal joints.

b. Destruction stage. It is marked by the tendon contraction when there is damage to the synovial tissue (Nasution, 2011).

c. deformity stage. At this stage, changes occur progressively and repeatedly, deformity and functional disturbances occur permanently (Nasution, 2011). The clinical manifestations of RA are divided into two categories, namely, articular manifestations and extra-articular manifestations (Suarjana, 2009). RA articular manifestations occur symmetrically in inflammation of the joints, bursa, and tendon sheaths that can cause pain, swelling, joint stiffness, and mild hydrops (Sjamsuhidajat, 2010). Cardinal signs of inflammation in the form of pain, swelling, redness, and warmth may be found early or during a relapse, but redness and heat may not be present in chronic RA (Surjana, 2009). Large joints, such as the shoulders and knees, are often a persistent clinical manifestation, although these joints may be asymptomatic years after onset (Longo, 2012).

Diagnosis

There are several criteria used, namely the criteria for the diagnosis of RA according to the American College of Rheumatology (ACR) in 1987 and the criteria for the American College of Rheumatology/European League Against Rheumatism (ACR/EULAR) in 2010 (Pradana, 2012). Laboratory tests required for the diagnosis of RA include serum examination for IgA, IgM, IgG, anti-CCP and RF antibodies, synovial fluid analysis, plain joint radiographs, MRI, and ultrasound (Longo, 2012).

Medication and Treatment

RA must be treated perfectly. Patients must be explained that this disease cannot be cured (Sjamsuhidajat, 2010). RA therapy should be started as early as possible to reduce the rate of worsening of the disease. Patients should be referred within three months of the onset of symptoms to confirm the diagnosis and initiation of DMARD (Disease-Modifying Anti-Rheumatic Drugs) therapy (Surjana, 2009).

RA therapy aims to:

a. To reduce the pain experienced by the patient

b. Maintaining its functional status

c. Reduce inflammation

d. Controlling systemic involvement

e. Protection of joints and extra-articular structures

f. Holding disease progression

g. Avoid complications associated with therapy

Pharmacologic Therapy of Rheumatoid Arthritis

In the journal "The Global Burden Of Rheumatoid Arthritis In The Year 2000", drugs in RA therapy are divided into five groups, namely (Symmons, 2006):

1. NSAIDs (Non-Steroid Anti-Inflammatory Drugs) to reduce joint pain and stiffness.

2. Second-line agents such as gold injection (gold injection), Methotrexate, and Sulphasalazine. These drugs belong to the DMARD group. This group of drugs will serve to reduce the disease process and reduce the acute phase response. These medications have side effects and should be monitored carefully.

3. Steroids, these drugs have the advantage of reducing symptomatic symptoms and do not require monitoring but have serious long-term consequences.

4. Immunosuppressant drugs. These drugs are required in small proportions for patients with systemic disease.

5. A new biologic agent, this drug is used to inhibit inflammatory cytokines.

There are no standard rules regarding this group of drugs in the therapy of RA. DMARD (Disease-Modifying Anti-Rheumatic Drugs), the selection of the type in the patient must consider adherence, disease severity, doctor's experience, and comorbidities. The most commonly used DMARDs are MTX (Metrothexate), hydroxychloroquine or chloroquine phosphate, sulfasalazine, leflunomide, infliximab, and etarnecept. (Suarjana, 2009).

Non-Pharmacological Therapy of Rheumatoid Arthritis

Non-pharmacological therapy includes modality therapy and complementary therapy. Treatment modalities include diet (cod liver oil supplementation), hot and cold compresses and massage to reduce pain, exercise and rest, and irradiation using infrared light. Complementary therapies include herbal medicines, acupressure, and progressive relaxation (Afriyanti, 2009). Surgical treatment is performed in chronic conditions, when severe pain, extensive joint damage, a significant limitation of motion, and tendon rupture occur.

The surgical method is used in synovectomy if the joint destruction is not extensive; if extensive, arthrodesis or arthroplasty is performed. The use of orthopedic aids is used to support daily life (Sjamsuhidajat, 2010).

Reference

Rheumatoid Arthritis. http://digilib.unila.ac.id/2424/9/2.%20Bab%202.pdf