The major goals of treatment of arthritis are as follows: (1) reduce pain and discomfort; (2) prevent deformities and loss of joint function; and (3) help the patient maintain a productive and active life. Inflammation must be suppressed and mechanical and structural abnormalities corrected or compensated for with assistive devices. Treatment options include reduction of joint stress, physical and occupational therapy, drug therapy, and surgical intervention.

There are several general classes of drugs (Table 1) traditionally used in the treatment of RA. A newer class of agents for treatment of RA, recombinant fusion proteins, selectively modulates the CD80 or CD86-CD28 costimulatory signal required for full T cell activation. Other drugs may also be used for treatment.

Table1. Drugs for Treatment of Rheumatoid Arthritis

Nonsteroidal Antiinflammatory Drugs

Traditional treatment of RA consists of nonsteroidal antiinflammatory drugs (NSAIDs; e.g., salicylates, ibuprofen). The major effect of these agents is to reduce acute inflammation. Aspirin is the oldest drug of the nonsteroidal class, but the use of aspirin as the initial choice of drug therapy has largely been replaced by the newer NSAIDs.

Prostaglandins are a group of related compounds that are important mediators of a wide variety of physiologic processes, including immunomodulation. Prostaglandins are derived primarily from arachidonic acid via the cyclooxygenase enzymes (COX) pathway. NSAIDs inhibit prostaglandin synthesis by blocking two isoforms of COX, COX-1, and COX-2. Newer NSAID agents (e.g., Vioxx, Celebrex) selectively block the COX-2 enzyme that is primarily upregulated in response to tissue damage during inflammation but preserves COX-1 activity and enhances the safety profile.

Corticosteroids and Glucocorticoids

Corticosteroids (e.g., cortisone and prednisolone [prednisone]) have antiinflammatory and immunoregulatory activity. Glucocorticosteroids pass through the cell membrane into the cytoplasm and activate the cytoplasmic glucocorticosteroid receptor, which represses gene expression through the transcriptional interference of activator protein 1 (AP-1) and nuclear factor kappa B (NF-κB). The proteins inhibited by glucocorticoste roids include interleukin-1 (IL-1), IL-2, IL-6, IL-8, TNF-α, and IFN-γ. Glucocorticosteroids were the original selective COX-2 inhibitors. Oral corticosteroids can produce a variety of complications, including high blood pressure, increased susceptibility to infection, and osteoporosis.

Disease-Modifying Antirheumatic Drugs

 The disease-modifying antirheumatic drugs (DMARDs) include methotrexate, intramuscular gold salts, hydroxychloro quine, sulfasalazine, d-penicillamine, and immunosuppressive and other cytotoxic drugs (e.g., cyclosporin A, cyclophosphamide, azathioprine). Newer drugs for the treatment of RA include leflunomide, etanercept, adalimumab, infliximab (Remicade), and anakinra Antimalarials may be used as well.

Methotrexate has become the most popular DMARD because of its early onset of action (4 to 6 weeks), good efficacy, ease of administration, and high patient tolerability. Methotrexate is a folic acid antagonist. The immunosuppressive and cytotoxic effects of methotrexate are caused by the inhibition of dihydrofolate reductase.

Immunosuppressive and cytotoxic drugs other than methotrexate are used only for patients who have aggressive disease or extra-articular manifestations such as systemic vasculitis. The most common drugs are azathioprine (Imuran), cyclophosphamide (Cytoxan), and cyclosporin A. Because of the potential for high toxicity, these agents are used for life-threatening extra-articular manifestations or severe articular disease refractory to other therapy.

• Azathioprine is a purine analogue that can cause severe bone marrow suppression, particularly in patients with renal insufficiency or when used concomitantly with allopurinol or angiotensin-converting enzyme (ACE) inhibitors.

• Cyclophosphamide is an alkylating agent associated with serious toxicities, including bone marrow suppression, hemorrhagic cystitis, premature ovarian failure, infection, and secondary malignancy, particularly an increased risk of bladder cancer. Thus, cyclophosphamide is not used in the treatment of uncomplicated RA.

• Cyclosporine (cyclosporin A) is an immunosuppressive agent approved for use for preventing renal and liver allograft rejection. Cyclosporine inhibits T cell function by inhibiting the transcription of IL-2.

Other Drugs

Antimalarial drugs are rapidly absorbed, relatively safe, well tolerated, and often effective remittive agents in the treatment of RA, particularly mild to moderate disease. The mechanism of action of antimalarial drugs in the treatment of patients with RA is unknown.

Recombinant fusion proteins represent a new class of drugs that selectively modulate specific cell surface receptors, CD80 or CD86, on the surface of an antigen-presenting cell that binds to CD28 on the T cell. A recombinant fusion protein, abatacept, has been modified to prevent complement fixation. It competes with CD28 for CD80 and CD86 binding and can be used to modulate T cell activity selectively. This selective costimulation modulator has been proposed to be useful for patients who have an inadequate response to anti–TNF-α therapy.

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مواضيع ذات صلة

Juvenile Idiopathic Arthritis

Diagnostic Evaluation of Rheumatoid Arthritis

Immunologic Manifestations of Rheumatoid Arthritis

Signs and Symptoms of Rheumatoid Arthritis

Treatment of Systemic Lupus Erythematosus

Diagnostic Evaluation of Systemic Lupus Erythematosus

Immunologic Manifestations of Systemic Lupus Erythematosus

Signs and Symptoms of Systemic Lupus Erythematosus

Different Forms of Lupus

Renal Disorders

Neuromuscular Disorders

Autoimmune Hematologic Disorders