Drugs and Prescription Medications For RA
Drug treatments are an essential part of managing RA, especially during periods when the disease is active. DMARDs, both traditional drugs and newer biologics, have been shown to slow and prevent damage to joints, thereby preserving function and improving quality of life. Drug treatment generally fall into two categories, symptomatic treatments (those drugs whose main focus is relief of symptoms) and disease-modifying treatments (those drugs that can modify the course of RA and slow or prevent joint destruction in addition to providing relief of symptoms).
Choice of drug treatment, as well as intensity of treatment (whether one or more drugs are used and drug dosages), will depend on individual factors including how severely RA affects you and any side effects associated with treatment. Your doctor will work closely with you to strike the right balance in suppressing RA-related inflammation (and symptoms), while keeping side effects to a minimum. This is the key challenge of drug treatment in RA. To get the balance right, your doctor may adjust the dose of your RA medication or switch to another that has a different track record for efficacy or side effects.1
There are several classes of drugs that are commonly used to treat RA and its symptoms. Symptomatic drug treatments include NSAIDs, glucocorticoids (also called corticosteroids or just steroids), and pain medications. Drugs that slow bone erosion may also be considered symptomatic treatments. DMARDs (including traditional agents, such as methotrexate, and newer biologics, such as TNF-inhibitors) comprise the group of medications that provide relief of symptoms and protection against the damaging affects that RA inflammation has on joints and related structures.1
You may find NSAIDs, which include ibuprofen (Advil, Motrin), naproxen (Aleve), or indomethacin (Indocin), as well as aspirin, very useful in providing fast relief of RA symptoms such as pain and minor inflammation. However, NSAIDs have no effect on the long-term damage to joints that can result from chronic inflammation associated with RA. To have an effect on inflammation, an NSAID must be taken continuously (at a specified dose) and must be taken for a couple of weeks for the anti-inflammatory effect to be fully achieved. Talk to your doctor about the appropriate dose to use for whichever NSAID you are taking. Remember that two NSAIDs should not be taken at the same time.1
Glucocorticoids (also called corticosteroids or just steroids) are very effective at controlling inflammation. They may be taken orally, by injection into a vein, or by direct injection into a joint cavity. Steroids (examples include prednisone, prednisolone, methylprednisolone) have been shown to provide rapid improvement of RA symptoms, including pain and tenderness, stiffness, swelling, and inflammation. However, unlike DMARDs, they do not slow or prevent RA-related damage to joints and other structures.1
Steroids are typically used during an RA flare, when disease activity is at its highest and you may find it hardest to function normally. Because steroids take effect rapidly, they are often used in combination with RA drugs that act more slowly, such as methotrexate, which may take a month to achieve full efficacy, or newer biologics, which may take a couple weeks to achieve full efficacy. Steroids are typically used at the lowest dose possible and only for a limited period of time because of the potential for a variety of side effects, including exacerbation of diabetes, weight gain, bone loss (osteopenia and osteoporosis), increased risk of infection, and increased risk for cataracts.1
Several different classes of drugs provide pain relief in RA but do not have any effect on inflammation. These include analgesics such as acetaminophen (Tylenol), the narcotic-like pain medication tramadol (Ultram), capsaicin cream or ointment, and narcotic pain relievers, such as codeine, oxycodone, and hydrocodone.1
Use of the narcotic pain relievers in patients with RA is generally discouraged due to the potential for addiction with long-term use and because of the fact that they have no effect on inflammation. However, narcotic pain relievers may be useful in certain circumstances, such as in RA patients with joints that are badly damaged and who are not candidates for joint replacement surgery. Use of narcotics in these patients must be closely monitored by a rheumatologist or pain specialist.1
DMARDs (disease-modifying anti-rheumatic drugs) are effective at reducing inflammation associated with RA and slowing or preventing damage to joints and enabling a patient to maintain function and quality of life. This is why they are called “disease-modifying,” because they can interrupt the processes that cause damage in rheumatic diseases. The introduction of DMARDs for the treatment of RA has significantly changed and improved the prospects for patients with RA. Before the availability of drugs like methotrexate, damage to joints and related structures from chronic inflammation associated with RA was inevitable for many patients.1
A number of agents known as traditional DMARDs include methotrexate, hydroxychloroquine, sulfasalazine, and leflunomide.1 Newer biologics are also considered DMARDs because they modify the course of RA and slow or prevent joint damage.
One limitation associated with traditional DMARDs is the time it takes for them to achieve full effect. For instance, methotrexate may take 4 to 6 weeks to improve RA symptoms and hydroxychloroquine 2 to 3 months. This is why glucocorticoids are often used in concert with DMARDs during RA flares for acute (short-term) control of inflammation and associated symptoms.1
DMARDs are associated with a range of side effects, which is why your doctor will work closely with you to adjust the dose of whichever DMARD you use to balance the therapeutic effect with safety concerns or side effects.1
The introduction of biologics is the latest advance in the treatment of RA, and one that has significantly broadened and improved the drug treatment options for patients. These treatments also fall under the category of DMARDs, because they can change or modify the disease course in RA and slow or prevent damage to joints and related structures.1
The term “biologics” is used for these treatments because they are designed to target specific molecules on immune system cells, such as receptors on T- or B-cells, to block the actions of these cells and, thereby, dampen the out-of-control inflammatory process that characterizes an autoimmune disease like RA. There are several types of biologics available to treat RA, including tumor necrosis factor (TNF)-inhibitors (also called anti-TNF agents), B-cell inhibitor, T-cell inhibitor, interleukin-6 (IL-6) inhibitor, and JAK inhibitor. Often, these agents are only used in patients who cannot use or who have failed to derive benefit from traditional DMARDs. However, they can be used in combination with traditional DMARDs and are often used with NSAIDs and short-term glucocorticoid treatment.2
TNF-inhibitors are the largest groups of biologics now available to treat RA and include etanercept (Enbrel), adalimumab (Humira), infliximab (Remicade), certolizumab (Cimzia), and golimumab (Simponi). Toclizumab (Actemra) is an IL-6 inhibitor, rituximab (Rituxan) is a B-cell inhibitor, and abatacept (Orencia) is a T-cell inhibitor.2 First in a new class of treatment, tofacitinib (Xeljanz), a JAK inhibitor available as an oral pill taken twice daily, was approved by the FDA in November 2012.
Biologics take somewhat less time to achieve full effect than traditional DMARDs, with time to effect ranging from 2 to 6 weeks, depending on the specific drug. All biologics must be taken by injection or infusion. Some are available for injection through the skin and may be taken at home. Others must be infused at your doctor’s office, with an infusion taking anywhere from 1 to 6 hours.1
Biologics are associated with several side effects. The most important and potentially dangerous have to do with their effect on the immune system. Because biologics are designed to dampen the immune response, they can increase your risk of developing infections or certain cancers.1