The Autoimmune Connection: Essential Information for Women on Diagnosis, Treatment, and Getting On With Your Life

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Authors: Rita Baron-Faust, Jill Buyon
rules. Ultimately, your rheumatologist will rely on his or her judgement and your input. And your input is critical.
Analgesic (Pain) Medications
    Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the drugs your rheumatologist will likely reach for first to treat joint pain and swelling. They include aspirin and aspirin-like drugs such as over-the-counter ibuprofen (Motrin, Advil) and naproxen (Aleve) , prescription-only naproxen (Naprosyn, Anaprox) , naproxen sodium (Naprelan) , and diclofenac sodium (Voltaren) .
    NSAIDs have both painkilling and anti-inflammatory properties, but they can also raise heart risk and cause gastrointestinal symptoms such as upset stomach or, in some cases, bleeding ulcers.
    That’s because they work by blocking enzymes in the body called cyclooxygenase-1 (COX-1) and cyclooxygenase-2 (COX-2) . While the COX-2 enzyme is related to inflammation, COX-1 protects the lining of the stomach and helps platelets to form clots. Because most NSAIDs block both COXenzymes, they can erode the stomach lining and lead to bleeding, especially among women using corticosteroids and women over age 75 who may have a thinned stomach lining. These complications can be minimized by taking NSAIDs with meals and using acid reducers like omeprazole (Prilosec, Nexium) or cimetidine (Tagamet) , or a prostaglandin such as misoprostol (Cytotec) .
    However, recent research suggests prescription-strength Nexium (40 mg) can lead to bone thinning, so discuss its use with your rheumatologist.
    NSAIDs that only block the COX-2 enzyme have a slightly reduced risk of serious gastrointestinal side effects (such as bleeding ulcers), but studies show around the same incidence of minor GI problems as the nonselective drugs. COX-2 inhibitors are also much more expensive. Prescription selective COX-2 inhibitors include celecoxib (Celebrex) and meloxicam (Mobic), a less selective COX-2 inhibitor.
    Because COX-2 inhibitors don’t have the blood-thinning properties of aspirin, they do not lower the risk of blood clots and heart attack (and may potentially increase it). This is a special concern for women, since RA can lead to early heart disease (see pages 55 to 57 ). If you already have heart disease and need antiplatelet therapy, the ACR recommends using low-dose aspirin (81 mg a day).
    Nonaspirin NSAIDs in general can raise your risk of heart attack and other cardiovascular problems—even as early as the first week you take them, according to the FDA. 16
    The American College of Gastroenterology (ACG) and EULAR, among others, recommend that NSAIDs be used at the lowest possible dose for the shortest amount of time—and PPIs (or misoprostol ) used for gastroprotection, even with COX-2 selective inhibitors. 17
Disease-Modifying Antirheumatic Drugs (DMARDs)
    Disease-modifying antirheumatic drugs (DMARDs) can literally alter the course of RA, preventing damage and destruction of the joints, bones, and cartilage. While many of these drugs work in nonspecific ways to modulate the immune system, newer DMARDs known as biological agents target specific cytokines.
    The standard of care is now treatment with DMARDs 18 as soon as a diagnosis of RA is made, says Vivian P. Bykerk, MD, director of the InflammatoryArthritis Center of Excellence at the Hospital for Special Surgery in NYC and an associate professor of medicine at the Weill Cornell Medical College.
    Early treatment can often slow the disease process and arrest further bone and joint destruction, improving function and reducing disability in RA, says Dr. Bykerk.
    The DMARD most commonly used for early and established RA is methotrexate (Trexall) , often called MTX for short. MTX is the “anchor” drug used to treat RA, alone or in combination with other therapies.
    “In RA, it works by inhibiting adenosine, interfering with the production of inflammatory cells and chemical mediators of inflammation with the net result of less inflammatory infiltrates in the joint,” explains Dr.

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