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Tennis Star Swings Back at Rheumatoid Arthritis

<ѻý class="mpt-content-deck">— Caroline Wozniacki hopes her nearly debilitating condition inspires others
MedpageToday
A photo of Caroline Wozniacki playing tennis

Danish professional tennis star Caroline Wozniacki was riding high early in 2018. After winning the Australian Open in January, she was once again ranked number one by the Women's Tennis Association, a position she had held in 2010 and 2011. But over the course of the year, she was besieged by injuries and debilitating fatigue.

"After Wimbledon, I really wasn't feeling well," last October. "I thought it was the flu. I thought it was fine; I'm going to get over it. I got to Washington, and my knees are hurting, my leg is hurting. Okay, I'll just move on. I play in Montreal and something really doesn't feel right. I can't lift my arms over my head. I go to see the doctor, and they tell me everything is fine, and then I know that I'm not fine. I thought maybe I had mono. It turns out that I have an autoimmune disease, rheumatoid arthritis."

In January 2019, Wozniacki told The Telegraph that she . "My condition is a day-to-day thing but I'm ready for the new season. I always work hard. I'm always on the court and go to the gym every day, but if my body doesn't feel perfect then I'll work on some technical things -- so I've had to adjust a little bit." So far, her results this year have been mixed. Although she hasn't won any singles titles this year, she has made it to the round of 16 on three occasions and has netted almost $750,000 in prize money.

Overview of Rheumatoid Arthritis

Rheumatoid arthritis is a disease that causes chronic abnormal inflammation, primarily affecting the joints. The most common signs and symptoms are pain, swelling, and stiffness of the joints. Small joints in the hands and feet are involved most often, although larger joints (such as the shoulders, hips, and knees) may become involved later in the disease. Joints are typically affected in a symmetrical pattern: if joints in the hand are affected, both hands tend to be involved.

Rheumatoid arthritis can also cause inflammation of other tissues and organs, including the eyes, lungs, and blood vessels. Additional signs and symptoms of the condition can include loss of energy, low-grade fever, weight loss, and anemia. Some affected individuals develop rheumatoid nodules, which are firm lumps of noncancerous tissue that can grow under the skin and elsewhere in the body.

The signs and symptoms of rheumatoid arthritis usually appear in mid- to late adulthood. Many affected people have episodes of symptoms (flares) followed by periods with no symptoms (remissions) for the rest of their lives. In severe cases, affected individuals have continuous health problems related to the disease for many years. The abnormal inflammation can lead to severe joint damage, which limits movement and can cause significant disability.

Rheumatoid arthritis affects about 1.3 million adults in the U.S. Worldwide, it is estimated to occur in up to 1% of the population. The disease is two to three times more common in women than in men, which may be related to hormonal factors.

Rheumatoid arthritis probably results from a combination of genetic and environmental factors, many of which are unknown.

Rheumatoid arthritis is classified as an autoimmune disorder. In people with rheumatoid arthritis, the immune system triggers abnormal inflammation in the synovium and tendon sheath. Inflammation causes pain, swelling, and stiffness of the joint. In severe cases, the inflammation also affects the bone, cartilage, and other tissues within the joint, causing more serious damage. Abnormal immune reactions also underlie the features of rheumatoid arthritis affecting other parts of the body.

Variations in dozens of genes have been studied as risk factors for rheumatoid arthritis. Most of these genes are known or suspected to be involved in immune system function. The most significant genetic risk factors for rheumatoid arthritis are variations in human leukocyte antigen (HLA) genes, especially the gene.

Diagnosis of Rheumatoid Arthritis

Rheumatoid arthritis can be difficult to diagnose in its early stages for several reasons:

  • There is no single test for the disease.
  • Symptoms differ from person to person and can be more severe in some people than in
  • others.
  • Symptoms can be like those of other types of arthritis and joint conditions, and it may take some time for other conditions to be ruled out.
  • The disease develops over time, and only a few symptoms may be present in the early
  • stages.
  • As a result, doctors use a variety of the following tools to diagnose the disease and to rule out other conditions including medical and family history, physical examination, laboratory tests, and imaging exams.

Useful laboratory tests include:

  • Rheumatoid factor (RF): RF is an antibody most people with rheumatoid arthritis eventually have in their blood. Not all people with rheumatoid arthritis test positive for RF, and some people test positive for RF but never develop the disease. RF also can be positive in some other diseases. However, a positive RF in a person who has symptoms consistent with rheumatoid arthritis can be useful in confirming a diagnosis. Also, high levels of RF are associated with more severe rheumatoid arthritis.
  • Anti-CCP antibodies: This blood test detects antibodies to cyclic citrullinated peptide (anti-CCP). This test is positive in most people with rheumatoid arthritis and can even be positive years before rheumatoid arthritis symptoms develop. When used with the RF, this test's results are very useful in confirming a rheumatoid arthritis diagnosis.

Other common blood tests include:

  • White blood cell count
  • Blood test for anemia, which is common in rheumatoid arthritis
  • Erythrocyte sedimentation rate
  • C-reactive protein

Treatment of Rheumatoid Arthritis

Doctors use a variety of approaches to treat rheumatoid arthritis. However, no matter which treatment is chosen, the goals are the same:

  • Relieve pain
  • Reduce inflammation
  • Slow down or stop joint damage
  • Improve well-being and ability to function

In 2015, the American College of Rheumatology published recommended guidelines for the treatment of rheumatoid arthritis (A 2019 update is anticipated in late 2019/early 2020). Treatment choices are based upon whether a patient is newly diagnosed or an established RA patient, and whether there are high-risk comorbidities (such as Hepatitis B or C, history of/current malignancy, congestive heart failure, or previous serious infections).

They also strongly recommend the use of "tight control" i.e. using a treat-to-target strategy, with a goal of remission or low disease activity. Measure of disease activity can include a number of instruments such as the Patient Activity Scale (PAS or PASII), Routine Assessment of Patient Index Data 3 (RAPID3), Clinical Disease Activity Index (CDAI), etc.

Drugs used in the treatment of RA include pain relief and anti-inflammatory drugs -- such as analgesics, nonsteroidal anti-inflammatory drugs, (NSAIDs) and systemic and intraarticular glucocorticoids -- and disease-modifying anti-rheumatic drugs (DMARDS).

DMARDs may act to slow disease progression. They are frequently a first-line drug in the treatment of new patients with RA. They are classified as either nonbiologic or biologic. Common nonbiologic DMARDs include:

  • Hydroxychloroquine
  • Leflunomide
  • Methotrexate (The most common first-line treatment)
  • Sulfasalazine

Biologic response modifiers are genetically engineered medications that help reduce inflammation and damage to the joints by interrupting the inflammatory process. They generally target cytokines or their receptors, or other cell surface molecules. Currently, several biologic response modifiers are approved for rheumatoid arthritis, including:

TNF-α inhibitors:

  • Adalimumab
  • Certolizumab
  • Etanercept
  • Golimumab
  • Infliximab

Interleukin receptor antagonists:

  • Tocilizumab (IL-6)
  • Anakinra (IL-1)

Others:

  • Rituximab (anti-CD20 B-cell depletion)
  • Abatacept (T-cell co-stimulation blocker)

Another DMARD, tofacitinib (Xeljanz), is from a new class of drugs called Janus kinase (JAK) inhibitors. It is an inhibitor of the enzyme Janus kinase 1 (JAK1) and Janus kinase 3 (JAK 3). It interferes with the JAK-STAT signaling pathway that affect cytokine functions.

Michele R. Berman, MD, and Mark S. Boguski, MD, PhD, are a wife and husband team of physicians who have trained and taught at some of the top medical schools in the country, including Harvard, Johns Hopkins, and Washington University in St. Louis. Their mission is both a journalistic and educational one: to report on common diseases affecting uncommon people and summarize the evidence-based medicine behind the headlines.