15 Early Signs of Rheumatoid Arthritis ( courtecy;- medicineNet.com )

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15 Early Signs of Rheumatoid Arthritis
Early symptoms can vary from person to person. Learn about 15 characteristic early symptoms of rheumatoid arthritis




Rheumatoid Arthritis (RA)



A woman suffers hand pain due to rheumatoid arthritis (RA).

What is rheumatoid arthritis (RA)?

Rheumatoid arthritis (RA) is a type of inflammatory arthritisRA disease is characterized by chronic joint inflammation (in the fingers, hands, knees, feet, for example). RA may also be called rheumatoid disease because at times rheumatoid arthritis causes systemic illness that impacts many organs of the body.

What are early signs and symptoms of rheumatoid arthritis, and what areas of the body are affected?

  •  
While early symptoms of RA can be mimicked by other diseases, the symptoms and signs are very characteristic of rheumatoid disease. The 15 early RA symptoms and signs discussed in this article include the following:



Picture of a man with arthritis joint pain

What is the treatment for rheumatoid arthritis (RA)?

There is no known cure for rheumatoid arthritis. To date, the goal of treatment in rheumatoid arthritis is
  • to reduce joint inflammation and pain,
  • maximize joint function, and
  • prevent joint destruction and deformity.
Fatigue is a common symptom of rheumatoid arthritis (RA).

Fatigue

Fatigue is a very common symptom in all stages of rheumatoid arthritis, particularly when the joint inflammation is active. Fatigue in rheumatoid arthritis can be caused by the body's reaction to inflammation, poor sleepanemia, and medications.
The fatigue of rheumatoid arthritis that results in lack of energy can adversely affect emotions and mood, occupation, relationships with people, sex drive, productivity, attentiveness, creativity, and happiness. Fatigue from rheumatoid arthritis can also be associated with poor appetite and weight loss.

A man experiences rheumatoid arthritis (RA) joint pain in his wrist.

Joint pain

Joint pain from rheumatoid arthritis is caused by the inflammation present in a joint when the disease is active. Joint pain can also occur when the disease is inactive or controlled if the joint has been damaged by rheumatoid arthritis in the past.
Active rheumatoid arthritis causes the joint to swell because of both thickening of the joint lining tissue (synovium) and because of excess joint fluid. The swollen, inflamed joint stretches and irritates the capsule that surrounds the joint. The joint capsule has nerves endings within it that immediately send pain signals to the brain.
Past rheumatoid arthritis can lead to permanent joint destruction with damaged cartilage, bone, and ligaments. When the damaged joint is used, it can cause intense pain.

A patient feels joint tenderness as a doctor examines her hand for rheumatoid arthritis (RA).

Joint tenderness

Rheumatoid arthritis characteristically leads to tenderness of involved joints. This is because the inflamed joint lining tissue has irritated the nerves in the joint capsule. When the irritated joint capsule is compressed by external pressure, such as from touching the joint, it is frequently tender. The pain elicited from compression is immediate. This is one of the reasons that rheumatoid arthritis can lead to difficulty sleeping and insomnia.
A woman's hands show swollen finger joints due to rheumatoid arthritis (RA).

Joint swelling

Swollen joints are very common in rheumatoid arthritis. Sometimes the joint swelling is minimal and can be difficult to appreciate. Other times the joint swelling is very apparent. Generally, people who are affected by rheumatoid arthritis can easily tell when their joints are swollen. The joint swelling can lead to loss of range of motion of the joint. Joint swelling in the fingers can make it hard to get rings off and on easily.

Red, inflamed toe joints may indicate rheumatoid arthritis.

Joint redness

Redness occurs over joints when they are inflamed. The redness in the skin over an inflamed joint from rheumatoid arthritis occurs because the capillaries of that skin are widened by the adjacent inflammation. These widened capillaries are referred to as dilated capillaries.Joint redness does not occur in all inflamed joints from rheumatoid arthritis. Sometimes the inflammation in the joint is inadequate to cause the capillaries in the skin to dilate.
A doctor examines a patient for joint warmth, a symptom of active rheumatoid arthritis (RA) inflammation.

Joint warmth

Warmth of the joints affected by rheumatoid arthritis is a sign of active inflammation. Doctors look for joint warmth as they monitor the activity of the disease. As rheumatoid arthritis responds to treatment, joint warmth resolves. Sometimes joint warmth is present without visible joint swelling or redness.

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Joint stiffness may be a result of RA pain.

Joint stiffness

Stiffness is a typical rheumatoid arthritis symptom. Joints that are affected by active rheumatoid arthritis are inflamed and characteristically stiffer in the morning than later in the day. Doctors use the duration of the morning stiffness as a measure of the severity of the active joint inflammation. As rheumatoid arthritis responds to treatment, the duration of the morning joint stiffness diminishes.

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Rheumatoid arthritis can cause a loss of joint range of motion.

Loss of joint range of motion

As the joints of rheumatoid arthritis become more inflamed with active disease, they tend to have incomplete range of motion. The range of motion is limited by the swelling within the joint. This is typically associated with weakness in the involved areas.
Joints affected by longstanding rheumatoid arthritis commonly lose range of motion permanently.



A person suffering from RA has multiple swollen joints on both hands and wrists.

Many joints affected (polyarthritis)

Usually, but not always, rheumatoid arthritis affects many joints. Classically, RA affects the small joints of the hands and wrists and balls of the feet. Also, not uncommonly, knees, elbows, hips, ankles, and shoulders can be inflamed.
Sometimes, only a few joints are involved. Less frequently, a singular joint is involved. Both of these scenarios are more common in childhood inflammatory arthritis (juvenile rheumatoid arthritis).
When four or more joints are inflamed, the condition is referred to as polyarthritis. When only a few joints are inflamed, it is referred to as oligoarthritis. When a single joint is inflamed, it is referred to as monoarthritis.

A man with rheumatoid arthritis (RA) limps after retrieving his newspaper.

Limping

Limping from poor lower extremity function can be caused by many diseases of the nerves, muscles, and bones of the lower extremities. Limping frequently occurs when rheumatoid arthritis affects the hips, knees, ankles, or feet. Pain, loss of range of motion, and joint swelling all can cause a person with rheumatoid arthritis to have a noticeable limp. It is not unusual for a young child with rheumatoid arthritis to have a painless limp as the first sign of the rheumatoid disease.
A radiograph of the hand of a 71-year-old woman with rheumatoid arthritis (RA) shows joint deformity.

Joint deformity

Joint deformity can occur from chronic rheumatoid arthritis. Deformity in rheumatoid arthritis occurs because the unchecked inflammation leads to both erosion of cartilage and bone as well as ligament loosening (laxity). Early detection and treatment of rheumatoid arthritis is critical to prevent permanent joint destruction and joint deformity.

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This X-ray of hands affected by rheumatoid arthritis (RA) shows colorized symmetry of affected joints on both hands.

Both sides of the body affected (symmetric)

Typically, the distribution of the joints involved in a person with rheumatoid arthritis is similar on both sides of the body. This symmetric joint involvement is a feature of classic rheumatoid arthritis. This does not mean that joint involvement is always symmetric, but it is common.
Rheumatoid arthritis usually (not always) involves many joints on both sides of the body. It is, therefore, sometimes referred to as a symmetric polyarticular form of arthritis. Accordingly, the small joints of the hands, wrists, and feet are commonly affected. The knees, ankles, shoulders, hips, and elbows can also be involved in early disease. Rheumatoid arthritis is characterized by inflammation in these joints. Early manifestations of this inflammation can be gradual or rapidly intense. The joint inflammation causes stiffness, usually worse in the morning or after being sedentary. It also causes warmth, swelling, redness, and pain in varying degrees. The joint can be very subtly affected with slight swelling or markedly affected with substantial loss of range of motion. The pain level can be completely disabling and does not always correlate with the degree of apparent inflammation.
As described above, the manner that each of the symptoms affects an individual can be very different from individual to individual and can vary during the day. The intensity and effect of each of the symptoms is dependent upon the patient's age, activity, the medications he or she takes, as well as any additional medical conditions that are present.



Loss of joint function may occur with rheumatoid arthritis due to joint pain and swelling.

Loss of joint function

Because rheumatoid arthritis leads to pain, swelling, and tenderness of the involved joints, there is loss of joint function. The swelling and sensitivity impedes the full motion and stability of the joint and it becomes incapable of carrying the movement with confidence, balance, and completeness. This loss of joint function leads to limping, lack of coordination, loss of grip and dexterity, and disability.



The inflammation of RA may cause anemia.

Anemia

The chronic inflammation of rheumatoid arthritis commonly causes the bone marrow to decrease the release of red blood cells into the circulation. This lowers the red blood count to cause anemia when rheumatoid arthritis is active. It is not unusual for the anemia of rheumatoid arthritis to spontaneously correct as the inflammation of the disease is quieted by treatment.


Fever may occur when RA is causing inflammation.

Fever

Fever, while not common in rheumatoid arthritis, does occur in some patients when the disease is actively causing inflammation. Typically, there is only mild low-grade temperature elevation and this corrects rapidly as the inflammation of rheumatoid arthritis is treated. Because patients with rheumatoid arthritis frequently require medications that can decrease the normal immune response, it is important that when they develop fever, infection is considered as a possible cause. Infections can require aggressive treatment and interruption of some underlying rheumatoid treatments.

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Initially, rheumatoid arthritis (RA) may affect one joint or a few joints.

What are the less common forms of rheumatoid arthritis?


Rheumatoid arthritis can begin in less common forms. For example, it can begin with involvement of only a single joint or a few joints. Sometimes, this can later evolve to the more common presentation of many joints on both sides of the body. Rarely, the earliest symptom of rheumatoid disease is inflammation of a body area that does not even involve a joint. For example, the lining of the lungs (pleura) can become inflamed to cause pleurisy many months before the arthritis develops. Occasionally, only a few joints are involved and the doctor may suspect another type of inflammatory arthritis. (There are over 100 forms of arthritis!) Again, this can sometimes only later evolve to become the more typical symmetrical polyarthritis by including many joints on both sides of the body. The caveat is that by recognizing early rheumatoid arthritis symptoms doctors and their patients can address the disease early, thereby affording optimal outcomes for those affected.
Medically Reviewed on 5/17/2018
References
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Juvenile Idiopathic Arthritis (Juvenile Rheumatoid Arthritis)

Juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA) facts

  • JIA was known in the U.S. in the past as JRA (juvenile rheumatoid arthritis or juvenile RA).
  • Epidemiologic studies estimate that approximately 294,000 American children are affected by JIA.
  • Children of European ancestry are more likely to develop the condition while those of Japanese and Filipino background are less likely.
  • When considering the manifestation options of JIA, those children with European background are more likely to experience the oligoarticular version of JIA (see below) while those of African-American heritage are more likely have the rheumatoid factor (RF) positive, polyarticular juvenile idiopathic arthritis version (see below).
  • Among Caucasian children developing oligoarticular JIA, younger girls (2-4 years of age) are the most commonly affected.
  • Genes seemed to play a role both in the development of JIA, as well as the clinical manifestations that may affect a child.

What is juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)?

Juvenile idiopathic arthritis (JIA) is the umbrella term under which several forms of chronic arthritis in children are categorized. Regardless of type, all of these conditions have several historical and/or clinical characteristics in common. One or more joints must demonstrate evidence of inflammation characterized by swollen joints, limitation in the range of motion of the involved joint(s), tenderness when the joint is moved, and increased warmth of the joint region. These symptoms must be present (even intermittently) for at least six weeks and affect a child less than 16 years of age.
JIA is the most frequent chronic rheumatologic disease of childhood, and the cause(s) are not well understood. Both environmental and genetic influences are felt to contribute to the development of signs and symptoms of JIA. Knowledgeable specialists (pediatric rheumatologists usually affiliated with pediatric teaching hospitals) can help to limit the possibility of complications of juvenile idiopathic arthritis including leg-length discrepancy, joint contractures, and destruction and blindness due to inflammation of the eye (iritis).
Until the late 1990s, JIA was known in the U.S. as JRA (juvenile rheumatoid arthritis) and JCA (juvenile chronic arthritis) in Europe. The revised name was devised in order to better distinguish the childhood disease from rheumatoid arthritis (RA) that affects adults. This new nomenclature has enabled the categorization of six JIA subtypes. This updated classification has helped to foster better communication among those doing research on causation, clinical manifestations, and therapy of JIA.
JIA is considered a diagnosis of exclusion; the diagnosis can only be confidently made when (1) the patient's history, physical exam, and laboratory findings are consistent with those described in the literature by the International League of Associations for Rheumatology and (2) other conditions have been excluded. These include infection, malignancytraumareactive arthritisimmunodeficiency, and other connective tissue/rheumatologic diseases (for example, systemic lupus erythematosus).



Learn about JRA symptoms and signs.

15 Early Symptoms and Signs of RA

While early RA symptoms can be mimicked by other diseases, the symptoms and signs are very characteristic of rheumatoid disease. The 15 early rheumatoid arthritis symptoms and signs discussed in this article include the following:
  • Fatigue
  • Joint pain
  • Joint tenderness
  • Joint swelling
  • Joint redness
  • Joint stiffness
  • Loss of joint range of motion
  • ...

What are the types of juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)?

There are six broad categories of JIA. These include
  1. systemic onset JIA,
  2. oligoarticular JIA (containing two subgroups),
  3. polyarticular JIA (containing two subgroups),
  4. psoriatic arthritis,
  5. enthesitis related arthritis, and
  6. undifferentiated arthritis.
The specific criteria necessary to establish a diagnosis and prognosis for each category are detailed below.

What are causes and risk factors of juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA) arthritis?

While no specific cause(s) of JIA have been determined, there is strong evidence of both genetic and environmental factors being implicated in the development of the disease. Studies of the frequency of JIA have shown that if one identical twin develops the disease that the likelihood of their identical sibling developing JIA is 25%-40%. Studies of nonidentical siblings show evidence that if one child develops JIA there is a 15 to 30 times increased risk that a sibling will develop the condition when compared to the general pediatric population.
The biologic and clinical manifestations of JIA provide strong evidence that a general theme of an immune system misdirection is evident. The immune system has two "arms" -- the cell based (lymphocytes, etc.) and humeral based (antibodies). Rheumatologists have demonstrated that both of these elements of the immune system react against the patient's own body structures (joints, muscles, eye tissues, etc.). Much research is currently focused in an effort to better understand this auto-inflammatory process in the hope that understanding the cause of JIA will enable better and more effective treatments and ultimately a cure for the condition.

What specialists treat juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)?

Members of the treatment team would include a pediatric rheumatologist, a pediatric ophthalmologist, physical and occupational therapists, a pharmacologist, and a social worker/family counselor.

What are juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA) symptoms and signs, and how are the different types of juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA) diagnosed?

The International League of Associations of Rheumatology has classified JIA into six distinct patterns that vary by clinical presentation and evolution of symptoms, laboratory implications, potential complications, and therapeutic options. While some similarities exist among these diseases, the uniqueness of each manifestation of JIA is strong enough to justify the breakdown into the six patterns. One characteristic common to all six forms of JIA is that of "morning stiffness" that improves during the day as more movement is done. Likewise, spontaneous patterns of worsening and lessening of symptoms (which may be independent of therapy) is characteristic.
1. Systemic onset JIA: By definition, systemic onset JIA must have arthritis (swelling, pain, and warmth) of one or more joints associated with a minimum of two weeks of daily spiking fevers. The fever is often greater than 102 F (39 C) and usually spikes once or twice a day and may have the unique pattern of returning to below normal between rises. In addition, a characteristic intermittent salmon-colored rashswollen lymph nodesliver, and spleen; and inflammation of the lungs, the pericardium (the "sack" surrounding the heart), and other organs may occur. During febrile episodes, children appear moderately sick, but with resolution of fever they are much improved. Systemic onset JIA affects approximately 10%-15% all children suffering from JIA. There is no gender preference (the frequency in boys and girls is equal), with symptoms generally starting between 3-5 years of age. There is no unique laboratory test for JIA, but children typically have anemia and elevation of white blood cell and platelet counts, as well as alterations of general markers of inflammation. Complications of systemic onset JIA may include slower than expected growth, weakening of bones, abnormalities of liver and lung function, and consequences of therapy (see below). The prognosis is generally noted to depend upon the severity of arthritis with many/most of the systemic symptoms resolving over months to years. The low mortality rate (<0.3% in North America) is reassuring. Since the diagnosis of systemic onset of JIA is one of exclusion, the possibility of infection, malignancy, collagen vascular disease, and rheumatic fever must also be considered.
2. Oligoarticular JIA: Oligoarticular is defined as arthritis that affects four or fewer joints in the first six months of the disease. This form of JIA accounts for about 50% of all cases of pediatric chronic arthritis and may be subdivided into two groups. One group consists of those children who continue throughout the entire course of their disease having four or fewer joints involved. The other group eventually develops greater than four-joint involvement after the first six months of illness. The onset of disease is between 2-4 years of age with a female gender bias of approximately 3:1. Children with oligoarticular JIA most commonly have a single large joint (knee in approximately 90% of cases) involvement. Symptoms of joint pain and tenderness are worse in the morning in association with the previously described morning stiffness (see systemic onset JIA). The primary complication of oligoarticular JIA is inflammation of the iris (the colored region of the eye). Iritis is found in approximately 15%-20% with this form of JIA and is often without symptoms. Complications of iritis may include clouding of the cornea (cataracts), glaucoma, and vision loss. Since outcome is linked to early diagnosis, it is imperative an ophthalmologist evaluate children with oligoarticular JIA every three to four months. Conditions that should be eliminated prior to establishing a diagnosis of oligoarticular JIA include trauma, infection, malignancy, and arthritis following an infection.
3. Polyarticular juvenile idiopathic arthritis: Children who have five or more joints involved with arthritis during the first six months of their disease are classified into the polyarticular JIA form of illness. Two subgroups of polyarticular JIA exist based upon a constellation of various laboratory studies. One group (rheumatoid factor "RF" positive) affects between 5%-10% of all patients with JIA. Late childhood through young teenage girls are the most likely to develop this pattern. Generally, small joints (such as the hands and feet) tend to be involved, and a more aggressive course has been observed. "RF negative" polyarticular JIA affected individuals tend to have a milder course and thus a better outcome. Fatigueanemia, suboptimal growth, and iritis (to a lesser degree than oligoarticular JIA) are complications. Other conditions that must be considered and eliminated prior to establishing the diagnosis of polyarticular JIA include infection, malignancy, and collagen vascular disease (including systemic lupus erythematosus).
4. Psoriatic arthritis (PsA): Establishing the diagnosis of psoriatic arthritis involves demonstration of both large and small joint arthritis and a characteristic rash (psoriasis). Should the rash not be present, two of the following must exist: (a) family history of psoriasis in an immediate family member, (b) diffuse swelling of the fingers, and (c) pitting of the nails. Children with psoriatic arthritis may also develop iritis and should have ophthalmologic evaluation every six months.
5. Enthesitis-related arthritis (ERA): Enthesitis (inflammation at the site of tendon insertion on the bone) most profoundly affects males over 8 years of age and often involves the lower back, sacroiliac joints, and joints of the legs, ankles, and feet. Patients with a particular genetic marker (HLA-B27) may also develop iritis, inflammatory bowel diseasepsoriasis, and/or ankylosing spondylitis (inflammation of the pelvic joints -- most commonly the sacroiliac region). The male to female ratio is 7:1.
6. Undifferentiated arthritis: Children who either do not fit clearly into the above unique subtypes of JIA or who have symptoms/laboratory studies that overlap more than one subtype are classified as having undifferentiated arthritis. By their nature, the patient population with this form of JIA often presents with nonclassical history and/or findings on physical exam and laboratory studies. Providing an accurate prognosis and developing a treatment program are challenges.

What is the treatment for juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)? What medications treat JIA/JRA?


While there currently is no cure for JIA, an integrated and coordinated approach has been shown to be helpful in lessening the morbidity (nonlethal side effects) of JIA. Goals include lessening pain, joint contractures, and growth disturbances (see above). Monitoring for the development of iritis and aggressive treatment are also paramount. Often patients are best served at a pediatric teaching hospital where access to pediatric rheumatologists, physical and occupational therapists, pharmacologists, and social support providers may allow "one stop shopping."
Therapies for JIA patients include the following:
1. Nonsteroidal anti-inflammatory drugs (NSAIDs) are commonly used as the first line of therapy due to their positive effect of reducing inflammation in arthritis and relatively few side effects. Medications such as ibuprofen (AdvilMotrin), naproxen (Aleve), and indomethacin (Indocin) are examples of this class of therapy.
2. Steroids are another common class of medications for those experiencing moderate to severe arthritis or nonarthritis inflammatory consequences of JIA. These medications may be administered orally (prednisone [Deltasone], prednisolone [Pediapred]), intravenously (methylprednisolone [Solu-Medrol], dexamethasone [Decadron], hydrocortisone [Solu-Cortef]), or injected directly into an involved joint (methylprednisolone [Depo-Medrol], triamcinolone [Kenalog]). Side effects of steroids may be considerable, and pediatric rheumatologists strive to use the lowest possible dosage. Side effects are most commonly seen at dosages over 20 mg/day and may include immune system depressionincreased appetite resulting in weight gainacne, mood changes, osteoporosis, bruising, cataractsglaucoma, and diabetes.
3. Antirheumatic medications (also known as disease-modifying antirheumatic drugs or DMARDs) are needed in approximately two-thirds of children to control the joint changes and prevent damage of JIA. These medications are generally considered when the medications previously described are not providing effective control of the illness. Medicines in this category include methotrexate (Trexall), now considered the "gold standard" for JIA, sulfasalazine (Azulfidine), azathioprine (Imuran), cyclosporine (SandimmuneNeoral), and others. These medications are administered orally or intravenously. Antirheumatic medications are more potent in effect but also can have significant side effects. All of these medications require regular blood testing to monitor for side effects. Problems include immune suppression, which may cause an increased risk of infection, certain cancers, bone marrow toxicity, pulmonary toxicity, liver function abnormalities, abdominal pain, and decrease in appetite.
4. Biologic agents can lessen the morbidity for children with JIA. These agents are administered either by superficial injection under the skin or intravenously. Their general chemical classification is that of "monoclonal antibodies" that work by accurately targeting various mechanisms of the immune system that are overactive and misdirected in JIA. They are associated with an increased risk of infections and (rarely) development of certain malignancies. As such, close clinical monitoring and various laboratory studies are required. Examples of biologics used in the treatment of JIA include etanercept (Enbrel), anakinra (Kineret), adalimumab (Humira), tocilizumab (Actemra), and abatacept (Orencia).
5. Autologous stem cell transplantation is reserved only for those children with JIA who have failed the above therapeutic options. This procedure requires hospitalization and is a two-step process. The initial goal is utilization of high-dose immune suppression medications to remove the patient's lymphocytes (a type of white blood cell) that are attacking the patient's joint(s). Once removed, new stem cells from the patient (autologous) that were previously harvested and treated are introduced back into the patient's body via the bloodstream. This process requires expertise found only in a few pediatric referral centers.
Rheumatoid Arthritis Symptoms and Treatment

What are complications of juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)?

Perhaps the most insidious and most devastating complication of JIA is a form of eye inflammation of the iris of the eye called iritis. The risk for iritis is variable depending upon the subtype of JIA. The highest risk group is oligoarticular JIA while patients with systemic onset JIA are at a low risk of this complication. It is imperative that all JIA patients have thorough ophthalmologic examinations in order to detect any changes that would herald the onset of iritis.
Another common complication of JIA is growth disturbances (such as a difference in leg lengths). Interestingly, the involved joint (such as the knee) has an increase in blood flow due to the inflammatory nature of the local arthritis. This increase in blood flow encourages the area of bone growth (growth plate) to maximum activity and thus the involved leg is longer than the non-involved limb. However, as the disease progresses, the chronic nature of arthritis can damage the growth plate region causing premature fusion and thus the involved leg will be retarded relative to the uninvolved limb. Many patients experience moderate pain of the joints involved resulting in limited use of the region. As a result, loss of calcium from the bone can result in osteoporosis.
These children and their parents may also fall victim to emotional stress associated with any chronic illness. Long-term low-grade pain may stimulate a sense of helplessness and hopelessness and thus depression. Children often have a limited social life (especially with their peers) due to school absenteeism.
It must also be remembered that the medical therapies commonly used to treat JIA can have many have prominent side effects (see above).

What is the prognosis of juvenile idiopathic arthritis (JIA)/juvenile rheumatoid arthritis (JRA)?

Approximately 50% of children with JIA continue to have active disease into adulthood. In patients who have active disease into adulthood, there can be significant disability with functional limitations. Outcome may reflect duration of disease, presence of polyarticular involvement, and the need for systemic steroids. In the United States and Canada, death is rare (29 out of 10,000 patients) and is most likely with systemic onset JIA.

Rheumatoid Arthritis (RA)

Rheumatoid arthritis (RA) facts


  • Rheumatoid arthritis is an autoimmune disease that causes chronic inflammation of the joints and other areas of the body.
  • Rheumatoid arthritis symptoms and signs include
  • Rheumatoid arthritis is a chronic disease characterized by periods of disease flares and remissions.
  • In rheumatoid arthritis, multiple joints are usually, but not always, affected in a symmetrical pattern.
  • Chronic inflammation of rheumatoid arthritis can cause permanent joint destruction and deformity.
  • Damage to joints can occur early and does not always correlate with the severity of RA symptoms.
  • The "rheumatoid factor" is an antibody that can be found in the blood of 80% of people with rheumatoid arthritis. Rheumatoid factor is detected in a simple blood test. Possible risk factors for developing rheumatoid arthritis include genetic background, smoking, silica inhalation, periodontal disease, and microbes in the bowels (gut bacteria).
  • There is no cure for RA. The treatment of rheumatoid arthritis optimally involves a combination of patient education, rest and exercise, joint protection, medications, and occasionally surgery.
  • Medications used in the treatment of rheumatoid arthritis include NSAIDs, DMARDs, TNF alpha inhibitors, IL-6 inhibitors, T-cell activation inhibitors, B-cell depleters, JAK inhibitors, immunosuppressants, and steroids.
  • Early RA treatment results in a better prognosis.
  • Rheumatoid arthritis can affect people of all ages. The cause of rheumatoid arthritis is not known.
Picture of hands affected by rheumatoid arthritis. Notice the joint deformity in the fingers.
Picture of hands affected by rheumatoid arthritis. Notice the joint deformity in the fingers; Image provided by Getty Images

What is rheumatoid arthritis (RA)?

Rheumatoid arthritis definition

Rheumatoid arthritis (RA) is an autoimmune disease that causes chronic inflammation of the joints. Autoimmune diseases are illnesses that occur when the body's tissues are mistakenly attacked by their own immune system. The immune system contains a complex organization of cells and antibodies designed normally to "seek and destroy" invaders of the body, particularly infections. Patients with autoimmune diseases have antibodies and immune cells in their blood that target their own body tissues, where they can be associated with inflammation. While inflammation of the tissue around the joints and inflammatory arthritis are characteristic features of rheumatoid arthritis, the disease can also cause extra-articular inflammation and injury in other organs in the body. Because it can affect multiple other organs of the body, rheumatoid arthritis is referred to as a systemic illness and is sometimes called rheumatoid disease. Rheumatoid arthritis is a classic rheumatic disease. Rheumatoid arthritis that begins in people under 16 years of age is referred to as juvenile idiopathic arthritis or JIA (formerly juvenile rheumatoid arthritis or JRA).
Pictures of Normal and Arthritic Joints - Rheumatoid Arthritis
Picture of a joint with rheumatoid arthritis

Learn about rheumatoid arthritis symptoms and signs.

15 Rheumatoid Arthritis (RA) Symptoms and Signs

While early symptoms of rheumatoid arthritis can actually be mimicked by other diseases, the symptoms are very characteristic of rheumatoid disease. Rheumatoid arthritis symptoms and signs include the following:
  • Fatigue
  • Joint pain
  • Joint tenderness
  • Joint swelling
  • Joint redness
  • Joint warmth
  • Joint stiffness
  • Loss of joint range of motion
  • Limping
  • Joint deformity
  • Many joints affected (polyarthritis)
  • Both sides of the body affected (symmetric)
  • Loss of joint function
  • Anemia
  • Fever

Rheumatoid arthritis vs. osteoarthritis - Differences

Rheumatoid arthritis is a destructive joint disease that is caused by inflammation in the tissue that normally produces lubrication fluid for joints. When this tissue remains inflamed, it leads to deformity by loosening joint ligaments and to joint destruction by eroding away cartilage and bone.
Osteoarthritis is a noninflammatory joint disease whereby the cartilage of the joint thins, typically asymmetrically -- so only one knee or hand may be affected. The illustration on the previous page demonstrates the difference between a normal joint and those of osteoarthritis and rheumatoid arthritis.
While rheumatoid arthritis is a chronic illness, meaning it can last for years, patients may experience long periods without symptoms. However, rheumatoid arthritis is typically a progressive illness that has the potential to cause significant joint destruction and functional disability.
A joint is where two bones meet to allow movement of body parts. Arthritis means joint inflammation. The joint inflammation of rheumatoid arthritis causes swelling, pain, stiffness, and redness in the joints. The inflammation of rheumatoid disease can also occur in tissues around the joints, such as the tendons, ligaments, and muscles.
In some people with rheumatoid arthritis, chronic inflammation leads to the destruction of the cartilage, bone, and ligaments, causing deformity of the joints. Damage to the joints can occur early in the disease and be progressive. Moreover, studies have shown that the progressive damage to the joints does not necessarily correlate with the degree of pain, stiffness, or swelling present in the joints.
Rheumatoid arthritis is a common rheumatic disease, affecting approximately 1.3 million people in the United States, according to current census data. The disease is three times more common in women as in men. It afflicts people of all races equally. The disease can begin at any age and even affects children (juvenile idiopathic arthritis), but it most often starts after 40 years of age and before 60 years of age. Though uncommon, in some families, multiple members can be affected, suggesting a genetic basis for the disorder.

What are rheumatoid arthritis causes and risk factors?

The cause of rheumatoid arthritis is unknown. Even though infectious agents such as viruses, bacteria, and fungi have long been suspected, none has been proven as the cause. The cause of rheumatoid arthritis is a very active area of worldwide research. It is believed that the tendency to develop rheumatoid arthritis may be genetically inherited (hereditary). Certain genes have been identified that increase the risk for rheumatoid arthritis. It is also suspected that certain infections or factors in the environment might trigger the activation of the immune system in susceptible individuals. This misdirected immune system then attacks the body's own tissues. This leads to inflammation in the joints and sometimes in various organs of the body, such as the lungs or eyes.
It is not known what triggers the onset of rheumatoid arthritis. Regardless of the exact trigger, the result is an immune system that is geared up to promote inflammation in the joints and occasionally other tissues of the body. Immune cells, called lymphocytes, are activated and chemical messengers (cytokines, such as tumor necrosis factor/TNF, interleukin-1/IL-1, and interleukin-6/IL-6) are expressed in the inflamed areas.

Gut bacteria, smoking, and gum disease

Environmental factors also seem to play some role in causing rheumatoid arthritis. For example, scientists have reported that smoking tobacco, exposure to silica mineral, and chronic periodontal disease all increase the risk of developing rheumatoid arthritis. There are theories about different gut bacteria (the microbiome of gut microbes that naturally inhabit the lining of the bowels) that might trigger the onset of rheumatoid arthritis in genetically susceptible individuals. No specific microbes have been identified as definite causes.

What are complications of rheumatoid arthritis?

Since rheumatoid arthritis is a systemic disease, its inflammation can affect organs and areas of the body other than the joints. Arthritis-related inflammation of the glands of the eyes and mouth can cause dryness of these areas and is referred to as Sjögren's syndrome. Dryness of the eyes can lead to corneal abrasion. Inflammation of the white parts of the eyes (the sclerae) is referred to as scleritis and can be very dangerous to the eye. Rheumatoid inflammation of the lung lining (pleuritis) causes chest pain with deep breathingshortness of breath, or coughing. The lung tissue itself can also become inflamed and scarred, and sometimes nodules of inflammation (rheumatoid nodules) develop within the lungs. Inflammation of the tissue (pericardium) surrounding the heart, called pericarditis, can cause a chest pain that typically changes in intensity when lying down or leaning forward. Rheumatoid arthritis is associated with an increased risk for heart attack. Rheumatoid disease can reduce the number of red blood cells (anemia) and white blood cells. Decreased white cells can be associated with an enlarged spleen (referred to as Felty's syndrome) and can increase the risk of infections. The risk of lymph gland cancer (lymphoma) is higher in patients with rheumatoid arthritis, especially in those with sustained active joint inflammation. Firm lumps or firm bumps under the skin (subcutaneous nodules called rheumatoid nodules) can occur around the elbows and fingers where there is frequent pressure. Even though these nodules usually do not cause symptoms, occasionally they can become infected. Nerves can become pinched in the wrists to cause carpal tunnel syndrome. A rare, serious complication, usually with longstanding rheumatoid disease, is blood vessel inflammation (vasculitis). Vasculitis can impair blood supply to tissues and lead to tissue death (necrosis). This is most often initially visible as tiny black areas around the nail beds or as leg ulcers.

What are rheumatoid arthritis symptoms and signs?


RA symptoms come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission). Remissions can occur spontaneously or with treatment and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and people generally feel well. When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies among affected individuals, and periods of flares and remissions are typical.

What does rheumatoid arthritis feel like?

When the disease is active, RA symptoms can include
  • fatigue,
  • loss of energy,
  • lack of appetite,
  • low-grade fever,
  • muscle and joint pain, and
  • stiffness.
Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity. This is referred to as morning stiffness and post-sedentary stiffness. Arthritis is common during disease flares. Also during flares, joints frequently become warm, red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis).
Rheumatoid arthritis usually inflames multiple joints and affects both sides of the body. In its most common form, therefore, it is referred to as a symmetric polyarthritis. Early rheumatoid arthritis symptoms may be subtle. The small joints of both the hands and wrists are often involved. Early symptoms of RA can be pain and prolonged stiffness of joints, particularly in the morning. Symptoms in the hands with rheumatoid arthritis include difficulty with simple tasks of daily living, such as turning door knobs and opening jars. The small joints of the feet are also commonly involved, which can lead to painful walking, especially in the morning after arising from bed. Occasionally, only one joint is inflamed. When only one joint is involved, the arthritis can mimic the joint inflammation caused by other forms of arthritis, such as gout or joint infection. Chronic inflammation can cause damage to body tissues, including cartilage and bone. This leads to a loss of cartilage and erosion and weakness of the bones as well as the muscles, resulting in joint deformity, loss of range of motion, destruction, and loss of function. Rarely, rheumatoid arthritis can even affect the joint that is responsible for the tightening of our vocal cords to change the tone of our voice, the cricoarytenoid joint. When this joint is inflamed, it can cause hoarseness of the voice. Symptoms in children with rheumatoid arthritis include limping, irritability, crying, and poor appetite.
Picture of rheuamtoid arthritis joint deformity in the feet
Picture of rheumatoid arthritis joint deformity in the feet; Image provided by Getty Images




What tests do physicians use to diagnose rheumatoid arthritis?

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There is no singular test for diagnosing rheumatoid arthritis. The diagnosis is based on the clinical presentation. Ultimately, rheumatoid arthritis is diagnosed based on a combination of the presentation of the joints involved, characteristic joint swelling and stiffness in the morning, the presence of blood rheumatoid factor (RF blood test or RA test) and citrulline antibody, as well as findings of rheumatoid nodules and radiographic changes (X-ray testing). It is important to understand that there are many forms of joint disease that can mimic rheumatoid arthritis.
The first step in the diagnosis of rheumatoid arthritis is a meeting between the health care professional and the patient. The doctor reviews the history of symptoms, examines the joints for inflammation, tenderness, swelling, and deformity, the skin for rheumatoid nodules (firm lumps or bumps under the skin, most commonly over the elbows or fingers), and other parts of the body for inflammation. Certain blood and X-ray tests are often obtained. The diagnosis will be based on the pattern of symptoms, the distribution of the inflamed joints, and the blood and X-ray findings. Several visits may be necessary before the health care professional can be certain of the diagnosis. A doctor with special training in arthritis and related diseases is called a rheumatologist.
It is the inflammation in the joint that helps to distinguish rheumatoid arthritis from common types of arthritis that are not inflammatory, such as osteoarthritis or degenerative arthritis. The distribution of joint inflammation is also important to the health care professional in making a diagnosis. In rheumatoid arthritis, the small joints of the hands and fingers, wrists, feet, and knees are typically inflamed in a symmetrical distribution (affecting both sides of the body). When only one or two joints are inflamed, the diagnosis of rheumatoid arthritis becomes more difficult. The doctor may then perform other tests to exclude arthritis due to infection or gout. The detection of rheumatoid nodules (described above), most often around the elbows and fingers, can suggest the diagnosis.
Abnormal antibodies can be found in the blood of people with rheumatoid arthritis with simple blood testing. An antibody called "rheumatoid factor" (RF) can be found in 80% of patients with rheumatoid arthritis. Patients with rheumatoid arthritis and rheumatoid factor are referred to as having "seropositive rheumatoid arthritis." Patients who are felt to have rheumatoid arthritis and do not have positive rheumatoid factor testing are referred to as having "seronegative rheumatoid arthritis." Citrulline antibody (also referred to as anti-citrulline antibody, anti-cyclic citrullinated peptide antibody, and anti-CCP antibody) is present in 50%-75% people with rheumatoid arthritis. It is useful in the diagnosis of rheumatoid arthritis when evaluating cases of unexplained joint inflammation. A test for anti-citrullinated protein antibodies is especially helpful in looking for the cause of previously undiagnosed inflammatory arthritis when the traditional blood test for rheumatoid arthritis, rheumatoid factor, is not present. Citrulline antibodies have been felt to represent the earlier stages of rheumatoid arthritis in this setting. Citrulline antibodies also have been associated with more aggressive forms of rheumatoid arthritis. Another antibody called the "antinuclear antibody" (ANA) is also frequently found in people with rheumatoid arthritis.
It should be noted that many forms of arthritis in childhood (juvenile inflammatory arthritis) are not associated with blood test positivity for rheumatoid factors. In this setting, juvenile rheumatoid arthritis must be distinguished from other types of joint inflammation, including plant thorn arthritis, joint injury, arthritis of inflammatory bowel disease, and rarely joint tumors.
A blood test called the sedimentation rate (sed rate) is a crude measure of the inflammation of the joints. The sed rate actually measures how fast red blood cells fall to the bottom of a test tube. The sed rate is usually faster (high) during disease flares and slower (low) during remissions. Another blood test that is used to measure the degree of inflammation present in the body is the C-reactive protein. Blood testing may also reveal anemia, since anemia is common in rheumatoid arthritis, particularly because of the chronic inflammation.
The rheumatoid factor, ANA, sed rate, and C-reactive protein tests can also be abnormal in other systemic autoimmune and inflammatory medical conditions. Therefore, abnormalities in these blood tests alone are not sufficient for a firm diagnosis of rheumatoid arthritis.
Joint X-rays may be normal or only demonstrate swelling of soft tissues early in the disease. As the disease progresses, X-rays can reveal bony erosions typical of rheumatoid arthritis in the joints. Joint X-rays can also be helpful in monitoring the progression of disease and joint damage over time. Bone scanning, a procedure using a small amount of a radioactive substance, can also be used to demonstrate the inflamed joints. MRI scanning can also be used to demonstrate joint damage.
The doctor may elect to perform an office procedure called arthrocentesis. In this procedure, a sterile needle and syringe are used to drain joint fluid out of the joint for study in the laboratory. Analysis of the joint fluid in the laboratory can help to exclude other causes of arthritis, such as infection and gout. Arthrocentesis can also be helpful in relieving joint swelling and pain. Occasionally, cortisone medications are injected into the joint during the arthrocentesis in order to rapidly relieve joint inflammation and further reduce symptoms.

What are the stages of rheumatoid arthritis?

The American College of Rheumatology has developed a system for classifying rheumatoid arthritis that is primarily based upon the X-ray appearance of the joints. This system helps medical professionals classify the severity of your rheumatoid arthritis with respect to cartilage, ligaments, and bone.
Stage I
  • No damage seen on X-rays, although there may be signs of bone thinning
Stage II
  • On X-ray, evidence of bone thinning around a joint with or without slight bone damage
  • Slight cartilage damage possible
  • Joint mobility may be limited; no joint deformities observed
  • Atrophy of adjacent muscle
  • Abnormalities of soft tissue around joint possible
Stage III
  • On X-ray, evidence of cartilage and bone damage and bone thinning around the joint
  • Joint deformity without permanent stiffening or fixation of the joint
  • Extensive muscle atrophy
  • Abnormalities of soft tissue around joint possible
Stage IV
  • On X-ray, evidence of cartilage and bone damage and osteoporosis around joint
  • Joint deformity with permanent fixation of the joint (referred to as ankylosis)
  • Extensive muscle atrophy
  • Abnormalities of soft tissue around joint possible
Rheumatologists also classify the functional status of people with rheumatoid arthritis as follows:
  • Class I: completely able to perform usual activities of daily living
  • Class II: able to perform usual self-care and work activities but limited in activities outside of work (such as playing sports, household chores)
  • Class III: able to perform usual self-care activities but limited in work and other activities
  • Class IV: limited in ability to perform usual self-care, work, and other activities



What are rheumatoid arthritis treatment options? What are types of rheumatoid arthritis medications?


There is no known cure for rheumatoid arthritis. To date, the goal of treatment in rheumatoid arthritis is to reduce joint inflammation and pain, maximize joint function, and prevent joint destruction and deformity. Early medical intervention has been shown to be important in improving outcomes. Aggressive management can improve function, stop damage to joints as monitored on X-rays, and prevent work disability. Optimal RA treatment involves a combination of medications, rest, joint-strengthening exercises, joint protection, and patient (and family) education. Treatment is customized according to many factors such as disease activity, types of joints involved, general health, age, and patient occupation. RA treatment is most successful when there is close cooperation between the health care professional, patient, and family members.
Two classes of medications are used in treating rheumatoid arthritis: fast-acting "first-line drugs" and slow-acting "second-line drugs" (also referred to as disease-modifying antirheumatic drugs or DMARDs). The first-line drugs, such as aspirin and cortisone (corticosteroids [Rayos, Celestone, Depo-Medrol, Kenalog]), are used to reduce pain and inflammation. The slow-acting second-line drugs, such as methotrexate (RheumatrexTrexall, Otrexup, Rasuvo) and hydroxychloroquine (Plaquenil), promote disease remission and prevent progressive joint destruction.
The degree of destructiveness of rheumatoid arthritis varies among affected individuals. Those with uncommon, less destructive forms of the disease or disease that has quieted after many years of activity ("burned out" rheumatoid arthritis) can be managed with rest plus pain control and anti-inflammatory medications alone. In general, however, function is improved and disability and joint destruction are minimized when the condition is treated earlier with second-line drugs (disease-modifying antirheumatic drugs), even within months of the diagnosis. Most people require more aggressive second-line drugs, such as methotrexate, in addition to anti-inflammatory agents. Sometimes these second-line drugs are used in combination.
The areas of the body other than the joints that are affected by rheumatoid inflammation are treated individually. Sjögren's syndrome can be helped by artificial tears and humidifying rooms in the home or office. Medicated eyedrops, cyclosporine ophthalmic drops (Restasis), are also available to help the dry eyes in those affected. Regular eye checkups and early antibiotic treatment for infection of the eyes are important. Inflammation of the tendons (tendinitis), bursae (bursitis), and rheumatoid nodules can be injected with cortisone. Inflammation of the lining of the heart and/or lungs may require high doses of oral cortisone.
In some cases with severe joint deformity, surgery may be recommended to restore joint mobility or repair damaged joints. Doctors who specialize in joint surgery are orthopedic surgeons. The types of joint surgery range from arthroscopy to partial and complete replacement of the joint. Arthroscopy is a surgical technique whereby a doctor inserts a tube-like instrument into the joint to see and repair abnormal tissues.
Total joint replacement is a surgical procedure whereby a destroyed joint is replaced with artificial materials. For example, the small joints of the hand can be replaced with plastic material. Large joints, such as the hips or knees, are replaced with metals.

"First-line" rheumatoid arthritis medications

Acetylsalicylate (aspirin), naproxen (Naprosyn), ibuprofen (Advil, Medipren, Motrin), etodolac (Lodine), and diclofenac (Voltaren) are examples of non-steroidal anti-inflammatory drugs (NSAIDs). NSAIDs are medications that can reduce tissue inflammation, pain, and swelling. NSAIDs are not cortisone. Aspirin, in doses higher than those used in treating headaches and fever, is an effective anti-inflammatory medication for rheumatoid arthritis. Aspirin has been used for joint problems since the ancient Egyptian era. The newer NSAIDs are just as effective as aspirin in reducing inflammation and pain and require fewer dosages per day. Patients' responses to different NSAID medications vary. Therefore, it is not unusual for a medical professional to try several NSAID drugs in order to identify the most effective agent with the fewest side effects. The most common side effects of aspirin and other NSAIDs include stomach upset, abdominal pain, ulcers, and even gastrointestinal bleeding. In order to reduce gastrointestinal side effects, NSAIDs are usually taken with food. Additional medications are frequently recommended to protect the stomach from the ulcer effects of NSAIDs. These medications include antacids, sucralfate (Carafate), proton-pump inhibitors (Prevacid and others), and misoprostol (Cytotec). Newer NSAIDs include selective Cox-2 inhibitors, such as celecoxib (Celebrex), which offer anti-inflammatory effects with less risk of stomach irritation and bleeding risk.
Corticosteroid medications can be given orally or injected directly into tissues and joints. They are more potent than NSAIDs in reducing inflammation and in restoring joint mobility and function. Corticosteroids are useful for short periods during severe flares of disease activity or when the disease is not responding to NSAIDs. However, corticosteroids can have serious side effects, especially when given in high doses for long periods of time. These side effects include weight gain, facial puffiness, thinning of the skin and bone, easy bruising, cataracts, risk of infection, muscle wasting, and destruction of large joints, such as the hips. Corticosteroids also carry some increased risk of contracting infections. These side effects can be partially avoided by gradually tapering the doses of corticosteroids as the individual achieves improvement in symptoms. Abruptly discontinuing corticosteroids can lead to flares of the disease or other symptoms of corticosteroid withdrawal and is discouraged. Thinning of the bones due to osteoporosis may be prevented by calcium and vitamin D supplements.



"Second-line" or "slow-acting" rheumatoid arthritis drugs (disease-modifying anti-rheumatic drugs or DMARDs)

While "first-line" medications (NSAIDs and corticosteroids) can relieve joint inflammation and pain, they do not necessarily prevent joint destruction or deformity. Rheumatoid arthritis requires medications other than NSAIDs and corticosteroids to stop progressive damage to cartilage, bone, and adjacent soft tissues. The RA medications needed for ideal management of the disease are also referred to as disease-modifying antirheumatic drugs or DMARDs. They come in a variety of forms and are listed below. These "second-line" or "slow-acting" medicines may take weeks to months to become effective. They are used for long periods of time, even years, at varying doses. If maximally effective, DMARDs can promote remission, thereby retarding the progression of joint destruction and deformity. Sometimes a number of DMARD second-line medications are used together as combination therapy. As with the first-line medications, the doctor may need to try different second-line medications before treatment is optimal.
Research suggests that patients who respond to a DMARD with control of the rheumatoid disease may actually decrease the known risk (small but real) of lymphoma (cancer of lymph nodes) that exists from simply having rheumatoid arthritis. The various available DMARDs are reviewed next.
Hydroxychloroquine (Plaquenil) is related to quinine and has also been used in the treatment of malaria. It is used over long periods for the treatment of rheumatoid arthritis. Possible side effects include upset stomach, skin rashes, muscle weakness, and vision changes. Even though vision changes are rare, people taking Plaquenil should be monitored by an eye doctor (ophthalmologist).
Sulfasalazine (Azulfidine) is an oral medication traditionally used in the treatment of mild to moderately severe inflammatory bowel diseases, such as ulcerative colitis and Crohn's colitis. Azulfidine is used to treat rheumatoid arthritis in combination with anti-inflammatory medications. Azulfidine is generally well tolerated. Common side effects include rash and upset stomach. Because Azulfidine is made up of sulfa and salicylate compounds, it should be avoided by people with known sulfa allergies.
Methotrexate (Rheumatrex, Trexall, Otrexup, Rasuvo) has gained popularity among health care professionals as an initial second-line drug because of both its effectiveness and relatively infrequent side effects. It also has an advantage in dose flexibility (dosages can be adjusted according to needs). Methotrexate is an immunosuppressive drug. It can affect the bone marrow and the liver, even rarely causing cirrhosis. All people taking methotrexate require regular blood tests to monitor blood counts and liver function. Taking folic acid as a supplement can reduce the risk of methotrexate side effects.
Gold salts have been used to treat rheumatoid arthritis throughout most of the past century. Gold thioglucose (Solganal) and gold thiomalate (Myochrysine) are given by injection, initially on a weekly basis, for months to years. Oral gold, auranofin (Ridaura), was introduced in the 1980s. Side effects of gold (oral and injectable) include skin rashmouth sores, kidney damage with leakage of protein in the urine, and bone marrow damage with anemia and low white cell count. Those receiving gold treatment are regularly monitored with blood and urine tests. Oral gold can cause diarrhea. These gold drugs have lost favor in the treatment of RA because of the availability of more effective treatments, particularly methotrexate.
D-penicillamine (DepenCuprimine) can be helpful in selected cases of progressive forms of rheumatoid arthritis. Side effects are similar to those of gold. They include fever, chillsmouth sores, a metallic taste in the mouth, skin rash, kidney and bone marrow damage, stomach upset, and easy bruising. People taking this medication require routine blood and urine tests. D-penicillamine can rarely cause symptoms of other autoimmune diseases and is no longer commonly used for the treatment of rheumatoid arthritis.
Immunosuppressive medicines are powerful medications that suppress the body's immune system. A number of immunosuppressive drugs are used to treat rheumatoid arthritis. They include methotrexate as described above, azathioprine (Imuran), cyclophosphamide (Cytoxan), chlorambucil (Leukeran), and cyclosporine (Sandimmune). Because of potentially serious side effects, immunosuppressive medicines (other than methotrexate) are generally reserved for those who have very aggressive disease or those with serious complications of rheumatoid inflammation, such as blood vessel inflammation (vasculitis). The exception is methotrexate, which is not frequently associated with serious side effects and can be carefully monitored with blood testing. Methotrexate has become a preferred second-line medication as a result.
Immunosuppressive medications can depress bone-marrow function and cause anemia, a low white cell count, and low platelet counts. A low white count can increase the risk of infections, while a low platelet count can increase the risk of bleeding. Methotrexate rarely can lead to liver cirrhosis, as described above, and allergic reactions in the lung. Cyclosporine can cause kidney damage and high blood pressure (hypertension). Because of potentially serious side effects, immunosuppressive medications are used in low doses, usually in combination with anti-inflammatory agents.
Combinations of traditional DMARDs, including sulfasalazine, methotrexate, and hydroxychloroquine, have been shown by researchers to be another potent method of stopping disease progression of rheumatoid arthritis.

What are newer rheumatoid arthritis medical treatments?

Newer "second-line" drugs (DMARDs) for the treatment of rheumatoid arthritis include leflunomide (Arava) and the "biologic" medications etanercept (Enbrel), infliximab (Remicade), anakinra (Kineret), adalimumab (Humira), rituximab (Rituxan), abatacept (Orencia), golimumab (Simponi), certolizumab pegol (Cimzia), tocilizumab (Actemra), and JAK inhibitors represented by tofacitinib (Xeljanz). Each of these medications can increase the risk for infections, and the development of any infections should be reported to the health care professional when taking these newer second-line drugs.
Leflunomide (Arava) is available to relieve the symptoms and halt the progression of the disease. It seems to work by blocking the action of an important enzyme that has a role in immune activation. Leflunomide can cause liver diseasediarrheahair loss, and/or rash in some people. It should not be taken just before or during pregnancy because of possible birth defects and is generally avoided in women who might become pregnant.
Biologic DMARDs represent a novel approach to the treatment of rheumatoid arthritis and are products of modern biotechnology. These are referred to as the biologic medications or biological response modifiers. In comparison with traditional DMARDs, the biologic medications have a much more rapid onset of action and can have powerful effects on stopping progressive joint damage. In general, their methods of action are also more directed, defined, and targeted.
Etanercept, infliximab, adalimumab, golimumab, and certolizumab pegol are biologic medications that intercept a messenger protein in the joints (tumor necrosis factor or TNF) that promotes inflammation of the joints in rheumatoid arthritis. These TNF-blockers intercept TNF before it can act on its natural receptor to "switch on" the process of inflammation. This effectively blocks the TNF inflammation messenger from recruiting the cells of inflammation. Symptoms can be significantly, and often rapidly, improved in those using these drugs. Etanercept must be injected subcutaneously once or twice a week. Infliximab is given by infusion directly into a vein (intravenously). Adalimumab is injected subcutaneously either every other week or weekly. Golimumab is injected subcutaneously on a monthly basis. Certolizumab pegol is injected subcutaneously every two to four weeks. Each of these medications is being evaluated by health care professionals in practice to determine what role they may have in treating patients in various stages of rheumatoid arthritis. Research has shown that biological response modifiers also prevent the progressive joint destruction of rheumatoid arthritis. They are currently recommended for use after other second-line medications have not been effective. The biological response modifiers (TNF-inhibitors) are expensive treatments. They are also frequently used in combination with methotrexate and other DMARDs. Furthermore, it should be noted that the TNF-blocking biologics all are more effective when combined with methotrexate. These medications should be avoided by people with significant congestive heart failure or demyelinating diseases (such as multiple sclerosis) because they can worsen these medical conditions.
Anakinra (Kineret) is another biologic DMARD treatment that is used to treat moderate to severe rheumatoid arthritis. Anakinra works by binding to a cell messenger protein (IL-1, a pro-inflammatory cytokine). Anakinra is injected under the skin daily. Anakinra can be used alone or with other DMARDs. The response rate of anakinra does not seem to be as high as with other biologic medications.
Rituximab (Rituxan) is an antibody that was first used to treat lymphoma, a cancer of the lymph nodes. Rituximab can be effective in treating autoimmune diseases like rheumatoid arthritis because it depletes B-cells, which are important cells of inflammation and in the production of abnormal antibodies that are common in these medical conditions. Rituximab is used to treat moderate to severely active rheumatoid arthritis in patients who have failed treatment with the TNF-blocking biologics. Preliminary studies have shown that Rituximab was also found to be beneficial in treating severe rheumatoid arthritis complicated by blood vessel inflammation (vasculitis) and cryoglobulinemia. Rituximab is an intravenous infusion given in two doses, two weeks apart, approximately every six months.
Abatacept (Orencia) is a biologic medication that blocks T-cell activation. Abatacept is used to treat adult patients who have failed treatment with a traditional DMARD medication. Abatacept is an intravenous infusion given monthly or a weekly subcutaneous injection.
Tocilizumab (Actemra) is approved for the treatment of adult patients with moderately to severely active rheumatoid arthritis (RA) who have had an inadequate response to one or more tumor necrosis factor (TNF) antagonist therapies. Tocilizumab is the first approved biologic medication that blocks interleukin-6 (IL-6), which is a chemical messenger of the inflammation of rheumatoid arthritis. Tocilizumab is an intravenous infusion given monthly or a weekly subcutaneous injection.
Tofacitinib (Xeljanz) is the first in a new class of medications used to treat rheumatoid arthritis called JAK inhibitors. Tofacitinib is used to treat adults with moderately to severely active rheumatoid arthritis in which methotrexate did not work well. Tofacitinib can be used with or without methotrexate. This prescription medicine is taken by mouth twice daily. Tofacitinib is considered a "targeted" medication that specifically blocks special enzymes of inflammation in joints (called Janus kinase) within cells. Tofacitinib is, therefore, referred to as a JAK inhibitor.
While biologic medications are often combined with traditional DMARDs in the treatment of rheumatoid arthritis, they are generally not used with other biologic medications because of the unacceptable risk for serious infections. Similarly, JAK inhibitor medication is not used with traditional biologic medications.

Rheumatoid arthritis diet, exercise, therapy, home remedies, and alternative medicine

Foods to avoid with RA

There is no special RA diet or diet "cure" for rheumatoid arthritis. One hundred years ago, it was touted that "night-shade" foods, such as tomatoes, would aggravate rheumatoid arthritis. This is no longer accepted as true. There are no specific foods or food groups that should be universally avoided by individuals with rheumatoid arthritis.
There is no evidence that gluten bothers rheumatoid arthritis. Nevertheless, for those who are definitely sensitive to gluten (wheat, barley, and rye), the gluten-free diet can prevent poor intestinal absorption of important nutrients because the small intestines can become inflamed in these individuals. Bowel inflammation can be detrimental for those also affected by rheumatoid arthritis if they become deficient in nutrients, such as vitamin D and folate.

Foods that fight RA inflammation

Nevertheless, there are some home remedies that may be helpful, although these are not considered as potent or effective as disease-modifying drugs. Fish oils, such as in salmon, and omega-3 fatty acids supplements have been shown to be beneficial in some short-term studies in rheumatoid arthritis. This suggests that there may be benefits by adding more fish to the diet, such as in the popular Mediterranean diet. The anti-inflammatory effects of curcumin in dietary turmeric, an ingredient in curry, may be beneficial in reducing symptoms of rheumatoid arthritis.

Supplements for RA

Supplements such as calcium and vitamin D are used to prevent osteoporosis in patients with rheumatoid arthritis. Folic acid is used as a supplement to prevent side effects of methotrexate treatment of rheumatoid arthritis. Alcohol is minimized or avoided in rheumatoid arthritis patients taking methotrexate.
The benefits of cartilage preparations such as glucosamine and chondroitin for rheumatoid arthritis remain unproven. Symptomatic pain relief can often be achieved with oral acetaminophen (Tylenol) or over-the-counter topical preparations, which are rubbed into the skin. Antibiotics, in particular the tetracycline drug minocycline (Minocin), have been tried for rheumatoid arthritis recently in clinical trials. Early results have demonstrated mild to moderate improvement in the symptoms of arthritis. Minocycline has been shown to impede important mediator enzymes of tissue destruction, called metalloproteinases, in the laboratory as well as in humans.

Exercises and home remedies for RA

Because impact loading the joints can aggravate inflamed, active rheumatoid arthritis and also be difficult when joints have been injured in the past by the disease, it is important to customize activities and exercise programs according to each individual's capacity. Physical therapy can be helpful. Movement exercises that are less traumatic for the joints, including yoga and tai chi, can be beneficial in maintaining flexibility and strength as well as lead to an improved general sense of well-being.
Proper regular exercise is important in maintaining joint mobility and in strengthening the muscles around the joints. Swimming is particularly helpful because it allows exercise with minimal stress on the joints. Physical and occupational therapists are trained to provide specific exercise instructions and can offer splinting supports. For example, wrist and finger splints can be helpful in reducing inflammation and maintaining joint alignment. Devices such as canes, toilet seat raisers, and jar grippers can assist in the activities of daily living. Heat and cold applications are modalities that can ease symptoms before and after exercise.

What about rheumatoid arthritis and pregnancy?

In general, rheumatoid arthritis often improves during pregnancy. It is commonplace for the rheumatoid joint inflammation to decrease and be minimized during pregnancy. Unfortunately, this reduction of joint inflammation during pregnancy is not usually sustained after delivery.
Medications that are commonly used to treat inflammation, such as non-steroidal anti-inflammatory drugs including ibuprofen (Motrin, Advil), naproxen (Aleve), and others, are not used during pregnancy. Drugs that are used to stop the progression of rheumatoid disease, such as methotrexate (Rheumatrex, Trexall) and cyclosporine (Neoral, Sandimmune), are not used during pregnancy and also must be discontinued well in advance of conception because of potential risks to the fetus. Biologic medications are avoided during pregnancy when possible.
When rheumatoid arthritis is active during pregnancy, steroid medications such as prednisone and prednisolone are often used to quiet the joint inflammation. These medications do not adversely affect the fetus.

What is the prognosis for patients with rheumatoid arthritis?

With early, aggressive treatment, the outlook for those affected by rheumatoid arthritis can be very good. The overall attitude regarding ability to control the disease has changed tremendously since the turn of the century. Doctors now strive to eradicate any signs of active disease while preventing flare-ups. The disease can be controlled and a cooperative effort by the doctor and patient can lead to optimal health.
Rheumatoid arthritis causes disability and can increase mortality and decrease life expectancy to lead to an early death. Patients have a less favorable outlook when they have deformity, disability, ongoing uncontrolled joint inflammation, and/or rheumatoid disease affecting other organs of the body. Overall, rheumatoid arthritis tends to be potentially more damaging when rheumatoid factor or citrulline antibody is demonstrated by blood testing. Life expectancy improves with earlier treatment and monitoring.
Finally, minimizing emotional stress can help improve the overall health in people with rheumatoid arthritis. Support and extracurricular groups provide those with rheumatoid arthritis time to discuss their problems with others and learn more about their illness.

Is there a cure for RA?

No, rheumatoid arthritis is not a curable disease at this time. As the science of genetics and disease as well as autoimmunity evolve, it is very likely that cures for rheumatoid arthritis will become available.

What are tips for living with rheumatoid arthritis?

  • Early and aggressive treatment tends to result in optimal outcome.
  • Understand how your rheumatoid arthritis, as well as the effects and side effects of its treatment, will be monitored.
  • Maintain a working relationship with your treating physician. Consider consulting with a rheumatologist.
  • Have a game plan for addressing flare-ups of the rheumatoid inflammation.
  • Preplan your treatment options for travel with your physician.
  • Review with your physician any concerns about your rheumatoid arthritis, its influence on your lifestyle activities, your avocations, and your long-term life goals.

Is it possible to prevent rheumatoid arthritis?

Currently, there is no specific prevention of rheumatoid arthritis. Because cigarette smoking, exposure to silica mineral, and chronic periodontal disease all increase the risk for rheumatoid arthritis, these conditions should be avoided.

What specialists treat rheumatoid arthritis (RA)?

The primary specialist for diagnosing, managing, and monitoring rheumatoid arthritis is a rheumatologist. The rheumatologist works together with the primary doctor and other specialists to maximize health outcomes and minimize comorbid health conditions. Other specialists that can be involved in the care of patients with rheumatoid arthritis include physiatrists, dermatologists, pulmonologists, cardiologists, nephrologists, radiologists, neurologists, endocrinologists, orthopedists, and general surgeons. Ancillary health care providers who can be involved in the care of patients with rheumatoid arthritis include physical therapists, occupational therapists, and massage therapists.

What new information about RA has come from the 2015 national meeting of the American College of Rheumatology?

There are many new biologic treatments for rheumatoid arthritis on the near horizon. Many of these are being studied with and without simultaneous methotrexate. Some block chemical messengers and some block specific cell types of inflammation.
The significant benefit of treating lipid/cholesterol profiles in patients with rheumatoid arthritis to improve long-term risks of stroke and heart attack was emphasized.
Diets that were higher in fish, grains, and vegetables were shown to decrease the risk of developing rheumatoid arthritis, while the Western diet, defined as including more processed meats increased the risk. It is not certain whether this is because of a direct anti-inflammatory effect of the fish, grains, and vegetables or because of changes in the natural bacteria in the gut.

What research is being done on rheumatoid arthritis?

Scientists throughout the world are studying many promising areas of new treatment approaches for rheumatoid arthritis. Indeed, treatment guidelines are evolving with the availability of newer treatments. These areas include treatments that block the action of the special inflammation factors, such as tumor necrosis factor (TNF alpha), B-cell and T-cell function, as well as interleukin-1 (IL-1), as described above. Many other drugs are being developed that act against certain critical white blood cells and chemical messengers involved in rheumatoid inflammation. Also, new NSAIDs with mechanisms of action that are different from current drugs are on the horizon.
Better methods of more accurately defining which patients are more likely to develop more aggressive disease are becoming available. Recent antibody research has found that the presence of citrulline antibodies in the blood (see above, in diagnosis) has been associated with a greater tendency toward more destructive forms of rheumatoid arthritis.
Studies involving various types of the connective tissue collagen are in progress and show encouraging signs of reducing rheumatoid disease activity. Finally, genetic research and engineering are likely to bring forth many new avenues for earlier diagnosis and accurate treatment in the near future. Gene profiling, also known as gene array analysis, is being identified as a helpful method of defining which people will respond to which medications. Studies are under way that are using gene array analysis to determine which patients will be at more risk for more aggressive disease. This is all occurring because of improvements in technology. We are at the threshold of tremendous improvements in the management of rheumatoid arthritis.

Are there support groups for people with rheumatoid arthritis?

There are support groups for rheumatoid arthritis in all major cities in the United States. Many are affiliated with local hospitals and/or local chapters of the Arthritis Foundation.
The Arthritis Foundation
P.O. Box 19000
Atlanta, Georgia 30326

Where can people get additional information on rheumatoid arthritis?

For more information about rheumatoid arthritis as well as living with RA and for support groups, please consider the following:
National Arthritis and Musculoskeletal and Skin Diseases Clearinghouse
Box AMS
Bethesda, Maryland 20892
301-495-4484

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