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Chapter I Rheumatoid arthritis
Chapter I Rheumatoid arthritis
1. Overview
Rheumatoid arthritis, sometimes referred to as rheumatoid disease, is achronic, progressive and disabling autoimmune disease that causes inflammation
and pain in the joints, the tissue around the joints, and other organs in the human
body. Rheumatoid arthritis usually affects the joints in the hands and feet first, but
any joint may become affected. Patients with rheumatoid arthritis commonly have stiff
joints and feel generally unwell and tired.
Rheumatoid arthritis is an autoimmune disease. Our immune system is a
complex organization of cells and antibodies designed to seek out and destroy
organisms and substances which harm us, such as infections. When our immune
system starts attacking our own bodies, mistaking body tissues for foreign invaders,
we have an autoimmune disease.
Individuals with an autoimmune disease have antibodies in their blood which
target their own body tissues, resulting in inflammation. The immune system of a
patient with rheumatoid arthritis attacks the lining of the joints, causing them to swell.
As opposed to the wear-and-tear damage which occurs with osteoarthritis,
rheumatoid arthritis affects the lining of the joints, resulting in painful swelling that can
lead to bone erosion and joint deformity. Eventually the affected joints may become
permanently damaged.
Rheumatoid arthritis is referred to as a systemic illness. Systemic means it
affects the entire body; in the case of rheumatoid arthritis, multiple organs in the body
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Chapter I Rheumatoid arthritis
can be affected. The patient may also have fevers and experience fatigue.
Rheumatoid arthritis may also produce diffuse (spreading) inflammation in the lungs,
the membrane around the lungs (pleura), pericardium (a double-walled sac that
contains the heart and the roots of the great blood vessels) and the tough white outer
coat over the eyeball (sclera); it can produce nodular lesions, most commonly in
subcutaneous tissue under the skin.
Rheumatoid arthritis is much more common that MS (multiple sclerosis) or
leukemia. However, awareness of the diseases effects and severity are more
restricted to patients, their caregivers and their relatives because it is not well
publicized.
Rheumatoid arthritis symptoms generally come and go. On some occasions
symptoms may be mild, while on others they may be severe and extremely painful. A
patient has aflare up when symptoms are bad. It is impossible to know when a flareup may come.
Rheumatoid arthritis can be a very painful condition, leading to considerable
loss of functioning and mobility. Diagnosis is made chiefly as a result of identifying
signs and symptoms, as well as rheumatoid factor blood tests and X-rays. Diagnosis
and the long-term management of the disease is generally carried out by a
rheumatologist; a specialist in rheumatology.
Rheumatoid arthritis affects all ages, races, and social and ethnic groups. It is
most likely to strike people 35-50 years of age, but it can occur in children,teenagers, and elderly people. (A similar disease affecting young people is known as
juvenile rheumatoid arthritis).
Worldwide, about 1% of people are believed to have rheumatoid arthritis, but
the rate varies among different groups of people. For example, rheumatoid arthritis
affects about 5%-6% of some Native American groups, while the rate is very low in
some Caribbean peoples of African descent.
The rate is about 2%-3% in people who have a close relative with rheumatoid
arthritis, such as a parent, brother or sister, or child.
As many as half of those with rheumatoid arthritis are no longer able to work
10-20 years after their condition is diagnosed. Although the disease has no cure,
early diagnosis and prompt subsequent treatment of symptoms may slow the
progression down, as well as making the patient more comfortable.
2. History
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The first known traces of arthritis date back at least as far as 4500 BC. A text
dated 123 AD first describes symptoms very similar to rheumatoid arthritis. It was
noted in skeletal remains of Native Americans found in Tennessee. In the Old World
the disease is vanishingly rare before the 1600s and on this basis investigators
believe it spread across the Atlantic during the Age of Exploration. In 1859 the
disease acquired its current name.
An anomaly has been noticed from investigation of Precolumbian bones. The
bones from the Tennessee site show no signs of tuberculosis even though it was
prevalent at the time throughout the Americas. Jim Mobley, at Pfizer, has discovered
a historical pattern of epidemics of tuberculosis followed by a surge in the number of
rheumatoid arthritis cases a few generations later. Mobley attributes the spikes in
arthritis to selective pressure caused by tuberculosis. A hypervigilant immune system
is protective against tuberculosis at the cost of an increased risk of autoimmune
disease.
The art ofPeter Paul Rubens may possibly depict the effects of rheumatoid
arthritis. In his later paintings, his rendered hands show, in the opinion of some
physicians, increasing deformity consistent with the symptoms of the disease.
Rheumatoid arthritis appears to some to have been depicted in 16th century
paintings. However, it is generally recognised in art historical circles that the painting
of hands in the sixteenth and seventeenth century followed certain stylised
conventions, most clearly seen in the Mannerist movement. It was conventional, for
instance to show the upheld right hand of Christ in what now appears a deformed
posture. These conventions are easily misinterpreted as portrayals of disease. They
are much too widespread for this to be plausible.
The first recognized description of rheumatoid arthritis was in 1800 by the
French physician Dr Augustin Jacob Landr-Beauvais (17721840) who was based
in the famed Salptrire Hospital in Paris. The name "rheumatoid arthritis" itself was
coined in 1859 by British rheumatologist DrAlfred Baring Garrod.
Notable cases
Dorothy Hodgkin, Nobel prize winning scientist, developed severe deforming
rheumatoid arthritis at age 28. In spite of this she continued her career and
developed X-ray crystallography, which underpins much of the information
known about rheumatoid arthritis. She also discovered the structure of insulin
and enabled the discovery of the genetic code.
Auguste Renoir, impressionist painter, whose later 'softer' style might have
reflected in some way his severe disability.
Christiaan Barnard, the first surgeon to perform a human-to-human heart
transplant had to retire owing to the condition. He also wrote a book on living
with arthritis.
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Chapter I Rheumatoid arthritis
James Coburn claimed to have healed the condition using pills containing a
sulfur-containing compound on his return to acting.
Erik Lindbergh, aviator and member of the X-Prize administration. Erik has
been a spokesman for the arthritis drug Enbrel, as a result of his success with
the treatment.
Bob MortimerBritish comedian and actor.
Kathleen Turnerand Aida Turturro have worked to raise public awareness of
the condition
Billy Bowden, international cricket umpire who had to retire from active play
because of rheumatoid arhtirits.
Melvin Franklin, bass singer of the Temptations. He treated RA with cortisone
shots so he could perform.
Jamie Farr, American actor, famous for his role as Max Klingeron the 1970s
television series M*A*S*H.
Sandy Koufax, An American Hall-of-Fame baseball pitcher who played from1955 to 1966 for the Los Angeles Dodgers.
Jeffrey Gottfurcht An American who is attempting to be the first person with
RA to climb to the top of Mt. Everest March 2011.
3. Signs and symptoms
A symptom is something the patient feels and reports, while a sign is
something other people, such as the doctor detect. For example, pain may be a
symptom while a rash may be a sign.
The symptoms of rheumatoid arthritis 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 arthritisvaries among affected individuals, and periods of flares and remissions are typical.
When the disease is active, symptoms can include fatigue, loss of energy, lack
of appetite, low-grade fever, muscle and joint aches, and stiffness. Muscle and joint
stiffness are usually most notable in the morning and after periods of inactivity.
Arthritis is common during disease flares. Also during flares, joints frequently become
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).
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Chapter I Rheumatoid arthritis
In rheumatoid arthritis, multiple joints are usually inflamed in a symmetrical
pattern (both sides of the body affected). The small joints of both the hands and
wrists are often involved. Simple tasks of daily living, such as turning door knobs and
opening jars, can become difficult during flares. The small joints of the feet are also
commonly involved. 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 jointdeformity, 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.
The most commonly affected joints are:
The proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints of
the hands (middle and base joints of the finger)
The wrists, especially the ulnar-styloid articulation
The shoulders
Elbows
Knees
Ankles
Metatarsophalangeal (MTP) joints (in the toes)
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Note: The distal interphalangeal (DIP) joints are not usually affected (top joint of
the finger)
The spine is never affected, except the atlanto-axial articulation in late disease.
Morning stiffness - morning stiffness is a hallmark symptom of rheumatoid arthritis,
especially if it lasts more than an hour. Experts say that the duration of morning
stiffness is usually a good indication of the inflammatory activity of the disease.
Although patients with other forms of arthritis may have early morning joint stiffness,
they tend not to last for more than an hour. There may be stiffness after long periods
of inactivity, which tends to last longer than in cases of degenerative arthritis.
Joint pain and swelling - the lining of the affected joint becomes inflamed - the skin
over the joint becomes warm, red and swollen. The area is painful and tender to the
touch.
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Anemia - according to The National Health Service (NHS), UK, approximately 80%
of patients with rheumatoid arthritis are anemic - there is a low number of red blood
cells; the blood is unable to carry enough oxygen.
Loss of appetite/Weight loss - a significant number of patients may experience loss
of appetite, and subsequent weight loss.
The patient may have red and puffy hands.
The following non-specific systemic flu-like symptoms may be felt weeks to
months before other symptoms appear:
Fatigue (tiredness)
Malaise
Depression
Fever - usually low grade (37 - 38C; 99 - 100F). Experts say that a higher
fever often indicates an infectious cause (another illness).
Flare-ups
The symptoms of rheumatoid arthritis tend to be intermittent (sporadic); they
come and go. Sometimes the patient will have a flare-up - the symptoms will be more
intense and severe.
Although flare-ups can occur at any time, they tend to be more painful in the
morning, when the patient wakes up. As the day progresses symptoms will start to
ease.
Rheumatoid arthritis is a systemic illness (one that affects the entire body)
Multiple organs in the body can be affected, including:
Inflammation in the lungs - this usually causes no symptoms. If the patient
develops shortness of breath medications may be prescribed to reduce
inflammation in the lungs.
Inflammation of the membrane around the lungs (pleura)
Inflammation of the pericardium - a double-walled sac that contains the
heart and the roots of the great blood vessels.
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Inflammation of the tough white outer coat over the eyeball (sclera) -
affects about 5% of patients. Symptoms may include red, painful and possibly dry
eyes.
Nodular lesions - about 1 in every 4 rheumatoid arthritis patients develops
lumps under the skin - rheumatoid nodules. They tend to occur on the skin over the
elbows and forearms. They may be painful, but not usually.
Inflammation of the tear glands
Inflammation of the salivary glands
Inflammation of the cricoarytenoid joint - this is a joint in the larynx (voice
box). When it is inflamed it can cause hoarseness.
4. Cause
The smooth lining of the membranes (thin layer of cells) that surround our
joints is called the synovium. A flexible joint is lined by a synovial membrane. The
synovium produces a clear substance - synovial fluid - which lubricates and
nourishes the cartilage and bones inside the joint capsule.
When the immune system attacks the synovium, rheumatoid arthritis may
occur. Antibodies attack the synovium, leaving it sore and inflamed - the synovium
becomes thicker and may eventually invade and destroy cartilage (the stretchy
connective tissue between bones) and bone inside the joint. The joint is held together
by tendons (tissue that connects bone to muscle) and ligaments (tissue that connects
bone and cartilage). These tendons and ligaments weaken and stretch, and the joint
eventually loses its shape and configuration. The joint may eventually be completely
destroyed.
Nobody really knows what starts off this process. Even though infectious
agents such as viruses, bacteria, and fungi have long been suspected, none hasbeen 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. It is also suspected that certain infections or factors in
the environment might trigger the activation of the immune system in susceptible
individuals. Environmental factors also seem to play some role in causing
rheumatoid arthritis. For example, scientists have reported that smoking tobacco
increases the risk of developing rheumatoid arthritis.
5. Diagnosis
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In its early stages rheumatoid arthritis may be difficult to diagnose. Its signs
and symptoms - especially stiffness and inflammation - are similar to several other
conditions.
A GP (general practitioner, primary care physician) will carry out a physical
examination. The doctor will carefully check the joints to see if there is any swelling
(e.g. pain on squeeze test on the knuckles), as well as determining how easily they
move. The patient will be asked about symptoms.
The doctor may also order the following tests:
Blood tests
Erythrocyte sedimentation rate (ESR or sed rate) - this blood test detects and
monitors inflammation in the body by measuring the rate at which red blood cells in
a test tube separate from blood serum over a set period, becoming sediment in the
bottom of the test tube. A high sedimentation rate is linked to more inflammation. In
other words, if the red blood cells sink faster to the bottom of the test tube, it could
mean that the patient has an inflammatory condition, such as rheumatoid arthritis.
C-reactive protein (CRP) - CRP is produced by the liver. A higher CRP level is
linked to the presence of inflammation in the body.
Anemia - a significant proportion of patients with rheumatoid arthritis also have
anemia; when not enough oxygen is carried in the blood, because of a lack of red
blood cells. If the patient is found to have anemia it does not necessarily mean they
have rheumatoid arthritis.
Rheumatoid factor - this blood test determines whether rheumatoid factor (an
antibody) is present in the patients blood. The majority of rheumatoid arthritis
patients have this abnormal antibody in their bloodstream. During the early stages
of the disease it is sometimes difficult to detect rheumatoid factor. As this antibody
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is present in a small proportion of people without rheumatoid arthritis, this test
cannot confirm the disease definitively.
Imaging scans and X-rays - an X-ray of the patients joints can help the doctor
determine what type of arthritis is present. Several X-rays can help track the
progression of rheumatoid arthritis in the joints over time.
MRI (magnetic resonance imaging) scans - can help the doctor determine
more specifically what damage has been done to a joint. A MRI machine uses a
magnetic field and radio waves to create detailed images of the body.
Signs of destruction and inflammation on ultrasonography and magnetic
resonance imaging in the second metacarpophalangeal joint in established
rheumatoid arthritis. Thin arrows indicate an erosive change; thick arrows indicate
synovitis. Ultrasonography (left side of image) in the (a) longitudinal and (b) the
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transverse planes shows both signs of destruction and inflammation. Axial T1-
weighted magnetic resonance images were obtained (c) before and (d) after contrast
administration, also demonstrating synovitis. Additionally, a coronal T1-weighted
magnetic resonance image (e) before contrast administration visualizes the same
bone erosion as shown in panels c and d.
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
rheumatoid arthritis.
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 aroundjoint
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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
Distinguishing rheumatoid arthritis from other medical conditions
Several other medical conditions can resemble RA, and usually need to be
distinguished from it at the time of diagnosis:
Crystal induced arthritis (gout, and pseudogout) - usually involves particular
joints and can be distinguished with aspiration of joint fluid if in doubt
Osteoarthritis - distinguished with X-rays of the affected joints and blood tests
Systemic lupus erythematosus (SLE) - distinguished by specific clinical
symptoms and blood tests (antibodies against double-stranded DNA)
One of the several types ofpsoriatic arthritis resembles RA - nail changes and
skin symptoms distinguish between them
Lyme disease causes erosive arthritis and may closely resemble RA - it may
be distinguished by blood test in endemic areas
Reactive arthritis (previously Reiter's disease) - asymmetrically involves heel,
sacroiliac joints, and large joints of the leg. It is usually associated with
urethritis, conjunctivitis, iritis, painless buccal ulcers, and keratoderma
blennorrhagica.
Ankylosing spondylitis - this involves the spine and is usually diagnosed in
males, although a RA-like symmetrical small-joint polyarthritis may occur in the
context of this condition.
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Hepatitis C - RA-like symmetrical small-joint polyarthritis may occur in the
context of this condition. Hepatitis C may also induce Rheumatoid Factor auto-
antibodies
Rarer causes that usually behave differently but may cause joint pains:
Sarcoidosis, amyloidosis, and Whipple's disease can also resemble RA.
Hemochromatosis may cause hand joint arthritis.
Acute rheumatic fever can be differentiated from RA by a migratory pattern of
joint involvement and evidence of antecedent streptococcal infection. Bacterial
arthritis (such as streptococcus) is usually asymmetric, while RA usually
involves both sides of the body symmetrically.
Gonococcal arthritis (another bacterial arthritis) is also initially migratory and
can involve tendons around the wrists and ankles.
6. Pathophisiology
The key pieces of evidence relating to pathogenesis are:
1. A genetic link with HLA-DR4 and related allotypes ofMHC Class II and the T cell-
associated protein PTPN22.
2. A link with cigarette smoking that appears to be causal
3. A dramatic response in many cases to blockade of the cytokine TNF (alpha).
4. A similar dramatic response in many cases to depletion ofB lymphocytes, but no
comparable response to depletion ofT lymphocytes.
5. A more or less random pattern of whether and when predisposed individuals are
affected.
6. The presence of autoantibodies to IgGFc, known as rheumatoid factors (RF), and
antibodies to citrullinated peptides (ACPA).
These data suggest that the disease involves abnormal B cell - T cell
interaction, with presentation of antigens by B cells to T cells via HLA-DR eliciting T
cell help and consequent production of RF and ACPA. Inflammation is then driven
either by B cell or T cell products stimulating release of TNF and other cytokines. The
process may be facilitated by an effect of smoking on citrullination but the stochastic(random) epidemiology suggests that the rate limiting step in genesis of disease in
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predisposed individuals may be an inherent stochastic process within the immune
response such as immunoglobulin or T cell receptor gene recombination and
mutation. (See entry underautoimmunity for general mechanisms).
If TNF release is stimulated by B cell products in the form of RF or ACPA -
containing immune complexes, through activation of immunoglobulin Fc receptors,
then RA can be seen as a form of Type III hypersensitivity. If TNF release is
stimulated by T cell products such as interleukin-17 it might be considered closer to
type IV hypersensitivity although this terminology may be getting somewhat dated
and unhelpful. The debate on the relative roles of immune complexes and T cell
products in inflammation in RA has continued for 30 years. There is little doubt that
both B and T cells are essential to the disease. However, there is good evidence for
neither cell being necessary at the site of inflammation. This tends to favour immune
complexes (based on antibody synthesised elsewhere) as the initiators, even if not
the sole perpetuators of inflammation. Moreover, work by Thurlings and others inPaul-Peter Tak's group and also by Arthur Kavanagh's group suggest that if any
immune cells are relevant locally they are the plasma cells, which derive from B cells
and produce in bulk the antibodies selected at the B cell stage
Although TNF appears to be the dominant, other cytokines (chemical
mediators) are likely to be involved in inflammation in RA. Blockade of TNF does not
benefit all patients or all tissues (lung disease and nodules may get worse). Blockade
of IL-1, IL-15 and IL-6 also have beneficial effects and IL-17 may be important.
Constitutional symptoms such as fever, malaise, loss of appetite and weight loss are
also caused by cytokines released in to the blood stream.
As with most autoimmune diseases, it is important to distinguish between the
cause(s) that trigger the process, and those that may permit it to persist and
progress.
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Chapter I Rheumatoid arthritis
Possible infectious triggers
It has long been suspected that certain infections could be triggers for this
disease. The "mistaken identity" theory suggests that an infection triggers an immune
response, leaving behind antibodies that should be specific to that organism. The
antibodies are not sufficiently specific, though, and set off an immune attack against
part of the host. Because the normal host molecule "looks like" a molecule on the
offending organism that triggered the initial immune reaction - this phenomenon is
called molecular mimicry. Some infectious organisms suspected of triggering
rheumatoid arthritis include Mycoplasma, Erysipelothrix, parvovirus B19 and rubella,
but these associations have never been supported in epidemiological studies. Nor
has convincing evidence been presented for other types of triggers such as food
allergies.
Epidemiological studies have confirmed a potential association between RAand two herpesvirus infections: Epstein-Barr virus (EBV) and Human Herpes Virus 6
(HHV-6). Individuals with RA are more likely to exhibit an abnormal immune
response to the Epstein-Barr virus. The allele HLA-DRB1*0404 is associated with low
frequencies ofT cells specific for the EBV glycoprotein 110 and predisposes one to
develop RA.
Psychological factors
There is no evidence that physical and emotional effects or stress could be a
trigger for the disease. The many negative findings suggest that either the triggervaries, or that it might in fact be a chance event inherent with the immune response,
as suggested by Edwards et al.
Continued abnormal immune response
The factors that allow an abnormal immune response, once initiated, to
become permanent and chronic, are becoming more clearly understood. The genetic
association with HLA-DR4, as well as the newly discovered associations with the
gene PTPN22 and with two additional genes , all implicate altered thresholds in
regulation of the adaptive immune response. It has also become clear from recent
studies that these genetic factors may interact with the most clearly defined
environmental risk factor for rheumatoid arthritis, namely cigarette smoking.Other
environmental factors also appear to modulate the risk of acquiring RA, and
hormonal factors in the individual may explain some features of the disease, such as
the higher occurrence in women, the not-infrequent onset after child-birth, and the
(slight) modulation of disease risk by hormonal medications. Exactly how altered
regulatory thresholds allow the triggering of a specific autoimmune response remains
uncertain. However, one possibility is that negative feedback mechanisms that
normally maintain tolerance of self are overtaken by aberrant positive feedback
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Chapter I Rheumatoid arthritis
mechanisms for certain antigens such as IgG Fc (bound by RF) and citrullinated
fibrinogen (bound by ACPA) (see entry on autoimmunity).
Once the abnormal immune response has become established (which may
take several years before any symptoms occur), plasma cells derived from B
lymphocytes produce rheumatoid factors and ACPA of the IgG and IgM classes in
large quantities. These are not deposited in the way that they are in systemic lupus.
Rather, they appear to activate macrophages through Fc receptor and perhaps
complement binding. This can contribute to inflammation of the synovium, in terms of
edema, vasodilation and infiltration by activated T-cells (mainly CD4 in nodular
aggregates and CD8 in diffuse infiltrates). Synovial macrophages and dendritic cells
further function as antigen presenting cells by expressing MHC class II molecules,
leading to an established local immune reaction in the tissue.
The disease progresses in concert with formation of granulation tissue at theedges of the synovial lining (pannus) with extensive angiogenesis and production of
enzymes that cause tissue damage. Modern pharmacological treatments of RA
target these mediators. Once the inflammatory reaction is established, the synovium
thickens, the cartilage and the underlying bone begin to disintegrate and evidence of
joint destruction accrues.
7. Treatement
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 treatment for the disease 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.
Treatment of rheumatoid arthritis is a team effort involving at its core:
The patient
The specialist (rheumatologist)
The nurse practitioner
Other members of the rheumatology team include the:
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Chapter I Rheumatoid arthritis
Chiropodist
GP (general practitioner)
Occupational therapist
Orthopaedic surgeon
Orthotist
Pharmacist
Physical therapist (UK: physiotherapist)
Podiatrist
Primary care nurse
Although not automatically part of every rheumatology team, patients may also
benefit from counseling services.
Medications
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), are used to reduce pain and inflammation.
The slow-acting second-line drugs, such as gold, methotrexate, and
hydroxychloroquine (Plaquenil), promote disease remission and prevent progressive
joint destruction, but they are not anti-inflammatory agents.
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 years of activity ("burned out" rheumatoid arthritis) can be
managed with rest and pain and anti-inflammatory medications alone. In general,
however, function is improved and disability and joint destruction are minimized whenthe 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. In some cases
with severe joint deformity, surgery may be necessary.
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Chapter I Rheumatoid arthritis
"First-line" medications
Acetylsalicylate (aspirin), naproxen (Naprosyn), ibuprofen (Advil, Medipren,
Motrin), and etodolac (Lodine) are examples of nonsteroidal 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 doctor to try
several NSAID drugs in order to identify the most effective agent with the fewest sideeffects. 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 asthe individual achieves improvement in symptoms. Abruptly discontinuing
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Chapter I Rheumatoid arthritis
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. For further information on
corticosteroids, please read the article on prednisone
"Second-line" or "slow-acting" 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
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 weeksto 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.
Recent 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 is also 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 thetreatment 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 has gained popularity among doctors 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 immune-suppression drug. It can affect the bone marrow and the
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Chapter I Rheumatoid arthritis
liver, even rarely causing cirrhosis. All people taking methotrexate require regular
blood tests to monitor blood counts and liver function.
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 rash, mouth 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 because of the availability of
more effective treatments, and many companies no longer manufacture them.
D-penicillamine (Depen, Cuprimine) can be helpful in selected cases of
progressive forms of rheumatoid arthritis. Side effects are similar to those of gold.They include fever, chills, mouth 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 (Rheumatrex, Trexall) 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 andcause 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 and allergic reactions in the
lung. Cyclosporine can cause kidney damage and high blood pressure. Because of
potentially serious side effects, immunosuppressive medications are used in low
doses, usually in combination with anti-inflammatory agents.
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Newer treatments
Newer "second-line" drugs 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), and tocilizumab
(Actemra). 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. Arava can cause liver disease,
diarrhea, hair 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 inwomen who might become pregnant.
Newer medications that represent a novel approach to the treatment of
rheumatoid arthritis 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. Certolizumabpegol is injected subcutaneously every two to four weeks. Each of these medications
is being evaluated by doctors 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 persons with significant congestive heart failure or
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Chapter I Rheumatoid arthritis
demyelinating diseases (such as multiple sclerosis) because they can worsen these
conditions.
Anakinra is another biologic treatment that is used to treat moderate to severe
rheumatoid arthritis. Anakinra works by binding to a cell messenger protein (IL-1, a
proinflammatory 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
cancerof the lymph nodes. Rituxan 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
conditions. Rituxan is now available to treat moderate to severely active rheumatoid
arthritis in patients who have failed treatment with the TNF-blocking biologics.Preliminary studies have shown that Rituxan was also found to be beneficial in
treating severe rheumatoid arthritis complicated by blood vessel inflammation
(vasculitis) and cryoglobulinemia. Rituximab (Rituxan) 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.
Orencia is now available to treat adult patients who have failed treatment with a
traditional DMARD or TNF-blocking biologic medication. Abatacept (Orencia) is an
intravenous infusion given monthly.
Tocilizumab (Actemra) has recently been 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 (Actemra) is the first approved biologic medication that blocks
interleukin-6 (IL-6), which is a chemical messenger of the inflammation of rheumatoid
arthritis. Tocilizumab (Actemra) is an intravenous infusion given monthly.
While biologic medications are often combined with traditional DMARDs in the
treatment of rheumatoid arthritis, they are generally not used with other biologicmedications because of the unacceptable risk for serious infections.
The Prosorba column therapy involves pumping blood drawn from a vein in
the arm into an apheresis machine, or cell separator. This machine separates the
liquid part of the blood (the plasma) from the blood cells. The Prosorba column is a
plastic cylinder about the size of a coffee mug that contains a sand-like substance
coated with a special material called Protein A. Protein A is unique in that it binds
unwanted antibodies from the blood that promote the arthritis. The Prosorba column
works to counter the effect of these harmful antibodies. The Prosorba column is
indicated to reduce the signs and symptoms of moderate to severe rheumatoid
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Chapter I Rheumatoid arthritis
arthritis in adult patients with long-standing disease who have failed or are intolerant
to disease-modifying antirheumatic drugs (DMARDs). The exact role of this treatment
is being evaluated by doctors, and it is not commonly used currently.
Other treatments
There is no special diet 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. Fish oil may have anti-inflammatory
beneficial effects, but so far this has only been shown in laboratory experiments
studying inflammatory cells. Likewise, the benefits of cartilage preparations 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 mildto 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.
The areas of the body other than the joints that are affected by rheumatoid
inflammation are treated individually. Sjogren's syndrome (described above, see
symptoms) can be helped by artificial tears and humidifying rooms of the home or
office. Medicated eyedrops, cortisporine 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.
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 inreducing 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.
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.
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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 orknees, are replaced
with metals.
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.
Future treatments
Scientists throughout the world are studying many promising areas of new
treatment approaches for rheumatoid arthritis. These areas include treatments that
block the action of the special inflammation factors, such as tumor necrosis factor(TNFalpha) and interleukin-1 (IL-1), as described above. Many other drugs are being
developed that act against certain critical white blood cells 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 is 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. Weare at the threshold of tremendous improvements in the way rheumatoid arthritis is
managed.
Lifestyle
When a flare-up occurs the patient should rest as much as possible. Exerting
very swollen and painful joints frequently results in worsening symptoms.
Generally, when flare ups are not present, the patient should exercise
regularly; this will help their general health and mobility. If rheumatoid arthritis hascaused muscles around the joints to become weak, exercise will help strengthen
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Chapter I Rheumatoid arthritis
them. Exercises that do not strain the joints are best, such as swimming. A qualified
physical therapist can teach the patient exercises that improve mobility.
Applying heat or cold - tense and painful muscles may benefit from the
application of heat. A 15 minute hot bath or shower may help. Some people find
that using a hot pack or an electric heating pad (set at lowest setting) helps.
Pain may be dulled with cold treatment. The numbing effect of cold may also
decrease muscle spasms. Patients with poor circulation or numbness should not
use cold treatments. Examples of cold treatment include cold packs, soaking the
affected joint in cold water, and ice massage. Some people benefit from placing the
affected joints in warm water for a few minutes, followed by cool water for one
minute; repeating the cycle for about 30 minutes, ending with a warm water soak.
Relaxation - finding ways of alleviating mental stress may help control pain.
Examples include hypnosis, guided imagery, deep breathing and muscle
relaxation.
Complementary therapies - these are commonly used by people with
rheumatoid arthritis. Few studies have been carried out on how effective they are.
Examples include:
o Acupuncture
o Chiropractic
o Electrotherapy
o Hydrotherapy
o Massage
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Chapter I Rheumatoid arthritis
o Nutritional supplements - for example, fish oil, glucosamine sulphate
and chondriotin.
o Osteopathy
8. Right price of the prescription
Prescription medication is an expense that many families cannot afford. If there
are some persons that dont have an insurance plan that will cover their
prescriptions and are a low-income family, then they are not alone. Fortunately, there
are some programs available to assist them with their medications, but finding them
can be a struggle. Here are a few options that could help this people afford their
medicines:
First of all, patients should communicate with their doctor on some aspects:
if they are without prescription coverage their doctor can truly be their greatest alley
and can help them in a variety of ways. If their doctor starts them on a new
prescription drug, there are a series of questions they can ask to make sure they get
the best deal. Patients should begin by asking their doctor if he has any free
samples they can have, to try the medication. Explain their insurance situation and
see if their doctor will offer them the medication for free. If their doctor does not have
any samples for them to take home, they should ask him if he could call the drugrepresentative from that company to send some samples to them. These drug
representatives stop in regularly to restock their supply and are happy to get more
clients under their belt. This can be a win-win situation for all the parties involved.
If samples are unavailable, they should ask their doctor if they can have a "trial
prescription," so that they can buy fewer of the tablets at first. This can be a good
way to find out if a medication will work for them and also to see if they can tolerate
any nasty side effects. If the drug does not work for them, they will not have invested
in a month's supply that they will be unable to use. There are also specific questions
that patients can ask about the medications they are taking. For example, to ask their
doctor if there is a generic equivalent to the medication they are taking because they
are exploring less expensive alternatives. If there are no generic equivalents to this
medication, they can also ask about over-the-counter (OTC) medications.
Sometimes, there are OTC medications patients can take that will achieve the same
results as the actual prescription drug. Another question patients can ask is if they
could buy a double dosage of the medication, in pill form, and split the tablets in half
for their regular dosage. There are many prescriptions that can be purchased and
then can easily be halved. This can result in a fifty-percent savings on patients
medication.
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Chapter I Rheumatoid arthritis
Their doctor may also know about specific aid from the drug manufacturer.
Many prescription companies have programs to give medication to patients who have
no way to pay for their prescription drugs. Programs vary from manufacturer to
manufacturer, but all require the doctor to submit the application for the patients.
Patients should explore this route with their doctor and see what the company
requirements are and if this type of aid is available for them. Finally, patients should
check in yearly with their doctor to see if cheaper versions of their medications have
becomeavailable.
Another alternative to get cheaper treatment is to try to buy the medications
online: online stores can offer a lot of savings for their customers, particularly
Canadian pharmacies where drug prices are much cheaper (savings of up to half on
many prescriptions). Patients must make sure that they research the company well to
ensure that the company is not a fake. Examples of things to look for are a toll free
number, real operators who answer their phone, a physical company address, and asecure website to do their shopping. They will also want to make sure the pharmacy
is approved by the organization that governs the state/country where the pharmacy is
located.
State assistance, can be a real help somtimes: make sure to investigate what
patients state offers in assisting with the cost of his/her prescription drugs. These
programs are typically available to the elderly, disabled, and low-income families.
People can obtain information about these programs through their state's website or
by calling the office of their state senator or representative.
Patients having cost problems with their medication, and should not be afraid or
ashamed to ask their doctor, the drug company, or their pharmacy about assistance
programs. There are great savings in asking and exploring for cheaper alternatives.
9. Prognosis
It isn't possible to predict exactly how rheumatoid arthritis will progress foreach patient. The inflammation in rheumatoid arthritis damages the cartilage and
sometimes the bone itself. It may also damage any ligaments within the joints.
Inflammation causes the tough capsules that surround joints to stretch. When
the swelling goes down the capsule remains stretched and can no longer hold the
joint in its proper position. As a result the joint becomes unstable and this can lead to
deformities of the joints. Some damage is done every time the joints are inflamed and
once joints are damaged they don't heal properly. This is why most treatment aims to
prevent joint damage by minimizing inflammation as early as possible in the disease.
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Chapter I Rheumatoid arthritis
Inflammation can sometimes affect the blood vessels, the lungs and, rarely,
the membrane around the heart. People with rheumatoid arthritis are also more at
risk of heart attack and strokes. This seems to be caused by the inflammation and
the risk is probably reduced by controlling the disease.
Most people follow a pattern of flare-ups with periods of months or even years
when there is little inflammation. There's likely to be some damage in a number of
joints. People whose disease follows this pattern are likely to have some problems
with their joints and may have to change their activities a little, but overall probably
won't notice too great an impact on their lives.
Some people, maybe as many as 1 in 5, always have very mild rheumatoid
arthritis that causes few problems. People in this group will usually have only minor
damage to a small number of joints.
A few people, no more than 1 in 20, will have rheumatoid arthritis that
becomes progressively worse, often quite quickly. These individuals are likely to
have severe damage to many of their joints, and are also more likely to have
inflammation in other parts of the body besides their joints.
The course of the disease varies greatly. Around 20%-30% will have
subcutaneous nodules (known as rheumatoid nodules); this is associated with a poor
prognosis.
Disability
Daily living activities are impaired in most individuals.
After 5 years of disease, approximately 33% of sufferers will not be working.
After 10 years, approximately half will have substantial functional disability.
Prognostic factors
Poor prognostic factors include persistent synovitis, early erosive disease,extra-articular findings (including subcutaneous rheumatoid nodules), positive serum
RF findings, positive serum anti-CCP autoantibodies, carriership of HLA-DR4
"Shared Epitope" alleles, family history of RA, poor functional status, socioeconomic
factors, elevated acute phase response (erythrocyte sedimentation rate [ESR], C-
reactive protein [CRP]), and increased clinical severity.
Mortality
Estimates of the life-shortening effect of RA vary; most sources cite a lifespan
reduction of 5 to 10 years. According to the UK's National Rheumatoid ArthritisSociety, "Young age at onset, long disease duration, the concurrent presence of
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other health problems (called co-morbidity), and characteristics of severe RA such
as poor functional ability or overall health status, a lot of joint damage on x-rays, the
need for hospitalisation or involvement of organs other than the joints have been
shown to associate with higher mortality". Positive responses to treatment may
indicate a better prognosis. A 2005 study by the Mayo Clinic noted that RA sufferers
suffer a doubled risk of heart disease, independent of other risk factors such as
diabetes, alcohol abuse, and elevated cholesterol, blood pressure and body mass
index. The mechanism by which RA causes this increased risk remains unknown; the
presence of chronic inflammation has been proposed as a contributing factor.
10. Prevalence of arthritis
Disability-adjusted life yearfor rheumatoid arthritis per 100,000 inhabitants in 2004.
no data less than 40 40-50 50-60 60-70 70-80 80-90 90-100
100-110 110-120 120-130 130-140 more than 140
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The incidence of RA is in the region of 3 cases per 10,000 population per
annum. Onset is uncommon under the age of 15 and from then on the incidence
rises with age until the age of 80. The prevalence rate is 1%, with women affected
three to five times as often as men. It is 4 times more common in smokers than non-
smokers. A study in 2010 found that those who drank modest amounts of alcohol
regularly were four times less likely to get rheumatoid arthritis than those who never
drank. Some Native American groups have higher prevalence rates (5-6%) and
people from the Caribbean region have lower prevalence rates. First-degree relatives
prevalence rate is 2-3% and disease genetic concordance in monozygotic twins is
approximately 15-20%.
It is strongly associated with the inherited tissue type Major histocompatibility
complex (MHC) antigen HLA-DR4 (most specifically DR0401 and 0404) hencefamily history is an important risk factor.
Rheumatoid arthritis affects women three times more often than men, and it
can first develop at any age. The risk of first developing the disease (the disease
incidence) appears to be greatest for women between 40 and 50 years of age, and
for men somewhat later. RA is a chronic disease, and although rarely, a spontaneous
remission may occur, the natural course is almost invariably one of persistent
symptoms, waxing and waning in intensity, and a progressive deterioration of joint
structures leading to deformations and disability.
11. Travel tips for people with Rheumatoid arthritis
Some people with arthritis develop a reluctance to try new things or
experience activities that their physical limitations might make more of a challenge.
For example, people with arthritis often become reluctant to travel. With forethought
and careful planning, people with arthritis can travel too.
If traveling with arthritis is a concern, it is wise to take short trips at first andhave someone along who could be of assistance if necessary. As short trips are
accomplished and enjoyed successfully, longer trips can be planned with confidence.
The short trips allow them to experience traveling and at the same time learn what
difficulties occur that can be either avoided or planned for.
Make their needs known
If a travel agent is utilized when planning more extensive trips, patients should
be specific about their restrictions and requirements. Do not assume that all will be
well and all will be understood. They must make their needs known. Ask the travelagent questions that will solve their concerns. Ask about:
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