Proiect Engleza Cap I

8/3/2019 Proiect Engleza Cap I

1/37

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

1 | P a g e


2/37


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

2 | P a g e
http://www.emedicinehealth.com/script/main/art.asp?articlekey=59059http://www.emedicinehealth.com/script/main/art.asp?articlekey=59059


3/37


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.

3 | P a g e
http://en.wikipedia.org/wiki/4500_BChttp://en.wikipedia.org/wiki/123_ADhttp://en.wikipedia.org/wiki/Symptomhttp://en.wikipedia.org/wiki/Tennesseehttp://en.wikipedia.org/wiki/Age_of_Explorationhttp://en.wikipedia.org/wiki/Peter_Paul_Rubenshttp://en.wikipedia.org/wiki/Piti%C3%A9-Salp%C3%AAtri%C3%A8re_Hospitalhttp://en.wikipedia.org/wiki/Alfred_Baring_Garrodhttp://en.wikipedia.org/wiki/Dorothy_Hodgkinhttp://en.wikipedia.org/wiki/X-ray_crystallographyhttp://en.wikipedia.org/wiki/Insulinhttp://en.wikipedia.org/wiki/Genetic_codehttp://en.wikipedia.org/wiki/Auguste_Renoirhttp://en.wikipedia.org/wiki/Christiaan_Barnardhttp://en.wikipedia.org/wiki/4500_BChttp://en.wikipedia.org/wiki/123_ADhttp://en.wikipedia.org/wiki/Symptomhttp://en.wikipedia.org/wiki/Tennesseehttp://en.wikipedia.org/wiki/Age_of_Explorationhttp://en.wikipedia.org/wiki/Peter_Paul_Rubenshttp://en.wikipedia.org/wiki/Piti%C3%A9-Salp%C3%AAtri%C3%A8re_Hospitalhttp://en.wikipedia.org/wiki/Alfred_Baring_Garrodhttp://en.wikipedia.org/wiki/Dorothy_Hodgkinhttp://en.wikipedia.org/wiki/X-ray_crystallographyhttp://en.wikipedia.org/wiki/Insulinhttp://en.wikipedia.org/wiki/Genetic_codehttp://en.wikipedia.org/wiki/Auguste_Renoirhttp://en.wikipedia.org/wiki/Christiaan_Barnard


4/37


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).

4 | P a g e
http://en.wikipedia.org/wiki/James_Coburnhttp://en.wikipedia.org/wiki/Erik_Lindberghhttp://en.wikipedia.org/wiki/X-Prizehttp://en.wikipedia.org/wiki/Enbrelhttp://en.wikipedia.org/wiki/Bob_Mortimerhttp://en.wikipedia.org/wiki/Kathleen_Turnerhttp://en.wikipedia.org/wiki/Aida_Turturrohttp://en.wikipedia.org/wiki/Billy_Bowdenhttp://en.wikipedia.org/wiki/Melvin_Franklinhttp://en.wikipedia.org/wiki/Jamie_Farrhttp://en.wikipedia.org/wiki/Maxwell_Klingerhttp://en.wikipedia.org/wiki/Televisionhttp://en.wikipedia.org/wiki/M*A*S*Hhttp://en.wikipedia.org/wiki/Sandy_Koufaxhttp://en.wikipedia.org/w/index.php?title=Jeffrey_Gottfurcht&action=edit&redlink=1http://en.wikipedia.org/wiki/James_Coburnhttp://en.wikipedia.org/wiki/Erik_Lindberghhttp://en.wikipedia.org/wiki/X-Prizehttp://en.wikipedia.org/wiki/Enbrelhttp://en.wikipedia.org/wiki/Bob_Mortimerhttp://en.wikipedia.org/wiki/Kathleen_Turnerhttp://en.wikipedia.org/wiki/Aida_Turturrohttp://en.wikipedia.org/wiki/Billy_Bowdenhttp://en.wikipedia.org/wiki/Melvin_Franklinhttp://en.wikipedia.org/wiki/Jamie_Farrhttp://en.wikipedia.org/wiki/Maxwell_Klingerhttp://en.wikipedia.org/wiki/Televisionhttp://en.wikipedia.org/wiki/M*A*S*Hhttp://en.wikipedia.org/wiki/Sandy_Koufaxhttp://en.wikipedia.org/w/index.php?title=Jeffrey_Gottfurcht&action=edit&redlink=1


5/37


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)

5 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=374http://www.medicinenet.com/script/main/art.asp?articlekey=2051http://www.medicinenet.com/script/main/art.asp?articlekey=374http://www.medicinenet.com/script/main/art.asp?articlekey=2051


6/37


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.

6 | P a g e


7/37


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.

7 | P a g e


8/37


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

8 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=11299http://www.medicinenet.com/script/main/art.asp?articlekey=11299


9/37


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

9 | P a g e


10/37


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

10 | P a g e
http://en.wikipedia.org/wiki/Medical_ultrasoundhttp://en.wikipedia.org/wiki/Magnetic_resonance_imaginghttp://en.wikipedia.org/wiki/Magnetic_resonance_imaginghttp://en.wikipedia.org/wiki/Metacarpophalangeal_jointhttp://en.wikipedia.org/wiki/Synovitishttp://en.wikipedia.org/wiki/File:Rheumatoid_arthritis_ultrasound_MRI_MCP_joint_ar1904-2.gifhttp://en.wikipedia.org/wiki/Medical_ultrasoundhttp://en.wikipedia.org/wiki/Magnetic_resonance_imaginghttp://en.wikipedia.org/wiki/Magnetic_resonance_imaginghttp://en.wikipedia.org/wiki/Metacarpophalangeal_jointhttp://en.wikipedia.org/wiki/Synovitis


11/37


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


Stage IV

on X-ray, evidence of cartilage and bone damage and osteoporosis aroundjoint

11 | P a g e


12/37


joint deformity with permanent fixation of the joint (referred to as ankylosis)

extensive muscle atrophy


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.

12 | P a g e
http://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Pseudogouthttp://en.wikipedia.org/wiki/Osteoarthritishttp://en.wikipedia.org/wiki/X-rayhttp://en.wikipedia.org/wiki/Systemic_lupus_erythematosushttp://en.wikipedia.org/wiki/Psoriatic_arthritishttp://en.wikipedia.org/wiki/Lyme_diseasehttp://en.wikipedia.org/wiki/Reactive_arthritishttp://en.wikipedia.org/wiki/Sacroiliachttp://en.wikipedia.org/wiki/Urethritishttp://en.wikipedia.org/wiki/Conjunctivitishttp://en.wikipedia.org/wiki/Iritishttp://en.wikipedia.org/wiki/Keratoderma_blennorrhagicahttp://en.wikipedia.org/wiki/Keratoderma_blennorrhagicahttp://en.wikipedia.org/wiki/Ankylosing_spondylitishttp://en.wikipedia.org/wiki/Gouthttp://en.wikipedia.org/wiki/Pseudogouthttp://en.wikipedia.org/wiki/Osteoarthritishttp://en.wikipedia.org/wiki/X-rayhttp://en.wikipedia.org/wiki/Systemic_lupus_erythematosushttp://en.wikipedia.org/wiki/Psoriatic_arthritishttp://en.wikipedia.org/wiki/Lyme_diseasehttp://en.wikipedia.org/wiki/Reactive_arthritishttp://en.wikipedia.org/wiki/Sacroiliachttp://en.wikipedia.org/wiki/Urethritishttp://en.wikipedia.org/wiki/Conjunctivitishttp://en.wikipedia.org/wiki/Iritishttp://en.wikipedia.org/wiki/Keratoderma_blennorrhagicahttp://en.wikipedia.org/wiki/Keratoderma_blennorrhagicahttp://en.wikipedia.org/wiki/Ankylosing_spondylitis


13/37


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

13 | P a g e
http://en.wikipedia.org/wiki/Hepatitis_Chttp://en.wikipedia.org/wiki/Sarcoidosishttp://en.wikipedia.org/wiki/Whipple's_diseasehttp://en.wikipedia.org/wiki/Hemochromatosishttp://en.wikipedia.org/wiki/Streptococcalhttp://en.wikipedia.org/wiki/Gonococcalhttp://en.wikipedia.org/wiki/Tendonshttp://en.wikipedia.org/wiki/HLA-DR4http://en.wikipedia.org/wiki/MHC_Class_IIhttp://en.wikipedia.org/wiki/PTPN22http://en.wikipedia.org/wiki/Tumor_necrosis_factorshttp://en.wikipedia.org/wiki/B_lymphocytehttp://en.wikipedia.org/wiki/T_lymphocytehttp://en.wikipedia.org/wiki/Rheumatoid_factorhttp://en.wikipedia.org/wiki/Anti-citrullinated_protein_antibodyhttp://en.wikipedia.org/wiki/Citrullinationhttp://en.wikipedia.org/wiki/Hepatitis_Chttp://en.wikipedia.org/wiki/Sarcoidosishttp://en.wikipedia.org/wiki/Whipple's_diseasehttp://en.wikipedia.org/wiki/Hemochromatosishttp://en.wikipedia.org/wiki/Streptococcalhttp://en.wikipedia.org/wiki/Gonococcalhttp://en.wikipedia.org/wiki/Tendonshttp://en.wikipedia.org/wiki/HLA-DR4http://en.wikipedia.org/wiki/MHC_Class_IIhttp://en.wikipedia.org/wiki/PTPN22http://en.wikipedia.org/wiki/Tumor_necrosis_factorshttp://en.wikipedia.org/wiki/B_lymphocytehttp://en.wikipedia.org/wiki/T_lymphocytehttp://en.wikipedia.org/wiki/Rheumatoid_factorhttp://en.wikipedia.org/wiki/Anti-citrullinated_protein_antibodyhttp://en.wikipedia.org/wiki/Citrullination


14/37


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.

14 | P a g e
http://en.wikipedia.org/wiki/Autoimmunityhttp://en.wikipedia.org/wiki/Fc_receptorhttp://en.wikipedia.org/wiki/Type_III_hypersensitivityhttp://en.wikipedia.org/wiki/Interleukin-17http://en.wikipedia.org/wiki/Type_IV_hypersensitivityhttp://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/IL-15http://en.wikipedia.org/wiki/IL-6http://en.wikipedia.org/wiki/IL-17http://en.wikipedia.org/wiki/Autoimmunityhttp://en.wikipedia.org/wiki/Fc_receptorhttp://en.wikipedia.org/wiki/Type_III_hypersensitivityhttp://en.wikipedia.org/wiki/Interleukin-17http://en.wikipedia.org/wiki/Type_IV_hypersensitivityhttp://en.wikipedia.org/wiki/Cytokineshttp://en.wikipedia.org/wiki/IL-15http://en.wikipedia.org/wiki/IL-6http://en.wikipedia.org/wiki/IL-17


15/37


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

15 | P a g e
http://en.wikipedia.org/wiki/Molecular_mimicryhttp://en.wikipedia.org/wiki/Mycoplasmahttp://en.wikipedia.org/wiki/Erysipelothrixhttp://en.wikipedia.org/wiki/Parvovirushttp://en.wikipedia.org/wiki/Rubellahttp://en.wikipedia.org/wiki/Herpesvirushttp://en.wikipedia.org/wiki/Epstein-Barr_virushttp://en.wikipedia.org/wiki/Human_Herpesvirus_Sixhttp://en.wikipedia.org/wiki/T_cellshttp://en.wikipedia.org/wiki/Glycoproteinhttp://en.wikipedia.org/wiki/PTPN22http://en.wikipedia.org/wiki/Molecular_mimicryhttp://en.wikipedia.org/wiki/Mycoplasmahttp://en.wikipedia.org/wiki/Erysipelothrixhttp://en.wikipedia.org/wiki/Parvovirushttp://en.wikipedia.org/wiki/Rubellahttp://en.wikipedia.org/wiki/Herpesvirushttp://en.wikipedia.org/wiki/Epstein-Barr_virushttp://en.wikipedia.org/wiki/Human_Herpesvirus_Sixhttp://en.wikipedia.org/wiki/T_cellshttp://en.wikipedia.org/wiki/Glycoproteinhttp://en.wikipedia.org/wiki/PTPN22


16/37


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:

16 | P a g e
http://en.wikipedia.org/wiki/Autoimmunityhttp://en.wikipedia.org/wiki/Pannushttp://en.wikipedia.org/wiki/Autoimmunityhttp://en.wikipedia.org/wiki/Pannus


17/37


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.

17 | P a g e


18/37


"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

18 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=795http://www.medicinenet.com/script/main/art.asp?articlekey=792http://www.medicinenet.com/script/main/art.asp?articlekey=778http://www.medicinenet.com/script/main/art.asp?articlekey=9520http://www.medicinenet.com/script/main/art.asp?articlekey=1908http://www.medicinenet.com/script/main/art.asp?articlekey=443http://www.medicinenet.com/script/main/art.asp?articlekey=711http://www.medicinenet.com/script/main/art.asp?articlekey=17349http://www.medicinenet.com/script/main/art.asp?articlekey=17349http://www.medicinenet.com/script/main/art.asp?articlekey=731http://www.medicinenet.com/script/main/art.asp?articlekey=9521http://www.medicinenet.com/script/main/art.asp?articlekey=8257http://www.medicinenet.com/script/main/art.asp?articlekey=2849http://www.medicinenet.com/script/main/art.asp?articlekey=302http://www.medicinenet.com/script/main/art.asp?articlekey=314http://www.medicinenet.com/script/main/art.asp?articlekey=795http://www.medicinenet.com/script/main/art.asp?articlekey=792http://www.medicinenet.com/script/main/art.asp?articlekey=778http://www.medicinenet.com/script/main/art.asp?articlekey=9520http://www.medicinenet.com/script/main/art.asp?articlekey=1908http://www.medicinenet.com/script/main/art.asp?articlekey=443http://www.medicinenet.com/script/main/art.asp?articlekey=711http://www.medicinenet.com/script/main/art.asp?articlekey=17349http://www.medicinenet.com/script/main/art.asp?articlekey=17349http://www.medicinenet.com/script/main/art.asp?articlekey=731http://www.medicinenet.com/script/main/art.asp?articlekey=9521http://www.medicinenet.com/script/main/art.asp?articlekey=8257http://www.medicinenet.com/script/main/art.asp?articlekey=2849http://www.medicinenet.com/script/main/art.asp?articlekey=302http://www.medicinenet.com/script/main/art.asp?articlekey=314


19/37


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

19 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=434http://www.medicinenet.com/script/main/art.asp?articlekey=6307http://www.medicinenet.com/script/main/art.asp?articlekey=809http://www.medicinenet.com/script/main/art.asp?articlekey=4225http://www.medicinenet.com/script/main/art.asp?articlekey=805http://www.medicinenet.com/script/main/art.asp?articlekey=44657http://www.medicinenet.com/script/main/art.asp?articlekey=409http://www.medicinenet.com/script/main/art.asp?articlekey=1992http://www.medicinenet.com/script/main/art.asp?articlekey=703http://www.medicinenet.com/script/main/art.asp?articlekey=13341http://www.medicinenet.com/script/main/art.asp?articlekey=509http://www.medicinenet.com/script/main/art.asp?articlekey=332http://www.medicinenet.com/script/main/art.asp?articlekey=434http://www.medicinenet.com/script/main/art.asp?articlekey=6307http://www.medicinenet.com/script/main/art.asp?articlekey=809http://www.medicinenet.com/script/main/art.asp?articlekey=4225http://www.medicinenet.com/script/main/art.asp?articlekey=805http://www.medicinenet.com/script/main/art.asp?articlekey=44657http://www.medicinenet.com/script/main/art.asp?articlekey=409http://www.medicinenet.com/script/main/art.asp?articlekey=1992http://www.medicinenet.com/script/main/art.asp?articlekey=703http://www.medicinenet.com/script/main/art.asp?articlekey=13341http://www.medicinenet.com/script/main/art.asp?articlekey=509http://www.medicinenet.com/script/main/art.asp?articlekey=332


20/37


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.

20 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=322http://www.medicinenet.com/script/main/art.asp?articlekey=835http://www.medicinenet.com/script/main/art.asp?articlekey=793http://www.medicinenet.com/script/main/art.asp?articlekey=826http://www.medicinenet.com/script/main/art.asp?articlekey=2015http://www.medicinenet.com/script/main/art.asp?articlekey=1900http://www.medicinenet.com/script/main/art.asp?articlekey=729http://www.medicinenet.com/script/main/art.asp?articlekey=361http://www.medicinenet.com/script/main/art.asp?articlekey=764http://www.medicinenet.com/script/main/art.asp?articlekey=12343http://www.medicinenet.com/script/main/art.asp?articlekey=45894http://www.medicinenet.com/script/main/art.asp?articlekey=45603http://www.medicinenet.com/script/main/art.asp?articlekey=6748http://www.medicinenet.com/script/main/art.asp?articlekey=378http://www.medicinenet.com/script/main/art.asp?articlekey=322http://www.medicinenet.com/script/main/art.asp?articlekey=835http://www.medicinenet.com/script/main/art.asp?articlekey=793http://www.medicinenet.com/script/main/art.asp?articlekey=826http://www.medicinenet.com/script/main/art.asp?articlekey=2015http://www.medicinenet.com/script/main/art.asp?articlekey=1900http://www.medicinenet.com/script/main/art.asp?articlekey=729http://www.medicinenet.com/script/main/art.asp?articlekey=361http://www.medicinenet.com/script/main/art.asp?articlekey=764http://www.medicinenet.com/script/main/art.asp?articlekey=12343http://www.medicinenet.com/script/main/art.asp?articlekey=45894http://www.medicinenet.com/script/main/art.asp?articlekey=45603http://www.medicinenet.com/script/main/art.asp?articlekey=6748http://www.medicinenet.com/script/main/art.asp?articlekey=378


21/37


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

21 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=7488http://www.medicinenet.com/script/main/art.asp?articlekey=8517http://www.medicinenet.com/script/main/art.asp?articlekey=12005http://www.medicinenet.com/script/main/art.asp?articlekey=19189http://www.medicinenet.com/script/main/art.asp?articlekey=22211http://www.medicinenet.com/script/main/art.asp?articlekey=15767http://www.medicinenet.com/script/main/art.asp?articlekey=58563http://www.medicinenet.com/script/main/art.asp?articlekey=119573http://www.medicinenet.com/script/main/art.asp?articlekey=119625http://www.medicinenet.com/script/main/art.asp?articlekey=119628http://www.medicinenet.com/script/main/art.asp?articlekey=7488http://www.medicinenet.com/script/main/art.asp?articlekey=110443http://www.medicinenet.com/script/main/art.asp?articlekey=1900http://www.medicinenet.com/script/main/art.asp?articlekey=10560http://www.medicinenet.com/script/main/art.asp?articlekey=42809http://www.medicinenet.com/script/main/art.asp?articlekey=2007http://www.medicinenet.com/script/main/art.asp?articlekey=7488http://www.medicinenet.com/script/main/art.asp?articlekey=8517http://www.medicinenet.com/script/main/art.asp?articlekey=12005http://www.medicinenet.com/script/main/art.asp?articlekey=19189http://www.medicinenet.com/script/main/art.asp?articlekey=22211http://www.medicinenet.com/script/main/art.asp?articlekey=15767http://www.medicinenet.com/script/main/art.asp?articlekey=58563http://www.medicinenet.com/script/main/art.asp?articlekey=119573http://www.medicinenet.com/script/main/art.asp?articlekey=119625http://www.medicinenet.com/script/main/art.asp?articlekey=119628http://www.medicinenet.com/script/main/art.asp?articlekey=7488http://www.medicinenet.com/script/main/art.asp?articlekey=110443http://www.medicinenet.com/script/main/art.asp?articlekey=1900http://www.medicinenet.com/script/main/art.asp?articlekey=10560http://www.medicinenet.com/script/main/art.asp?articlekey=42809http://www.medicinenet.com/script/main/art.asp?articlekey=2007


22/37


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

22 | P a g e


23/37


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.

23 | P a g e
http://www.medicinenet.com/script/main/art.asp?articlekey=685http://www.medicinenet.com/script/main/art.asp?articlekey=6092http://www.medicinenet.com/script/main/art.asp?articlekey=44632http://www.medicinenet.com/script/main/art.asp?articlekey=44238http://www.medicinenet.com/script/main/art.asp?articlekey=43322http://www.medicinenet.com/script/main/art.asp?articlekey=273http://www.medicinenet.com/script/main/art.asp?articlekey=11615http://www.medicinenet.com/script/main/art.asp?articlekey=56640http://www.medicinenet.com/script/main/art.asp?articlekey=82997http://www.medicinenet.com/script/main/art.asp?articlekey=283http://www.medicinenet.com/script/main/art.asp?articlekey=685http://www.medicinenet.com/script/main/art.asp?articlekey=6092http://www.medicinenet.com/script/main/art.asp?articlekey=44632http://www.medicinenet.com/script/main/art.asp?articlekey=44238http://www.medicinenet.com/script/main/art.asp?articlekey=43322http://www.medicinenet.com/script/main/art.asp?articlekey=273http://www.medicinenet.com/script/main/art.asp?articlekey=11615http://www.medicinenet.com/script/main/art.asp?articlekey=56640http://www.medicinenet.com/script/main/art.asp?articlekey=82997http://www.medicinenet.com/script/main/art.asp?articlekey=283


24/37


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

24 | P a g e
http://www.medicinenet.com/script/main/forum.asp?articlekey=497http://www.medicinenet.com/script/main/forum.asp?articlekey=498http://www.medicinenet.com/script/main/art.asp?articlekey=488http://www.medicinenet.com/script/main/forum.asp?articlekey=497http://www.medicinenet.com/script/main/forum.asp?articlekey=498http://www.medicinenet.com/script/main/art.asp?articlekey=488


25/37


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

25 | P a g e


26/37


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.

26 | P a g e


27/37


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.

27 | P a g e


28/37


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

28 | P a g e
http://en.wikipedia.org/wiki/UKhttp://en.wikipedia.org/wiki/UK


29/37


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

29 | P a g e
http://en.wikipedia.org/wiki/Mayo_Clinichttp://en.wikipedia.org/wiki/Diabeteshttp://en.wikipedia.org/wiki/Cholesterolhttp://en.wikipedia.org/wiki/Body_mass_indexhttp://en.wikipedia.org/wiki/Body_mass_indexhttp://en.wikipedia.org/wiki/Disability-adjusted_life_yearhttp://en.wikipedia.org/wiki/Mayo_Clinichttp://en.wikipedia.org/wiki/Diabeteshttp://en.wikipedia.org/wiki/Cholesterolhttp://en.wikipedia.org/wiki/Body_mass_indexhttp://en.wikipedia.org/wiki/Body_mass_indexhttp://en.wikipedia.org/wiki/Disability-adjusted_life_year


30/37


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:

30 | P a g e
http://en.wikipedia.org/wiki/Incidence_(epidemiology)http://en.wikipedia.org/wiki/Prevalencehttp://en.wikipedia.org/wiki/Indigenous_peoples_of_the_Americashttp://en.wikipedia.or

Proiect Engleza Cap I

Documents

Transcript of Proiect Engleza Cap I