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Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disorder that causes the immune system to attack the joints.
Rheumatoid arthritis is a
disabling and painful inflammatory condition, which can lead to substantial loss
of mobility due to pain and joint destruction. Rheumatoid
arthritis is also systemic in
that it often also affects many extra-articular tissues throughout the body
including the skin, blood vessels,
heart, lungs, and muscles.
Derived from the Greek rheumatos= flowing, -oid= in the shape
of, arthr= joint, itis= condition involving inflammation
Rheumatoid Arthritis Symptoms
The American College of Rheumatology has defined (1987) the
following criteria for Rheumatoid Arthritis:
- Morning stiffness of >1 hour.
- Arthritis and soft-tissue swelling of >3 of 14 joints/joint
groups
- Arthritis of hand joints
- Symmetric arthritis
- Subcutaneous nodules in specific places
- Rheumatoid factor at a level above the 95th percentile
- Radiological changes suggestive of joint erosion
Four criteria for Rheumatoid Arthritis
have to be met, although many patients are treated despite not meeting
Rheumatoid arthritis criteria.
The symptoms that distinguish
rheumatoid arthritis are
inflammation and soft-tissue swelling of many joints at the same time (polyarthritis).
The hands are generally affected in a symmetric fashion. The pain generally
improves with use of the affected joints, and there is usually stiffness of all
joints in the morning that lasts over 1 hour.
If the arthritis has been longstanding, the inflammatory
activity has led to erosion and destruction of the joint surface, which impairs
their range of movement and leads to deformity. The fingers are typically
deviated towards the little finger (ulnar deviation) and can assume unnatural
shapes.
Subcutaneous nodules on extensor surfaces, e.g. the elbows,
are often present.
It is recommended that Transfer
Factor Advanced Formula to be used in autoimmune conditions.
Transfer Factor Plus is generally preferred for
conditions caused by infection. Transfer Factors
suppress over acting immune system
to ease autoimmune conditions.
Rheumatoid Arthritis Diagnosis
When Rheumatoid Arthritis is being clinically suspected, immunological studies
are required, such as rheumatoid factor (RF, a specific antibody). A negative Rheumatoid Factor
does not rule out Rheumatoid Arthritis; rather, the arthritis is called seronegative.
During the
first year of illness, rheumatoid factor is frequently negative. 80% patients
eventually convert to seropositive status. Rheumatoid Factor is also seen in other illnesses,
like Sjogren's syndrome, therefore the test is not very specific. Because of
this low specificity, a new serological test has been developed in recent years,
which tests for the presence of so called anti-citrullinated protein (ACP)
antibodies.
Like RF, this test can detect approximately 80% of all Rheumatoid Arthritis
patients, but is rarely positive in non-Rheumatoid Arthritis patients, giving it a specificity of
around 98%. In addition, ACP antibodies
can be often detected in early stages of Rheumatoid Arthritis disease, or even before disease onset. Currently, most common test for ACP
antibodies is the anti-CCP (cyclic citrulinated peptide) test. Also, several
other blood tests are usually done to allow for other causes of arthritis, such
as lupus erythematosus. The erythrocyte sedimentation rate (ESR), C-reactive
protein, full blood count, renal function, liver enzymes and immunological tests
(e.g. antinuclear antibody/ANA) are all performed at this stage. Ferritin can
reveal hemochromatosis, which can mimic Rheumatoid Arthritis.
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Pathophysiology of Rheumatoid Arthritis
The cause of Rheumatoid Arthritis is unknown, but long
suspected to be infectious. Mycoplasma, Erysipelothrix, Epstein-Barr virus,
parvovirus and rubella have been suspected but never supported in
epidemiological studies. As in other autoimmune diseases, the "mistaken
identity" theory suggests that an offending organism causes an
immune response
that leaves behind antibodies that are specific to that organism. The antibodies
are not specific enough, though. They begin an immune attack against, in this
case, the synovium, because some molecule in the synovium "looks like" a
molecule on the offending organism that created the initial
immune reaction.
Autoimmune diseases require that the affected individual have
a defect in the ability to distinguish self from foreign molecules. This ability
is acquired in the first year of life. There are markers on many cells that
confer this self-identifying feature. However, some classes of markers allow for
Rheumatoid Arthritis to happen. 90% of patients with Rheumatoid Arthritis have the cluster of markers known as the
HLA-DR4/DR1 cluster, whereas only 40% of controls do. Thus, in theory,
Rheumatoid Arthritis
requires susceptibility to the disease through genetic endowment with specific
markers and an infectious event that triggers an
autoimmune response.
Once triggered, the
immune response causes inflammation of the synovium. Modern pharmacological treatments of
Rheumatoid Arthritis target these early and
intermediate molecular mediators of inflammation, including tumor necrosis
factor alpha (TNF-?), interleukin (IL)–1, IL-6, transforming growth factor beta,
IL-8, fibroblast growth factor and platelet-derived growth factor. Once the
inflammatory reaction is established, the synovium thickens, the cartilage and
the underlying bone begins to disintegrate and evidence of joint destruction
accrues.
It is recommended that Transfer
Factor Advanced Formula to be used in autoimmune conditions.
Transfer Factor Plus is generally preferred for
conditions caused by infection. Transfer Factors
suppress over acting immune system
to ease autoimmune conditions.
Pharmacological treatment of Rheumatoid Arthritis can be
divided into disease-modifying antirheumatic drugs (DMARDs),
anti-inflammatory
agents and analgesics. DMARDs have been found to produce durable remissions and
delay or halt disease progression. This is not true of anti-inflammatories and
analgesics.
DMARDs can be further subdivided into xenobiotic agents and
biological agents. Xenobiotic agents are those DMARDs that do not occur
naturally in the body, as opposed to biologicals.
Xenobiotics
Xenobiotics include:
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