Signs
and Symptoms of Rheumatoid Arthritis
The
onset of rheumatoid arthritis(RA) is mostly very gradual, but sometimes it might
start with an acute episode. It tends to affect the small joints in a diffuse
manner, called polyarthritis, as many joints of the hands and of the upper neck
are simultaneously affected. In the beginning it affects only perhaps three or
four of the "knuckles"of the hands. These are called metacarpophalangeal
joints or "MCP joints" for short. There will be pain, swelling, heat,
some redness of the overlying skin and loss of range of motion of the affected
small joints. The joints have effusions (fluid build-up) and the synovial membranes
get inflammed, a condition termed"synovitis". This process leads to
eventual scarring and joint stiffness. Unfortunately the inflammatory process
does not stop at the joint level at all, but it also involves the tendons that
travel across the joints in the hands and the support ligaments. Loss of these
support structures leads to the grotesque
deformities with ulnar deviation of the MCP joints. Tendons thicken
and show nodules and can even rupture due to a softening up of the structure as
a result of the inflammatory process (Ref. 1 and 2).
The RF titer (=rheumatoid factor
titer) It is poorly understood why the immune
system is changed in rheumatoid arthritis patients, but this seems to be the underlying
pathophysiological process that is behind all of these symptoms. We do
know that the immune system in rheumatoid arthritis patients is altered and produces
an abnormal antibody to altered immunoglobulins. This is called the rheumatoid
factor (RF) or rheumatoid antibody. If it is low, the disease process is not yet
systemic, if it is high, the disease is more aggressive and systemic spread into
all body joints is more likely. This blood test then together with the erythrocyte
sedimentation rate(=ESR) is a useful test to help diagnose and monitor the progress
of the treatment of rheumatoid arthritis. This antibody in RA is directed at altered
proteins in the synovial membrane of joints, tendon sheaths and in a few more
serious cases in other areas of the connective tissue including arterial walls.
This distinguishes RA from other connective tissue diseases such as Sjögren's
syndrome where the autoantibody is directed more against the salivary and lacrimal
glands resulting in a dry mouth and in dry eyes. There is ample evidence in the
immunological literature that the key to understanding RA and other connective
tissues diseases is found in the altered immune response (T helper cells, plasma
cells, macrophages, autoantibodies etc.). This leads to joint, cartilage and tendon
destruction. | The following summarizes
various other symptoms and signs of RA (modif. from Ref. 1 and 2): In the
spine the upper end of the cervical spine is often affected with subluxations
of the joints between the first and second vertebral bodies(atlantoaxial
subluxation).There is a danger of spinal stenosis
and/or spinal cord compression. Rheumatoid
nodules happen in about 20% of patients with RA. They are hardened
fibrotic lumps in the skin at the outside of the elbows
(extensor surface) where pressure occurs from leaning on them, as
well as the Achilles tendons, where shoes exert pressure onto the skin. Vascular
Damage from immune complexes that are deposited in the vascular
walls. A variety of different clinical signs are associated with this:
skin ulcers, occlusion of vessels going to fingers or toes with a threat of loss
of these. The nutritional vessels of nerves can be affected and a painful neuritis
of a nerve can develop. The minifiltration system of the kidneys can be damaged
(glomerular vessel infarcts), which makes the kidneys much more prone to toxicity
of drugs that are used to treat RA. In the final stage a rare condition, called
amyloidosis can lead to even more kidney damage.
Sjögren's
Syndrome (often spelled as "Sjögren's"
syndrome) In these patients there is a drying up of salivary
gland secretions and lacrimal gland secretions leading to a dry mouth and dry
eyes. It is important that these patients use artificial tears to prevent serious
corneal damage and blindness. Dryness can also develop in the skin, the mucous
membranes of the nose, throat, upper airways and bronchial tubes and the genitals.
This leads to more frequent bronchitis infections and pneumonias. The immune
system is so seriously altered that Sjögren's patients have a risk of about 40-fold
over the normal risk to develop lymphomas. Pancreatitis is common as this too
is a glandular organ. Joint involvement is similar to RA, but the joint
swelling and progression of symptoms is much more benign and self-limiting. Treatment
is conservative and concentrates on symptomatic control of the symptoms. Care
must be taken that the physician does not harm the patient by overzealous therapies.
For instance one has to be careful not to overuse corticosteroids and one should
not use methotrexate for Sjögren's syndrome patients as their immune system is
already compromised and these therapies could trigger the development of a lymphoma.
Eye Involvement: Episcleritis
is an irritation of the conjunctiva with reddening, irritation, light
sensitivity, increased tear flow and tenderness. It is self limiting and can also
present with some rheumatoid nodules. It does not threaten the vision. Scleritis:
This condition affects the deeper layers of the sclera (the
white of the eye). Pain with this condition is so severe that it can interfere
with sleep and appetite. There is sensitivity to light, a nodular redness, which
in time turns into scarring and thinning of the sclera, which gives it a bluish-grey
appearance. This is potentially a threat to vision as the scarring can permanently
damage the eye by spontaneous rupture of the eye.
Felty
Syndrome: This syndrome consisits of a combination of RA
, enlarged spleen and bone marrow suppression (with low white blood cell counts).
It leads to serious infections because of a weakness in the immune system and
vasculitis, which is associated with leg ulcers and nerve damage (mononeuritis).
Other findings are low platelets associated with prolonged bleeding and anemia.
The lymph glands can be enlarged and this needs to be separated from lymphomas
and leukemias. Neurological Problems: Nerve
entrapments are common such as carpal tunnel syndrome and ulnar neuropathy affecting
sensitivity and strength in the hands and wrists, tarsal tunnel syndrome in the
ankles/feet and other more rare signs. Nerve root compressions are also found,
more commonly in the cervical spine, but sometimes also in the lumbar spine from
subluxations and compression fractures of end stage RA of facet joints and osteoporosis.
There is a great danger to the spinal cord when the bony spinal support structure
has been eroded. Immunological Abnormalities: There
are a number of immunological abnormalities that are found in patients with RA.
The most well known is the already mentioned rheumatoid facor (RF), which is an
abnormal antibody directed against the altered immunogloblulins IgG and IgM.
The higher the titer, the more likely that there is an antibody/antigen reaction
and immune complexes form. These in turn will cause vasculitis, glomerulonephritis
(a kidney disease) and neuropathies, as was earlier indicated. About 80% of patients
have seropositive RA, where the RF is present. On the other hand 20% have seronegative
arthritis and they have all the clinical signs of RA. Other parts of the immune
system are also affected: The synovial membranes are infiltrated by T helper lymphocytes
that help the plasma cells to produce RF. Macrophages that process the synovial
membrane antigen are also present in the joint effusions of RA patients. The immune
complexes lead to release of prostaglandins and enzymes in the joints that destroy
cartilage, ligaments and tendons.
|
