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.
|
