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Introduction: CPPD, like gout, is a form of
arthritis caused by crystals that induce inflammation within
the joint space. For this reason, this condition is also
known as �pseudogout� (i.e. � mimicking gout). Unlike gout,
however, which is caused by uric acid crystals, CPPD is caused
by calcium-containing crystals.
These crystals have a tendency to accumulate along damaged
cartilage surfaces within joints. Deposits of these crystals
can be seen in up to 4% of the adult population at some time
during life, and the prevalence of these deposits increases
with age to the point that about 1/2 of those in their 80s
will demonstrate evidence for these deposits on x-ray. Most
individuals will experience no symptoms as a result of these
calcium deposits. Those who do, however, may develop joint
inflammation in a variety of different patterns.
Features of
CPPD:
CPPD may result in different degrees of
inflammation in different patients. Three basic types of
arthritis are observed: acute arthritis flares of one joint,
chronic inflammation of many joints, and rapidly progressive
degeneration of the cartilage of an affected joint.
Many patients with CPPD will develop acute episodes of joint
pain, swelling, warmth, and possibly redness. Fever may also
be present during these attacks. Surgery or serious illness
may trigger a disease flare. It is this form of CPPD that is
referred to as pseudogout because of the similarity of these
episodes with gout. The most commonly affected joint is the
knee, followed by the wrist. Less commonly, hand joints may
be involved, or the joint at the base of the big toe may
become inflamed (causing further confusion with gout).
Other patients may develop inflammation of several joints at
once. This inflammation is usually less intense but more
widespread. When hand and wrist joints are inflamed in this
manner, CPPD can resemble rheumatoid arthritis (RA), although
RA generally results in more joint destruction.
Finally, some individuals with CPPD appear to have a rapid
progression of joint damage that resembles severe
osteoarthritis (OA). Signs of inflammation are even less
pronounced in this subset of patients. It is believed that
the presence of the calcium crystals more rapidly strips away
the lining of the cartilage. In many, it may be difficult to
determine if the calcium deposits are causing any damage in
the joint or are simply present by coincidence. Again, the
knee is commonly affected, just as we see in those with
ordinary OA. Because the wrist, elbow, and certain knuckles
are rarely involved in OA alone, CPPD must be considered as a
diagnosis.
Diagnosis:
CPPD should be considered as a
possible diagnosis if patients exhibit any of the different
patterns of joint pain or swelling noted above. The findings
of swelling or warmth on physical examination suggest that any
kind of inflammatory arthritis could be present. It is only
by investigating further that CPPD can be sorted out from
other conditions.
X-rays often demonstrate calcium deposits in involved joints,
particularly the knee and the wrist. These deposits often
have the appearance of a thin white rim lining the cartilage.
While a swollen and inflamed joint coupled with the finding of
soft tissue calcium deposits within the joint suggests the
diagnosis, as mentioned above, many people over the age of 65
with no joint symptoms may demonstrate these calcium deposits
on x-ray.
Examining a sample of joint fluid is a more accurate way of
making a diagnosis. Not only can the diagnosis of CPPD be
confirmed, but other possible problems, such as acute joint
infection, can be ruled out. A drop of fluid can be examined
under a device know as a polarized light microscope for
calcium crystals, which can be distinguished from uric acid
crystals found in gout by an experienced physician. There
are certain obstacles to finding the calcium crystals within
the joint fluid sample. The crystals of CPPD are more
difficult to see under the microscope than the crystals found
in gout. If the fluid is not examined within about 6 hours,
the crystals may disappear. Also, the joints may not be as
inflamed in certain patients with CPPD, and there may be less
fluid to aspirate. To make matters more confusing, a certain
number of patients have both gout and CPPD.
Laboratory tests do not help diagnose CPPD, but they do help
investigate other diseases that may be associated with this
condition. Over-activity of the parathyroid gland, which
controls calcium levels in the body, under-activity of the
thyroid gland, low magnesium levels, and a disease causing
iron overload known as hemochromatosis are all seen in
increased frequency in patients with CPPD and should be
considered and screened for with blood tests. While
identifying these associated diseases is important, treating
them does not remove calcium crystal from the joint or reduce
joint symptoms. CPPD still must be treated separately.
Therapy:
Treatment of CPPD may be either
intermittent for acute flares or daily for chronic joint
disease. The inflammation of CPPD can be treated much in the
same way we treat gout. The major difference, however,
between the two disorders is that long-term therapy for gout
results in uric acid crystals being eliminated from the joint,
while no such therapy exists for CPPD.
Non-steroidal anti-inflammatory drugs (NSAIDs)
reduce symptoms and joint swelling in most individuals with
CPPD and may be sufficient to treat the majority of patients.
Ibuprofen (Motrin), naproxen (Naprosyn), and indomethacin (Indocin)
are commonly used NSAIDs but increase the risk for damage to
the stomach, potentially leading to ulcers in certain patients
at risk. This risk is reduced when using COX-2 selective
NSAIDs such as celecoxib (Celebrex) or valdecoxib (Bextra) as
well as the partially COX-2 selective drug meloxicam (Mobic).
Corticosteroids may
be administered in many different forms. Most often, these
agents are more appropriately given during an acute flare
rather than for chronic inflammatory joint disease due to the
side effects of long-term therapy (thinning of the bones,
elevation of blood sugar, weight gain, cataracts, etc.).
While withdrawing fluid from the joint, injecting steroids
directly into the joint often provides prompt relief of
swelling and pain. Intravenous infusions or injections into
the muscle are rarely required to treat severe flares
involving multiple joints. Oral corticosteroids can also be
given short-term with few side effects; when given
chronically, doses of less than 10 mg/day of prednisone or its
equivalent should be used.
Colchicine is usually
given orally for acute flares. Intravenous colchicine may be
more effective in this setting but has the potential risk of
suppressing the bone marrow�s production of blood cells. Low
doses of oral colchicine given once to twice daily for those
with frequent attacks of joint inflammation may reduce the
frequency and/or severity of these episodes. The response
seen in patients with chronic ongoing inflammatory arthritis
is variable, and diarrhea is a side effect that may limit this
approach. None-theless, low cost and relatively few side
effects make colchicine an option worth attempting in certain
patients with CPPD.
Phosphocitrate is a
medication in experimental stages of development that seems to
prevent formation of CPPD crystals as well as other less
common calcium crystals. Studies have not yet established
what role this agent may have in treating CPPD long-term. |
