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In the diagnosis of rheumatoid arthritis there is a meeting between the doctor and the patient. The doctor reviews the
history of symptoms, examines the joints for inflammation and deformity, the skin for rheumatoid nodules, and other parts
of the body for inflammation. Certain blood and x-ray tests are often obtained. The diagnosis will be based on the pattern
of symptoms, the distribution of the inflamed joints, and the blood and x-ray findings. Several visits may be necessary before
the doctor can be certain of the diagnosis. A rheumatology referrel is preferred,for accurate diagnosis.
The distribution of joint inflammation is important to the doctor in making a diagnosis. In rheumatoid arthritis, the
small joints of the hands, wrists, feet, and knees are typically inflamed in a symmetrical distribution (affecting both sides
of the body). When only one or two joints are inflamed, the diagnosis of rheumatoid arthritis becomes more difficult. The
doctor may then perform other tests to exclude arthritis due to infection or gout. The detection of rheumatoid nodules, most
often around the elbows and fingers, can suggest the diagnosis.
Abnormal blood antibodies can be found in patients with rheumatoid arthritis. A blood antibody called "rheumatoid factor"
can be found in 80% of patients. Another antibody called "the antinuclear antibody" (ANA) is also frequently found in patients
with rheumatoid arthritis. A blood test called the sedimentation rate (sed rate) is a measure of how fast red blood cells
fall to the bottom of a test tube. The "sed rate" is usually faster during disease flares, and slower during remissions. Another
blood test that is used to measure the degree of inflammation present in the body is the C-reactive protein. The rheumatoid
factor, ANA, sed rate, and C-reactive protein tests can also be abnormal in other systemic autoimmune conditions. Therefore,
abnormalities in these blood tests alone are not sufficient for a firm diagnosis of rheumatoid arthritis.
Joint x-rays may be normal or only show swelling of soft tissues early in the disease. As the disease progresses x-rays
can show bony erosions typical of rheumatoid arthritis in the joints. Joint x-rays can also be helpful in monitoring the progression
of disease and joint damage over time. Bone scanning, a radioactive test procedure, can demonstrate the inflamed joints. The
doctor may elect to perform an office procedure called arthrocentesis. In this procedure, a sterile needle and syringe are
used to drain joint fluid out of the joint for study in the laboratory. Analysis of the joint fluid, in the laboratory, can
help to exclude other causes of arthritis, such as infection and gout. Arthrocentesis can also be helpful in relieving joint
swelling and pain. Occasionally, cortisone medications are injected into the joint during the arthrocentesis in order to rapidly
relieve joint inflammation and further reduce symptoms. Useful laboratory tests for patients with
recent onset inflammatory polyarthritis may include complete blood count, erythrocyte sedimentation rate, rheumatoid factor
test, aspartate aminotransferase (AST) test, creatinine level and urinalysis. Erythrocyte sedimentation rate (ESR)is an inexpensive
measure of disease activity in those with rheumatoid arthritis; however, the test is not diagnostic and rates are not elevated
in all patients affected. A positive test result for rheumatoid factor is helpful but not essential to confirm the clinical
impression of rheumatoid arthritis in the setting of symmetrical inflammatory polyarthritis. If the arthritis has lasted more
than a year, the physician should consider taking radiographs of the hands and feet.
The importance of diagnosing rheumatoid arthritis cannot be overemphasized - early intervention with DMARDs has been
shown to improve long-term outcomes,and once joint damage has occurred erosion and joint instability are irreversible. If
rheumatoid arthritis is mild and in its early stages many rheumatologists favour using hydroxychloroquine because it is safe
and convenient. If control is suboptimal after 6 months, additional DMARDs are often prescribed. A recent study reported some
efficacy with minocycline for patients with early seropositive rheumatoid arthritis. However, long-term efficacy data for
patients treated with minocycline are not available, and radiographs show that damage progresses at the same rate as in placebo-treated
patients.
If a patient has moderate or severe rheumatoid arthritis, especially if the rheumatoid factor is positive, injectable
gold or methotrexate may be the preferred DMARD. Gold treatment has the important advantage of offering the potential for
disease remission, but methotrexate is more convenient and better tolerated. Sulfasalazine is safe as a second-line agent
and can be used in combination with methotrexate and other DMARDs. Many new DMARDs are becoming available.
There is frequently a delay between the presentation of polyarthritis and the confirmed diagnosis, and there is always
a delay before a prescribed DMARD has the expected benefit. When optimal DMARD therapy or a combination of DMARDs does not
control synovitis, low-dose prednisone can provide symptom relief, acceptable low toxicity and joint protection. Bisphosphonate,
either cyclical tidronate or daily alendronate, reduces the risk of steroid-induced osteoporosis and should be prescribed
prophylactically when the daily dose of prednisone is 7.5 mg or more.
Patients with active rheumatoid arthritis should be assessed by a rheumatologist on a regular basis, and clinical and
laboratory evaluations should be repeated to measure the efficacy and toxicity of treatment. The aim of therapy is to minimize
pain, stiffness and joint swelling; retard joint damage; and reduce future disability. In patients who are under 50 years
of age with joint pain and swelling lasting longer than 6-8 weeks the diagnoses to be considered include rheumatoid arthritis,
psoriatic arthritis, other seronegative spondyloarthropathies and SLE. In patients over 50 years of age,crystal-induced synovitis
should also be considered. Osteoarthritis may also cause considerable inflammation in the affected joints. For most of these
conditions specific therapies aimed at controlling inflammation, preserving range of motion in the joint and preventing joint
damage are successful in decreasing morbidity and improving quality of life.
The patient with symptoms in many joints requires a detailed history and physical examination. If there is morning stiffness
lasting more than 30 minutes or stiffness after sitting, the joint complaints are likely to be caused by inflammation; a convincing
history of joint swelling confirms the presence of inflammation . The physician should record the onset and progression of
symptoms and the distribution of joints affected. A history of psoriasis in the patient or a family member is an important
clue to the possibility of psoriatic arthritis. The physician should also inquire about a history of iritis or inflammatory
bowel disease, both of which are associated with seronegative spondyloarthropathies.
A recent episode of infectious diarrhea or genitourinary infection are clues to possible Reiter's syndrome. Does
the patient have symptoms suggestive of SLE (e.g., photosensitive or malar rash, alopecia or pleurisy)? Is there a past history
of acute episodes of arthritis or gout? Are the joints tender or swollen? Is movement limited? The choice of laboratory tests
that may help depend on the differential diagnosis.
Patients must be made aware of the need for monitoring. The incidence of serious side effects is markedly reduced with
regular monitoring, because adverse effects are more likely to be discovered before serious or irreversible consequences arise.
Despite the long list of side effects, which often intimidates patients, long-term series of rheumatoid arthritis patients
treated with DMARDs have found that serious side effects are rare.
When counselling a patient who expresses concern about potential side effects, it is also important to remind him or
her of the consequences of the alternative; doing nothing will result in irreversible disability, progressive joint damage
and premature death. It is also important to recognize that information on the use of antirheumatic drugs in other fields
of medicine may not be applicable to patients with rheumatic diseases. Drugs such as methotrexate and cyclosporine, which
are used in cancer therapy and transplant programs respectively, are used in lower doses for rheumatoid arthritis, and the
incidence of adverse events is lower.
Persistence in the use of DMARDs is of great importance. DMARDs are used to treat incurable, chronic diseases where treatment
will be lifelong and the number of available options is limited. Typically a patient with rheumatoid arthritis will use a
succession of DMARDs over the years. After an initial response, a drug is often eventually discontinued, either because of
adverse side effects or loss of effect. To ensure the best result, it is important to give each drug a full trial, namely,
the maximum dose for sufficient time, before declaring it not efficacious. In addition, there are a number of strategies for
dealing with common side effects. Rather than stopping treatment, the patient may be referred to a rheumatologist, or one
can be consulted by the physician, regarding the management of persistent side effects.
The use of a combination of DMARDs is now widely practised. Some rheumatologists advocate the use of combination therapy
from the onset of disease for early control, with a subsequent gradual withdrawal of therapy, as necessary to maintain control.
Others prefer the opposite strategy: successively adding DMARDs to agents to which the patient has shown a partial response.
Proponents of the latter view believe it prevents unnecessary exposure to potentially toxic drugs of patients who may respond
to single therapy. This approach may also be more acceptable to patients. Commonly used combinations include hydroxychloroquine
with most DMARDs, especially methotrexate or intramuscular gold; sulfasalazine and methotrexate with or without hydroxychloroquine;
and cyclosporine and methotrexate.
The treatment of early rheumatoid arthritis is now recognized as crucial to long-term outcome, and the selection of agents
is a complex task owing to the rapidly increasing number of treatments available, alone or in combination. When possible,
a rheumatologist should be involved in this decision-making process. There is no consensus as to the order in which DMARDs
should be chosen for the treatment of rheumatoid arthritis or other inflammatory arthritides. Choice must be tailored to the
patient's profile and preference, disease activity and prognostic markers of disease severity.
The use of corticosteroids results in rapid, potent and reliable suppression of inflammation. This explains their wide
use for the inflammatory manifestations of rheumatic diseases and for systemic vasculitis. However, their effect in suppressing
the synovitis in rheumatoid arthritis is not sustained and requires a progressive increase in dosage to maintain the benefit.
The precise role of orally administered corticosteroids in rheumatoid arthritis remains controversial. Short courses of low-dose
steroids can be useful as "bridging therapy" to control symptoms while waiting for DMARDs to take effect or to control severe
flare-ups. Patients can decrease the dose as soon as symptoms are under control. The injection of steroids into the most affected
joints can often alleviate the need for oral steroids (at the rate of 1-2 large joints every 2-6 weeks). Intramuscular injections
of corticosteroids are advocated by some to prevent difficulties in tapering off the dose of oral corticosteroids.
The use of an alternate-day regimen is associated with a lower incidence of some of the side effects Maintenance
of control of the disease can be a problem. Switching from daily to an alternate-day regimen must be done gradually (by tapering
off the dose on alternate days down to zero) to prevent both adrenal insufficiency and exacerbation of the disease. Administration
of the dose in the evening, a divided dose and the use of longer acting forms are associated with greater adrenal suppression.
It is useful to think of corticosteroid administration in 3 broad ranges: low dose (i.e., the equivalent of orally administered
prednisone, 15 mg daily or less), as used in the treatment of polymyalgia rheumatica, active arthritis and mildly active systemic
lupus erythematosus; moderate dose (i.e., 15-25 mg daily); and high dose (i.e., 25-60 mg daily), as used in the treatment
of acute manifestations of systemic vasculitis and the more severe manifestations of systemic lupus erythematosus.
Unfortunately,RA has the reputation that it is incurable-that nothing can be done. RA is currently incurable,it certainly
is treatable-at any stage-early the easier,and better. Health care systems are changing. The old system wherein physicians
made all the decisions is slowly disappearing. In the new system, patients,especially those with complex diseases,can be misunderstood,
The choice and the responsibilities,are yours. It is your health,and no one else will pay as much attention to it,or will
benefit from it as much as you.
If you have rheumatoid arthritis,you need to be proactive. You have to initiate contact with your health care providers
and get along with them. The right diagnosis is the start. You will most certainly require the services of a rheumatologist
for treatment and monitoring of your disease. Most of all you need to become more educated about your disease The most important
thing in management of the disease is to get it under control. If the inflammation associated with RA is controlled,most of
the other problems that occur as a result of the devastating effects of inflammation is gone or minimized. Don't accept you
have to live with it,(always) you may have to live with it up to a certain point.but understand your treatment options and
never accept treatments just because someone said it may work. They may not work for you.
Most RA patients get lost in a maze of treatmentment options (and unfounded opinions),valuable time and the opportunity
to control the disease is lost. It is your life and your disease. Make the decision to get the treatment you need to
get your disease under contol,and forget Uncle Jims's arthritis symptoms and treatment,or your friend's back problem treatments.
The first step,is seeing a rheumatologist. Family doctor's are one of the most valuable people in this world,but a good doctor
who have your sole interests will refer you to one. The average family doctor's training in rheumatology is very,low in terms
of time spent at medical training in rheumatology (estimated at less than 1 %-if the option in taken)and furthermore,some
do not take the rheumatology option offered at medical school. My family doctor admits it,and quickly refers when he is not
quite sure. of any complex problems of the human body,that what he is trained to do. A most valuable physician,we can not
afford to be without,but with limitations in regard to certain problems that may arise.
Dismantling The Treatment Pyramid:
Dismantling the treatment pyramid: Some patients may remember "Red Kelly" ,in the 70s,then coach of the Toronto Maple
Leafs hockey club of the NHL who tried "pyramid power" to motivate his team. It was a seventies fad based on vague interpretations
of mysteries,such as using crystals to "realign your aura" The mix of specious reasoning and hokey,pokey data was enough to
convince students and athletes to sit under pyramids as a way of increasing their prowess in studies and sport. The practise,
fortunately, has gone the way of the "model-A Ford automobile",but the pyramid did have one serious application: as a symbol
for rheumatoid arthrtis management
The "pyramid approach to treatment" is a visual for the administeration of sequentially more powerful interventions:
The base of the pyramid is rest, physical therapy,ASA,and other NSAIDs. Next up are progressively stronger disease-modifying
anti-rheumatic drugs (DMARDs-slow acting anti-rheumatic drugs-then referred to as SAARDs) capped,at the apex of the pyramid,by
experimental drugs and procedures. The pyramid approach has long been part of the fabric of rheumatology, certainly for as
long as Dr. James F. Fries can remember. Fries is director of ARAMIS (Arthritis Rheumatism and Aging Medical Information System)
based at Stanford University Medical Centre,where,for the past decades or so,he and his colleagues have been building databases
on arthritis. Their research has contributed to a new understanding of RA,and a recognition that the pyramid approach to tretment
was based on some false notions about the disease.
The first was the view that RA is a relatively mild disease,followed a leisurely course,that doesn't amount to much in
most people,and often goes into remission by itself. Then there was the belief,Fries says "that ASA and NSAIDs wer very benign
drugs,and that disease modifying drugs-like intramuscular gold and,even worse,methtrexate or azathioprine-were too dangerous
in a benign disease." Incorrect,and wrong again. On the basis of such false premises says Fries,"we accepted the pyramid strategy".
In recent years,anumber of studies-many of them drawing on the remarkable ARAMIS database-have led to a very different
conclusions. What they've learned has led to what Fries calls "a 180-degree change in the way we therapeutically approach
RA",similar to the change in the way heart attack victimins are treated: Years ago,heart patients were prescribed six weeks
of absolute bed rest,which seemed logical at the time. But outcomes took a leap foward when cardiologists started hauling
their patients out of bed and up into treadmills and out running marathons. "Those of us who have seen both eras",Fries says,"realize
we were flatly wrong in the way we approached coronary artery disease-and we were flatly wrong in RA. So,we're at a time when
we made a 180-degree shift,in this case with the treatment pyramid".
"Initially,the pyramid approach was useful because at the base of the pyramid you had one drug,ASA " says Dr. Bill Benson
a rheumatologist a St. Joseph's Hospital in Hamilton Ontario. "And then,of course,you went very quickly from ASA ti the disease-modifying
drugs. Where things got complicated was in the "70s and "80s,when we had 13 other NSAIDs come into the market. It made the
base of the the pyramid so deep that many physicians started to go with the concept that you just keep trying these non-steriodals,which
would give you up to two or three years' worth of alternatives before you move on to a stronger, slow-acting,anti-rheumatic
drug. And this led to immense,damaging delay in the management of RA." At the same time,it was clear that NSAIDs weren't stopping
the disease in most people,while the slower acting drugs showed greter potential to put the disease to rest,if not temporarily,
and sometimes permanently. In addition, doctors were becoming aware,from clinical experience if not from academic studies,that
DMARDs also worked best with early-stage RA-before it caused irreversible cartilage or bone damage.
A rheumatologist at the University of Birmingingham,England wrote in the British Journal of Clinical Practise in 1995,"There
is now great deal of evidence that inflammatory arthritis is at its most active soon after onset: The conventional delay in
therapy until disease becomes severe is therefore a missed opportunity. The appearance of erosions ( in cartilage and bone
) also peaks early in disease. A further stimulus for early therapy has come from evidence that systemic disease itself is
harmful: For example,patients who maintain a high acute phase response over two years lose approximately 10 % of the bone
from the hips". -Dr. Paul Emery.
"There was a feeling 20 years ago that you could sort of start anytime and these drugs would work and slow things down"
Says rheumatologist Dr.Benson from Hamilton,"so there was no particular rush, I think people appreciate now that,if you want
to stop the disease,you have to treat early and slam the barn door before the horse gets out." Since that realization,there
have been a number of new ways of looking at RA management. Two researchers at the University of Washington were among the
first to suggest (in the Journal of Rheumatolog ,in 1989) "remodelling the pyramid". In its place,they propsed a "step-down
bridge" approach to RA,in which treatment is initiated "with a combination of rapid-acting anti-inflammatory medications and
slower-acting second-line drugs. this provides erly control of inflammation and a "bridge" until slower-acting medications
can take effect". Medications are then sequentially withdrawn,in contrast to the traditional pyramid,in which they're sequentially
added.
A year later in the early 1990s A researcher-rheumatologist Dr. Fries suggested a slightly different strategy. (saw-tooth) One
of the problems with previous strategies,he said, was that patients didn't recieve DMARDs before they had "substantial erosive
disease and disability. Such drugs have most typically first been prescribed six to eight years into the disease course;too
little,too late,for too few". That course was based on the assumption that NSAIDs were relatively harmless in terms of side
effects compared to DMARDs. In fact,ARAMIS (data base) data showed that there's really little to choose between the two drugs
in that regard. The data also provided a new view of oain relief. It was always ssumed that NSAIDs provided fast relief from
the pain,while DMARDs worked on the underlying disease
While that's essentially true,Fries noted that "pain in RA is a consequence of the inflammatory process and of prior
destructive eents in the joints". So, while NSAIDs provide day-to-day relief from the pain,the ultimate pain reliever is the
best medication that best "reduces Inflammation and retards bone and cartilage destruction and prevents future pain". An ARAMIS
study that examined pain levels nine months after therapy began in some 10,000 courses of treatment with different agents
found that pain relief from NSAIDs was "at best modest,while (treatments) with DMARDs were three times more substantial".
Fries also emphasizes that RA isn't benign as people used to think It does,in fact,increase moratality rates,a "long-established
but neglected observation" that negates another frequent argument for the old therapeutic pyramid:"that drugs with the ( extremely
rare ) potential for fatal reactions should not be used in a 'nonfatal" disease unless absoslute necessary."- which proved
wrong. Fries asserts that old rheumatologists' dominant therapeutic strategy "had been an illogical one,based upon premises
that can now shown to be false,in which we treted patients symtomatically until their joints had sustained irreversable damage.
Only then did we employ,slowly and ferfully,our most effective agents. We took a short-term view of analgesia in a long-term
diseae. We accepted rather uncritically the view that NSAIDs were safe and DMARDs were dangerous. We allowed slow month-to-month
deteriation to pass unobserved until the best point to change therapy had long passed. We are using new stratgy,rolted in
the relevant clinical facts and dedicated to the improvement of long-term outcome".
The sawtooth strategy Fries initially proposed advocated the serial use of DMARDs,introducing one or more as the therapeutic
benefit of the earlier drug is lost,but that strategy has yet to prove more effective than the step-down approach. Since
then,variations have been suggested ,with clinicians employing different tactics to affect patient outcomes; rheumatologist
no longer talk about "reversing the pyramid".
Dr Keystone-researcher-rheumatologist generally starts patients on methotrexate: "It used to be be you started with gold
and then went to chloroquine (replaced by plauenil),then you went maybe to azathioprine or sulfasalizine,and finally you think
about a agent like methotrexate. "Even if their joint swelling remains the same,people feel better,they're less symptomaticc.
And a proportion of people go into remission" Fries in contrast starts patients with relativelu mild hydroxychloroquine (
an approach more common in U S than in Canada) Keystone generally starts patients on methotrexate
Keystone contends that Canadians "are more aggressive than Americans by far" in their treatment philosophy. As soon as
we make a diagnosis,we put patients on DMARD, What's different is,we're using methotrexate earlier,and we're combining DMARDs
earlier. So, in a sense,we are reversing,the pyramid,because we're not waiting to get to the top,we're starting DMARD from
Day One".
Most present day rheumatologist,follow,and believe in Keystones' approach.
Are there any key findings in the evaluation of a rheumatoid patient that
are known to correlate with a more aggressive pattern? Fortunately, studies have confirmed several prognostic indicators suggestive
of an adverse progression in a rheumatoid patient. Onset of RA at an early age, high titers of rheumatoid
factor, elevated acute phase reactants such as erythrocyte sedimentation rate (ESR) or C-reactive protein (CRP), swelling
of multiple joints (usually 20 or more), and the presence of rheumatoid nodules are some of the indicators of poor prognosis.
In addition, extra-articular features of RA such as vasculitis, rheumatoid lung disease, and ocular manifestations (episcleritis,
to name one) also carry a poor prognosis. Prompt recognition of these signs in a rheumatoid patient warrants aggressive implementation
of DMARD (Disease Modifying Anti-Rheumatic Drug) therapy.
Although the presence of rheumatoid factor can be seen in up to 85% of
RA patients, it cannot be used to monitor disease response to therapy. Titers of rheumatoid factor rarely correlate with disease
activity. Furthermore, its presence can be seen in other conditions such as malignancy, infections, and even aging, and thus
is not specific for the diagnosis of RA.
The most common isotype of rheumatoid factor is IgM, generally directed
at the Fc binding site of another immunoglobulin, typically IgG. The presence of rheumatoid factor in RA suggests the loss
of immune tolerance, ie, the immune system's unresponsiveness to self-antigens. It is postulated that the physiologic role
or production of rheumatoid factor is in response to an antigenic stimulus. Unfortunately, even after numerous attempts to
identify it, the particular antigen that is a common denominator among all rheumatoid patients remains elusive.
In a 5-year study that followed 732 patients with early RA (diagnosed for <2 years and no use of DMARDs), Scientists assessed
factors that affect which patients with early RA stop working. Overall, 9% of patients had marked functional loss at
presentation, with work disability seen in 27% of patients who were employed at onset of RA. After 5 years, almost one
third of patients (29%) employed at onset of RA had retired because of RA.
Using logistic regression analysis, the authors found that the patients most likely to stop working were those who performed
manual work (odds ratio of 4.9), and those who had worse baseline Stanford Health Assessment Questionnaire (HAQ) scores (greater
than 1.5; odds ratio of 3.6). Other factors associated with increased work disability included increased erythrocyte sedimentation
rate, female sex, and moderately increased HAQ scores. On the other hand, presence of erosions and the patients age at RA
onset were relatively weak predictors of work disability at 5 years, with odds ratios of 1.9 and 1.1, respectively.
Patients with RA show rapid functional decline that begins early in the course of RA. Using the HAQ Functional Disability
Index, investigators assessed functional disability in 1274 patients with RA who were followed longitudinally for up to 12
years. The rate of functional loss increased sharply after the first clinic visit. Half of the patients with RA reached HAQ
scores of about 1 (moderate loss of function) within 2 years. Half of the patients reached scores of 2 (severe loss of function)
within 6 years. Half of the patients reached scores of 2.5 (very severe loss of function) within 10 years after the first
clinic visit. These data show that disability increases most rapidly during the early years of the disease; the decline in
functional disability slows thereafter.
Another study reviewed 31 studies of mortality in RA to determine the predictors of mortality that can be modified with
treatment and medical care. Although measures of disease activity such as TJC and ESR were found to be significant predictors
of mortality in half to two thirds of the studies, patient and physician measures of functional disability were reported to
be significant in more than two thirds of the studies. These measures include patient questionnaires, physicians' global assessment
of disease, physical functional status, patients' global assessment of disease, and patient psychological distress.
Pain score and RF were found to significantly predict mortality in less than half of all studies. Pincus and Sokka have suggested
that better control of quantitative markers that significantly predict early mortality could provide a valuable approach to
improving outcomes in RA.
A number of clinical and laboratory variables have been related to disease activity/severity in patients with RA. Clinical
factors that have been correlated with more aggressive or severe disease include duration of RA and number of swollen joints.
The presence/severity of joint erosions and rheumatoid nodules is also a predictor of disease severity. Laboratory variables
associated with more aggressive/severe RA include higher rheumatoid factor titer, the presence of anticyclic citrullinated
peptides (anti-CCP), high levels of CRP, and elevated ESR. The presence of one or two shared epitope DRB1 alleles has also
been associated with increased disease severity in patients with RA.
A team of investigators carried out a more extensive comparison of the ability of sonography versus conventional radiography
to detect erosions in the MCP joints of patients with RA. Their study included 100 RA patients (40 with early disease defined
as <12 months duration and no DMARD therapy). Sonography detected 127 definite erosions in 56 of 100 RA patients, compared
with radiographic detection of 32 erosions in 17 of 100 patients.
In early disease, sonography detected 6.5-fold more erosions than did radiography, in 7.5-fold the number of patients.
In late disease, these differences were 3.4-fold and 2.7-fold, respectively. These investigators concluded that sonography
reliably detects more erosions than conventional radiography, especially in early RA, and that this technology has the potential
to greatly assist in identification of candidates for early intervention. On the other hand, conventional x-rays detected
erosions in only 14% of patients at baseline and in 29% after 1 year. Information obtained with MRI was also useful in establishing
a prognosis for these patients. Baseline findings that predicted carpal MRI erosions at 1 year included a total MRI score
=6 (sensitivity, 93.3%; specificity, 81.8%; positive predictive value, 93.3%), MRI bone edema, and MRI synovitis. Thus, MRI
scans may be more effective at detecting erosions in early RA, and may be useful in identifying patients for aggressive disease
intervention.
In the Arthritis, Rheumatism, and Aging Medical Information System (ARAMIS) databank to model the relationship between
a wide range of variables and cost of treatment over the succeeding 5 years. The results of this analysis indicated that disability,
as measured by HAQ DI was a much stronger predictor of treatment cost than any other variable, including age, sex, disease
duration, or education level. After disability was entered into the prediction model, no other variables evaluated had significant
predictive value.
Disability drives up the major costs associated with RA, including hospitalization, surgery, loss of employment, and
the need for long-term care. In the United States, 2.1 million people have been diagnosed with RA, while worldwide, 165 million
people are affected. The majority of studies on the economic consequences of RA have been conducted in the United States.
The economic costs of RA were estimated to be $8.74 billion in 1994, an amount that represented about 0.3% of the gross domestic
product. Yelin and Wanke estimated that the direct medical costs of RA in the United States are $5,919 per case per year.
Indirect costs of RA primarily are the result of lost income from work due to the high incidence of work disability in
patients with RA. Other indirect costs result from the significant limitations in both the instrumental and nurturing functions
experienced by a homemaker in managing a household. According to one estimate, indirect costs of RA (mainly lost wages) are
3 to 4 times higher than direct costs. In a study of 133 employed patients with early RA, indirect costs (the cost of
sick leave and lost productivity) averaged $11,750 per person-year for the entire duration of the study (mean of 2.5 years).
The lifetime costs of RA are as high as those related to coronary artery disease or stroke.
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