Features

Sock's Rheumatoid Arthritis Page 1:

Although we do not know the cause of RA joint damage is caused by inflammation in the synovial membrane. This normally,thin synovial membrane becomes inflamed with cells called lymphocytes,macrophages,polymorphs,and fibroblasts. After the attack,this, now, thick,inflamed synovial membrane is called the pannus.

The cells within the pannus become activated and release enzymes and chemicals (cytokines ) that permanently damage the cartilage and the bone and also attract more cells into the inflamed tissue. In RA this inflammatory process is like a one way highway;the inflammation can continue indefinitely,causing more and more damage,leading to joint destruction and deformity. Thus the need for disease modifying drugs ( DMARDs).

This inflammatory process is part of the body's immune system. The immune system is a natural defense against invaders such as bacteria,viruses,and even cancerr.

Although the immune system is normally activated by a foreign agent,it can be activated to attack normal,healthy cells. In RA,for some unknown reasons,the immune system becomes activated and causes marked inflammation in the synovial membrane.

There is non-erosive,short-lived RA,but the majority of patients have the erosive,on-going,progressive destructive , and delibitating type of disease.

RA affects women more than men,with the peak incidence between ages 40 and 60,although the disease can appear at any time of life. Onset can be gradual and insidious,ocurring over a period of days or weeks. Usually it begins in the small joints of the hands or the feet. A woman may notice that her shoes do not fit quite as well as they used to or experience pain while wearing high heels. The pain is usually a "dull" type of pain. The hands appear mildly swollen to the patients,but not to others,they may have difficulty taking rings on and off.

Many patients with early RA take over-the-counter medications,such as acetaminophen or ibuprofen,for a period of time before seeking medical attention. Since the clinical picture at this stage may still be vague,the family doctor may simply prescribe a nonsteroidal anti-inflammatory (NSAID ) drug and recommend continued follow-up.

The arthritis may be asymmetric at first ( i.e., limited to one side of the body ) but over a period of weeks to months tends to become symmetric. Patients may experience stiffness-a hallmark of the disease,and complain of diminished energy and fatigue. Eventually they will begin to manifest more over-all features of synovitis or swelling and tenderness in the involved joints.

With time,disease manifestations will become objective and more obvious to those around the patient (family,friends ). Examination typically shows involvement of the small joints of the hands,feet,or both. In the hands,there is characteristically involvement of PIP or MCP joints but sparing of the distal interphalangeal ( DIP) joints,may be the background. X-rays at this stage may or may not show features of the disease. Some patients will have normal radiographs while others demonstrate erosions and sometimes joint space narrowing within six months to a year after onset. Symptoms vary among patients.

Laboratory studies initially may not contribute to the diagnosis. The rheumatoid factor assay ( RF) is initially negative in many patients,and in up to 30 %,the assay is never positive. The ESR may or may not be elevated at presentation;the elevation may not occur for weeks or even months,later.

The other diagnostic possibily that the physician should consider is systemic lupus erythematosus (SLE). Findings should show the lack of findings consistent with SLE ( e.g., photosensitivity,cutaneous disease,internal organ involvement). It is also important to make sure that a patient that may show some symptoms at the start,does not have parvovirus B 19,or hepatitis B or, C infection.

Formal diagnosis of RA requires that the case meet at least four of the seven ACR criteria:

1) Morning stiffness lasting at least one hour. In fact,even stiffness for more than 30 minutes strongly suggests inflammatory disease. Alleviations of morning stiffness with activity is a hallmark of inflammtory arthritis. Later in the day,continued activity will aggravate the problem and exacerbate the pain.

2) Swelling in three or more joints simultaneously (polyarthritis ).

3) Swelling in the hand joints ( PIP,MCP,or wrist).

4) Symmetric arthritis. Initially,joints on only one side may be involved,but the arthritis tends to spread to the other side of the body.

5) Erosions or decalcifications on x-rays of the hand.

6) Subcutaneous rheumatoid nodule

7) A positive serum rheumatoid factor.

X-ray may not help in the initial diagnosis,but they provide a baseline. After one or two years,the physician can obtain another x-ray to see whether the disease has continued to progress radiographically. Ths can occur independently of clinical manifestations ; even patients whose symptoms have responded well to therapy may continue to show radiographic progression. Second,if erosions or joint space narrowing had already been present,it would have helped to predict the disease course and to determine the therapeutic strategy. This procedure is often,not done. As one old grumpy,misinformed, said "We know all about the disease,we can see with our eyes if ra is present ". Unfortunately, not.

Even if a patient does not meet four criteria,the primary physician should entertain the possibility of RA.

Patients whose disease features characteristic of RA may merit referral to a rheumatologist. During the past few years,there has been a much greater emphasis on early diagnosis. Underlying that emphasis is the realization that some patients experience early functional and radiographic decline that ultimately produces significant impairement in their ability to function. The sooner the diagnosis is made and disease-modifying ( DMARDs ) therapy initiated,the better off the patient is likely to be, over both the short and long term. Seeking alternative therapy at this stage is simply, foolish,and ignorant of the facts,involved in ,true,rheumatoid disease.

Damage (erosions ) to joints once done,is not reversible !! A few patients may have the non-erosive type. We turn our attention to the majority of patients.

Rheumatoid arthritis seldom goes away. Eighty percent or more of patients will continue to live with it. When its initial symptoms appear,it's almost impossible to tell who will do well and who will not. But we do know that joint damage occurs early on,and that we have only a very short period of time-a year or less-to prevent this damage with a effective treatment program ("window of opportunity").

This means that treatment is divided into two phases:

1) an initial phase (preferably short) where RA is suppressed as completely as possible;

2) A long-term surveillance phase where local complications of RA is seen and dealt with before damage can occur,and where major flare-ups are anticipated and prevented as much as possible

Treatment involves long-term contract between physician and patient. Each must understand the other as fully as possible. Communications must be open There will be times when contact is interrupted because the disease may turn stable,but it must be re-established when necessary. And the patient must be able to judge when that time has come.

It's important for the patient to learn as much as possible about the disease,its complications and its treatment. The side effect of the medications,when therapy is effective and when it is not/becomes non effective.The patient is the "driver",not a passenger.

Features:

Approximately 15 % of cases of RA will "explode" over a matter of a few days. Although not all the joints that will eventually cause trouble will be inbolved in the first attack,there will be quite a number-24 is typical. They will include both large and small joints,and especially the MCPs and MTPs. Similar joints on both right and left sides will be involved. Morning stiffness and fatigue will dominate.

About 75 % of the time,the picture is less spectacular. A wrist becomes swollen and for some time it's the only problem. Or a patient develops maeked tenderness under the balls of both feet (the MTP joints),particularily when first getting up in the morning. Gradually,over several week to several months,more and more joints join the picture. Fatigue and morning stiffness appear. It may take a year before a clear diagnosis is made.

In 10 % of cases,RA starts off much like gout. A single joint,such as a knee,wrist or shoulder,suddenly becomes very painfu,swollen and warm. Often the pain is so severe the joint is not useable. Two or three days later,its back to normal. After a month or so,another attack strikes,usually in another joint. As time goes by,the attack becomes more frequent. Gradually they are less and less severe but more and more frequent,and instead of clearing up,the swelling and pain start to persist. One day,perhaps after a year or more,it becomes obvious that it is RA. This pattern is called palindromic rheumatism,and while it doesn't always turn out to be RA,it more often does.

Very rarely,RA first appears in an ""extra-articular" (non-joint) site,with joint symptoms appearing months later. When it does,it usually takes the form of chest complications,and the patient is usually male.

The symptoms of rheumatoid arthritis come and go, depending on the degree of tissue inflammation. When body tissues are inflamed, the disease is active. When tissue inflammation subsides, the disease is inactive (in remission).

Remissions can occur spontaneously or with treatment, and can last weeks, months, or years. During remissions, symptoms of the disease disappear, and patients generally feel well.

When the disease becomes active again (relapse), symptoms return. The return of disease activity and symptoms is called a flare. The course of rheumatoid arthritis varies from patient to patient, and periods of flares and remissions are typical.

When the disease is active, symptoms can include fatigue, lack of appetite, low grade fever, muscle and joint aches, and stiffness. Muscle and joint stiffness are usually most notable in the morning and after periods of inactivity.

Arthritis is common during disease flares. During flares, joints frequently become red, swollen, painful, and tender. This occurs because the lining tissue of the joint (synovium) becomes inflamed, resulting in the production of excessive joint fluid (synovial fluid). The synovium also thickens with inflammation (synovitis).

Signs of disease remission:

*Morning stiffness that lasts less than 30 minutes.

*No pain when at rest.

*Little or no pain or tenderness with moving joints.

*Normal energy level.

Rheumatoid factor (RF) is a protein that can be detected in the blood of most patients with RA. It's an antibody-a type of protein that is normally produced to fight off infections. In the case of RF,however,there is no obvious infecting agents,so scientists don't know what triggers the antibody production. It is produced by lymphocytes,a type of white blood cell that collects in great numbers in the inflamed joints in rheumatoid arthritis,RF certainly plays a role in the inflammation and the damage in the joint,and elsewhere,that results. Its precise role is under study.

RF is found in the blood of about 60 % of new cases of RA,and these patients are called "seropositives" In general,patients who are "seropositive" right from the beginning are affected much more severely than "seronegatives". As the disease progresses,more and more patients change from "seronegative" to "seropositive". (The reverse is very rare.) Even then,though,up to 20 % remain RF negative.

RF is also found in other diseases,with and without arthritis,and in some normal people (much lower levels) Clearly, rheumatoid factor has a lot to do with RA,but it is not the cause.

The most typical change observed using X-rays is an erosion of bone at the margins of a joint. These changes can be seen in any joint that is inflamed long enough. While a few patients are remarably resistant to this development,70 % of those who develop erosions will show the first evedence of this within 3 years. One research study showed that thican happen by the end of the first year. This is the main reason why doctors tend to treat RA much more aggressively than they used to. Now doctors realize that it's a lot easier to prevent damage than to reverse it (We can't reverse damage)

The reasons why so few RA patients on steroids are receiving osteoporosis treatment have been unclear. Both patient factors and physician factors are felt to be involved. To address these issues, a group of investigators studied the factors associated with steroids and osteoporosis treatments and reported their findings recently in the journal Arthritis & Rheumatism².

The investigators studied the medical records of 539 patients who were treated by rheumatologists at a major teaching hospital. Of these patients, 236 (44%) were taking glucocorticoids. Of these steroid-treated patients, less than 1 in 4 were evaluated with bone density tests for osteoporosis. Patients who had taken more steroids, or had been taking them for longer, did not appear to be evaluated more frequently for osteoporosis.

Although fewer than 1 in 4 patients were evaluated for osteoporosis, a higher percentage (42%) of patients were actually prescribed medications used to treat osteoporosis. The rates of osteoporosis treatment were higher for post-menopausal women than for younger women and men. Patients who had additional medical problems beyond RA were less likely to be receiving osteoporosis treatment.

From these findings, this group of investigators concluded that rates of evaluation and treatment of glucocorticoid-induced osteoporosis remain very low. The lower rates of evaluation and treatment in men and younger women were anticipated, since little research in osteoporosis has been performed in RA patients. They hypothesized that the decreased rates in patients with other illnesses may result from resistance by both patients and physicians to add further medications to their current treatments.

These findings highlight the need for a better understanding of those factors influencing the decision to treat steroid-associated osteoporosis, as well as the need for increased awareness for appropriately applying therapy for this condition when it is warranted.