There are a number of reasons why I chose the topic of osteoporosis for my article this month. I have written many articles on osteoporosis over the past 29 years in which tremendous changes have occurred in both the diagnosis and treatment of the disease. Today I would like to focus on the latest things you should know about osteoporosis.

When I first started in the area of osteoporosis the diagnosis was made using an extremely primitive method of bone biopsy. This was a painful, time consuming and very impractical procedure. There was very little reason to do this diagnostic procedure because other than calcium and sodium fluoride, the treatment was extremely limited with very limited benefits.

However, little did I know how an area that I had chosen to be involved in over the years would become one of the most exciting areas in the field of medicine. Today we can diagnose osteoporosis with minimal time, effort and cost. Osteoporosis is by definition characterized by low bone mass and structural deterioration of bone tissue, which leads to an increased susceptibility of fractures of all the bones in particular, the hips, spine and wrist.

The diagnostic procedure of choice is bone densitometry. This is performed in about twenty minutes and the procedure can show as little as a 1% change in bone mass over one year either for better or for worse. The procedure is now readily available in multiple locations and essentially there is no excuse for every female who has reached menopause not to have a bone density in the same fashion as they would have a mammogram or a PAP smear. There are indications to do bone densitometry on women prior to menopause, for example, if they have a history of thyroid or other hormonal imbalances, if they have had an eating disorder, or if they have a strong family history or are on long-term medications which affect the bones. Males may also benefit from a bone density because osteoporosis is not a disease limited to women alone.

Males who have similar problems to the ones I have just mentioned, including hormonal issues such as thyroid disease, chronic illness and use chronic medications for other conditions, for example, corticosteroids, may also be at high osteoporosis fracture risk.

I make a plea that everybody who has a bone densitometry should have both the hip and spine measured. The use of bone density models that simply analyze a finger or a heel is a very primitive screening process. In this day and age and certainly in areas such as Miami and Aventura, there is no reason not to get a complete bone density of the hip and spine as the time and cost are minimally, different for a more complete test result.
Furthermore, it is very important to emphasize that the interpretation of the bone density is as important as the test itself. I would strongly suggest when having a bone density test that the question as to who will be doing the interpreting of the test be asked. Unfortunately, there are many very marginal reports generated which even when bone loss is present are being interpreted as within normal limits. No bone loss should be regarded as within normal limits. One bone density by itself is also really of little benefit. It is the ability to compare the changes in bone mass from year to year, which ultimately makes the most difference in deciding therapy changes. Ideally the individual reading bone densities should be certified by one of the two national bodies in technical competency of bone densitometry.

At the moment, probably close to 28 million Americans are affected by osteoporosis. This is almost one out of every 2 women over the age of 50. By the age of 75 1/3 of all men will be affected by osteoporosis. Osteoporosis causes nearly 1.6 million fractures annually resulting in cost directly and indirectly of nearly $10 billion dollars.

In my next column I will talk about the treatment of osteoporosis, but it is very important for people who have a family history, have had early menopause, who smoke tobacco regularly, drink large amount of caffeine or carbonated beverages or have small body mass, to have a bone density as soon as possible in their adult lives to try and establish their baseline for bone mass.

The truth is that individuals suffering hip fractures have a 5 to 20% greater risk of dying within their first year following an injury than other individuals in their age group. A woman’s risk of hip fracture is equal to her combined risk of breast, uterine and ovarian cancer. The point is that this can be totally prevented and ultimately osteoporosis is a disease that can be eradicated if we make an early diagnosis and aggressively treat people who have bone loss.

Author: Norman B. Gaylis, M.D., F.A.C.P., M.A.C.R.

Dr. Norman B. Gaylis

In my several years as a practicing rheumatologist, I have noticed that many people with arthritis -and sometimes, their doctors -harbor the mistaken notion that arthritis confines its symptoms to the joints alone. Certainly, the most common arthritic disorders relate to pain and swelling of the joints, but in many instances, this is just the tip of the iceberg. Extra-articular (outside the joint) manifestations of rheumatoid arthritis can, in some cases, cause extreme discomfort.

Actually, the term ‘rheumatoid arthritis’ is a misnomer. The condition should be called rheumatoid disease because of the wide range of symptoms and findings that can appear, without any apparent, direct relationship to the joints themselves. Obviously, this is because rheumatoid arthritis is not a joint disease, but is rather a generalized, inflammatory disease of the immune system, and thus can affect just about any organ system. In my view, a thorough knowledge of potential problems, no matter how rare, through consultation with a rheumatologist, will ultimately promote better health and reduced medical bills for the person with R.A.-and hopefully will not cause undue worry at every twinge or cough.

Most of the extra-articular manifestations of rheumatoid arthritis can be ascribed to either vasculitis, rheumatoid nodules, or serositis.

In vasculitis, which is an inflammation of the small blood vessels, findings may vary from skin ulceration (the

death of skin cells caused by the lack of blood flow) to inflammation of the nerve endings, which may cause weakness or abnormal sensations in the fingers and toes ranging from a pins-andneedles feeling to total numbness. In very severe cases, bleeding from the gastrointestinal tract and even stroke can result. It is important to recognize these symptoms in a very early state, because appropriate treatment can correct and very often reverse the problem.

Large rheumatoid nodules-hard clumps of tissue-are often seen on pressure points such as the elbows. While they are usually asymptomatic, though detectable, they may become painful and if the skin breaks down, or ulcerates, there rises the possibility of a secondary infection. Nodules are particularly uncomfortable when they appear over pressure points such as the buttocks.

The most serious extra-articular manifestation of R.A., however, is serositis -either pleuritis (an inflammation of the lining of the lungs) or pericarditis (an inflammation of membranes which cover the heart). The latter may result in the person having severe chest pain, fever and coughing. With the former, the clinical picture is very similar to that of pneumonia: fluid build-up, fever, coughing and, at times, the coughing up of blood.

Other manifestations of R.A. include anemia, enlargement of the lymph nodes (especially around an inflamed joint), inflammation of the eye, and, due to involvement of the joints of the larynx, hoarse voice, pain on swallowing, and shortness of breath.

Finally, in people whose rheumatoid arthritis has affected the cervical spine, neurological manifestations must he considered. Cervical spine involvement can cause severe pain in the neck and head, and weakness in the arms and legs. People with R.A. should take particular care in looking after the neck, preventing any form of trauma or whiplash injury. Many physicians advise such people to wear a cervical collar. Surgical stabilization of the spine is employed only on those rare occasions when, due to spinal cord compression, severe and definite neurological signs appear.

Fever, weakness in the extremities, chest pain-quite a catalog of symptoms. But keep in mind that such problems can also stem from everyday disorders such as a common virus, totally unrelated to your arthritis. Therefore it is very important to keep your rheumatologist informed of any change in your symptoms to help distinguish your arthritis symptoms from any other problems. For the most part, these problems are treatable, and even reversible.

Dr. Norman B. Gaylis

Scott Bridgeman has led an active lifestyle in the Miami area for the past six years. As Vocal Director for Royal Caribbean, he has supervised large cast rehearsals and choreography for review shows aboard cruise ships. The 45 year old regularly walked 4-5 miles per day until he began experiencing pain in his knees, which eventually spread to his ankles and feet. By the time he was diagnosed with Rheumatoid Arthritis (RA) thirteen months ago, he was walking with two canes and no longer able to work.

Scott’s primary physician began a course of Methotrexate, a medication commonly prescribed to reduce the pain and inflammation associated with RA. After failing to see improvement after three months, Scott was referred to Dr. Norman Gaylis, a Board Certified Rheumatologist in Aventura, Florida. Though temporarily sidelined with the effects of RA, Scott is one of the lucky ones, receiving an early referral to a rheumatologist who incorporates objective imaging in the management of this debilitating disease.

Dr. Gaylis began treating Scott with Remicade, a relatively new medication for RA given intravenously in the physician’s office, and ordered a MRI exam of his extremities. Scott recalls, “I had a previous MRI that was long, loud, and scary, so I wasn’t too excited until I saw the size of the MagneVu system. My exam was done right there in Dr. Gaylis’ office with a small MRI unit, and it was very comfortable and convenient. I met with Dr. Gaylis one week later to review the MagneVu images, and I saw for myself the bone erosions found by the radiologist. I am impressed that the physician treating me has this objective data, and I am confident about our course of treatment”. According to Dr. Gaylis, a repeat MRI will be done after six months to evaluate Scott’s response to treatment.

Scott Bridgeman has been on Remicade for seven months now, and says the difference is “like night and day”. He no longer walks with a cane, and has returned to work supervising Country, Jazz and Pop review shows for throngs of cruise vacationers. And the band plays on.

Dr. Norman B. Gaylis

This is an article that I have written many times in my life. It appears that when I look back and see what my articles reflected on the management of Rheumatoid arthritis initially twenty years ago and then more recently ten years ago. It is amazing that there was almost no change in my articles for both of those time periods. Now however, it is essentially an entirely new article.

This is because in the last years the treatment for Rheumatoid arthritis has undergone a major breakthrough. The new therapeutic discoveries have resulted in tremendous improvement for the patients suffering from Rheumatoid arthritis. The prevention of the disability and the joint damage that almost always occurred in these patients was unrealisticup until very recently. From my perspective the new treatments make it a lot more satisfying and gratifying to treat my patients with. Rheumatoid arthritis.

Rheumatoid arthritis is the second most common type of arthritis after osteoarthritis. It can affect the entire body, not only the joints. In fact it should probably be called rheumatoid disease rather than Rheumatoid arthritis. It has the potential to cause serious damage to any joint in the body and it can affect any age group. I have seen 3-month-old babies and elderly people as old as 95 years suffer from the disease.

The most, common complaint is simply pain, swelling and stiffness in the joints often with chronic fatigue. In the beginning, patients may feel that this is just simply due to over utilizing a joint. Once the condition sets in, it tends to involve more joints, be more persistent and cause more disability. This is because of the inability to perform ones basic needs at a fundamental level.

Rheumatoid arthritis is in fact, a disease of the immune system. Ironically, while the, immune system normally protects us against outside foreign bodies such as bacteria and viruses, in Rheumatoid arthritis, as in other autoimmune diseases, the immune system becomes confused. It is unable to recognize the difference between these foreign invaders and one’s own natural normal cells, and as a result, the immune system starts to attack our own natural tissues hence, the definition autoimmune disease.

Up until very recently, efforts to treat rheumatoid arthritis were at a lower level in the immune system. We obviously try to treat the pain and swelling of the joints with anti-inflammatories, corticosteroids, joint injections, which utilize cortisone-like medications, and moderate immune modulators which work to a certain extent to stop the symptoms of the disease. Medications such as methotrexate, gold and others like them certainly helped stop the symptoms of the disease but over the course of time, did not prevent progressive

damage and deformity that the disease caused.

The exciting breakthroughs, that I referred to in my first paragraph occurred approximately three years ago with the introduction of a medication known as Enbrel. Shortly thereafter, Remicade was approved for Rheumatoid arthritis and more recently a third drug, Anakinra has been introduced.

All three of these drugs, in different ways, work to not only suppress the immune system that is responsible for the pain and inflammation in rheumatoid arthritis, but also to prevent the joint damage that partially had been accepted as a normal process of the diseases progression. Studies are now showing that using these drugs not only prevent further deterioration of the joint, but in fact, reverse damage that has already occurred. From my perspective, the results of using this drugs on my patients have been dramatic. The benefit that has been provided in these patients who have previously been disabled and are now able to get out and work, play sports and perform activities that they had been unable to do for so many years is incredible.

As with any new medication, one needs to be cautious that. there are possible. side effects that we have not yet seen that we will see after long-term use. However, in the short term it would appear that the results are very dramatic. I believe any patient/individual with rheumatoid arthritis can look to the horizon with a lot more hope than ever before. Also, it is important that they be treated as soon as possible and the insurance companies should pay for these medications as soon as possible. If anybody has rheumatoid arthritis ‘and would like more information, or has rheumatoid arthritis and is not being treated with one of these new medications, I believe they should speak to their rheumatologist. They can certainly call my office to find out how to obtain one of these treatments, and if it is indeed appropriate for them or a loved one.

Dr. Norman B. Gaylis

Many people are surprised to hear that a condition, namely psoriasis, that has been historically always associated with affecting the skin only, may in fact also be one of the more common causes of arthritis. It is known as psoriatic arthritis.

This is a condition that may be seen with either the typical skin changes of psoriasis with associated pain and swelling of the joints or alternatively may in fact at times present itself with pain and swelling of the joints without the skin lesions being present. It is only after evaluating the patients fairly typical joint presentation, performing further blood tests and x-rays that the diagnosis of psoriatic arthritis is made. If the correct diagnosis is missed, the patient is given more than one diagnosis and the treatment, which in recent times has become much more beneficial and is capable of reversing the joint damage, is not utilized.

In the characteristic cases there may well be a family history of psoriasis, particularly on the male side passed from males to males. However, it is not specific to males only, as many females may also be subject to developing psoriasis and psoriatic arthritis.

The condition may occur at any age. It is often present at a very young age and usually has manifested itself by the time the patient reaches middle age. There is an association of a specific gene called HLA B27. This in particular is in the type of psoriasis that affects the spine in a similar way to ankylosing spondylitis. These patients present more commonly with neck and back pain rather than involvement of the peripheral joints.

Another form of psoriatic arthritis mimics the arthritis seen in rheumatoid arthritis and will affect primarily the joints involving the toes and the hands. Classically, these patients may develop what we call “sausage toes” as their toes swell up like small cocktail sausages and very often there will be typical nail changes in the hands and the feet which help the physician to make a diagnosis. The condition can be very painful, cause severe damage of the joints if not treated early enough and result in crippling disabilities.

The diagnosis is confirmed by typical x-ray findings. The x-rays show fairly specific abnormalities that are not necessarily seen in other forms of arthritis.

The blood tests are nonspecific which is in its own way a diagnostic feature because in conditions such as rheumatoid arthritis one will usually have positive blood tests that support the diagnosis of rheumatoid arthritis.

The joints that are involved in the hands are usually the ones closest to the nail bed, the distal interphalangeal joint as opposed to the findings in rheumatoid arthritis where you may well have more involvement of the joints further away from the nail bed. In both conditions, the distribution of the disease can be called “bilateral and symmetrical”, in other words, affecting both hands in almost a mirror image like fashion. The condition is often aggravated by stress and worsens in the presence of other co-existing diseases.

It is critical to make an early diagnosis and start conventional treatment using the so-called nonsteroidal antiinflammatory drugs. The use of these drugs still forms a basis for the reduction in pain that is required. The nonsteroidals that one would use today are the Cox-2 specific group of anti-inflammatories, which have fewer side effects than the older traditional nonsteroidal antiinflammatory drugs.

Unfortunately, these drugs do nothing to affect the course of the disease, nor do they reverse the disease. In order to do this we have used other medications. In particular, for many years we have used Methotrexate, which is a drug used for rheumatoid arthritis predominately and types of cancer. This drug in low doses does help both the skin and the joint disease in psoriatic arthritis. Careful monitoring of the patient during use of Methotrexate is needed to prevent unexpected side effects especially on the liver.

Recently, a tremendous exciting breakthrough has introduced the use of biologic anti-TNF Alpha Blocking drugs. This new group of drugs is revolutionizing the treatment of arthritis. In this category in particular, we have Enbrel, which already has been approved for psoriatic arthritis.

Remicade and Humira which are about to be approved and are currently being used in clinical research studies in our office are showing outstanding results. The use of these three drugs has allowed us to dramatically reverse both the skin changes and the joint disease. We have made many patients with psoriatic arthritis much more functional and much less symptomatic.

At this point in time I believe psoriatic arthritis is a condition that should be treated early and intensively. But it is never too late to begin therapy. We are currently conducting a clinical trial for psoriatic arthritis in our office. If you would like more information or have any questions, please don’t hesitate to call our office for an evaluation and suggestions.

Dr. Norman B. Gaylis

Polymyalgia rheumatica is an inflammatory disorder of the muscles characterized by pain and stiffness in the shoulders, neck, arms, lower back and legs. It occurs mainly in people over the age of 50 and is more common in woman than in men. Many people, when developing the symptoms initially believe that their aches and pains are simply due to a flu-like illness or possibly getting older. Unfortunately, this leads to a somewhat simple diagnosis being left untreated in many people for far longer than is necessary. It is because the symptoms are so nonspecific that the diagnosis is often times missed.

As the condition progresses, the pain including the stiffness may increase to the point where the sufferer cannot lift his/her arms or get out of a chair without great pain; evening turning over in bed or getting off the toilet seat may be very difficult and painful. At times, this condition may be associated with fatigue, depression, sweats and a total feeling of debilitation.

It is unfortunate that many times this diagnosis takes awhile to be made as it is a very simple illness that can be treated once other problems have been ruled out. A person having the symptoms I have just described should have a thorough examination to exclude other causes of muscle pain, fatigue and weakness. In particular, one should rule out more serious conditions such as malignant disorders, other arthritis disorders and an autoimmune inflammation of the muscles called polymyositis. In addition to a thorough physical exam, blood tests and x-rays may be needed to help make a diagnosis but the most pertinent blood test that helps clench the diagnosis is an abnormally elevated sedimentation rate.

The medicine used for the treatment of polymyalgia rheumatica is exclusively and specifically prednisone. This medicine is a cortisone derivative and significantly reduces inflammation in the muscles. It is the one and only drug used to treat polymyalgia rheumatica and, while there are obviously side effects-to prednisone, the therapeutic benefit that it provides compared to other treatments, makes the choice easy. The response to prednisone is dramatic and diagnostic in and of itself.

The role of the rheumatologist is to find a balance between the effects of the disease versus the potential side effects of the medication. This is done watching the course of the disease by periodically testing the blood sedimentation rate and maintaining the lowest possible dose of prednisone. The ultimate objective is to wean the patient off the medication when the disease goes into remission which usually happens 6 months to 2 years after the initial onset of symptoms.

In a small number of patients, an associated condition causing inflammation of the blood vessels on the side of the head, namely the temporal artery, can occur. This is a disease known as temporal arteritis which needs to be recognized as it can lead to blindness.

If you think you have symptoms that could be caused by polymyalgia rheumatica, please speak to your physician as this is a very treatable condition and there is no reason for patients to suffer unnecessarily from the debilitating pains and functional loss of polymyalgia rheumatica.

Dr. Norman B. Gaylis

De Quervain’s tendonitis is a fairly common condition that I see in my office. The patient presents with pain at the base of the thumb, which radiates up the forearm, in particular. The pinching or grasping the thumb or finger also aggravates the condition. Any up and down movement of the wrist causes exquisite pain in the tendon at the base of the thumb. There is appositive test known as the Finkelstein Test, which essentially stretches the tendon, and performing this test will illicit severe pain from the patient.

The treatment for this condition will consist of the use of ice, nonsteroidal anti-inflammatory drugs and rest. In the absence of this being sufficient, a local anti-inflammatory steroid injection is very effective when injected into the tendon sheath. Very rarely surgery may be indicated to reduce the pain.

Another very common condition seen in my practice is the so-called trigger thumb or finder. The patient will notice, especially in the morning, that he/she has difficulty straightening their thumb or fingers completely or will have them snap when straightened out. On examination, these patients will have tenderness in the palm side of the hand over the tendon sheath and this can be palpated. This is equivalent to having a rusty pulley where the tendon sheath runs over the bones in the hand. This results in trigger fingers or tendonitis of the fingers and thumbs. The management consists of the use of anti-inflammatory steroid injections of the flexor tendon sheath, which is very effective and very rarely, if this does not cause relief, the use of surgery is successful.

In the hand, we also see a relatively common condition called Dupuytren’s contracture, which is characterized by the thickening and hardening of the palmar fascia along the outer aspect of the hand, primarily affecting the 5th and 4th fingers. The patient will notice progressive tightening of the skin in that area with progressive difficulty in straightening the 5th and 4th fingers. This has been seen in families and is often noted in both hands. It is more commonly seen in patients with diabetes. The condition runs a variable course, sometimes remaining unchanged over a period of years while other times rapidly resulting in severe deformity of the hand. The treatment depends on how rapidly the condition is progressing.

Initially, treatment with heat, stretching exercises and the use of protective gloves is helpful. At times, if the condition progresses too rapidly, a surgical release of the fibrous tissue causing the contraction is necessary.

Dr. Norman B. Gaylis

What is Osteoarthritis? How does it happen? Why you? How will it affect your daily life?…

…If you recently learned that you have Osteoarthritis, these are probably some of the questions you have been asking. In this column I will try to help you understand Osteoarthritis and learn to live with it. The most important thing for you to understand is that while Osteoarthritis is not curable, it is very treatable and, in most cases, there is no reason for the condition to significantly lower your quality of life.

Osteoarthritis is a condition that results when the smooth lining that covers the bones and joints, the cartilage, starts to wear out. When this happens, bones rub against bones. This friction can also cause small spurs to form within the joints. As a result of this process, cartilage, our body’s shock absorber, is destroyed and pain and discomfort occur when moving joints. The natural reaction to this pain is to protect one’s joints by not moving them. This, in turn, weakens the muscles that support the joints.
Osteoarthritis is prevalent among people over the age of 60 because of the wear the body is subjected to over the years. The condition can also occur in younger people. Between 30 and 40 million people in the U.S. today suffer, from Osteoarthritis.

Osteoarthritis and its symptoms vary for each individual. The pain can be mild or very severe. It may come and go. Some people may be disabled by it, while others may feel only a few twinges during damp, humid or cold weather. The joints most commonly effected by Osteoarthritis are those subject to the most wear and tear during our lives. This includes all weight bearing joints, particularly the hips, knees and feet. Osteoarthritis often effects the thumb, the most actively used joint in the body. The spine, especially the back and the neck are also commonly affected by the condition. Osteoarthritis of the spine is usually a result of bad body mechanics and bad habits, including watching television in bed, sleeping on one’s stomach, wearing the wrong prescription lenses, being overweight and lifting or bending over without first bending at the knees.

There is a hereditary form of Osteoarthritis which effects the joints at the ends of the fingers causing swelling and deformities of the knuckles. These deformities are called Heberden’s Nodes.

Osteoarthritis develops slowly and worsens over time. Therefore, it is important to diagnose and treat the condition early, to eradicate causitive factors and to begin therapy to prevent long-term problems.

Diagnosis begins with a physical examination by a specialist in the field of Arthritis. At times certain blood tests are ordered to rule out other Arthritic conditions. X-rays of the involved joints are usually suggested and fluid from the joints is examined. Once the diagnosis is established, the treatment goals are to ease pain and discomfort, reduce or prevent disability and help the patient to continue his or her routine activities as independently as possible. It is important for the patient to recognize that treatment of Osteoarthritis does not rely on drugs alone. Anti-inflammatory medications and aspirin-like drugs can be very helpful in reducing symptoms, but they do not correct the problem, nor do they prevent long-term disability. When I see a patient for the first time my primary goal is to educate him/ her as to why Osteoarthritis developed and how to eradicate those reasons. For example, someone who has osteoarthritis of the hips and knees cannot walk five miles per day. That is not to say that exercise is no good. Once the inflammation is reduced with the aid of medication, exercise is very important to strengthen the muscles that support the joints. In general, non-weight bearing or non-active exercises are suggested. The ideal exercises are swimming, riding a bicycle or range-of-movement exercises without any need to prevent overuse of painful joints. Therapies such as hit, ultrasound and massage may also help to reduce the pain and disability of Osteoarthritis. While all of these therapies can provide symptomatic relief, it is important to remember that they will not cure Osteoarthritis.

There is no “magic formula” which a physician can prescribe to suit all Osteoarthritis patients. A blend of rest, exercise, therapy and medication must be tailored for each individual patient according to his or her own special needs and lifestyle. I strongly emphasize the need to sit down with your doctor and explain your personal circumstances and needs. Together you will develop the best therapeutic program for you.

In most instances, if you are getting good medical advise, taking your medications as directed and following your rest and exercise program, you will be able to enjoy a fairly comfortable lifestyle and slow the progressive destruction of the disease. Of course, if you seek a physician’s help after you have had Osteoarthritis for many years there may be irreversible damage done to the joint. At that point, one must consider other medical options, such as joint replacement surgery. Total joint replacement has been performed with grit success on the hip and to a lesser extent on the knee, shoulder and small joints of the hand and foot. I generally recommend that surgery be performed only after all other forms of therapy have been exhausted. This is not because that surgery will not be successful, but simply, because the replacement joint has a limited life span.

I want to make a plea to you to avoid using unproven drugs or following the advise of untrained friends and neighbors who recommend various miracle cures such as D. 4. S. D.. (v hr*+^ 4e .. devil’-, claw.-.snake venom and the like. Such “cures” can actually do more harm than good simply because they delay participation in more valid forms of therapy.

Despite claims to the contrary, there is no known diet that will cause, prevent or cure Osteoarthritis. The best dietary advice I can offer is that a well-balanced diet is important for all physical fitness and that one can eat basically anything in moderation. Remember, excess weight puts stress on the joints and that stress can accelerate pain and Osteoarthritis.

While Osteoarthritis is a painful and sometimes crippling disorder, most individuals should be able to live fairly normally and comfortably with some form of therapy. The condition may slow you down once in a while, you may even need to change the way you do certain things, but by working hard and being properly motivated, you should be able to keep up with what is important to you. With medication, rest and exercise, most of my patients are able to control their symptoms and continue with most, if not all of their daily activities and live full and productive lives.

If you have any questions about Osteoarthritis, feel free to contact me through this column. Until next time, when I will discuss Rheumatoid Arthritis, try to stay as “loose” as possible!

Dr. Norman B. Gaylis

I talked about osteoarthritis in my last article, how it presents itself and how it is the most common form of arthritis affecting 25 to 30 million Americans. In fact, 14 million Americans alone suffer from osteoarthritis of the knee. There have been some major breakthroughs in the medical treatment of osteoarthritis in the last few years. I would like to discuss the most common forms of treatments used today but certainly not all of the types of treatments.

Aspirin-like anti-inflammatory drugs, the so called nonsteroidal anti-inflammatory drugs, were the most commonly used drugs to treat osteoarthritis for many years. Unfortunately, while they were effective, they had a very high incidence of gastrointestinal side effects including peptic ulceration and bleeding. We are very fortunate in that, in the last few years, we have had a new group of (rugs developed, the so called COX-2 specific inhibitors. This group of drugs, which includes Celebrex and Vioxx, is able to provide the same anti-inflammatory benefits of the older group of drugs without causing as many gastrointestinal side effects.

As we move towards the future, these medications are going to be progressively refined to become more effective and more tolerable. It is my, belief that, at this point it time as we enter a new millennium, there is no reason not to use this new COX-2 grout of anti-inflammatory drugs as the basis of medical therapy for osteoarthritis.

There are a number of over the counter medications available for the treatment of arthritis. Caution should be exercised in treating oneself because the use of over-the counter anti-inflammatory drugs is fraught with potential problems, in particular, because of the side effects that these drugs can cause. I would urge all of you thinking about treating yourselves, to please speak to your physician before going tout and buying an over-the-counter medication which, when taken in accumulative dosages, can be extremely toxic. My personal thought is that the availability of these drugs over the counter does the patient population a disservice because of the high number of side effects that occur when these drugs are taken in an uncontrolled situation.

I should also mention the use of chondroitin sulfate and glucosamine as one of the most recently touted breakthroughs in the treatment of osteoarthritis. There is some marginal anti-inflammatory benefit and improvement of symptoms in patients with osteoarthritis who use these substances. It seems in the early cases of osteoarthritis where the pain and stiffness have just developed in the joints, the use of chondroitin sulfate and glucosamine may have a beneficial effect in reducing discomfort as well as in prevention further progression of the disease. However, in the majority of cases, the improvement is minimal and does not really benefit the more advanced cases of osteoarthritis.

For all of the above therapies to work, the patient needs to have in sight into the cause of their problems. For example, if there is osteoarthritis of the hip or the knee, walking may be aggravating the problem in their joints and, therefore, should be avoided. Likewise, any aggravating factor that may affect the involved joints in a negative way needs to be reversed or discontinued to allow for the best outcomes. Also, patients who have a weight problem will certainly cause stress to their weight bearing joints over the period of a life time and, therefore, treating arthritis in the knees and the hips involves getting the patient to try and keep their weight at an acceptable level for themselves.

In conclusion, osteoarthritis is a very treatable and, at times, preventable disorder. If anyone has pain, stiffness or swelling of any of their joints, please see your physician as soon as possible as the longer it takes to be treated, the more difficult it is to have a positive outcome.

Steven G. Ostrov, Robert M. Quencer, Norman B. Gaylis, Roy D. Altman

Cerebral Atrophy in Systemic Lupus Erythematosus:
Steroid- or Disease-Induced Phenomenon?

Thirty-two patients with systemic lupus erythematosus were evaluated clinically and with computed topography in order to determine whether the occurrence of cerebral atrophy in systemic lupus erythematosus was due to the steroid therapy or the cerebral manifestations of the disease itself. Of these patients, 14 had central nervous system manifestations of the disease (lupus cerebritis) and 12 of the 14 were on long-term steroid therapy. Eighteen patients had no clinical evidence of lupus cerebritis and all were on long-term steroids. Of the 14 lupus cerebritis patients, 10 showed moderate cerebral atrophy, four minimal atrophy, and none were normal. Of the 18 patients without lupus cerebritis, none had moderate atrophy, six (33%) showed minimal atrophy, and 12 (67%) had normal CT scans. This data suggest that it is the lupus cerebritis rather than the steroid therapy that is responsible for the moderate cerebral atrophy. In patients suspected of lupus cerebritis, steroids should not be withheld because of concern for steroid-induced atrophy. Rather, the dose pay need to be increased.

A significant number of patients with systemic lupus erythematosus (SLE) have central nervous system (CNS) involvement, which is expressed in many ways, including infarction, intracerebral hemorrhage, aneurysms, cerebral atrophy, aseptic meningitis, pseudotumor cerebri, convulsions, cranial nerve palsies, visual loss, intractable headaches, peripheral neuropathy, tremor, chorea, transverse myelopathy, organic brain syndrome, depression, and psychosis [1 -9]. We noticed a high incidence of cerebral atrophy on computed topographic (CT) scans obtained in patients with SLE. Since these patients are frequently treated with corticosteroids, it was unclear in many cases whether the cerebral atrophy was secondary to the systemic disease process or to the long-term steroid treatment. Therefore, we reviewed a large group of SLE patients to determine whether the cerebral atrophy was related to their primary disease or to its treatment.

Subjects and Methods

Clinical and CT evaluations were undertaken of 32 patients who met at least four of the criteria for SLE established by the American Rheumatism Association [10]. The 28 females and three males were 14-51 years old (average age, 28 years).

Axial CT scans were obtained on the GE 8800 and EMI 1010 units. The scans were classified as normal, minimal, or moderate atrophy. Minimal cerebral atrophy was defined as focal or diffuse sulcal widening without ventricular enlargement. Moderate cerebral atrophy was defined as sulcal widening with lateral ventricular enlargement. Ventricular enlargement was determined by the criterion of Evans [11 ], using the ratio of the maximum transverse diameter of the frontal horns to the greatest internal transverse diameter of the skull. Although this criterion was originally developed with pneumoencephalography, later authors [12, 13] have shown a direct correlation between ventricular size on pneumoencephalography and CT.

The clinical cerebral manifestations of SLE were termed ”cerebritis” and included any abnormality of central neurologic function with a change from the prior state in the absence of other possible etiologies. Patients with clinically active renal disease or hypertension were not included. Longcterm steroid therapy was defined as continuous prednisone treatment for 6 months or longer or greater than 40 mg/day for at least 3 months.

Results

Of the 32 SLE patients, 14 had clinical lupus cerebritis, and, of these, 12 were on long-term steroids. The two not on steroids were seen with lupus cerebritis and were placed on steroid therapy following CT. The 18 patients who had no clinical evidence of lupus cerebritis were all on long-term steroid therapy.

Of the 14 patients with lupus cerebritis, three had normal CT scans at the time of their initial neurologic signs, but each eventually showed moderate atrophy. Seven other patients in the cerebritis group had moderate atrophy at the time of the initial CT scan, yielding a total of 10 patients with moderate cerebral atrophy. Four cerebritis patients had minimal atrophy. None of the patients with lupus cerebritis had normal CT scans (table 1).

In the group of 18 patients without lupus cerebritis, 12 had normal CT scans, six showed minimal atrophy, and none had moderate atrophy. Statistical analysis of the significance of the difference between the two groups revealed a p value of less than 0.001. None of our 32 patients had CT evidence of hemorrhage or areas of diminished attenuation suggestive of a cerebral infarction.

The number of years of steroid therapy was essentially the same in the cerebritis and noncerebritis groups (average, 2.9 and 3.1 years respectively). The cerebritis group received an average of about 19% more corticosteroids than the noncerebritis group and had SLE an average of 2 years longer (6.8 and 4.8 years, respectively).

Table 1: Steroid- vs. Disease-Induced Cerebral Atrophy with SLE
CT Results	No. Patients
	Cerebritis		Noncerebritis (All Steroids)
	Steroids	No Seroids
Normal	0	0	12
Minimal atrophy	4	0	6
Moderate atrophy	8	2	0
Totals	12	2	18

Discussion

In recent years there has been debate over the significance of corticosteroid therapy versus cerebritis as a cause of cerebral atrophy in patients with SLE [6, 7, 9, 14]. Momose et al. [14] showed a high degree of cerebral and cerebellar cortical atrophy in patients with endogenous Cushing syndrome. Bentson et al. [9] noted that cerebral atrophy in a patient with SLE did not imply diffuse microinfarcts, “since the appearance may be related to the prolonged use of steroids.” Gonzalez-Scarano et al. [7] suggested that the association of sulcal enlargement and lupus cerebritis may be of importance in confirming the clinical diagnosis of lupus cerebritis and in following the course of the disease. No authors have related the degree of cerebral atrophy with the presence of lupus cerebritis. Neither has there been an attempt to use the CT demonstration of cerebral atrophy in the management of patients with SLE.

In our study, which sought specifically to address these two important issues, we found that moderate cerebral atrophy was seen only in patients with lupus cerebritis (71 %). In the noncerebritis patients, the CT scans were either normal (67%) or showed minimal atrophy (33%). Since nearly all the patients in both the cerebritis and noncerebritis groups had been on long-term steroid treatment, we concede that minimal atrophy may be related to the corticosteroid therapy, but believe that moderate atrophy is related to the disease process itself. The relatively small excess of corticosteroids (19%) received by the cerebritis patients could not account for the moderate atrophy demonstrated in 71 %. Although the length of disease may influence to some degree the development of cerebral atrophy, the facts that there were some cerebritis patients with moderate atrophy who had had SLE for a short time (less than 4 years) and that there were noncerebritis patients with minimal atrophy who had had SLE for a long time (up to 15 years) indicate that the important factor in the eventual development of moderate atrophy is cerebritis per se rather than the duration of systemic disease.

Previous authors have proposed mechanisms to explain the minimal atrophy observed in patients on steroid therapy. Heinz et al. [15] stated that protein catabolism with resultant decrease in intravascular colloid osmotic pressure can cause the movement of fluid from the intravascular to the extravascular spaces, thus expanding the subarachnoid spaces, while Bentson et al. [9] mentioned that chronic steroid use may result in relative cerebral dehydration, possibly secondary to alterations in vascular permeability. While we agree that these theories can explain the presence of the minimal atrophy that we observed, the moderate atrophy in our cerebritis cases requires an alternate explanation. We believe that moderate atrophy in lupus cerebritis may be accounted for by small vessel vasculitis or perivasculitis that results in a decrease of the neuronal population. Although we do not have histologic proof of this assumption, moderate cerebral atrophy was seen only in patients with clinical central nervous system abnormalities.

Acceptance of this interpretation of the data could alter the therapeutic approach to patients with lupus cerebritis. Cerebritis should be given diagnostic preference in a lupus patient with CNS symptoms and moderate cerebral atrophy. It may warrant increasing the patient’s steroid dose. On the other hand, in a lupus patient exhibiting similar symptoms but without moderate atrophy, the CNS features cannot definitely be ascribed to SLE. Change in steroid treatment may be less imperative.

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