Doctor...What Are The Effects Of Alcohol On Rheumatoid Arthritis?

Could a glass of wine at dinner time be the next major arthritis breakthrough?

Possibly... according to a recent Swedish study. A diet of 10% ethanol had a protective effect on mice that would otherwise have developed collagen-induced arthritis (CIA), Swedish researchers report in Proceedings of the National Academy of Sciences. CIA is often used as an animal model of human rheumatoid arthritis (RA.)

Andrej Tarkowski, MD, the senior author and a faculty member in the department of rheumatology and inflammation research, Goteborg University, in Sweden, stated that the primary finding was that, in male mice, long term consumption of 10% ethanol delayed the onset and progression of CIA.

The underlying mechanism appears to be a reduction in inflammation due to decreased NF-kB activation (a primary inflammatory pathway) caused by upregulation- or increased production -of testosterone secretion.

The research team fused a CIA model in mice by immunizing male DBA/1 mice with collagen type II (CII). To determine whether drinking ethanol has any impact on the development of CIA, the mice were provided with either 10% ethanol or water alone to drink. Mice were sacrificed after 5 to 6 weeks. All four paws from DBA/1 mice were sectioned, stained, and examined for inflammation of the joint including damage to the joint lining and erosion of bone and cartilage.

The investigators report that development of arthritis due to inflammation was markedly reduced in the ethanol-drinking mice. Ethanol had no such effect on mice with arthritis induced by injection with a mixture of four monoclonal anti-CII antibodies. "These data suggest that ethanol affects the start or initiation rather than the perpetuation of immune responsiveness during CIA," mentioned the researchers.

Joints from the water-drinking mice developed frequent bone and cartilage erosions. Those from the ethanol-drinking mice were "histologically ...intact," meaning no significant damage occurred. In addition, ethanol prevented the arthritis-induced loss of bone mineral density associated with CIA.
"The major surprise in this study was the outstanding effect of ethanol on saving cartilage and bone, suggesting that apart from regulation of inflammatory mediators, matrix metalloproteinases (i.e., tissue destroying enzymes) might be a direct target for ethanol," commented Dr. Tarkowski.

Dr. Tarkowski cautions, "This dose of ethanol was chosen for mice with an exact knowledge regarding the toxicity. This was further confirmed by intact liver function at the end of experiments. In contrast, exchanging water for 10% ethanol in humans eventually will lead to liver disease (cirrhosis). Thus, the optimal dose of ethanol in the human setting to prevent/delay RA is presently unknown. For practical purposes, one could speculate on the use of doses of ethanol similar to those sometimes suggested for prevention of cardiovascular diseases--i.e., something in the range of 1 to 2 glasses of wine per day," he suggested.

"We are presently analyzing whether female mice with arthritis have the same effect from ethanol.
The investigators also compared castrated to intact male mice and found that mice drinking 10% ethanol had significantly elevated levels of testosterone and decreased levels of IGF1 and cortisol. "These observations, considered together with the cellular anti-inflammatory properties of testosterone that lead to a decrease of NF-kB activation, point to testosterone as a potential link mediating the anti-inflammatory effects of ethanol."

So... what are the implications for patients with RA?

The first is that perhaps, a prescription of a glass or two of wine a day is not necessarily bad.

However, there are cautions. The first is that patients who are taking methotrexate need to absolutely limit their consumption of alcoholic beverages because of the danger of developing cirrhosis. Second, patients taking non-steroidal anti-inflammatory drugs are at increased risk for developing stomach ulcers and alcohol increases that risk.

(Jonsson I-M, Verdrengh M, Brissiert M, et al. Ethanol prevents development of destructive arthritis. PNAS. 2007;104:258-263)

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland (http://www.aocm.org/). He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: Arthritis Treatment

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New Guidelines For Osteoarthritis - What Do They Mean?

Osteoarthritis is the most common type of arthritis and the leading cause of chronic musculoskeletal pain and limited mobility in older people worldwide.

It is a disease that causes cartilage in weight-bearing areas such as the neck, low back, hips, knees, and the base of the thumbs to deteriorate and wear away.

Since it is so common, many treatments have been advocated. Some treatments work and others don't. However, the sheer number of claims of efficacy can be overwhelming to both physicians as well as patients.

Guidelines are often created by various organizations in medicine to help both the patient as well as the physician arrive at decisions. These guidelines are formulated to let the physician and patient know what types of diagnostic criteria or treatment methods have enough evidence behind them to be recommended for use.

A new set of treatment recommendations for knee and hip osteoarthritis have been released by a scientific organization, the Osteoarthritis Research Society International (OARSI).

These are evidence-based recommendations - meaning they have the power of scientific data backing them up. A subcommittee of OARSI was given the task of coming up with specific guidelines to help clear the confusion and clutter surrounding what really works and what doesn't for osteoarthritis of the hip and knee.

The goals of the committee were (1) to review all of the published national and international treatment guidelines together with the more recent evidence from clinical trials and (2) to produce a single set of up-to-date, evidence-based recommendations for the worldwide treatment of knee and hip osteoarthritis.

The guidelines were accompanied by "grades", ie. percentages, to indicate how much evidence was behind each criterion.

The first of OARSI's 25 evidence-based recommendations was that that best treatment requires both non-drug and drug modalities. The remaining 24 recommendations fall into three categories - non-drug, drug, and surgical.

The following are the recommendations:

Non-drug - These 11 recommendations include education and self-management (97%); regular telephone contact (66%); referral to a physical therapist (89%); aerobic, muscle strengthening and water-based exercises (96%); weight reduction (96%); walking aids (90%); knee braces (76%); footware and insoles (77%); thermal modalities [heat or cold] (64%); transcutaneous electrical stimulation (58%); and acupuncture (59%).

Drug - These eight recommendations include acetaminophen (92%); non-selective and selective oral nonsteroidal anti-inflammatory drugs (NSAIDs)(93%); topical NSAIDs and capsaicin (85%); intraarticular injections of corticosteroids [joint injections of "cortisone"](78%); intraarticular injections of hyaluronans [joint injections of various lubricants](64%); glucosamine and/or chondroitin sulphate for symptom relief (63%); glucosamine sulphate, chondroitin sulphate and/or diacerein for possible structure-modifying effects (41%); and the use of weak opioids and narcotic analgesics for the treatment of refractory pain (82%).

Surgical - These five recommendations include total joint replacement (96%); unicompartmental knee replacement (76%); osteotomy and joint preserving surgical procedures (75%); joint lavage and arthroscopic debridement in knee OA (60%); and joint fusion as a salvage procedure when joint replacement had failed (69%).

According to Dr. Francis Berenbaum, president elect of OARSI and a faculty member in the Department of Rheumatology at Pierre & Marie Curie University, APHP Saint-Antoine Hospital in Paris, "Our goal was to make these guidelines as simple as possible so that healthcare providers could determine which therapies would be most useful for an individual patient."

In recent years, there has been a decline in the use of NSAIDs by physicians because of concerns related to the potential for causing gastrointestinal side effects and the possible cardiovascular risks associated with these drugs.

However, OARSI committee members found that NSAIDs are often effective pain relievers and their short-term use should be considered on a case-by-case basis and not as a long-term option.

The guideline committee was made up of experts from six countries, including 11 rheumatologists, two primary care physicians, one orthopedic surgeon, and two experts on evidence-based medicine.

While these guidelines are helpful in regards to current therapies, there are weaknesses.

For example, research into osteoarthritis is constantly advancing and newer types of therapies exist for which there is still insufficient evidence to say whether they are effective or not.

An illustration might be cold laser where insufficient numbers of well-controlled clinical trials exist to say for sure whether it works and how well.

Second, one therapy, arthroscopic debridement has much evidence supporting its use, yet payers such as CMS (Medicare) will not pay for it citing the very few studies that don't show benefit as their evidence.

Also... the guidelines are just that. They don't say whether a given treatment will work for a specific individual.

Finally, there are cutting edge therapies such as stem cells and the use of platelet rich growth factors which show a lot of promise but for which it is much too early to know how effective they will be.

So... stay tuned!

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland ( http://www.aocm.org ). He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: Arthritis Treatment

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Stem Cell Treatment For Osteoarthritis - What is it All About?

While many new and amazing therapies for rheumatoid arthritis have been developed in recent years, very little progress has been made in the treatment of osteoarthritis.

Osteoarthritis (OA) is the most common form of arthritis and affects approximately 30 million Americans. OA is a disease of articular cartilage, the gristle that caps the ends of long bones. Cartilage has both gliding as well as shock absorbing properties.

It is this flexibility of function that enables a joint to work properly.

Normal cartilage is composed of cells called chondrocytes that sit inside a matrix consisting of collagen and glycosaminoglycans... much like grapes inside Jello.

Osteoarthritis develops when the chondrocyte begins to malfunction and starts to produce destructive enzymes. At the same time water content inside the matrix changes making it more susceptible to stress. Small cracks, called "fissures" develop. Also, local inflammation involving the lining of the joint- called the synovium- begins. The end result is a gradual and premature wearing away of cartilage.

This process is most apparent in weight-bearing areas such as the neck, low back, hips, and knees.

Current approaches to the treatment of OA involve the use of analgesics (pain-relieving medicines), non-steroidal anti-inflammatory drugs (NSAIDS), physical therapy, proper weight management, exercises, injections of steroids, injections of viscosupplements (lubricants), and surgery.

While many of the above treatments help relieve pain, they do nothing to prevent cartilage loss... and more importantly, they do nothing to restore cartilage.

Orthopedic techniques such as chondrocyte transplantation and cartilage plug surgery are helpful for discrete, relatively small areas of cartilage loss but are generally reserved for younger people who have had traumatic injuries to cartilage. But what about the older person who suffers from osteoarthritis?

In recent years there has been much interest in the role of regenerative techniques to rebuild cartilage.

The topic of much study are stem cells. Stem cells are pluripotential cells, meaning they are cells that can become any kind of tissue, given the right stimulus. Stem cells can be obtained from embryonic tissue, which is a source of much controversy. Or they can be obtained from adults. The adult body has a small number of stem cells in many tissues. They are activated by injury or illness. Adult stem cells, as a rule, do not have the ability to differentiate as well as embryonic stem cells.

However, in recent years, techniques have been developed to harvest mesenchymal stem cells- stem cells found in the bone marrow. These mesenchymal stem cells cells, when properly prepared and concentrated, have the ability to differentiate into cartilage and bone.

Stem cells are harvested from the the patient's iliac crest bone marrow using local anesthetic and a special type of biopsy needle. The stem cells are then specially concentrated.

After the stem cells are prepared, the physician, using ultrasound guidance and local anesthetic, finds the area of arthritis involvement and irritates the area using a special large needle. This irritation is important because it initiates an inflammatory reaction which is the prelude to healing and regeneration. The areas that are irritated include the capsule, tendon insertions, pericapsular soft tissue, as well as cartilage.

Blood is drawn from the patient and spun in a special centrifuge in order to obtain platelet rich plasma. Platelets are blood cells that contain multiple growth and healing factors.

Once the irritation has been completed, stem cells as well as the platelet rich plasma are injected into the prepared area.

The growth factors within the platelet rich plasma act on receptors found on the surface of stem cells and cause the stem cells to differentiate and multiply.

The end result is cartilage regeneration as well as lessening of pain. While the data is preliminary, the early results appear to be very promising.

Nathan Wei, MD, FACP, FACR is a nationally known rheumatologist. For more info: Arthritis Treatment and Tendonitis Treatment Tips

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What is "PRP" and How Does it Work - Will it Help Me?

One exciting approach to wound healing, variously described as "regenerative medicine" or "tissue engineering" has been the use of platelet rich plasma (PRP) either alone or in conjunction with stem cells.

PRP got recent notoriety when it was mentioned that Hines Ward, the Pittsburgh Steeler's star wide receiver had received this treatment for an injury prior to the Super Bowl.

As it turns out, PRP has been used for quite some time now, particularly at our center, to help accelerate the healing of conditions such as tendonitis, ligament strains, muscle strains, arthritis, synovitis (inflammation inside the joint), and cartilage defects.

Platelet rich plasma is employed as a matrix graft, often referred to as an autologous tissue graft. This platelet-rich plasma (PRP) matrix is defined as a "tissue graft incorporating autologous growth factors and/or autologous undifferentiated cells in a cellular matrix where design depends on the receptor site and tissue of regeneration." (Crane D, Everts PAM. Practical Pain Management. 2008; January/February: 12- 26) 2008)

The reason PRP is so useful is that platelets, which are a normal blood cell, contain multiple growth factors that stimulate tissue growth. In particular, PRP stimulates the growth of collagen which is the main component of connective tissue such as tendons and cartilage. These factors include transforming growth factor-Β (TGF-B), fibroblast growth factor, platelet-derived growth factor, epidermal growth factor, connective tissue growth factor, and vascular endothelial growth factor.

These growth factors recruit undifferentiated cells to the site of injury and stimulate their growth. Another constituent of platelets, stromal cell derived factor I alpha causes newly recruited cells to adhere to the area.

In addition, when used with stem cells harvested from the patient's bone marrow, PRP "fires off" the stem cells to multiply quickly. This inflammatory response is what drives healing.

To use an analogy, PRP- particularly when used in conjunction with stem cells- sends the healing process into "warp drive."

PRP needs to be prepared in a way to ensure a maximal amount of platelets along with a high concentration of growth factors. Obviously, the more growth factors that can be delivered to the site of injury, the more likely tissue healing takes place.

This regenerative approach is diametrically opposite to the traditional method of healing tissue injuries which has been to use non-steroidal-anti-inflammatory drugs as well as steroid injections, which, while reducing inflammation, also markedly impede the healing process.

PRP is often used in conjunction with percutaneous tenotomy. This is a procedure where there is purposeful needle irritation of the affected area using ultrasound guidance after which PRP is then slowly injected into the site.

The use of diagnostic ultrasound has revolutionized the field of musculoskeletal medicine in allowing tissue healing procedures like tenotomy which often prevent the need for open surgical procedures with their attendant morbidity and mortality. In the successful use of PRP and/or stem cells in tissue engineering, is imperative that diagnostic ultrasound be used to guide the "needling" as well as the placement of the PRP.

The PRP is prepared by drawing 20 cc's of whole blood from the patient and then spinning the blood in a special centrifuge that layers out the platelets. This 20 cc's of whole blood generally yields about 2-10 cc's of platelet rich plasma.

Contraindications to the administration of PRP include platelet dysfunction, low platelet count, infection, anemia.

The average number of treatments required is two to three separated by four to eight week intervals. The need for another treatment can be determined by using Doppler ultrasound to see if the area remains inflamed (good) or has gone "cold" (bad).

Prior to a PRP procedure, a patient needs to hold their non-steroidal anti-inflammatory drugs for at least 3-4 days. They may resume them one week after. Also, patients with rheumatoid arthritis should hold their methotrexate for at least one week before and one week after the procedure. Patients on biologic medicines may need to hold their medicines longer, particularly when it comes to adalimumab (Humira), and infliximab (Remicade) because of the long half life of these drugs.

Following the procedure, patients must rest the affected area to prevent leakage of the PRP from the site.

Pain at the injection site is common for a 1-2 day period following the procedure.

For more information on platelet rich plasma (PRP) and stem cells, call the Arthritis Treatment Center at (301) 694-5800

Nathan Wei, MD, FACP, FACR is a nationally known board-certified rheumatologist with extensive experience in the use of platelet-rich plasma and stem cells. For more information: Arthritis Treatment and Arthritis Treatment Center

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Why is Osteoarthritis So Darned Hard to Treat?

Recent research efforts from both Northwestern University in Chicago and the University of Pittsburgh Medical Center have described work on the use of a new nanofiber gel that promotes cartilage growth in joints.

The material is injected into the damaged joint and stimulates bone marrow stem cells to produce natural cartilage.

The nanofibers allow stem cells from bone marrow to produce cartilage containing type II collagen and repair a damaged joint.

Type II collagen is the major protein component in articular cartilage, the gristle that caps the ends of long bones within a joint.

This is distinctly different from the Type I collagen produced as a result of another procedure used to heal cartilage damage called microfracture. Microfracture is a surgical procedure where small holes are drilled into the bone beneath the area of cartilage damage. This leads to bleeding from the bone marrow.

Ostensibly, stem cells from the marrow create new cartilage.

Microfracture causes the production of cartilage having predominately type I collagen. Type I collagen is the type found most commonly in scar tissue.

Type II collagen is weaker than Type I collagen and probably does not hold up as well. This may be one explanation why microfracture surgery has not been as successful as first thought.

Another type of procedure called autologous chondrocyte transplantation has also been used. In this procedure, cartilage is harvested from a non-weight-bearing part of the joint. The cartilage is then specially treated in a laboratory so that individual cartilage cells multiply. The cartilage cells are then put back into the joint under a small flap of tissue that is sewn into place. Recovery is long and the cartilage produced also appears to contain mostly Type I collagen.

Mosaicplasty where multiple cartilage plugs are fitted into the cartilage defect has also been used. Results are mixed.

Stem cell treatment has the appeal of being less invasive and requiring less recovery time. However, controlled data is nonexistent. Supportive evidence consists of case studies and small numbers.

One issue that has plagued researchers and clinicians alike is the mechanical forces present within weight-bearing joints such as the hip and knee.

When asked his opinion regarding the nanofiber issue, Dr. William Arnold, a Chicago-based rheumatologist stated, "This isn't the first 'cartilage growth stimulator'...and it won't be the last. There's no way that cartilage regrows on the surface of the medial femoral condyle (of the knee) without a mechanical correction accompanying the "regrowth". The shear compression forces in the medial compartment are formidable... and would quickly chew up any flimsy cartilage surface beginning to grow on the surface of the condyle."

Dr. Nathan Wei, a rheumatologist specializing in stem cell treatment for osteoarthritis, concurs with Dr. Arnold to a point. He states, "The impact loading forces on weight-bearing joints such as the knee and hip are one thing to contend with but with the hip there is the added stress of rotational movement and in the knee there are gliding and rotational forces to deal with as well."

He argues though, "Animal models have demonstrated that stem cell procedures are effective. And while human data is sparse, early evidence supports further investigation... I do agree that mechanical forces need to be dealt with through various means in order to allow stem cells to 'take'. We are currently attempting to address this issue. Our results so far are very encouraging."


He argues though, "Animal models have demonstrated that stem cell procedures are effective. And while human data is sparse, early evidence supports further investigation... I do agree that mechanical forces need to be dealt with through various means in order to allow stem cells to 'take'. We are currently attempting to address this issue. Our results so far are very encouraging."

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland. For more info: http://www.aocm.org and Arthritis Treatment

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Remission in Rheumatoid Arthritis - Is it Possible?

Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis. It is a chronic, autoimmune driven, systemic disease that affects approximately two million Americans.

While it is obviously a painful debilitating condition, RA also negatively impacts the quality of life and reduces functionality in affected individuals.

The goals of treatment are pretty straightforward. They are to reduce pain and inflammation, prevent further deterioration of joint damage, and restore functional capacity.

The advent of newer biologic drugs has enabled rheumatologists to offer remission- the absence of disease- to their patients with RA.

Aside from the symptomatic relief and restoration of function, there are other significant benefits of remission induction, They are extension of life span, since several studies have correlated disease activity with structural damage and structural damage with reduced functional disability status and reduced functional disability with shortened lifespan.

Also, the reason for this shortened lifespan appears to reside not only in functional status, but also in the accelerated cardiovascular disease that patients with active RA have.

So, it is imperative that patients with RA undergoing treatment be monitored to ensure they achieve remission.

The problem is that there are so many methods of disease activity measurement and there is no consensus among rheumatologists as to which measurement tool is the best.

Nonetheless, the two most common methods for quantifying disease activity are the American College of Rheumatology criteria and the Disease Activity Score. An additional measurement device is the Health Assessment Questionnaire (HAQ) which is designed to look at functional status only.

Each of these tools has its strengths and weaknesses.

It is clear from a number of studies that remission has many definitions, depending on who you talk to. It is also pretty clear that even a low grade amount of disease can still lead to poor outcomes because joint damage is still progressing and that eventually leads to long term disability.

Another problem is that the measurement devices mentioned above are cumbersome and difficult to routinely use in an office or clinic setting. Also, consistency of measurement can be an issue. What is a "1" to one rheumatologist may be a "2" to another.

On the other hand, biologic drugs are extremely expensive and many physicians as well as patients are not easily swayed by long term data but are more concerned with how they feel and function in the moment. This becomes even more of an issue as some rheumatologists offer "drug holidays" to patients who are "in remission."

A recent study from the Annals of Rheumatic Disease studied a group of patients with severe RA who had remission established with infliximab (Remicade) and then had the drug discontinued and still remained in remission.

The measurement devices they used were the DAS 28, x-rays, and HAQ. They concluded, "that more than half of patients who maintained a low disease state for more than 24 weeks on infliximab could discontinue the drug for a year or longer without radiographic or functional disease progression."

Bottom line: You can't go wrong shooting for remission. It may be possible to take a "drug holiday." There needs to be a balance between the goal of total remission and practical life style considerations.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis Treatment Center
(http://www.arthritistreatmentcenter.com). He is a both a former Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine as well as consultant to the National Institutes of Health. For more info: Arthritis Treatment

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How Safe Are Prescription Topical Non-Steroidal Drugs?

The treatment of osteoarthritis is essentially palliative.

Osteoarthritis is a degenerative disease where the articular cartilage- the gristle that caps the ends of long bones wears away. More than 20 million Americans suffer from osteoarthritis, making it the most common form of arthritis.

While the therapeutic approach varies from practitioner to practitioner, the general thrust is similar.

Patients are treated with analgesics or non-steroidal anti-inflammatory drugs, physical therapy, injections of glucocorticoids, injections of hyaluronic acid ("rooster comb") lubricants, and then have surgery.

In patients with relatively mild disease, physicians may also prescribe topical agents.

Many doctors feel that topical non-steroidal drugs may be safer to use than oral anti-inflammatory drugs.

A recent study assessed the efficacy and safety of diclofenac gel in the treatment of osteoarthritis of the knee in people aged 65 and older. This was actually a compilation of data from three large randomized studies that enrolled a total of 538 patients. Four hundred and thirty three of the volunteers had associated medical problems such as diabetes, high blood pressure, and cardiovascular disease. The data was reported by Dr. H. Richard Barthel and colleagues at the annual meeting of the American Medical Directors Association.

The patients applied either the topical diclofenac gel in a dose of four grams per day or placebo.
The time frame evaluated was 12 weeks of therapy.

Analysis of the data showed that 56 per cent of the patients who received diclofenac gel had side effects compared with 44 per cent of the placebo group.

One patient, an 80-year old woman, developed a blood clot in the leg and a subsequent pulmonary embolism that was felt to possibly be related to drug therapy.

Non-steroidal anti-inflammatory drugs are associated with an increased incidence of cardiovascular disease, particularly in older individuals with an underlying history of hypertension, diabetes, and other cardiovascular disease.

The systemic absorption of topical diclofenac gel is forty times less than the absorption of oral diclofenac according to Dr. Roy Altman, professor of medicine at the University of California, Los Angeles. While topical agents may reduce the risk of these problems compared with oral preparations, they do not eliminate them totally.

Also found in the analysis was a much higher rate of skin reactions related to the diclofenac gel. Reactions at the site of application occurred in 8.8 per cent of diclofenac gel patients and only 1.1 per cent of placebo treated patients.

Adverse cardiovascular problems occurred in 2.6 per cent of the diclofenac patients versus 1.1 per cent of placebo treated patients.

Besides the currently available Volteren gel, another recent FDA approved topical preparation is Pennsaid, another diclofenac-based rub.

This article points out the inadequacies of our current therapies for osteoarthritis.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis Treatment Center
ArthritisTreatmentCenter . He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: Arthritis Treatment

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What is the Future of Stem Cell Treatment For Regrowing Cartilage?

Osteoarthritis is the most common form of arthritis. Estimates of its prevalence among Americans vary from 20 million to 40 million.

The underlying pathophysiology is the premature deterioration of articular cartilage, the gristle that caps the ends of long bones. Cartilage is a form of connective tissue. It is unique in that it receives its nourishment from the lining of the joint- the synovium. Cartilage itself has no blood vessels or nerves.

The pain that arises from osteoarthritis is due to irritation brought about by local inflammation. These local inflammatory changes occur as a result of the production of destructive enzymes as well as local irritation due to altered biomechanics.

Until recently, the treatment of osteoarthritis has been purely symptomatic. Non-steroidal anti-inflammatory drugs either in oral or topical form, local joint injections of glucocorticoids, or intra-articular injections of viscosupplements (lubricants).

While helpful for alleviating pain temporarily, these approaches also are associated with potential side effects, and do not address the underlying problem- loss of articular cartilage.

In the 1990's there was interest in developing what are called disease modifying osteoarthritis drugs (DMOADS). However, research efforts directed at these disease modifying remedies were disappointing.
More recently there has been interest in the use of stem cells (SCs) to help with cartilage regeneration.

The questions, though, with this line of thinking have been many. What type of SCs should be used? What keeps the SCs inside the joints? How can the SCs be made most productive? When do they stop working? How do you provide the right environment for the SCs to make cartilage? What are the dangers of involved? What criteria are involved in selecting the right SCs expert?

The major breakthrough recently has been in the field of human pluripotent stem cells (hPSCs). The original work done by Shinya Yamanaka in 2007 has laid the groundwork for some excellent investigations involving the use of this techniology. Basically what Yamanaka was able to demonstrate was the ability to take adult stem cells, and reprogram them- essentially rewinding the biologic clock- so that the adult stem cells now behave like embryonic stem cells. The advantage is that these induced adult stem cells can become any type of tissue given the right environment.

However, there are technical problems with this approach and the reality of being able to use these types of stem cells, particularly for arthritis, is way off in the future.

So what is available now and how good is it? Currently, the use of mesenchymal stem cells (MSCs), adult stem cells located in the bone marrow and, which, if placed in the right location with currently available growth stimulators, appears to be effective.

MSCs are multipotential. They can become a limited number of tissue organs. Fortunately, cartilage appears to be one of them.

How effective the approach is, is difficult to say since there are no good long term randomized controlled studies. What is available are anecdotal reports. Unfortunately, these anecdotal reports fall far short of what would be considered good science.

Also, the application of MSCs where there is no cartilage left and there is an angulation deformity is problematic. In our hands, these patients do not respond.

Age and body mass index (weight) are two other important factors to consider.

What is known is that the approach is safe and appears effective for the short term (2-3 years). Clinical measurements, along with cartilage thickness improve.

Also, there is no evidence of cancer, which is the concern using the induced pluripotential approach.
So... the bottom line...the best current approach appears to be the use of adult MSCs made by concentrating marrow, along with growth factors derived from platelet rich plasma. In addition, the utilization of adipose tissue (fat) to serve as a scaffold is strongly advised.

Finally, the technical harvesting and administration of MSCs using diagnostic ultrasound guidance by an experienced and expert physician seems to be the most important ingredient necessary for a successful outcome.

Nathan Wei, MD FACP FACR is a board-certified rheumatologist and nationally known arthritis expert. He is an acknowledged authority on tissue regeneration and the use of stem cells and platelet-rich plasma for arthritis and related disorders. For more free info, go to: Arthritis Treatment and Arthritis Treatment Center

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What Other Diseases "Masquerade" as Rheumatoid Arthritis? Part 2 - The Infectious Group

While rheumatoid arthritis (RA) is the most common form of inflammatory arthritis, the diagnosis is not always easy to make. The reason is that there are more than 100 different kinds of arthritis. Most of them involve inflammation. When a patient goes to a rheumatologist to get a diagnosis, there is a process of elimination in order to arrive at the proper diagnosis. This process of elimination is called "differential diagnosis."

Differential diagnosis can be a difficult undertaking because so many forms of arthritis, particularly inflammatory forms of arthritis look alike. Generally it is helpful to divide the differential diagnosis of rheumatoid arthritis into two groups. The first group are the non-infectious diseases to consider and the second group are the infection-related conditions.

In part 1 of this article, I discussed the non-infectious causes of arthritis that need to be considered when assessing a patient with possible rheumatoid arthritis. In this article I will discuss those types of arthritis that are directly or indirectly due to infections.

Many infections can present with arthritis due to either direct inoculation of a joint (either from the outside or from a bloodstream infection) or due to autoimmune reactions. In many instances, infections lead to acute single joint arthritis; however, in some cases, chronic single or multiple joint arthritis can be present.

Missed infections can lead to significant complications; therefore, it is important to have a high index of suspicion for infection in any patient presenting with acute or chronic arthritis.

Here are some examples:

Gonococcal arthritis is an infection due to the organism that causes gonorrhea (N. gonorrhea). It usually affects a single joint (in 90% to 95% of cases). Symptoms include:

o Joint pain that migrates (jumps around) for 1 to 4 days;

o Pain in the hands/wrists due to inflammation of tendons;

o Sometimes a single joint can be inflamed;

o Fevers;

o Skin rash;

o Burning on urination;

o Lower abdominal pain.

The diagnosis of gonorrhea is made by taking the history and by culture or DNA polymerase chain reaction (PCR) analysis of areas of possible infection, including the throat, genitals, and anus. Since the organism that causes gonorrhea is difficult to grow, it can often be missed on culture. Gonococcal arthritis can usually be distinguished from rheumatoid arthritis (RA) by clinical presentation, blood tests, and cultures.

Lyme disease is a bacterial infection due to the spirochete Borrelia burgdorferi. It presents with a skin rash, swollen joints and flu-like symptoms, caused by the bite of an infected tick. Symptoms may include:

o A skin rash, often resembling a bulls-eye; the rash may be more widespread, though;

o Fever;

o Headache;

o Muscle pain;

o Stiff neck;

o Numbness and tingling

o Bell's palsy

o Swelling of knees and other large joints.

The diagnosis of Lyme disease is typically made by blood tests. Standardization of Lyme tests has improved greatly in the last few years. If chronic single joint arthritis develops, joint fluid analysis or joint tissue biopsy may be necessary for diagnosis. Lyme arthritis can usually be distinguished from RA by clinical presentation and blood testing.

Acute rheumatic fever (ARF) is an inflammatory disease that may develop after an infection with Streptococcus, the bacteria that causes strep throat and scarlet fever. The disease can affect the heart, joints, skin, and brain. Symptoms include:

o Fever;

o Arthritis (mainly affecting the knees, elbows, ankles, and wrists);

o Skin rash and skin nodules;

o A peculiar movement disorder, called Sydenham's chorea;

o Epistaxis (nosebleeds);

o Heart problems;

o Abdominal pain;

ARF is diagnosed by history, physical exam, and blood testing for antibodies against streptococcus. ARF and RA can have similar clinical features including arthritis and nodules. But, ARF can usually be distinguished from RA. For instance, rash and migratory arthritis (arthritis that moves from joint to joint) are unusual in RA. Blood tests are also useful for making the distinction.

Bacterial endocarditis (BE) happesn when bacteria from the skin, mouth or intestines enter the bloodstream and infect the heart valves and heart lining. Symptoms include fever, chills, and other flu-like symptoms as well as unexplained weight loss and weakness. Diagnosis is made by blood cultures and ultrasound imaging of heart valves. Rheumatoid factor can be elevated in endocarditis, so it is not useful for distinguishing BE from RA.

Arthritis may be a symptom of many viral illnesses. The duration is usually short. Clinical features in adults include:

Joint symptoms occur in up to 60%. Joint pains are more common than true joint inflammation. The joint pains usually don't last long. They are symmetric, and affect small joints of the hands, wrists, knees, and ankle joints. Morning stiffness and swelling can be present. A rash may be present

The most common cause of viral arthritis is probably Parvovirus B19.

Diagnosis of viral arthritis is usually made by blood testing.

RF testing is not helpful in distinguishing between hepatitis C infection and RA because RF levels can be elevated in patients with hepatitis C. However, in these situations, testing for anti-cyclic citrullinated peptide (anti-CCP) can be useful since these antibodies are not significantly elevated in hepatitis C infections.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland (http://www.aocm.org). He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: http://www.arthritis-treatment-and-relief.com/arthritis-treatment.html

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What Other Diseases "Masquerade" as Rheumatoid Arthritis? Part 1 - The Non-Infectious Group

Rheumatoid arthritis (RA) is the most common form of inflammatory arthritis and affects more than 2 million Americans. The diagnosis is not easy to make in many instances. There are more than 100 different kinds of arthritis. Most of them involve inflammation. When a patient goes to a rheumatologist to get a diagnosis, there is a process of elimination in order to arrive at the proper diagnosis. This process of elimination is called "differential diagnosis."

Differential diagnosis can be a difficult undertaking because so many forms of arthritis, particularly inflammatory forms of arthritis look alike. Generally it is helpful to divide the differential diagnosis of rheumatoid arthritis into two groups. The first group are the non-infectious diseases to consider and the second group are the infection-related conditions.

Since the discussion is rather long I have chosen to divide the article into two parts.

The following is a partial list of forms of inflammatory arthritis that can be seen and must be considered when evaluating a patient with inflammatory symptoms of arthritis and are not infection related.

RA is an autoimmune chronic inflammatory disease, primarily involving the peripheral joints (hands, wrists, elbows, shoulders, hips, knees, ankles, and feet). It can also affect non joint structures such as the lung, eye, skin, and cardiovascular system.

RA may start slowly with nonspecific symptoms, including fatigue, malaise (feeling "blah"), appetite loss, low-grade fever, weight loss, and vague joint pains, or it may have an explosive onset with inflammation involving multiple joints. The joint symptoms usually occur bilaterally- both sides of the body equally involved- and symmetric. Erosions- damage to the joint- can be seen with x-ray. In about 80% of cases, elevated levels of rheumatoid factor (RF) or anti-cyclic citrullinated antibodies (anti-CCP) are present in the blood. There appears to be a correlation between the presence of anti-CCP antibodies and erosions.

Juvenile rheumatoid arthritis (JRA) occurs in children under the age of 16. Three forms of JRA exist, including oligoarticular (1-4 joints), polyarticular (more than 4 joints), and systemic-onset or Still's disease. The latter condition is associated with systemic symptoms -- including fever and rash in addition to joint disease.

Polyarticular JRA has similar characteristics to adult RA. It causes about 30% of cases of JRA. Most children with polyarticular JRA are negative for RF and their prognosis is usually good.

Approximately 20% of polyarticular JRA patients have elevated RF, and these patients are at risk for chronic, progressive joint damage.

Eye involvement in the form of inflammation- called uveitis- is a common finding in oligoarticular JRA, especially in patients who are positive for anti-nuclear antibody (ANA), a blood test that is often used to screen for autoimmune disease. Uveitis may not cause symptoms so careful screening should be performed in these patients.

SLE is an inflammatory, chronic, autoimmune disorder that can involve the skin, joints, kidneys, central nervous system, and blood vessel walls. Patients may present with 1 or more of the following: butterfly-shaped rash on the face, affecting the cheeks; rash on other parts of the body; sensitivity to sunlight; mouth sores; joint inflammation; fluid around the lungs, heart, or other organs; kidney abnormalities; low white blood cell count, low red blood cell count, or low platelet count; nerve or brain inflammation; positive results of a blood test for ANA; positive results of a blood test for antibodies to double-stranded DNA or other antibodies.

Patients with lupus can have significant inflammatory arthritis. As a result, lupus can be difficult to distinguish from RA, especially if other features of lupus are not present. Clues that favor a diagnosis of RA over lupus in a patient presenting with arthritis affecting multiple joints include lack of lupus features, erosions (joint damage) seen on x-rays, and elevations of RF and anti-CCP antibodies.

Polymyositis (PM) and dermatomyositis (DM) are types of inflammatory muscle disease. These conditions typically present with bilateral (both sides involved) large muscle weakness. In the case of DM, rash is present. Diagnosis consists of finding the following: elevation of muscle enzyme levels in the blood [the two enzymes that are measured are creatine kinase (CPK) and aldolase], signs and symptoms, electromyograph (EMG)- an electrical test- alteration, and a positive muscle biopsy.

In addition, in many cases abnormal antibodies specific for inflammatory muscle disease can be elevated.

In both PM and DM, inflammatory arthritis can be present and can look like RA. Both inflammatory muscle disease and RA can affect the lungs. In RA, muscle function will usually be normal. Also, in PM and DM, erosive joint disease is unlikely. RF and anti-CCP antibodies are typically elevated in RA but not PM or DM.

SAs -- psoriatic arthritis, reactive arthritis, ankylosing spondylitis, and enteropathic arthritis -- are a category of diseases that cause systemic inflammation, and preferentially attack parts of the spine and other joints where tendons attach to bones. They also can cause pain and stiffness in the neck, upper and lower back, tendonitis, bursitis, heel pain, and fatigue. They are termed "seronegative" types of arthritis. The term 'seronegative' means that testing for rheumatoid factor is negative. Symptoms of adult SAs include:

o Back and/or joint pain;

o Morning stiffness;

o Tenderness near bones;

o Sores on the skin;

o Inflammation of the joints on both sides of the body;

o Skin or mouth ulcers;

o Rash on the bottom of the feet; and

o Eye inflammation.

Occasionally, arthritis similar to that seen in RA can be present. Careful history and physical examination can often distinguish between these conditions, especially if an obvious disease that is promoting inflammation is present (psoriasis, inflammatory bowel disease, etc.). In addition, RA rarely affects the DIP joints- the last row of finger joints. If these joints are involved with inflammatory arthritis, the diagnosis of an SA is possible. (Note of caution: a condition known as inflammatory erosive nodal osteoarthritis can also affect the DIP joints). RF and anti-CCP antibodies are negative in SAs, although, rarely, in cases of psoriatic arthritis there may be elevations of RF and anti-CCP antibodies.

Gout is caused by deposits of monosodium urate (uric acid) crystals into a joint. Gouty arthritis is acute in onset, very painful, with signs of significant inflammation on exam (red, warm, swollen joints). Gout can affect almost any joint in the body, but typically affects cooler areas including the toes, feet, ankles, knees, and hands. Diagnosis is made by drawing fluid from an inflamed joint and analyzing the fluid. Demonstrating monosodium urate crystals in the joint fluid is diagnostic, although finding elevated serum levels of uric acid can also be helpful.

In most cases, gout is an acute single joint disease that is easy to distinguish from RA. However, in some cases, chronic erosive joint inflammation where multiple joints are involved can develop. And, in cases where tophi (deposits of uric acid) are present, it can be difficult to distinguish from erosive RA. However, crystal analysis of joints or tophi and blood tests should be helpful in distinguishing gout from RA.

Calcium pyrophosphate deposition disease (CPPD), also known as pseudogout, is a disease is caused by deposits of calcium pyrophosphate dihydrate crystals in a joint. The presence of these crystals in the joints leads to significant inflammation. Establishing the diagnosis includes using:

o Detailed medical history;

o Withdrawing fluid from a joint to check for crystals;

o Joint x-rays to show crystals deposition in the cartilage (chondrocalcinosis); and

o Blood tests to rule out other diseases (e.g., RA or osteoarthritis).

In most cases, CPPD arthritis presents with single joint inflammation. In some cases, CPPD disease can present with chronic symmetric multiple joint erosive arthritis similar to RA. RA and CPPD disease can usually be told apart by joint aspiration demonstrating calcium pyrophosphate crystals, and by blood tests, including RF and anti-CCP antibodies, which are usually negative in CCPD arthritis. A complicating feature is that RA and CPPD can coexist!

Sarcoidosis is an inflammatory joint disorder. The majority of patients with this disease have lung disease, with eye and skin disease being the next most frequent signs of disease. Although the diagnosis of sarcoidosis can be made on clinical and x-ray presentation alone, sometimes the use of tissue biopsy with the demonstration of "noncaseating granulomas" is necessary for diagnosis.

Arthritis is present in 15% of patients with sarcoidosis, and in rare cases can be the only sign of disease. In acute sarcoid arthritis, joint disease is usually of rapid onset. It is symmetric involving the ankles, although knees, wrists, and hands can be involved. In most cases of acute disease, lung and skin disease are also present. Chronic sarcoid arthritis can be difficult to distinguish from RA. Although RA-specific blood tests, such as RF and anti-CCP antibodies, can be helpful in distinguishing RA from sarcoidosis, in some cases a biopsy of joint tissue may be required for diagnosis.

Polymyalgia Rheumatica (PMR) is a disease that leads to inflammation of tendons, muscles, ligaments, and tissues around the joints. It presents with large muscle pain, aching, morning stiffness, fatigue, and in some cases, fever. It can be associated with temporal arteritis (TA), also known as giant-cell arteritis, which is a related but more serious condition in which inflammation of large blood vessels can lead to blindness and aneurysms. Also, a peculiar syndrome where use of the arms and legs leads to cramping because of insufficient blood flow (limb claudication) can occur. PMR is diagnosed when the clinical picture is present along with elevated markers of inflammation (ESR and/or CRP). If temporal arteritis is suspected (headache, vision changes, limb claudication), biopsy of a temporal artery may be necessary to demonstrate inflammation of blood vessels.

PMR and TA can present with symmetric inflammatory arthritis similar to RA. These diseases can usually be distinguished by blood testing. In addition, headaches, vision changes, and large muscle pain are uncommon in RA, and if these are present, PMR and/or TA should be considered.

In part 2 of this article, I will discuss infectious diseases that need to be considered in the differential diagnosis of rheumatoid arthritis. When RA is suspected, it is critical to consult with an expert rheumatologist.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland (http://www.aocm.org). He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: http://www.arthritis-treatment-and-relief.com/arthritis-treatment.html

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New Guidelines For Rheumatoid Arthritis - Good Or Bad?

The American College of Rheumatology (ACR) is the national organization that represents much of the current thinking when it comes to arthritis care. One of their major commitments has been to develop guidelines for treatment of various types of arthritis. These guidelines are meant to instruct and perhaps give people an indication of what is considered "standard of care".

They are not set in concrete nor are they meant to restrict other therapies. Guidelines for the treatment of rheumatoid arthritis (RA) were last made by the ACR in 2002... before the general use of biologic therapy.

Rheumatoid arthritis is a chronic, systemic, autoimmune disorder for which there is no known cure. It affects roughly 2 million Americans.

Up until the turn of this past century, disease-modifying anti-rheumatic drugs (DMARDS) were the mainstay of treatment. Because of the advent of newer more effective biologic therapies, the ACR felt it was time for a major re-evaluation of the use of DMARD therapy in rheumatoid arthritis.

They issued a set of guidelines that were recently published. (Saag KG, et al. Arthritis Care and Research 2008; 59: 762-784).

These recommendations on the use of non-biologic and biologic DMARDs in RA have recently been published and focus on 5 key areas: indications for use, monitoring for side-effects, assessing the clinical response, screening for tuberculosis (a risk factor associated with biologic DMARDs), and under certain circumstances (i.e. high disease activity) the roles of cost and patient preference in choosing biologic agents. When formulating these recommendations, RA disease duration, disease severity, and prognostic features were also considered.

The authors of these guidelines stated that, "Applying these recommendations to clinical practice requires individualized patient assessment and clinical decision-making. The recommendations developed are not intended to be used in a 'cookbook' or prescriptive manner or to limit a physician's clinical judgment, but rather to provide guidance based on clinical evidence and expert panel input."

The ACR 2008 recommendations include:

o Initiation of methotrexate or leflunomide (Arava) therapy was recommended for most RA patients.

o Methotrexate plus hydroxychloroquine (Plaquenil) was also endorsed for patients with moderate to high disease activity.

o The triple DMARD combination of methotrexate plus hydroxychloroquine plus sulfasalazine (Azulfidine) for patients with poor prognostic features and moderate to high levels of disease activity was suggested.

o Recommended the prescription of anti-TNF agents such as etanercept (Enbrel), infliximab (Remicade), or adalimumab (Humira) along with methotrexate in early RA (less than 3 months) only for patients with high disease activity who had never received DMARDs. In intermediate- and longer-duration RA, anti-TNF agents were recommended for patients who had failed to respond adequately to methotrexate therapy.

o Reserving the use of second line biologic therapies such as abatacept (Orencia) and rituximab (Rituxan) for patients with at least moderate disease activity and poor disease prognosis for whom methotrexate in combination with or sequential administration of other non-biologic DMARDs did not lead to an adequate response.

o Avoiding the initiation or resumption of treatment with methotrexate, leflunomide, or biologic agents for patients with active bacterial infection, active herpes-zoster viral infection, active or latent tuberculosis, or acute or chronic hepatitis B or C.

o Not prescribing anti-TNF agents to patients with a history of heart failure, with a history of lymphoma, or with multiple sclerosis or demyelinating disorders.

o Avoiding the initiation or resumption of methotrexate, leflunomide, or minocycline for RA patients planning for pregnancy and throughout the duration of pregnancy and breastfeeding.

The authors continued on, "These recommendations are extensive but not comprehensive... and it is intended that they will be regularly updated to reflect the rapidly growing scientific evidence in this area along with changing practice patterns in rheumatology."

Personally, I feel the guidelines are too little too late. While I agree with the main body of their recommendations for the most part, I do disagree with some of their thoughts. For instance, I have disagreement with the use of triple therapy since I don't think it works and is potentially more toxic than the use of biologic therapies. In addition, the use of second-line drugs like Orencia and Rituxan should be given to patients who fail the combination of a TNF-inhibitor and methotrexate.

Newer biologic agents such as Actemra and Cimzia which are currently awaiting FDA approval will also alter the way rheumatologists approach treatment.

Progress in the field of rheumatoid arthritis research has been astounding. With the advent of newer techniques designed to diagnose and customize therapies, the possibility of a cure is not too far down the road.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis and Osteoporosis Center of Maryland (http://www.aocm.org). He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: http://www.arthritis-treatment-and-relief.com/arthritis-treatment.html

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So, What's New in 2010 For Rheumatoid Arthritis?

Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune-based disease that affects approximately two million Americans. The pathogenesis seems to implicate both genetic as well as environmental factors.

The chronic inflammatory response leads not only to joint destruction but also to damage involving internal organs.

Because of the complicated nature of the disease, no one therapy has been found to be curative.

In the early 1980's methotrexate revolutionized our treatment approach to rheumatoid arthritis. Prior to methotrexate, patients had limited options. Among them were gold salts, d-penicillamine- a highly toxic medicine, and hydroxychloroquine (Plaquenil).

What really allowed rheumatologists to achieve remission though was the development of highly targeted biologic therapies in the mid-1990's.

So... the upshot is that RA treatment has progressed rapidly with the introduction of biologic drugs such as the TNF-inhibitors (Enbrel, Humira, Remicade, and more recently, Simponi and Cimzia), rituximab (Rituxan), and abatacept (Orencia).

These drugs have greatly improved the quality of life for RA sufferers.

A number of new studies presented at the American College of Rheumatology meeting in Philadelphia has shed some light on predictors.

The first example is a study demonstrating that patients having a rapid response to Cimzia were more likely to have long-term control of disease.

Another study showed that patients with very high levels of rheumatoid factor, a protein that is elevated in the blood of 80 per cent of patients with RA predicted a better response to Remicade.

Another paper showed that older patients, particularly those with more aggressive disease had less of a response to TNF-inhibitor therapy than those patients who were younger and had milder disease.

Another study showed that restarting TNF-inhibitor therapy after loss of remission was effective in regaining remission. This paper was quite controversial in that most practitioners have found just the opposite to be true.

One study demonstrated that patients intolerant to TNF-inhibitor treatment were more likely to respond to Rituxan than they were to another TNF-inhibitor.

A significant predictor of x-ray progression of disease were two markers: rheumatoid factor positivity and age.

One encouraging paper showed that between 35 per cent to 50 per cent of patients who began treatment with biologics stayed on the same biologic for an extended period of time, sometimes many years.

The same meeting produced a study that expressed the idea that patients who were treated with a combination of methotrexate plus a biologic were more likely to stick with the biologic than if they were treated with the biologic alone.

Other studies showed that "small molecule" drugs... drugs that can be taken orally but which have biologic effects are promising.

Nathan Wei, MD, FACP, FACR is a rheumatologist and Director of the Arthritis Treatment Center (http://www.aocm.org). He is a former Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and consultant to the National Institutes of Health. For more info: Arthritis Treatment

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Who Else Wants General Information on Arthritis?

Today there are about 70 million Americans with arthritis...that's one person out of every four who suffer both pain and the expense of this crippling disease. In one year alone, arthritis will be responsible for over half a billion dollars in lost wages. The economic consequences of arthritis are important to review because each year, arthritis takes a devastating financial toll on our society.

Over the course of ten years, arthritis related work loss has been associated with a 37% drop in income for arthritics - all those without arthritis had a 90% rise in income over the same period of time!

If you...a friend...or a relative has arthritis, it's important to know that early treatment can help sufferers continue with their normal daily lives and remain productive members of the community.

The term "arthritis" is derived from the Greek: "arthron" meaning "joint" and "itis" meaning inflammation. Arthritis is a word that describes over 100 different conditions, some involving inflammation and others not.

Arthritis is not a single disease. It encompasses about 100 different conditions, that affect joints and that pose unique problems for diagnosis and treatment.

Some common types of arthritis include osteoarthritis, rheumatoid arthritis, gout, pseudo-gout, ankylosing spondylitis, polymyalgia rheumatica, psoriatic arthritis, Reiter's disease, systemic lupus erythematosus, and fibromyalgia.

Most types of arthritis involve joint inflammation. Inflammation is the body's natural response to injury or infection.

For an example of inflammation, take a simple scratch...your body automatically releases chemicals that cause fluids to accumulate and white blood cells to gather around the area of the scratch. As your body fights foreign substances and bacteria, inflammation... redness...heat...swelling...and pain occur at the sight of the injury.

In arthritis, unfortunately, this natural defense mechanism goes awry. Elements from the blood designed to fight infection and repair injury attack the body instead.

And, unless this inflammatory process is halted, it will continue to attack the body and cause joint destruction.

So you can begin to see how treatments that just relieve the pain associated with arthritis - but that do not reduce inflammation - may not adequately treat this disease.

Getting proper treatment early on is important...because proper care can help arthritis sufferers lead more active and comfortable lives.

Yet many people with arthritis delay going to a physician. Either they have fear about going to a doctor or they feel that nothing can be done for arthritis. Other reasons include the notion that all arthritis medicines are harmful or arthritis is just a normal part of aging.

Some people try unproven remedies which also delay proper diagnosis and treatment.

Since arthritis may evolve gradually, people often ignore its early warning symptoms or signs. These include persistent pain, tenderness, or swelling in one or more joints...symptoms that should not be dismissed as signs of age.

Other warning symptoms are joint pain and stiffness...especially when they appear in the morning.

Low back pain is one of the earliest symptoms of arthritis. For people over the age of 60, arthritis is the most frequent cause of low back pain.

The activity of arthritis varies unpredictably. Symptoms are cyclic in nature and seem to come and go.

Therefore, it is important to remember that any symptoms or signs of arthritis that last for more than six weeks - no matter how mild - should be checked by a physician. And, if symptoms are severe, then even waiting six weeks might be too long.

The two most common types of arthritis are osteoarthritis and rheumatoid arthritis. Joint inflammation is involved in both.

But, these types of arthritis differ in terms of...age of patients who are affected...the joints involved...the pattern of stiffness...and the potential for disability.

Close to 16 million Americans have osteoarthritis - the most common type of arthritis. Although osteoarthritis can occur at any age, it most often begins in people in their 50's and 60's.

Osteoarthritis or degenerative disc disease is a disorder of cartilage - the gristle that covers the ends of long bones. Cartilage is made of cell called chondrocytes which sit inside a framework made up of collagen and proteoglyens. Under normal conditions, chondrocytes make collagen and proteoglycens - in other works - they make the framework they sit inside. With osteoarthritis, chondrocytes behave abnormally and begin to make destructive enzymes such as collagenasese, stromelysin and others. These enzymes degrade cartilage...these enzymes also attract inflammatory cells which secrete substances called cytokines which cause further inflammation and damage to cartilage, underlying bone, and the joint lining.

This process results in progressive pain, stiffness, and loss of function.

Joint pain and stiffness are the most noticeable symptoms of osteoarthritis. Morning stiffness is usually brief lasting less than 15 minutes. Osteoarthritis usually affects weight bearing areas particularly the neck, low back, hips and knees.

It may also affect the fingers and hands and bony knobs may appear at the finger joints. The base of the thumb may also be affected. The typical pattern of osteoarthritis in the hands involves the distal and proximal interphalangeal (DIP and PIP) joints of the fingers, and the carpometacarpal (CMC) joint of the thumb.

Osteoarthritis is considered to be a degenerative joint disease. Along with inflammation, there is wear and tear on the inside of the joint.

This causes damage to the cartilage (the substance that forms the surface of the joints and works as a shock absorber). As the cartilage wears thin, the underlying bone is damaged. This process results in progressive pain, stiffness, and loss of function.

Osteoarthritis does not need to be disabling and with the proper medical care can be managed easily.

Rheumatoid arthritis is the other most common type of arthritis. It is more common in women and affects 7 million Americans...or one out of every five arthritis patients. It may affect any age group, although onset is most common in middle age.

Rheumatoid arthritis is usually characterized by heat, swelling, and pain in multiple joints in both the right and left sides of the body, including the hands, wrists, elbows, hips, knees, ankles, and feet. Spinal involvement also occurs on occasion.

The typical pattern of rheumatoid arthritis in the hands involves the proximal interphalangeal (PIP) joints, the metacarpal phalangeal (MCP) joints, the wrists, and the elbows.

Unlike osteoarthritis, rheumatoid arthritis can affect the entire body. People with this disease may feel sick all over...tire easily...lose their appetite...and lose weight.

In rheumatoid arthritis, the tissue that surrounds and nourishes the joints is attacked by the body's immune system. The body mistakenly perceives its own tissue as foreign, and it reacts by sending special white blood cells and toxic chemicals called cytokines to destroy the foreign material. (The cytokine abnormalities that cause the damage in rheumatoid arthritis are different from the abnormalities seen in osteoarthritis.) This process of white cell migration and cytokine release damages the joint.

Although we do not know the cause of rheumatoid arthritis, researchers are investigating several possibilities.

Another interesting point about rheumatoid arthritis is that this disease can affect the internal organs including the lungs, skin, blood vessels, spleen, heart, and muscles.

If rheumatoid arthritis is not well controlled it can damage the joints irreversibly and cause serious disability.

To diagnose rheumatoid arthritis, the rheumatologist establishes the presence of joint pain and inflammation lasting at least six weeks and then looks for signs of the course of the disease that are characteristic for rheumatoid arthritis.

There are also blood tests that aid in the diagnosis of rheumatoid arthritis.

Patients with rheumatoid arthritis have a series of flare-ups followed by a period where there are mild or no symptoms. Usually, the pain and disability of rheumatoid arthritis progresses gradually.

Morning stiffness generally lasts longer than half an hour and may last several hours depending on the severity of the condition.

Most forms of arthritis persist for the patient's lifetime. Medication cannot usually reverse the bone and soft tissue damage caused by arthritis.

However, new methods of measuring inflammation and its response to medication and other treatments offer valuable information to physicians...and can help to evaluate the arthritis sufferer's discomfort.

Magnetic resonance imaging is one such technique. This method using the effects that strong magnets have on water molecules to provide exquisite images of the interior of the body. MRI has been used to diagnose and also assess the degree of damage within joints of patients suffering from arthritis. It is also helpful for evaluating the effect of new drugs.

Although there is no cure for arthritis, proper treatment can help tremendously. The goal of arthritis treatment is to relieve the pain and stiffness due to the progressive destruction caused by inflammation, and to maintain or increase freedom of movement.

Among the advancements that have taken place in the medical treatment of arthritis are various disease-modifying medications that not only relieve symptoms but also help slow down the progression of disease.

Other advances include various cartilage sparing drugs, cartilage growing drugs, and also biologic remedies. These drugs act by blocking the destructive effects of enzymes such as metalloproteases in osteoarthritis and cytokines in rheumatoid arthritis. By targeting specific processes, relief of symptoms and healing of damage can take place with presumably fewer side effects.

What can you do if you think you have arthritis?

First, you can consult your doctor. This is important because medical issues are complicated and your doctor, who understands your health needs, can prescribe the best treatment for you.

The type of doctor who can best evaluate arthritis is called a rheumatologist. These are physicians who have completed four years of medical school, three years of internal medicine residency, and three years of rheumatology fellowship.

While arthritis can be a serious disease that can progress and cause disability, science has come up with some new answers for arthritis sufferers. It is now up to the arthritis sufferer to recognize early warning signs and symptoms and to see a rheumatologist. With proper medical care, the course of this crippling disease may change and people can help to be returned to fully active lives - without pain and crippling disability.
 

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Dr. Wei (pronounced “way”) is a board-certified rheumatologist and Clinical Director of the nationally respected Arthritis and Osteoporosis Center of Maryland. He is a Clinical Assistant Professor of Medicine at the University of Maryland School of Medicine and has served as a consultant to the Arthritis Branch of the National Institutes of Health. He is a Fellow of the American College of Rheumatology and the American College of Physicians. For more information on arthritis and related conditions, go to: Arthritis Pain Relief

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