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Posts Tagged ‘ankles’

I’m still in the midst of recovering from cervical fusion surgery on May 15 and am currently completing physical therapy. The process seems to be going well, pain and numbness is almost completely gone, and I’m slowly regaining muscle strength. After dealing with it for over 8 months, the neck and associated parts finally feels much better. But RA is never silent and has a way of rearing its ugly head just when you think things are calm. Sure, there is always the ongoing “background noise” of RA – fatigue, joint and muscle pain, finger swelling and pain, joint locking, and the persistent ankle pain after having three surgeries. But now the left hip is begging – no screaming – for attention.

Hip problems became apparent almost two years ago when I began getting steroid injections for trochanteric bursitis from my rheumatologist. Bursae are sac-like structures that are found in some joints and aid in providing friction reduction.[1] I had a bursa removed as part of an ankle surgery. The trochanteric bursa is on the outside of the hip and is commonly involved in RA.[2]

While my neck was healing, the left hip progressively grew worse. Sitting for any length of time was impossible, getting in and out of a chair and car was difficult, sleeping on the left side was not feasible, and the left side was favored while walking. At a recent rheumatology appointment, a fourth cortisone steroid injection was given into the trochanteric bursa. But the injection brought no relief. My rheumatologist referred me to an orthopedic specialist.

The orthopedic surgeon examined x-rays and noted that the space in the ball and socket joint, while somewhat reduced, looked fine. There was no bone erosion perceived. We spent some time discussing my earlier problems with the trochanteric bursa, the multiple steroid injections, and my current symptoms of groin and buttock pain. He then laid me down on my back and began to examine my hip movement through a series of tests. I couldn’t lift my leg off the table and extreme pain was felt when he manipulated it in various ways. After the physical exam his entire line of inquiry changed from the more external trochanteric bursa to focusing on tissues around the joint itself. He immediately began to suspect a labral tear. The labrum is cartilage that surrounds the hip joint.[3] But a physical exam and x-ray cannot directly pinpoint what’s really going on so an MRI is needed. A traditional MRI can’t always detect soft tissue in the complex hip joint so an arthrogram is added. Before the MRI, a radiologist injects a combination of fluid, steroid, and a contrast into the hip joint under the guidance of an x-ray. After the injection, you go directly to the MRI machine. The steroid can also provide a therapeutic purpose in reducing inflammation and pain. I am scheduled for an MR arthrogram tomorrow and hopefully it will help solve the mystery.

In addition to the more traditional bone erosion, I have a history of developing soft tissue damage to the musculoskeletal system from RA. This episode with the hip seems to be following that story.

[1] http://orthoinfo.aaos.org/topic.cfm?topic=a00409

[2] https://www.rheumatology.org/Practice/Clinical/Patients/Diseases_And_Conditions/Tendinitis_and_Bursitis/

[3] http://www.hss.edu/condition-list_labral-tears-hip.asp#.U_zH9WRDvA4

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In an earlier post, I outlined how RA can impact much more than bones including many organs and soft tissues. One group of soft tissues that can be damaged by RA includes those involved with the musculoskeletal system. The musculoskeletal system involves a complex interaction between muscles, bones, joints, and various connective soft tissues – all which can be the target of RA.

Erosion of bone tissues in joints is on of the trademark symptoms of rheumatoid arthritis. Through complex autoimmune biochemical processes, the body’s immune system attacks it’s own tissues like it was a foreign invader. A cascade of signaling chemicals promotes the production of bone cells called osteoclasts that erode bone tissue and surrounding cartilage. This kind of gross damage…

Read more at http://rheumatoidarthritis.net/living/attack-on-connective-tissues/

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491px-Muscle_posteriorSeveral recent observations caused me to wonder about the impact of RA on muscles. In the almost five years since being diagnosed with RA, I’ve seen a steady decrease of muscle strength coupled with an increase in periodic pain and aching in muscle tissue. I’ve thought that the aching could be caused by either overuse (comparatively speaking) or by biomechanical processes since the muscles are attached to RA-damaged joints via tendons. I can feel myself getting weaker as time goes on. In fact, muscle strength in RA patients can be reduced by up to 75% of normal (see this study from 1992). During a follow-up visit about one of my ankle surgeries a few years back, the orthopedic surgeon noted in my chart that my calf muscles were getting atrophied. I no longer have the strength to open jars, dig a hole, or even maintain extended use of a muscle on a given task. I began to wonder about the impact of rheumatoid arthritis on muscles.

While muscles haven’t been a primary research target, there have been a few studies about muscles and RA. As far back as 1951, researchers found that inflammation of arteries in muscle tissue was observed in RA patients. In a study of 350 RA patients in Spain, weakness, muscle atrophy, and muscle inflammation were commonly observed in those suffering from RA. A detailed research study by Helliwell and Jackson published in 1994 documented RA’s impact on muscle tissue. They concluded, “Although there is significant muscle wasting in RA, it is likely that reduction in strength is also attributable to joint deformity and pain leading to inhibition of grip directly and, indirectly, by arthrogenous muscle inhibition. Doubts remain about the quality of muscle in RA”. Arthrogenous refers to “starting from a joint”. In 1993, Young produced a model demonstrating the connection between joint damage and muscles.

In addition to biomechanical problems, it is entirely plausible that biochemical processes involved with RA may negatively impact muscle tissue. According to some researchers, RA related cytokines including IL-1 and TNF are involved with breaking down the protein in muscles. According to Rall, et al (1996), “Adults with RA have increased whole-body protein breakdown, which correlates with growth hormone, glucagon, and TNFα production.” They concluded…”And although progressive resistance training led to improved strength and functional status in patients with RA and in controls, we saw no changes in protein metabolism or hormone levels as a result of the training intervention among any of the groups of subjects.” In other words, muscle breakdown continued even in midst of exercise. This mirrors a study by a group from Finland who noted that exercise helped RA patients’ muscle strength but not bone density. In 1974, a group of researchers from Sweden noticed changes in the muscle tissue of RA patients. They stated, “It is emphasized that the type II atrophy must be the result of a more complex mechanism than simple ‘disuse’.”

My suspicions about the biochemical impact and connectedness to RA impacted joints are both confirmed in the research literature. The question then remains as to what may be done to stop or reverse the impact of RA on muscles. Some argue that RA patients should engage in regular exercise in order to maintain muscle tone (see Mayo Clinic, NCHPAD). In a 2003 review of research studies on the impact of exercise on RA patients, it was found that most studies demonstrated that exercise positively impacted muscle strength without negatively impacting pain or daily activities. These results are interesting to me personally because every time I try to engage in exercise or strenuous activity, I feel worse and daily activities are limited (see recent post). Regarding exercise, many experts now recommend, “If you can, you should; if you can’t, you shouldn’t.” (Dr. Borogini Health Central RA website).

The evidence is clear – rheumatoid arthritis does impact muscle tissue. But more research is needed to identify the specific causes and to develop long term solutions. Of course, a bona fide cure for RA would do the trick. Fortunately, there are still researchers seeking answers as attested to by the fact that funding is being provided to study muscles in RA patients (see recent grant award in the UK).

Creative Commons Photo Credit – Public Domain: http://commons.wikimedia.org/wiki/File:Muscle_posterior.png

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The last four days have been a grand time of celebrating our oldest son’s college graduation. It’s been a whirlwind of events including his senior engineering project presentation, three formal ceremonies of various sizes and durations, dinners, and a large party hosted at our house. This meant much physical activity around the yard and house the principal of which was 10 hours of smoking five large pork shoulders for 50 people (it was tasty and you should check out the website http://www.amazingribs.com/).

Tired_brown_bear_050701_01Going into this set of events, a nagging thought persisted…”I’m going to pay for this later.” Sure enough, by Sunday evening I could barely walk, my fingers were swollen and throbbing in pain, and sheer exhaustion washed over my body causing me to collapse. I knew that going to work Monday morning would not be possible.

Many argue that movement and exercise is critical medicine for arthritic joints stating that it relieves pain and stiffness (see these websites – Mayo Clinic, NCHPAD). In addition to potential positive impact on joints and muscles, exercise is obviously important for other reasons include cardiovascular and mental health. But my experience over the years has been that exercise and movement causes rebound pain and stiffness. Yet, I know that I’m missing out on the benefits of exercise.

It’s interesting to read some of the recommendations from medical websites. From WedMD…“Regular exercise can actually reduce overall pain from rheumatoid arthritis.” In my experience with RA, exercise always causes more pain. There are many times when I’ve had to stop movement because the pain got worse. WebMD also makes this statement, “Regular exercise improves functional ability and lets you do more for yourself.” This may be true for some but the functional ability of my ankles and Achilles tendons actually got worse after exercising. The tendons tore at a quicker rate and my orthopedic surgeon and physical therapist both recommended that I avoid any activity that puts stress on the tendons.

Can exercise actually be contraindicated for RA? Kelly Young at RA Warrior has an excellent series of posts about this topic. She concludes, “If you can, you should; if you can’t, you shouldn’t.” At the Health Central RA website, Dr. Borogini wrote a balanced article about the topic and makes an excellent suggestion which is in alignment with Kelly Young’s statement, Rest More When RA Is Active, Exercise More When It Is Not. The Johns Hopkins Arthritis Center website makes a great observation about movement and RA.

Acutely, resting of involved joints can assist with pain management and decrease the inflammation of the involved joint. However, the potential side effects of inactivity include decrease range of motion, loss of strength, altered joint-loading response, and decrease aerobic capacity.

This leaves those with active disease in a real quandary.

The conclusion that must be drawn from the recent set of weekend experiences is that my RA is not under control and I should probably avoid strenuous physical activity. But of course, I already knew that going into the weekend. The difficulty lies in the fact that life must go on and I was not about to miss this once-in-a-lifetime celebration. I just have to be ready to pay the consequences afterwards.

Creative Commons Photo Credit: http://commons.wikimedia.org/wiki/File:Tired_brown_bear_050701_01.JPG

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laptop and stethoscopeMy first systemic autoimmune symptom was in 2004 – I was not formally referred to a rheumatologist. Three years later I had ankle surgeries in both ankles which later was attributed to RA. Again, I was not referred to a rheumatologist. In late 2008 I started having additional symptoms that drove me to my primary care physician. He put all the symptom pieces together and immediately sent me to a rheumatologist resulting in a formal diagnosis five years after the first symptoms appeared. After diagnosis, I progressed rather quickly through a series of treatments (that journey continues today but that’s a story for another post). Now I am nowhere near clinical remission and have a severe level of disease activity that caused permanent joint damage and is dramatically impacting my life. I only wish I knew more about RA back in 2004. The good news is that there are some quality resources available that are designed to encourage early diagnosis and aggressive treatment.

One such resource is an online presentation from Dr. Martin Jan Bergman, a rheumatologist from Drexel University. He recently gave an excellent, relatively short, and non-technical presentation in October 2012 titled Rheumatoid Arthritis: Diagnosis, Treatment and Monitoring. The presentation was sponsored by Quest Diagnostics. His presentation is a superb resource for primary care physicians, RA patients, and care givers to better understand the disease and treatment processes.

One key point made by Dr. Bergman is that RA is more serious than most people think and there is a lack of public awareness of this severity. He points out that RA leads to disability, reduced work capacity, and lower quality of life. He strongly asserts that RA is a lethal disease and he shows how the survival rates of patients with high RA disease activity is similar to coronary artery disease and Hodgkin’s lymphoma. RA also brings about an increased risk of heart attacks, strokes, infection, and lymphoma.

Dr. Bergman is emphatic about early and aggressive diagnosis and treatment of RA. His says that his most common referrers are orthopedic surgeons but argues that this is often too late and primary care providers need to be more aware of RA symptoms. He stated that “there’s no such thing as arthritis- it’s a field of study.” He compares the loose use of the term arthritis to getting a diagnosis of a “belly problem” for a heart attack. With over 100 kinds of arthritis, keying in on the exact nature of the symptoms and diagnostic keys is critical to helping the patient. He discusses common diagnostic tests but warns that lab tests are normal in 35% of patients with RA. Common inflammatory tests like ESR and CRP are also normal 40% of time and should never be used to exclude a diagnosis.

Once diagnosed with RA, Dr. Bergman states that it should be treated aggressively. Waiting only results in permanent loss of function and poorer responses to treatment over time. He describes how the ACR/EULAR classification criteria should be used and he states that monitoring the disease using detailed criteria rather than just asking patients how they’re feeling provides a quicker response to treatments. His goal is to get patients as close to “normal” as possible.

Awareness of these issues discussed by Dr. Bergman is critically important for patients’ well-being. I only hope that more physicians will diagnose early, treat aggressively, and monitor carefully. Patients and care givers will find Dr. Bergman’s presentation enlightening.

Creative Commons Photo Credit: http://www.flickr.com/photos/67272961@N03/6123892769/

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My rheumatologist believes that I may have a combination of rheumatoid arthritis (RA) and ankylosing spondylitis (AS). I have had a positive rheumatoid factor (RF) test and I present classic examples of inflammation and damage in joints commonly associated with RA including in the proximal interphalangeal (PIP) and metacarpophalangeal (MCP) joints in both hands. Add to that list, symmetrical joint presentation in the wrists, shoulders, hips, and knees along with fatigue and it seems like RA. At the same time, my rheumatologist noted limited spinal mobility and many problems with my ankles and Achilles’ tendons which are common with AS. My first autoimmune symptom, which occurred years before joint problems, was inflammatory uveitis in both eyes. While Achilles tendon problems and uveitis can be associated with RA, they are more commonly seen in AS patients. But a test for HLA-B27, a common genetic test related to ankylosing spondylitis (AS), was negative. These blood tests are not 100% accurate and the official diagnosis in my chart is RA (diagnosis code 714).

photo (8)Muddying the water is the fact that I have been through a slew of RA treatments over the past four years in an effort to find a combination that works for the long term. I’m currently on Actemra infusions and now going back to add leflunomide (Arava) in an effort to capture the earlier success with Actemra. While many RA patients find relief from the most common treatments like methotrexate, Enbrel, and Humira, it seems to elude 30-40% of patients.[i] Every person seems to respond differently to various medicines and doses.

This personal evidence leads me to believe that there may be different sub-types of RA. In a recent conversation at the RA site on HealthCentral, the notion of sub-types of RA was mentioned. We already know that there are different types of inflammatory arthritis including RA, AS, psoriatic arthritis.[ii] And each of these diseases presents different patterns and may be treated with similar and/or different medications. But there seems to be a lack of scientifically defined sub-types of RA.

According to researchers from the Netherlands, “Rheumatoid arthritis (RA) is a heterogeneous disease with unknown cause.[iii] Differences in genetic expressions of RA patients were seen by these researchers lending some credence to a genetic link to sub-types of RA. In an earlier study of the genetics of RA in 1989, researchers found a gene called HLA-DR was found in 83% of 149 patients with classical or definite RA.[iv] But no explanation is given for the 17% of RA patients who did not show the gene. In 2010, a group of researchers found four genetic sub-types of RA.[v] Japanese scientists found genetic differences at the molecular level. They stated, “Data from genome-wide screening, transcriptional profiling, and animal models indicate that RA consists with heterogeneous disease subsets.”[vi] Some researchers even found different emotional responses in RA patients.[vii]

While the causes of RA are not completely evident, most scientists suspect a combination of factors including genetic and environmental (see earlier post on the triggers of RA). Scientists are now beginning to unravel the complexities of RA and find that there may actually be a variety of sub-types of the disease. I hypothesize that future research into RA and other autoimmune diseases will reveal that genetics and environmental factors impact the way individuals present symptoms and respond to treatments. This knowledge may lead to definitions of RA sub-types and better treatments in the future. In the meantime, I’ll keep experimenting with treatments in order to find a combination that works.

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450px-Walking_ManThe other day I walked into the kitchen and my wife laughingly said to me, “You’re walking like Frankenstein”. I laughed back because I knew that I was like the “living dead” for many reasons but mostly because of changes in my joints. I have bursitis in both hips which radiates pain down the thigh and in the buttocks (I got two cortisone shots recently and they did nothing – but that’s another story), cartilage damage in both knees, and three surgeries on my ankles. Add to that, I could barely get out of bed and walk around this morning due to sharp pain in the same area of the right ankle that’s had two surgeries. I’ve felt that pain before which was from erosion in the heel bone causing spurs to dig into the Achilles tendon. Yep, I was walking stiffly and probably looked like a monster from a movie.

It’s a natural tendency to make adjustments due to pain or joints that aren’t working as designed. Joint changes from rheumatoid arthritis seem to be inevitable As bone and soft tissues are attacked, damaged, and eroded, the joints can no longer work as they should. Fortunately, disease modifying medications can slow down the damaging biochemical processes. In spite of being on medications, changes are still affecting my movement and activity.

When the term arthritis is mentioned, the first thing that comes to most people’s mind is probably bone damage. With the more common osteoarthritis (OA), there may be damaged cartilage causing bone to rub together. But with rheumatoid arthritis (RA), the immune system attacks the body’s own tissue. The capsule surrounding the joint, called the synovium, becomes enlarged due to an increase of immune cells. Eventually an overproduction of bone eroding cells and enzymes begins to erode bone tissue and soft tissues.[i] The soft tissues that hold the joint together including tendons, ligaments, and cartilage are also damaged.[ii] [iii] When all of these tissues become affected, the entire skeletal structure designed for movement cannot work properly. Add to that stiffness caused by RA, and the result is walking like Frankenstein!

My joints used for walking are changing and the effects are becoming noticeable not just to me, but to those around me. Add to that the fact that any hope for strenuous physical activity is pretty much gone for now. My daughter wants to go snow skiing but the best I could do is drive her there and sit in the lodge drinking cocoa. The hope is that treatments can keep the process at bay long enough so I can avoid more surgeries and using assistive devices just to carry out that common, everyday task we take for granted – walking.

Photo Credit: By Stefan Eggert (User:Berreu) (Own work) [GFDL (http://www.gnu.org/copyleft/fdl.html) or CC-BY-SA-3.0 (http://creativecommons.org/licenses/by-sa/3.0/)], via Wikimedia Commons

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