Posts Tagged ‘sulphasalazine’

20121205-061120.jpgI received an official rheumatoid arthritis diagnosis almost four years ago. In that period of time I went through multiple treatment schemes (see the My Meds page) including four biologicals (Enbrel, Cimzia, Humira, and Orencia) and three DMARD chemicals (sulphsalazine, methotrexate, and Arava) in addition to numerous NSAIDS and the obligatory prednisone. As mentioned in blog posts over the past couple of months, it became increasingly apparent that the combination of Orencia and Arava was just not working. Sticking my head in the sand and ignoring the signs could only last so long while my wife and doctor tried to convince me that it was time to try something else. The evidence was becoming overwhelming…unrelenting fatigue beyond comprehension, increase in the number and intensity of swollen and tender joints, new joints including one shoulder and both hips presenting with signs of attack by RA, missed work, and a level of brain fog never experienced before. In addition, it felt like the monthly Orencia infusions might just as well have been plain saline solution as there was no improvement afterwards. On top of that, Arava was wrecking havoc on my digestive system and the bathroom and I became quite friendly.

While driving into the doctor’s office today, the inevitable started sinking in and I got nervous wondering what would happen. Most of this anxiety is probably grounded in the fact that I’ve been through a slew of treatments and I was feeling like options were beginning to run out. After an exam and conversation about symptoms, my rheumatologist emphatically stated that it’s time to change treatment. She continually expresses hope that we can find a medicine combination that will work for me. She got out a piece of paper and made two lists. The one on the left was for DMARDS that I haven’t tried yet and she wrote down Imuran and Cellcept. On the right she listed biologicals that I haven’t tried and she listed Remicade, Rituxin, and Actemra. In the middle she listed the newly approved oral biological Xeljanz which she dismissed as a possibility for now stating that she wanted to see more long-term data on efficacy and safety before widely using it. She recommended Imuran since it’s been around longer and has better efficacy data for treating RA. Imuran is an immunosuppressant commonly used to help organ transplant patients avoid tissue rejection. It is also used to treat many autoimmune diseases including RA, lupus, and MS. Since three TNF blockers didn’t seem to work well for me, she argued against Remicade but said that we’d keep that option on the list just in case we want to try it later. She said that Rituxan helps some of her RA patients but not as many as she would like. Actemra is the newest antibody biological for RA approved in the United States and she said that she’s seen it help some of her patients. It’s different from the TNF blockers and Orencia in that it targets interleukin 6 which is part of the autoimmune processes linked to RA. So we landed on the Imuran/Actemra combination and await insurance approval to begin the infusions. A trip to the lab for blood tests to establish baselines were ordered. In the meantime, doses of prednisone are prescribed to knock down inflammation.

Changing treatments brings about many questions but also hope that maybe it will provide some relief. Because relief would be a good thing right now!

Creative Commons photo credit: http://www.flickr.com/photos/busy-pochi/5170100206/

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There is no cure for rheumatoid arthritis or for most autoimmune diseases for that matter. This is primarily because the specific underlying causes of autoimmune diseases are unknown.

The germ theory of disease, the idea that diseases are caused by microorganisms such as bacteria and viruses, was hypothesized by Louis Pasteur[i] and further described by Robert Koch via his Postulates.[ii] While not applicable to all diseases, the theory has been successfully applied to a myriad of diseases leading to amazing treatments, cures, and vaccines.


Microorganisms, primarily bacteria, have been hypothesized as a cause of rheumatoid arthritis for years. In fact, some early treatments of RA included antibiotics and similar drugs like sulphasalazine (still prescribed today). But, using Koch’s Postulates, no germ could be isolated or identified as triggering the disease. Some still propose using antibiotic protocol to treat RA (see http://www.roadback.org/). I’m curious about this approach and plan to write about it in the future. Now bacteria, as a possible trigger of RA, are back in the scientific news.

As I wrote about in an earlier post, researchers taking a systems approach hypothesize that there are three possible triggers of autoimmune diseases – genetics, bacteria, and a “leaky gut” (proteins from food leaking through intestinal wall and causing an immune response). This work is primarily directed by Dr. Fasano at the University of Maryland.[iii] Now researchers from Harvard University and New York University report research on mice that demonstrated a relationship between the presence of a common bacteria found in the gut and an immune response leading to arthritis.[iv] [v] Mice genetically susceptible to autoimmune arthritis were raised in germ-free environments. They demonstrated a lack of arthritic symptoms. The mice were then exposed to a single type of gut bacterium and they immediately began to show symptoms of arthritis. They also found that a certain type of T cell connected to the production of arthritis-causing antibodies was connected to the presence of bacteria. The researchers argued that the mice didn’t “catch” arthritis from bacteria, but that there’s an interaction between the genetic make-up of the mouse and the autoimmune response to bacteria. This finding supports Fasano’s work and also lends evidence to the genetic link due to the fact that all people don’t get autoimmune diseases when exposed to certain bacteria.

What does this mean for those of us with RA? Probably nothing for the immediate future. We can’t live in germ-free environments like the mice in the study. A general wiping out of bacteria in the gut would wreck havoc on the digestive system and current antibiotic treatments don’t work for everyone with RA. But perhaps this research will spark more attention and funding on these issues leading to potential discoveries of causes of autoimmune diseases leading to the development of effective treatments.

[i] http://www.accessexcellence.org/RC/AB/BC/Louis_Pasteur.php

[ii] http://www.medterms.com/script/main/art.asp?articlekey=7105

[iii] http://somvweb.som.umaryland.edu/absolutenm/templates/?a=837&z=2

[iv] http://www.focushms.com/?p=206

[v] http://cbdm.hms.harvard.edu/assets/Publications/2010/JoyceWImmunity.pdf

Photo Credit: Creative Commons License http://www.flickr.com/photos/worldworldworld/

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Many of the first medical treatments for RA were chemical drugs that were actually developed for other diseases. Disease-modifying anti-rheumatic drugs, or DMARDs, are the hallmark chemical treatments for RA.[ii] These small molecule chemicals attack or incapacitate the enemy of RA, inflammation, using various processes. Many of these processes are not fully understood by scientists but suppression of the immune system resulting in less inflammation is suspected.

Methotrexate, plaquenil, sulfasalazine, Arava, cyclosporine, Imuran, Cytoxan, and gold salts are commonly used to treat RA. All of these are rather simple chemicals in terms of design, development, and production. This also tends to make them less costly relatively speaking. In heavier doses, some of these drugs are used as chemotherapies for various cancers. Plaquenil is used to treat malaria. If you ever want to help the uninformed really understand the seriousness of RA, let them know that you are taking a chemotherapy drug! Because they are somewhat harsh chemicals, the lists of side effects are rather lengthy.

Sulfasalazine was originally used as an antibiotic. But it is also thought to impact inflammation in the gastrointestinal tract. As mentioned in an earlier post, it is thought that 2/3 of the immune system lies around the intestines so it makes sense that sulfasalazine may reduce inflammation by impacting this area. This was the very first drug prescribed for my RA. No chance was given to see its impact because about 7 days into popping these large pills, I developed a severe allergic reaction. This occurred over the weekend and I was very close to heading to the emergency room. It took over a week for the sulfa to get out of my system. Also during this time, the symptoms of RA stepped it up many levels…that’s when methotrexate was prescribed.

I like to call methotrexate (MTX) the “chemical weapon” of choice against RA. At higher doses, it serves as a chemotherapy drug for some forms of cancer. In this use, it actually acts as a cell killer…attacking cells that divide quickly (like cancer cells). At lower doses, MTX acts as an anti-inflammatory by affecting T-lymphocytes. Methotrexate is probably used by more RA patients than any other treatment and is regularly used in combination with biological treatments (a future post).

My experience with MTX was short-lived. I took the first dose (7.5mg) on a Saturday as many do in an effort to fight the common side effects of nausea and headaches. By week three, it was clear that I couldn’t tolerate it at all. Besides the constant nausea and headaches, my brain was in a state of fog, my body hurt (not just from the RA), and I was totally nonfunctional. My rheumatologist said that a portion of patients cannot tolerate MTX. I knew it would be me because of my sensitively to every medicine under the sun. That’s when Enbrel was started.

Even though I’m no longer taking any small molecule chemicals for RA, I’m glad that they exist and provide relief for many. But the side effects are many and patients need to be fully aware of them in an effort to weigh benefits and costs.


[ii] http://www.webmd.com/rheumatoid-arthritis/modifying-medications

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The causes of rheumatoid arthritis (RA) and most autoimmune diseases are unknown. This includes celiac, type 1 diabetes, lupus, multiple sclerosis, and ulcerative colitis. That’s a sad thing since these diseases are insidious.

Because of the lack of definitive information about these diseases, there are many speculations running wild around the internet and unsuspecting sufferers look for answers from any place they can find it. I was recently eating in a restaurant and the TV on the wall was running a product infomercial and there was a claim at the bottom of the screen…”Arthritis can be cured”. One of my friends pointed and said, “Look, you better check it out!” Of course, at the bottom of the product’s website is this fine print *The statements on this page have not been evaluated by the Food & Drug Administration. This product is not intended to diagnose, treat, cure or prevent any disease.

Since being diagnosed with rheumatoid arthritis, my curiosity and scientific training pushed me deep into the research literature. By far the best work I’ve found is from Alessio Fasano from the University of Maryland School of Medicine. He has an excellent article called “Surprises from Celiac Disease” in the August 2009 issue of Scientific American (you have to suscribe to read it but here is a link to story about the article).

While most of Fasano’s research is with celiac disease (a problem digesting the gluten protein in wheat), his work is beginning to shed light on other autoimmune diseases. He notes that a trio of triggers seems to be present. 1. an environmental trigger, 2. a genetic susceptibility, and 3. a “leaky gut”.

With rheumatoid arthritis, scientists has long suspected that an infection of some sort, an environmental trigger, sets off the immune system. That’s why some of the early medicines, like sulphasalazine, were derived from antibiotics. Some still advocate long term antibiotic therapy for RA (check out the Roadback website). But infectious triggers have never been pinpointed nor fully explained the causes of the disease.

Genetics also seem to be connected. Many people suffering from autoimmune diseases show a genetic marker for some type of histocompatibility leukocyte antigen (HLA). HLA proteins bind to objects that they mistakenly recognize as foreign in the body.  This sets off an immune response where T lymphocytes recognize the “foreign object”, call in reinforcements, and the immune system then fights the “invaders.” During this process powerful inflammatory chemicals called cytokines are released. These cause the symptoms of RA. Cytokine receptors, like tumor necrosis factor (TNF), have been the target of RA research for the past 20 years and resulted in powerful drugs like Enbrel. I’m very thankful that scientists figured this much out because I’m a recipient of their hard work. Enbrel seems to be working well for me thus far. A detailed description of the process can be found at Johns Hopkin’s.

This leads us to the third factor in the trio of triggers – the “leaky gut”. This one has been getting airplay in the internet for some time and I was suspicious when I first heard about it. It does sound rather weird. Up to 2/3 of the immune system lies around the intestines. That makes sense because we ingest so many things into our bodies through our mouths. Our defense system must be ready to combat invaders. The intestines normally have a tight wall that keeps particles from leaking into the rest of the body. Fasano’s work with celiacs is shedding light on how increased permeability of the intestines allows proteins to leak out into the body where they are immediately attacked by the immune system. The role of this in RA is speculative at this point but some relief has been found in some people by controlling their diet (milk and wheat proteins being the most common).

Creative Commons License http://www.flickr.com/photos/jkunz/

Creative Commons License http://www.flickr.com/photos/jkunz/

There are many more questions than answers right now. A quote from the editors about Fasano’s article sums it up, “Surprisingly, essentially the same trio …seems to underlie other autoimmune disorders as well. This finding raises the possibility that new treatments for CD (celiacs) may also ameliorate other conditions.” This gives me hope. Perhaps not for me directly since new and complicated medicines take many years to develop, test, and market. But I have hope for the millions of future sufferers of autoimmune disorders.

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I want to blog about arthritis for three reasons. 1. Its therapeutic to write about what’s going on with me. 2. To communicate with my friends and family. 3. Bring awareness to autoimmune arthritis.

First Signs

In May 2004, I started having severe eye pain, redness, and blurred vision. I ended up at an ophthalmologist and within 1 minute he pronounced that both eyes had acute anterior iritis – an inflammation of the iris. After performing some tests and prescribing continuous doses of prednisone steroid, he asked me if I ever had joint problems. I thought that this was odd coming from a physician dedicated to treating eye problems. He stated that iritis is a common symptom in autoimmune disorders. He said that there are blood tests but since I had no other symptoms, I could just wait and see what happens. I quickly forgot all about it.

Next Signs

In the fall of 2006, I began to have problems with my Achilles tendons. They were swollen, inflamed, and very painful to the touch. The left tendon was worse than the right. It affected my ability to exercise. After visiting an orthopedic surgeon who specializes in ankles, he suspected that there was tendonitis and/or tearing in the tendon. Upon examination, he stated that the problem was likely congenital because I have long leg bones causing the tendon to stretch. An MRI of the tendon revealed tears in the tendon. Surgery on the left tendon was performed in January 2007. He repaired the torn section and also performed a lengthening of the tendon in order to reduce the tension. I mentioned that the right tendon was also hurting and the doctor indicated that we should just keep an eye on it while the other one healed from the surgery. I was hiking by the summer of 2007 and snow skiing that next winter. However, by that time, my right tendon was bothering me enough so I headed back to the orthopedic surgeon. A MRI revealed tearing and the same surgery was performed on the right leg in April 2008. I recovered and was back to snow skiing by December 2008. Never the less, my legs never felt the same way before the surgery.

Putting it all Together

In January of 2009, I began to experience pain in the middle joints of my fingers on both hands. This was accompanied by morning stiffness and a lot of fatigue. I also had chronic hives, usually in the evenings, on my arms and legs. I visited my regular doctor and told him of my symptoms. After describing my history with the eye problems and Achilles tendon tearing, he began to suspect that I had an autoimmune disease – like rheumatoid arthritis (RA). One clue is that symptoms presented symmetrically on both sides of the body…iritis in both eyes, Achilles tendon problems on both sides, etc. He mentioned that fatigue is also a common symptom. He referred me to a rheumatologist – a specialist in arthritis and associated diseases.

After completing a long medical history survey, multiple office visits, numerous blood tests, and hand x-rays, the rheumatologist said that I have some sort of autoimmune arthritis. My blood tests were negative for rheumatoid arthritis factor (about 20-30% of people are negative but have the symptoms). But the bottom line is that this is a clinical diagnosis based on symptoms. There is no single blood test. He initially called it seronegative arthritis or spondylarthropathy. Some call it seronegative rheumatoid arthritis. Sometimes, blood tests convert to positive over time. Doesn’t matter to me – I knew I felt bad.

Autoimmune means that your body’s own immune system is attacking itself. There is no known reason why this happens. Similar autoimmune diseases include ankylosing spondylitis, psoriasis, Crohns disease, and lupus. Autoimmune arthritis differs from the more common osteoarthritis in that its cause is immunological, not trauma induced. Most people will have some osteoarthritis by the time they are in their 60s. Autoimmune arthritis affects millions of Americans and can start anywhere from the 20s-50s.

Since x-rays of my fingers revealed the start of bone erosion, the doctor started me on a medicine called sulfasalazine which was supposed to reduce inflammation. I had a terrible allergic reaction so that got halted and I was put on methotrexate. This is an immunosuppressant drug that is supposed to slow the progression of joint damage. After three weeks on that drug, my body clearly told me it didn’t like it…constant nausea, headache, feeing like a truck ran over me, etc. So, off to the doctor I went again. By this time, joint pain had extended to the base of my fingers, both wrists, both elbows, and my knees. My ankles were always hurting since before the surgeries. At times, I could not lift heavy objects and even climbing the stairs was laborious. My joints popped and cracked when moved. I was stiff most of the day and the fatigue was worsening. The fatigue is the hardest part for people to understand. I describe it like having the flu. I was prescribed prednisone steroids to check the inflammation. This is fine for a short period of time but not long term.

The doctor finally put me on a “biological” drug called Enbrel. It’s a protein designed to attach itself to inflammation-causing chemicals released by white blood cells in the joints. It must be self-injected once a week – it doesn’t hurt too much. The drug is made via a recombinant DNA process where an engineered human gene designed to produce the protein is grown and harvested. The retail cost is $1,800 a month! Thank God for insurance coverage and a $25 co-pay!

At this point, I slowed down on work, church, and other activities in an effort to rest and give some time for the Enbrel to work. After about 2 weeks, today is the first day that I didn’t wake up too terribly stiff and I actually had energy the entire day – didn’t even take a nap! I’m hoping this is a sign that Enbrel is starting to work – it usually starts working in a couple of weeks with full impact over a few months. But time will tell. Enbrel and related drugs suppress the immune system so I have to stay vigilant for infections. There is no cure for arthritis. But people successfully receiving treatment go on to live normal lives. My goal is to snow ski again next winter!

Some of the hardest parts of dealing with this are the drawn out processes of diagnosing, figuring out treatments, and explaining to people what’s going on. And you never know what’s around the corner. Flares can come and go. But through all of it, I’ve come to rely on God, family and friends. I have hope for the future. I have hope that medical treatments will work. I have hope that God will heal me. There is no big celebrity carrying the flag for arthritis. There is no special ribbon to be worn (maybe a DNA-shaped helix ribbon would work!). But I hope everyone reading this will be more aware of the issues. Ask questions. And above all, pray for me.

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