Antibiotics as a Treatment for RA?

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Using the Germ Theory of Disease (discussed in my previous post), microorganisms such as bacteria have been suspected for many years as being the cause of RA. But a direct link has never been found. Lately, some researchers found evidence that common bacteria found in the gut, along with genetics, may serve as triggers of autoimmune diseases. [i]

Another small group of primitive bacteria called mycoplasmas have also been implicated as a causative agent of various diseases generally[ii] and RA specifically.[iii] These bacteria don’t have cell walls and only live inside the body of another organism as a parasite (plant, animal, etc.). They are extremely hard to isolate in people but one set of researchers examining mycoplasmas stated,

The results suggest that a high percentage of RA patients have systemic mycoplasmal infections. [iv]

While mycoplasmas may be present in patients, this does not prove a direct cause and effect link between these bacteria and RA. Never the less, some researchers state that,

“Further study is necessary to prove that M. fermentans is a causative microorganism of RA; however, the new mechanisms of disease pathogenesis provides hope for the development of effective and safe immunotherapeutic strategies…”[v]

If bacteria are linked to RA, then antibiotic therapy would logically follow suit. The tetracycline family of antibiotics, which is effective in treating mycoplasmas, is proposed for antibiotic protocol therapy. The most commonly used tetracycline antibiotic used in treating RA is minocycline.

Some studies show that patients given antibiotic protocol did not show benefit.[vi] [vii] [viii] Other studies demonstrate a reduction in RA symptoms. [ix] [x] Two fairly recent reviews of controlled experimental studies on the efficacy of the antibiotic tetracycline family revealed mixed results leading to insufficient conclusions.[xi] [xii] The exact reason why antibiotics may impact RA is not fully understood but it may include antibiotics killing off bacteria that are causing RA or it may simply be that antibiotics cause a reduction of inflammatory cytokines.[xiii] The scientific evidence for the use of at least the tetracycline family of antibiotics is unclear at this time.

Antibiotic protocols (AP) are not widely espoused by official medical rheumatology societies and non-profit arthritis organizations. In spite of this, there are several groups devoted to antibiotic treatments for autoimmune diseases and some rheumatologists will prescribe AP (see http://www.roadback.org/, http://rheumatic.org/, http://www.rheumaticsupport.net/index.php).

In conclusion,

1. Bacteria are not yet clearly linked as a direct cause of RA. Mycoplasmas may be one group of bacteria eventually implicated in autoimmune diseases.
2. Bacteria in the gut, along with genetics, may serve as a trigger for autoimmune diseases.
3. The efficacy of antibiotic treatments for RA is unclear at this time.
4. More research is needed to pinpoint the cause(s) of RA. All possible causes, including bacteria, should continue to be investigated.

The gut bacteria/genetics combination recently discovered shows the most promise. But I suspect that any resultant treatments from this line of research (many years down the line) are not likely to be generic, whole body administration of antibiotics. They are more likely to be genetic-based treatments designed to impact some biochemical process connected with bacteria’s impact on the immune system.

Personally, if I ever get to the spot where the spectrum of biologic and other current RA treatments don’t work for me, I will definitely raise the topic of antibiotic protocol with my rheumatologist. In the meantime, you can read about one person’s experience with antibiotic protocol at her blog http://rheumforgod.wordpress.com/ap-diary/.

Disclaimer: This short post is not meant to serve as an exhaustive review of the topic and related studies. My personal goal is to learn a little, share information with others, and keep discussions ongoing. I am neither promoting nor refuting the use antibiotic treatments for RA.

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

[ii] http://microbewiki.kenyon.edu/index.php/Mycoplasma

[iii] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2433307/

[iv]http://www.ncbi.nlm.nih.gov/pubmed/10402069?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

[v] http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WBK-4RXK6BC-3&_user=10&_coverDate=05%2F02%2F2008&_rdoc=1&_fmt=high&_orig=search&_origin=search&_sort=d&_docanchor=&view=c&_searchStrId=1444535875&_rerunOrigin=scholar.google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=40fa71c12bc87f80e946de33d9b718d2&searchtype=a

[vi] http://onlinelibrary.wiley.com/doi/10.1002/art.1780140607/abstract

[vii] http://www.jrheum.org/content/28/9/1967.short

[viii] http://www.ncbi.nlm.nih.gov/pubmed/8434246

[ix] http://www.annals.org/content/122/2/81.full

[x] http://www.okmicro.co.jp/Abt/MinocyclineERA1.pdf

[xi] http://www.formularymonographs.com/PDF/fandc-olf5026.pdf

[xii] http://www.jrheum.org/content/30/10/2112.abstract

[xiii] http://www.formularymonographs.com/PDF/fandc-olf5026.pdf

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A Bacterial Trigger for RA?

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.

bacteria

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.

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[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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Suffering with a Chronic Illness

About a year ago, in the midst of a bad RA flare and medications that weren’t working, a friend in his late 20s asked how I was doing. I proceeded to tell him about the pain and fatigue that were plaguing me. He got a perplexed look on his face and stated that he couldn’t understand how I could live like that. He avowed that he would not be able to handle it. I found this intriguing because at the time, I had lived with the pain so long and it never dawned on me that I couldn’t handle it. Sure, there were tough times, but it seemed to just become part of my life. I realized that my friend’s response was really based on his lack of experience with suffering. His life was relatively stress-free and he never experienced any major type of suffering. Of no fault of his, he simply lacked perspective.

According to research on life events, personal illness makes the list as one of the major contributors of stress (its rank depends on the currency of the research). [i] [ii] My young friend saw my RA as too stressful. He was seeing it from an acute, one time perspective. Chronic health issues like rheumatoid arthritis are different than acute ones in that they happen over time causing the person to make slow adjustments in perceptions. So how was it that I didn’t perceive my struggles with RA the same way as my young friend? A recent conversation with another friend more experienced with life in general, and various kinds of suffering specifically, reminded me of a verse from the New Testament.

And we rejoice in the hope of the glory of God. Not only so, but we also rejoice in our sufferings, because we know that suffering produces perseverance; perseverance, character; and character, hope. And hope does not disappoint us, because God has poured out his love into our hearts by the Holy Spirit, whom he has given us. Romans 5: 2b-5

Rejoice in our sufferings? This sounds crazy! I would never ask for suffering and would not wish it on anyone. However, I’ve come to learn that constant suffering with a chronic illness such as RA can lead to a level of perseverance, character building, and eventually hope. Anyone who suffers with a chronic illness learns to persevere and cope. It’s a survival mechanism. Over time, this builds one’s character. I’m always amazed at the patience and wisdom of those who experienced suffering. It’s like they have a quiet understanding…a secret of sorts. Think of a terminally ill person or someone who experienced the horrors of war first hand. And finally, there’s hope. Even in the midst of seemingly hopeless situations where RA pain and fatigue are constant, there’s always hope of a better day, new treatments, and no more suffering. Sure, I want RA to go away. But for the time being, I can be thankful for the perspective-giving lessons of suffering with a chronic illness.

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[i] http://occmed.oxfordjournals.org/cgi/reprint/51/4/287.pdf

[ii] http://www.rrrcc.org/pdf/GetFitRioHolmesRahe.pdf

Photo credit: Creative Commons License http://www.flickr.com/photos/dexxus/

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Celebrations

Today is a time for multiple celebrations. Here are a few of the reasons. Upon waking this morning, it was clear that the nasty flare of the past couple of weeks backed off enough that I could go about the business of living without RA screaming too loudly at me all day. The weather in Seattle was near perfect…70 degrees, sunny, and no humidity. It’s what we live for the other 9 months of the year. My 12 year old daughter’s soccer team is tearing it up at a tournament and she scored an amazing goal…in the air, over the defense and keeper, and into the corner of the goal. My friend of 20 years, Lee, was in town on business and we were able to meet for a true Pacific Northwest dinner…crab. Lee truly understands my battle with RA. While mostly in remission, he suffers with ankylosing spondylitis, an autoimmune disorder similar to RA which tends to affect the spine and other large joints. I’m very thankful for all of these things.

Finally, I wish to thank all of the readers of my blog which has been recently recognized on several fronts. My blog was approved this week as a member of the Patient Blogger Code of Ethics. My blog was chosen as one of the top 40 arthritis blogs by the Medical Assistant Schools. Michelle, who writes the blog Life and Times of a Girl with RA MCTD, and Sara who writes the Single Gal’s Guide to Rheumatoid Arthritis (who, by the way, has the best cartoons about her life), nominated my blog for the One Lovely Blog Award. Part of the award is to identify blogs that impact me and pass on the award. Here’s a list of some of my favorites (some have already been recognized).

The Seated View – Lene truly inspires me as she’s struggled with RA for many years and maintains a positive attitude. She is a regular contributor as an Expert at MyRACentral.

Dual Sport Life – I love reading Terry’s stories of kicking back at RA by getting on a motorcycle for some long ride in the country. We seem to have similar experiences with RA and medications and I love to hear from another man with RA.

Living it, Loving It – Lana tells it like it is without holding back. And, I love hearing the music playing in the background when opening her blog (I’m especially fond of Rascal Flatts).

Rheum for God – This author weaves faith into her posts and I’m interested in learning how antibiotic protocol treatment works for her (plus the pics of her babies are sweet).

RheumaBlog – Wren is a long time RAer with a deep mind and always posts thoughtful replies on my blog.

RAwarrior – Kelly is a tireless RA Warrior. She and I started our blogs about the same time.

∞itis – I can really relate to posts by “Warmsocks”. Plus, we both live in Washington state!

Frozen Woman: Life with RA – Laurie presents a real professional blog.

RAguy – His 60 second Guide to RA is still the best! Use it!

There are so many more excellent blog writers out there and I can’t mention them all. Thanks to everyone of them and for the service provided to the RA community. I just wish we could all get together in person sometime!

Andrew

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RA Pain – Types, Causes, and Treatments

I’m at a loss about how to describe the various types of pain I’ve experienced with RA. As I prepare this post, all of my PIP finger joints (middle joint) are swollen and tender to the touch. The DIP joint (tip) on my left pinky smarts. The MCP joint (base of finger) on my left middle finger lets me know when I grab the steering wheel. Both wrists hurt when I flex them. My right elbow displays a sharp pain right above the joint. Both knees ache and crunch when moved. My calf muscles feel stretchy and stiff. Both Achilles tendons sting…the right one is bad enough that it was difficult to drive home from work today. The sides of my feet hurt when I press on them. While this day may not typical, one thing is certain…some sort of pain is always present with RA.

Sometimes I find it hard to pinpoint the source or cause of the pain. Yet my analytical mind wants to understand the underlying reasons. Perhaps knowledge can lead to pursuit of the right treatment. But it’s probably more curiosity than anything since my stomach can’t handle oral NSAIDs, I try to avoid taking inflammation-reducing prednisone as much as possible, and I tend to shun narcotic pain relievers for their side effects.

Pain is the body’s way to telling you something is wrong. According to one source,

“[Pain is] an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage. While it is unquestionably a sensation in part or parts of the body, it is always unpleasant and, therefore, an emotional experience.”[i]

Pain can be classified as either acute – short term, or chronic – long term.[ii] While some RA induced pain may be acute, it can come and go depending on what joint is being affected, much of it is chronic. Pain sources can be nociceptive – caused from the stimulation of local nerve receptors, or non-nociceptive – caused by problems with the central nervous system.[iii] RA pain is nociceptive since it tends to be localized to various inflamed or damaged tissues. Nociceptive pain can be further divided into somatic – localized to an area resulting from damage to the musculoskeletal system, and visceral – non localized pain.[iv] With somatic pain,

“Patients may describe this as sharp, aching, and/or throbbing pain that is easily localized.” [v]

Pain associated with RA is typically chronic, nociceptive, and somatic. Management for this type of pain is facilitated through the use of analgesics like acetaminophen (Tylenol), non-steroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, or narcotics.[vi]

Another type of pain caused when the nervous system is damaged, called neuropathic pain, may also be associated with RA. [vii] For example, the tingling sensation associated with carpal tunnel syndrome I’ve experienced lately is caused by pressure on, or damage to the median nerve that enters the hand.

With RA, the first and foremost goal is to treat the cause of the pain – inflammation. In this regard, my thought is, “Humira, do your thing so inflammation and pain is reduced.” If not, I’ll be forced to take more drastic actions such as treating the pain symptoms directly. That’s where my treatment options become less available. I guess I’m left with Tylenol, the hottub, topical Voltaren gel (an NSAID), and rest! If that doesn’t work, perhaps I’ll pull out the prednisone tomorrow. I’d prefer to treat the cause directly and not the pain symptoms. In the meantime, I’ll try “taking” some of those peanut M&Ms my daughter brought home for me from back-to-school shopping!

Photo credit: Creative Commons License http://www.flickr.com/photos/azariusrex/

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[i] American Pain Society. Principles of Analgesic Use in the Treatment of Acute Pain and Cancer Pain. 5th ed. Glenview, IL: American Pain Society; 2003.

[ii] http://www.texmed.org/Template.aspx?id=1462

[iii] http://www.ehow.com/about_5393798_somatic-pain-vs-visceral-pain.html

[iv] http://www.painbalance.org/nociceptive-pain-overview-1956304245

[v] http://endoflife.northwestern.edu/pain_management/part_one.cfm

[vi] http://www.medterms.com/script/main/art.asp?articlekey=10933

[vii] http://www.painbalance.org/neuropathic-pain-overview-2772791

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RA and Tendons – My Achilles Heel

Walking is just not the same as it used to be. In an earlier post, rubbery legs were mentioned. Knees with damaged cartilage cause them to buckle and make it difficult to climb stairs. Tender toe and ankle joints make walking slow. Stiffness in the joints caused by inflammation cause an awkward gait. But these symptoms pale in comparison to what RA is doing to my Achilles tendons.

When joints become inflamed during RA, tissue damage on many fronts can occur. Most people familiar with RA are aware that hard bone tissue can become eroded (like has occurred in my finger joints). But joints are a conglomeration of multiple tissues such as bone, cartilage, and tendons and all can be damaged from RA-induced inflammation. Cartilage protects bones from rubbing on each other. Tendons connect muscles to bones.

Generally speaking, inflammation in a tendon is called tendonitis.[i] Many people experience tendonitis from repetitive use…have you ever gardened too long and had painful hands afterwards? Or think tennis elbow. In RA, ongoing tendon inflammation is caused by the messed up immune system attacking the tissues. According the Johns Hopkins website on rheumatoid arthritis, “Persistent tenosynovitis and synovitis leads to the formation of synovial cysts and to displaced or ruptured tendons.”[ii] Soft tissues, including tendons, can be damaged by RA. Many people with RA have tendonitis of the flexor tendon in the hand. When tendons are damaged, movement becomes difficult if not impossible.

In 2006, before an official RA diagnosis, I experienced chronic tendonitis in my Achilles tendons, the largest tendon in the body that connects the calf muscles to the heel. After a long history with conservative treatments that didn’t help (ice, ibuprofen, rest), an orthopedic surgeon discovered via MRI that I had a partially torn tendon. He performed surgery (see photo of one of the scars) to repair the tear and even “lengthened” the tendon by disconnecting it from the muscle and reattaching it lower down the leg. This is called a gastroc slide procedure[iii]…think of taking the tension off a rubber band. The tears in the tendons were attributed to my build and genetics. Within a year, the other ankle had the same problem and another surgery was in order. Long story made short…additional symptoms of RA appeared and the puzzle began to be put together. My primary care doc was the first to connect the Achilles tendon problems with potential autoimmunity and a diagnosis finally came after seeing a rheumatologist. Now I knew the reason for the tendon problems.

Hope that the surgeries repaired my Achilles tendons forever was shot down by the fact that, despite being on disease modifying drugs (currently Humira) designed to slow down inflammation, they continue to be tender, swollen, stiff, and painful, with heel spurs forming. During a flare, my tendons are among the first to “scream” at me. Movement of my legs is just not what is used to be and I oftentimes find myself walking in a stiff way that avoids stretching the Achilles tendon and calf muscles. Of the myriad RA symptoms, this indeed has become my “Achilles heel”![iv]

Photo #1 Credit: Creative Commons License http://www.flickr.com/photos/natashavora/

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[i] http://www.webmd.com/osteoarthritis/guide/arthritis-tendinitis

[ii] http://www.hopkins-arthritis.org/arthritis-info/rheumatoid-arthritis/rheum_clin_pres.html

[iii] http://www.footeducation.com/gastrocnemius-slide-straver-procedure

[iv] http://wordsmith.org/words/achilles_heel.html

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RA and Type A Personality – Not a Good Mix

Our house was built in 1980. The structure has strong bones and suits our needs just fine. But in 2004 when we bought it, it was clear that the doors and woodwork were tired and needed updating. Besides that, I really hate those hollow doors made of cheap plywood. In 2006 we bought interior solid 4-panel pre-hung doors for the entire house including all rooms and closets. Those got finished and installed within a few months (see photo). The baseboard and casing trim woodwork was the next project. After careful measuring and re-measuring, I ordered over 3,000 linear feet of fir trim which was quickly delivered to my garage. It was about this time that the symptoms of RA began creep in. Before being officially diagnosed, I had surgery on both Achilles tendons. The surgeries, coupled with increasing fatigue put all woodworking work on hold.

The pile of wood in my garage ate at my psyche…I wanted it done and installed. But RA had caused a change in those plans. Finally this spring, one of my sons and I began to tackle to job. Stations were set up and I taught him how to finish the wood which involved numerous steps. Piles of high quality finished wood began to appear (see photos). I was proud of my son for his attention to detail. With a few days off from work planned this week, my other son and I set out to start installing the trim. Yesterday was spent teaching him how to remove the old trim wood. A large pile of old junky wood was created. By evening, I could barely move. My wife warned me to take something for either pain and/or sleep when I went to bed but I promptly ignored her. By 5:00 a.m. I was awake and stiff as a board. With all of the old trim removed, I was determined to start installing the new wood today. My wife gently reminded me to take it slow today or even take the day off. My type A personality got in the way and I again ignored her.

Now I sit here with pain in every arm, hand, fingers, knees, and ankles…stiff as a board and with no energy. Getting out of my chair is downright difficult. Alright, I’m hard headed and refuse to learn. I still think that I’m healthy enough to tackle any project. I never learn my lesson. Sure, I’ll take a day or two away from the project. But I’ll likely “forget” and be right back in the same place tomorrow…the deck needs its annual staining! So much for the recommendation for RAers to “pace yourself”.

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Kinase Inhibitors – New Potential Disease Modifying Drugs for RA

For those of us with RA who regularly self-inject medicines (biologicals and/or methotrexate), a new set of oral medications are being developed. These are called kinase inhibitors and they show potential in treating the inflammation caused by RA. Kinases are molecules that have been linked to cellular pathways that produce inflammation-causing cytokine proteins. In RA, it’s these cytokines that ultimately cause the tissue destroying symptoms (see earlier post). If you’d like to read more about the biochemical processes involved with kinases, download on this brief article from the Journal of Rheumatology.

kinase signaling

Kinase inhibitor drugs are being developed for multiple diseases including some forms of cancer, diabetes, and inflammatory diseases including rheumatoid arthritis. A recent book published in 2009[i] documents over 100 potential kinase inhibitor medicines. It is reported that this class of drugs have huge marketing and profit potentials (upwards of $58 billion in 2010). [ii]

In a recent video, Dr. Gray Firestein from the University of California San Diego mentions the potential of two oral kinase inhibitors for RA currently in human clinical trials. The first group is called Spleen tyrosine kinase (STK) inhibitors. [iii] [iv] The pharmaceutical company AstraZeneca is already preparing for the manufacture and distribution of a new STK inhibitor called fostamatinib disodium.[v]

Another class of drugs are called janus kinase (JAK) inhibitors. According one group of researchers working with a JAK drug being tested by the pharmaceutical company Pfizer,

“Researchers tested several doses of the Pfizer drug in 24-week, Phase II studies, with some proving highly effective in providing relief from rheumatoid arthritis symptoms and near remission of disease activity…”[vi]

Comparisons between the JAK oral kinase inhibitors and common biological drugs like Humira are being planned. There have been a few side effects noticed in the clinical trials including diarrhea, increased cholesterol levels, and increased blood pressure. [vii] But according to one published study,

“If the results seen in phase 2 studies are confirmed in larger phase 3 studies, we may soon have new, oral DMARD therapies available.”[viii]

I’m encouraged by the new potential kinase inhibitor oral treatments for RA. Perhaps someday in the near future, I’ll be popping pills instead of injecting Humira. This is good news because a large group of RA patients do not respond to the biological therapies. [ix]

A reader send me an informative article on Kinase inhibitors (click here for PDF file on oralkinaseinhibitors).

Postscript to my last post…all tests for diabetes and hypothyroidism were negative!

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[i] http://www.wiley.com/WileyCDA/WileyTitle/productCd-0470278293.html

[ii] http://www.drugresearcher.com/Research-management/Report-predicts-kinase-market-to-reach-58.6bn-in-2010

[iii] http://www.ncbi.nlm.nih.gov/pubmed/18447591

[iv] http://jpet.aspetjournals.org/content/319/3/998.full

[v] http://www.nature.com/nrd/journal/v9/n4/full/nrd3155.html

[vi] http://www.reuters.com/article/idUSN1631123820091017

[vii] http://www.ncbi.nlm.nih.gov/pubmed/18447591

[viii] http://journals.lww.com/co-rheumatology/Abstract/2010/05000/Kinase_inhibitors__a_new_approach_to_rheumatoid.16.aspx

[ix] http://www.nature.com/nature/journal/v423/n6937/full/nature01661.html

Photo credit, Creative Commons License http://www.flickr.com/photos/thejcb/

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Autoimmunity – The Battle Inside My Body

A recent experience got me thinking about autoimmunity once again. Last week a lingering tingling in my hands prompted a call to my rheumatologist. He called back on Friday evening at 7:00 (after most people already called it a work week!) and asked me to come in the following week. After a few minutes in the exam room, he quickly pronounced that I had carpel tunnel syndrome…nerve damage (parasthesia) to the median nerve in the wrist. Although it could’ve been a side effect of taking Humira, the diagnosis was not a much of a surprise as I guessed this was the culprit. Carpel tunnel syndrome is commonly associated with RA.[i]

During the process of the doctor visit, I mentioned to the nurse and doctor that I had lost about 10 pounds in the past few months. For most folk, this would be a welcome thing. But I was not trying to lose weight and nothing else in my life had really changed lately. Unlike the mentioning of a few other symptoms (e.g. a recent flare including increased joint pain), this garnered attention and prompted a slew of questions and digging through the doctor’s notes which included my most recent blood work. The rheumy noted that my glucose level was slightly elevated previously (yes, I remembered him telling me this a few months back). This, of course, turned the discussion towards diabetes. Another glucose test along with a c-peptide test was ordered. He also mentioned thyroid problems as a possibility. My mother had autoimmune hypothyroidism (Hashimoto’s Disease) years ago eventually resulting in the removal of her thyroid. A complete battery of thyroid tests was also ordered. Off to the lab I went for a new blood draw.

While the lab test results are pending and I try to avoid thinking too much about it, I remembered that type I diabetes and Hashimoto’s Disease both have an autoimmune basis (specific organs are attacked in both). My recent set of symptoms may simply be part of RA and I can’t draw any definitive conclusions at this time. I’ve been down this road before as several years ago my first autoimmune symptom was uveitis– inflammation of the eyes. But once again I found myself asking the question, “Why does the body attack itself?” The simple answer is that scientists don’t really know although environmental and genetic factors are implicated (see earlier post on suspected triggers). But once a trigger occurs, the immune system mistakenly identifies your own tissue as foreign and then attacks it (see biochemistry of RA post). There are dozens of autoimmune diseases – rheumatoid arthritis, type I diabetes, lupus, Crohn’s disease, and psoriasis are among the more common. Patients with one autoimmune disease tend to be more prone to get another and there appears to be a genetic disposition.

The American Autoimmune Related Diseases Association (AARDA) is the only non-profit group devoted to autoimmunity. This organization provides a wealth of relevant information and support materials. According to their website, 50 million Americans suffer from an autoimmune disease. That’s about 20% of the population! Below are some surprising statistics about autoimmune diseases that are posted on the AARDA website. I encourage readers to pass this information onto friends and health care providers. The bottom line in my mind…

• Autoimmune diseases affect large numbers of people
• The symptoms can be serious and chronic
• Causes and cures are unknown at present
• More research is needed
• There is much ignorance about autoimmune diseases and how they affect people

Autoimmune Disease…is a major health problem.
• Researchers have identified 80-100 different autoimmune diseases and suspect at least 40 additional diseases of having an autoimmune basis. These diseases are chronic and can be life-threatening.
• Autoimmune disease is one of the top 10 leading causes of death in female children and women in all age groups up to 64 years of age.
• A close genetic relationship exists among autoimmune disease, explaining clustering in individuals and families as well as a common pathway of disease.
• Commonly used immunosuppressant treatments lead to devastating long-term side effects.
• The Institute of Medicine reports that the US is behind other countries in research into immune system self recognition, the process involved in autoimmune disease.
• Understanding how to modulate immune system activity will benefit transplant recipients, cancer patients, AIDS patients and infectious disease patients.

…faces critical obstacles in diagnosis and treatment.
• Symptoms cross many specialties and can affect all body organs.
• Medical education provides minimal learning about autoimmune disease.
• Specialists are generally unaware of interrelationships among the different autoimmune diseases or advances in treatment outside their own specialty area.
• Initial symptoms are often intermittent and unspecific until the disease becomes acute.
• Research is generally disease-specific and limited in scope. More information-sharing and crossover among research projects on different autoimmune diseases is needed.

…offers surprising statistical comparisons with other disease groups.
• NIH estimates up to 23.5 million Americans have an AD. In comparison, cancer affects up to 9 million and heart disease up to 22 million.
• NIH estimates annual direct health care costs for AD to be in the range of $100 billion (source: NIH presentation by Dr. Fauci, NIAID). In comparison, cancers costs are $57 billion (source: NIH,ACS), and heart and stroke costs are $200 billion (source: NIH, AHA).
• NIH research funding for AD in 2003 came to $591 million. In comparison, cancer funding came to $6.1 billion; and heart and stroke, to $2.4 billion (source: NIH).
• The NIH Autoimmune Diseases Research Plan states; “Research discoveries of the last decade have made autoimmune research one of the most promising areas of new discovery.”
• According to the Department of Health and Human Services’ Office of Women’s Health, autoimmune disease and disorders ranked #1 in a top ten list of most popular health topics requested by callers to the National Women’s Health Information Center.[ii]

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[i] http://www.webmd.com/pain-management/carpal-tunnel/carpal-tunnel-syndrome

[ii] http://www.aarda.org/autoimmune_statistics.php

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What is an RA Flare?

I can never sit for longer than an hour or so without getting quite stiff. Yesterday, I got up from my chair at church in order to move around a little. As I arose from the chair and put weight on my legs, a sharp pain hit my left knee causing me to almost buckle and fall down. I could barely walk. My right knee has always been the “problem child”…an MRI demonstrated damaged articular cartilage in that joint. But the problems with the left knee were new. On top of this new experience, I noticed an increase in pain and swelling in my fingers, wrists, elbows, and ankles and a decrease in energy. I’ve also experienced tingling in my hands to past few weeks (See earlier post. On a side note, my doctor called me back on Friday evening at 7:00 p.m. – how’s that for service? He didn’t think that the tingling was a side effect of Humira but wanted to see me as soon as possible – I have an appointment tomorrow at noon). I found myself reaching for the prednisone yesterday in an effort to knock down the inflammation and applying Voltaren gel to affected joints. I hadn’t done that in a long time. It became obvious that I’m experiencing a rheumatoid arthritis flare.

The term flare is bantered around routinely. Yet a clear understanding seemed to elude me. Dictionary.com’s medical dictionary gives the following definition for the term flare:

Function: n
1 :  a sudden outburst or worsening of a disease flare s  in rheumatoid arthritis —

Interestingly, this definition is applied to RA. But it doesn’t define what it looks and feels like. I suspect that the vagueness of the term is because of the lack of its use in science and the fact that RA affects people differently. One website describes it as “acute episodes of pain and inflammation.” [i] Scientists routinely use the term “flare” in the research literature but fail to adequately define it. (see this study for example). In one research study, the scientists stated,

“A flare was defined per protocol as an increase of five in active joint count or an increase from zero to three compared with the situation at week 28 (an active joint is swollen or tender on pressure; counting of joint groups in one hand or foot as above)”.[ii]

This definition, while perhaps practical for documenting the efficacy of a particular treatment, doesn’t seem to capture the essence of a flare. In 2009, one group of researchers attempted to develop a standardized definition. Using interviews with 120 rheumatologists and 11 patients, they proposed the following definition:

“(a) flare is any worsening of disease activity that would, if persistent, in most cases lead to initiation or change of therapy; and a flare represents a cluster of symptoms of sufficient duration and intensity to require initiation, change, or increase in therapy.” [iii]

While lacking clarity regarding duration (how long is a flare?), this definition starts to provide meaning with which I can relate. RA patients could fill in the blank on this sentence, “I know I’m having a flare when….”. For me, it’s when I reach for the prednisone and Voltaren gel and feel worn down. That’s a sure sign of a flare. How long will the current flare last? Who knows. But it will pass and I’ll hopefully return to “normal”…as normal as it can be with RA!

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[i] http://www.arthritistoday.org/conditions/rheumatoid-arthritis/self-help-for-ra/arthritis-flare.php

[ii] http://www.cobratherapie.nl/pdf/Boers%20et%20al%20Lancet%201997.pdf

[iii] http://www.jrheum.org/content/36/10/2335.abstract

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