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Ed Harris – My Story
Diagnosis and Early Symptoms
I was diagnosed with CREST syndrome in January of 1990, but had initial symptoms for
several years before diagnosis. My approach from the onset has been to read
everything I could find on the disease and decide on my own course of treatment. (I had
to change physicians before I could find one who was willing to let me take charge of
my own treatments!) I am a computer expert and was fortunate enough to be able to
obtain a free subscription to Medline on CD ROM and thus have had access to all of the
research literature worldwide even before it was readily available on the Internet.
The conventional medical approach for treating this disease is to wait until symptoms develop and then try to treat the symptoms. This made no sense to me at the time of diagnosis and still does not. Even before I understood what I now do about the disease, it was obvious to me that trying to prevent the disease from progressing would potentially be “easier” than dealing with symptoms after they arose. In 1991, I began to have severe heartburn, which is characteristic of CREST syndrome. This is because the lower esophageal sphincter loses muscle tone as part of the disease, resulting in acid reflux, i.e., the backup of stomach acid into the esophagus, which is what heartburn is. At the time I was taking Procardia to treat my Raynaud’s symptoms. My physician had either not known or failed to mention to me that Procardia and all other similar medications have a side effect of reducing the lower esophageal sphincter pressure, thus increasing heartburn! I dropped the Procardia, which improved the heartburn, but my Raynaud’s got worse. So, back to the research literature. I quickly discovered that some researchers were experimenting with a drug called Yohimbine for treating Raynaud’s (the drug has been used for centuries as a natural aphrodisiac and is now mostly used to treat certain forms of impotence!). It turns out that it does not have the side effect problem that Procardia does, and I have been using it with reasonably good results since 1992. Meanwhile, my heartburn continued to get worse and was not fully controlled by large doses of Prilosec. Also, by late 1992 I had become chronically chilled, to the point where I was wearing sweaters in the summer and raising the heat in my car so much my family was constantly complaining about suffocating from the heat! Search for a Potential Treatment
In early 1993, I began a much more thorough literature search to see if I could get a
better understanding of the disease process and perhaps discover a way to either stop
or delay the normal progression. I located some little known articles from the
Netherlands that showed a very significant finding about scleroderma that appears to
have been missed by virtually all scleroderma researchers. It turns out that in
scleroderma patients with Raynaud’s, these researchers had discovered that the red
blood cells clump together very abnormally as compared to either normal people or even people with primary Raynaud’s (same symptoms, but no underlying serious disease). They were using a treatment called plasmapheresis to treat the Raynaud’s, and had discovered that it had a significant effect on scleroderma related Raynaud’s but no effect on primary Raynaud’s. Of even more import, the plasmapheresis treatment resulted in a return to normal red blood cell aggregation that lasted for a significant time following treatment. I called the researchers as well as a clinician in the Netherlands and learned that they had been using it clinically there for a while with good success with CREST patients, but not as good results with diffuse scleroderma patients. The treatment appeared to work even for the more severe patients, but the treatment had to be done so often there were bad side effects from the treatment after 12 to 18 months. This gave me a clue as to what might be going on in scleroderma. By doing significantly more literature research, I was able to satisfy myself that most, if not all, scleroderma symptoms could be accounted for simply by the potential long-term effects of abnormal red blood cell aggregation. I won’t go into detail here, but I have access to literature to support this theory. Ironically, at the time I did this, the idea of progressive damage was not generally discussed in the literature, but in the past few years, I have noticed that this is now the generally accepted theory as to why there is long-term damage. However, I have not seen any mention of the abnormal red blood cell aggregation as a potential “first cause”. Plasmapheresis, by the way, is a very crude but effective procedure. What is done is to insert one needle into a vein on one arm, and another needle into a vein on the other arm. A continuous flow machine removes blood from one arm, separates out the red and white blood cells from the plasma, discards the plasma, re-mixes the red/white blood cells with either sterilized albumin or donated plasma, and puts the new mixture back in the other arm. It takes about two hours, is somewhat uncomfortable once they get the needles in (I am hard to stick, unfortunately), and leaves me feeling weird and tired for a few hours after treatment. Scleroderma, as well as other autoimmune diseases, involves antibodies that attack the body instead of foreign cells. The treatment supposedly “cleans” about 80% of the blood during each treatment, removing most of the antibodies. My own theory at this point is that the antibodies themselves are directly causing the abnormal red blood cell aggregation, and removing many of them returns the blood to close to normal for a time until more antibodies are generated. I put together a treatment plan, submitted it to my physicians, and after months of effort actually managed to convince my insurance company to fund the treatment. I began treatments in the fall of 1993. Based on the research results from the original studies, I decided on an initial treatment cycle that consisted of one treatment per week for four weeks, followed by a two month layoff, then the cycle repeats, for a total of 16 treatments per year. Initial Results
After one year of treatments my reflux was significantly improved and while I was still
somewhat chronically chilled it was not as bad as it had been before starting the
treatments. After two years of treatments my reflux was under complete control with a very low dose of Prilosec (later switched to Prevacid). And, I was no longer chronically cold at all. These are nice results, but they are subjective. Of much more significance is the fact that my hematocrit value (a quantitative measure of the percentage of red blood cells), which had been abnormally low for the previous 8 years, returned to a normal range following treatment. With continued treatment, my hematocrit values now are generally in the normal range for at least two months following each round of treatments! One other significant quantitative measure that supports the theory that the plasmapheresis treatments are stopping the progression of the disease is the results of repeated pulmonary function tests (PFT). In June 1994, I had an initial PFT that showed that while most measures, e.g., lung capacity, were normal or above normal (I exercise a lot), the gas exchange ability of my lungs had declined to about 68% of the expected value. This is common with CREST and if it continues can be very serious, leading to pulmonary fibrosis and pulmonary hypertension, which is currently untreatable. One year later, in May 1995, I repeated the PFT. The results of this critical measure were unchanged. At that time I considered this to be the best possible result since these changes to the lungs are normally irreversible and progressive. In August 1997 I repeated the PFT again. Again, all other measures except gas exchange were normal or above normal. However, this time my gas exchange measure had increased significantly, up to about 76% of expected. This was an unexpected result and certainly very good news. It suggested that my lungs were slowly healing. My most recent PFT was done in December 2000. This time my gas exchange measure had increased to 81% of the expected value! This result is actually in the normal range of 80% to 120%. Experimenting with Antibiotic Therapy
In 1995, while continuing regular plasmapheresis treatments, I turned my attention to
the research and anecdotal information on the theory that a mycoplasma infection or
other slow bacterial infection triggers rheumatoid arthritis, lupus, scleroderma, and other
similar autoimmune diseases. Recent well-controlled studies have shown that
appropriate antibiotic treatment shows beneficial effects for rheumatoid arthritis patients.
Anecdotal reports are widespread of similar effects with lupus and scleroderma. The
basic method of treatment is long term treatment with a tetracycline family antibiotic,
typically minocycline. Henry Scammell best explains this approach in the book “The
Arthritis Breakthrough”. If you get the book, you should be aware that a major study
published in the January 15th, 1995 issue of the “Annals of Internal Medicine” partially
validated the effectiveness of the treatment, but the mechanisms of the treatment are
still considered controversial.
After reviewing the literature on this approach, I started a one-year course of treatment with minocycline, while continuing with my plasmapheresis treatments for the time being. My initial dosage was 100 m.g., once per day. In addition to monitoring changes in symptoms, I also closely monitored my ANA titer level. My ANA titer had not changed much as a result of any of the treatments I have tried to date. The research literature as well as the anecdotal literature sometimes shows a reduction in ANA level and sometimes a return to a negative ANA titer after several years of treatment, indicating the disease is no longer active. At 3 months and 6 months after beginning antibiotic treatments, there was no change to the ANA level. However, at 10 months the ANA level dropped significantly from 2560:1 to 640:1. Unfortunately, at thirteen months the ANA level had returned to baseline again. Additional later tests showed the ANA level unchanged, suggesting that the apparent improvement was probably a lab error. I also had mycoplasma tests done at 6 months and after 1 year of treatment. No significant changes were noted in this important measure. After about 2 years of treatment with Minocycline, I stopped treatments since there appeared to be no obvious improvements in symptoms or objective measures. I was disappointed that the antibiotic approach had not worked for me since the anecdotal literature indicated that for some people it could actually cure the disease. It now appears likely that a number of different events can trigger scleroderma. For some people the trigger may be a mycloplasma infection, and in these cases antibiotic treatments can be very effective. For other people with a different trigger, it makes sense that this treatment approach would have no effect. Evidence for Effectiveness of Treatments - Part 1
In 1997 I was forced to stop my plasmapheresis treatments against my wishes, While
my internist and rheumatologist were now becoming increasingly convinced that the
treatments were effective at stopping or at least delaying the progression of the CREST,
one of the physicians who was in charge of the transfusion services unit where my
treatments were done had always been hostile to the treatments, considering them a
waste of time and that all of my so-called improvements were placebo effect. He
convinced my physicians to stop the treatments to see what would happen. The results
were very significant. At six months after I stopping treatments, my severe,
uncontrollable heartburn started to return. This gave my main physicians enough
“ammunition” to justify putting me back on the treatments. As before, it took about one
year of treatments for the reflux to get under full control again. While this forced
vacation from the treatments was not of my liking, it actually had a major impact on how
my physicians viewed the effectiveness of the treatments.
[Technical digression… In addition to being a computer expert, I am trained as a clinical psychologist. During my psychology training we learned how to correctly design research experiments. Obviously a single case study is never any more than suggestive. However, there is a single subject research design that can be used to establish that a treatment is effective and not just a placebo effect. Basically, if you take a baseline measure of a condition, add a treatment and get a change in that measure, then remove the treatment and return to the baseline condition, and then re-introduce the treatment and get the same change in the measure, then there is a very significant likelihood that the treatment caused the change. This is called an ABAB Reversal design and is well established as a valid research measure. And this is exactly what happened when my treatments were removed and then reintroduced.] Evidence for Effectiveness of Treatments - Part 2
In 2003, things were continuing to go extremely well. I had no residual symptoms other
than very mild Raynaud's and slight reflux easily controlled by low doses of OTC
Prilosec. So I decided to see if I could cut back the frequency of treatments a bit. I had
historically followed a treatment cycle of one one treatment per week for four weeks,
followed by a lay off alternating between 8 and 9 weeks, so as to average a two month
gap between treatment rounds. I decided to gradually increase the interval between
treatment rounds. I started by doing two treatment rounds with a 9-week gap with no
problems. This was followed by two treatment rounds with a 10-week gap. This also
seemed to go well so I increased the gap again, to 11 weeks. However, this time we
noticed that my Hematocrit (Hct), which had been in the low normal range, dropped
noticably. Historically, the Hct has been a leading marker for disease activity, dropping
back into the abnormal range before other symptoms start to re-occur. I immediately
went back to the original treatment cycle, and after two treatment cycles with an 8-week
gap, my Hct went back to normal. Since then I have stayed at the original two month
treatment gap with no other problems.
Back to Baseline Treatment Protocol
As I edit this (August 13, 2012), I just turned 65 and am now on Medicare (more about
this in a bit.). I am just about to leave for the second week of another treatment cycle. I
have now been receiving regular plasmapheresis treatments for almost 19 years and
am now more than 22 years after my initial diagnosis of Limited Scleroderma (CREST).
My health remains excellent. I am very active (I play tennis for more than two hours a
day on average) and other than mild Raynaud's I have no residual symptoms left. Also,
my once skeptical rheumatologist is now completely convinced that the treatments are
effective and is hoping to get another suitable CREST patient to try this treatment
approach. I believe that she would be willing to talk with other physicians about using
plasmapheresis treatments if they are interested in considering this treatment approach.
For now, I plan on continuing plasmapheresis treatments indefinitely until something else comes along that is more effective. I remain optimistic that I will remain stable as long as I do so. However, Medicare may prove to be my next challenge. My private insurance has been paying for my plasmapheresis treatments since October 1993, when I first started. It is not clear if Medicare will consider this approach "experimental" and refuse to pay for the treatments, at least initially. However, since plasmapheresis is actually listed as a possible treatment for scleroderma if other treatments don't work, my rheumatologist is optomistic that we will win on appeal if it proves necessary. I don't expect to know what will happen for a number of months and will update this article appropriately when I have additional information. Update: 10/12/2012 – I just received a Medicare Explanation of Benefits form which
included my first round of plasmapheresis treatments. Total hospital billing for each
treatment, by the way, is currently about $4000. It was around $2000 when I started
treatments in 1993. Medicare is paying for treatments without my even needing to
appeal and my supplemental Medicare insurance is covering the portion that Medicare
is not directly covering. It appears that Medicare is actually reimbursing the hospital about $1200, which is probably close to the actual cost to the hospital. The fact that Medicare is covering this may have significant benefit to other people that are in early stages of limited scleroderma and want to try regular plasmapheresis treatments. In general, most health insurance plans will cover everything that Medicare covers so they will not be able to reject plasmapheresis treatments as “experimental” if Medicare is covering it. Contact me for more thoughts on this if you are interested in considering plasmapheresis treatments. If anyone has questions, I can be reached by email at:

Source: http://www.synnovation.com/scleroderma/ed.pdf


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