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I get so disappointed when I see so many people talking about surgery or RadioIodine therapy and never see them speak of meds. I will let everyone know right now (I appologize for those that already know this)but if you have Grave’s Disease, THERE IS USUALLY NOTHING WRONG WITH YOUR THYROID!!! Many Doctor’s do not tell you the whole mechanics of the disease, and you need to know the whole mechanics so that you can understand the treatments.
Grave’s Disease is widely accepted as an autoimmune system problem, not a thyroid problem, in where anti-bodies called thyroid stimulating antibodies attach themselves to the thyroid and stimulate it to produce excess amounts of thyroid hormones. Typically, your thyroid is functioning normally.
Knowing this, I have come to some opinions: (everyone may not agree)
1. If there is nothing wrong with my thyroid why should I have it cut out when there are alternate forms of therapy that can be tried before resorting to an operation?
2. A very good endocrinologist who spends time with you can get your grave’s under control within a couple of months. If your’s can’t…well, no comment.
3. I believe that there are three stages of treatments, and these three types should be explained in full to you by your doctor so that you can make an educated decision. The first is the meds, that for most of the people I have talked to have sent them into remission, completely controls their condition (granted #2 has been satisfied), or has sent them into a hypo state (usually because theit doctor took them off of the meds too fast). The second is the radioiodine treatment that usually is not regulated well. I say this because I have seen the most inacurate results. I still believe this should be before an operation. In fact I have personally talked to several endo’s who don’t really believe that an operation is necessary. I believe that everyone seeking the best results from their treatments should take each treatment in it’s stages. First they should try the meds. Some 50% eventually go into remission or hypo, and again if you have a dedicated doc, they work in most cases. Second, if the meds don’t work, or cause unwanted side-effects, one should try the RadioIodine Treatment. Everyone that I have talked to who had a doc that took the time with them, only needed one treatment and ended up either euthyroid or hypothyroid. Lastly is the operation, which should be reserved for those that the first two treatments didn’t work for(very, very rare), or for those that have growths or other abnormalities. In almost all the cases that I have seen that the individual had only grave’s and no growths or other abnormalities, the operation caused a hypo state with other syptoms specific to gland removal prevailing, and were not satisfied with the results. Regretfully, I have spoken to numerous people (way too many) that said they were never given all the options.
This really frustrates me.
These are only opinions. I am not a doctor, so don’t use this as a recomendation. Use it to come up with your own questions! This is not a recomendation, it is only an opinion. In the end, you must find out all the information you can, and make the best judgement for yourself. I really believe the key is your doctor.Good Luck,
Ron
Saying that there is nothing wrong with the thyroid is, to me, missing the point. The way I see this whole process is to relate to transplant issues. When someone gets a kidney transplant, for instance, they are given drugs to suppress their immune systems so that their body will not produce an antibody to the new tissue. But if this fails, and an antibody is created by the body, the new kidney (and there is nothing “wrong” with this kidney, either, in functional terms) is doomed. The body “rejects” it, kills it off. In Graves, our bodies are rejecting our own thyroids, and causing them to malfunction, and die. And the antibodies are already there. In my reading of medical texts I have encountered, more than once, statements that we can all, no matter what treatment we choose, expect our thyroids to stop functioning sufficiently, as a result of the Graves antibody attack. Eventually, we can all expect to go hypo. The antibody attack will burn our thyroids out. Each and every one of the treatments available to us simply are designed to stop our bodies from being battered by too much thyroid hormone. None of them are designed to stop the antibody attack, and “save” our thyroids. So there really IS something “wrong” with our thyroids.
Again, from readings, it can take as long as fifteen years for the thyroid to be sufficiently damaged by the antibodies so that we no longer have too much thyroid hormone to worry about. As in everything else with this disease, I’m sure there can be variations in the timing. This is probably why some people go into permanent remission with ATDs and others are faced with being hyper again, after a period of remission. If you take them long enough, you will be faced with a period where you won’t need them any more. But not because they “saved” your thyroid. By blocking the thyroid’s ability to absorb iodine to make hormone, they will have kept you alive through the over-production of hormone phase. Then, when enough of your thyroid will have died off, you may not have to take them, ever again. But you should very much be on the alert for the development, perhaps some years in the future, of hypo symptoms.
That said, I don’t think any of us should try to PERSUADE others on this board to follow one treatment plan or another for this disease. What happened to us, may not happen to someone else. What worked for us may not work for someone else. While it has been extremely helpful to me to hear of the experiences of other people on the different types of treatments, I don’t find it at all helpful to have someone trying to persuade me to do something different, when it isn’t based on a factual knowledge of my specific situation (both medical and personal). When I was trying to decide what treatment to choose, and I read persuasive-type comments, it confused my emotions and my logic. There are good medical and personal reasons for choosing ANY of the three options. And, there are perhaps BAD reasons for choosing one or the other. Sometimes, medically, the best option may not be the one that we personally would prefer to choose. We need to try to be as realistic about what is happening to our bodies here, as we can be, so that we can make a good choice for ourselves, taking everything into consideration..
Bobbi
I don’t know if you have ever posted before, RON, but your opinion is certainly as welcome as anyone else’s. You acknowledged it as an opinion, and that is important. I agree with your frustration that many people are not told of the various options.
Bobbi’s point is well taken that no one should presume to give advice as to what any one particular person should specifically do…as many personal factors are different and our biological responses to any of the treatments are not equal. However as a general effort at bringing info to someone who may be new to GD, Ron’s post stands.
Bobbi, I wonder what prompted your speculation that the remissions following ATD’s are simply burned out thyroids? If someone, for example, had an eight year remission then was hyper again..would you think,the thyroid had recouped? Or is it more likely that the anti-bodies were absent or overcome for a time and then reasserted themselves?
Many people in remission are on no thyroid replacement, as their thyroids are functioning at a lab ascertained level of normal. Many report feeling well too. Remission with an intact thyroid, for however many years left in their thyroid, is real for some people. people who went through the ardours of hanging on to their thyroids. We wouldn’t want to dissuade others who have that hope from achieving what may be possible for them.
Although Bobbi’s analogy to organ transplant is interesting, as Ron said, the thyroid is not essentially the culprit. In organ transplants, people go through very serious blockade drugs in efforts to keep their new organs.As far as thyroids eventually pooping out anyway, many people, without any particular disease process, have reduced thyroid functioning as they age. But if one prefers to hang onto an organ until its actual failure, that does not seem like a radical approach. Well I’ll save the rest of my breath to cool my porridge.
There is a misunderstanding of the basic nature of Graves disease here.
In GD, the antibodies are targeted against the receptor for TSH,
or thyroid stimulating hormone. These receptors reside on or in the thyroid cells
and the gland is overstimulated to produce hormones beyond what it
would normally do. There is NO damage to the thyroid gland itself which
is why many people can take ATD’s for the 2 to 2 1/2 year active course
of the disease and do not need treatment or replacement thyroid hormone
afterwards. Their gland is still okay and producing hormones at a normal
level. ATD’s are the only treatment which does not remove or destroy the
gland itself.
A totally separate disease, known as Hashimoto’s thyroiditis, has anti-
bodies which do destroy thyroid glandular tissue and these people eventually
become hypothyroid because their glands are no longer working. They will
need to take thyroid hormones for the rest of their life.
Thought I would clear that up.
Hope this helps the discussion.
Right on RON!!!!Ron I really appreciated hearing your opinions on the different treatments
and I felt you made yourself very clear in stating that they were only your
opinions. Good job!!Hi, Jeannette:
In response to your question: why should an eight year remission after using ATDs, for instance, be any different than the situation in which I found myself this year? I had what I was told was a moderately large dose of RAI the week before Thanksgiving last year. My doctor and I had agreed to ablate the thyroid. I went hypo in January. Distinctly hypo. By April, I was mildly hyperthyroid again. OK. That could simply have been too much replacement hormone. So it was reduced. It was reduced again in July. It was reduced again in November. Last week I was taken off it altogether. The blood levels of thyroid hormone remain relatively unchanged through all of this. So what this now means is that the portion of my thyroid that did NOT get killed off with the RAI has been activated sufficiently by the antibodies to overproduce enough that right now I cannot take replacement hormone. And all other evidence suggests rampaging antibody levels. So, yes. I believe that in long-term remissions from ATDs that it is POSSIBLE that enough of the thyroid pooped out, as a result of the antibody attack, to allow us to go on without the meds, and that it is possible that at some future time, the continued antibody attack can rev up the remaining tissue, if there is enough of it left, to bring about hyper again.
Also, antibody levels, according to my endo, fluctuate for no known reason. Boy, I do wish there were more immunologists out there figuring out why this is. Anyway, none of the reading I did about ATDs even remotely suggested that they had any impact whatsoever on antibody levels. (You have to distinguish between WBC suppression here and antibodies–they are not the same thing.) So some remissions could simply coincide with lower overall antibody levels, and have nothing to do with thyroid destruction.
I don’t see that it matters. There are still good reasons to try ATDs for a lot of people, and I was not making my comments to Ron in any attempt to knock ATDs. Saying that I don’t think they “save” the thyroid, doesn’t mean that keeping it around longer (if you don’t have adverse side effects to the meds) isn’t a possitive thing. I just think we need to be realistic about what they are actually accomplishing, and not spin ourselves a fabric of false hopes. It would be particularly bad if someone went into remission on the ATDs, and at a later date ignored hypo symptoms until they had been in that state for a while, believing that they have “saved” their thyroids. The evidence suggests that we aren’t going to be able to save them, unless research turns up a way to suppress specific antibodies without compromising the entire immune system.
Thank You for the information.
I believe that what you are saying is true in some cases, and that ATDs do not suppress antibody action- that’s not how they are supposed to work in the first place. The truth about most remissions is that they usually happen within 18-24 months, and they leave the thyroid completely healthy. I also know that thousands of people go miss-diagnosed each year and are told that they have GD, when they also have another thyroid disease on top of GD. This also causes a problem with treatment of GD. Most of the time, if you are seen quickly and treated quickly, it is easier for you to go into remission without any thyroid damage. I agree that GD can cause thyroid damage, but I also know that the ATDs cause thyroid damage much less than the other two treatments, because the other two treatments are designed specifically to damage or remove part or all of the thyroid. ATDs do not always and in most cases don’t cause thyroid damage. And in most cases, the GD does not either. The pooping out usually is only in conjunction with a super-overproducing thyroid, and is usually found with other thyroid conditions on top of GD.What is such a possitive thing that we must all remember is that there are thousands and thousands of people out there with this disease that are perfectly healthy, and will never post at this BB. The majority of GD people are perfectly fine and never will have problems again. I must say that I don’t believe that most of the people here, including me, are the norm for this disease.
Typically the reason a thyroid goes into remission is that the body, or immune system, stops targeting the thyroid. This usually happens because the meds suppress the thyroid production and the conversion of T4 and T3 enough that the body “gives up” trying to stimulate the thyroid. (that’s in laymens terms I guess) It has nothing to do with WBC, suppression of WBC is sometimes a nasty side-effect of the ATDs.
Whether you take ATDs or RAI, your body still has the antibodies present, and lots of people have the RAI and continue to be overstimulated until they have the whole thyroid killed. Typically there is no remission with RAI, just euthyroidism. But with the ATDs there is a chance that the antibodies will stop attacking the thyroid, and one may never have a problem again. Or the antibodies can come back, and you can go through the motions again.
Just remember that we here with problems are not the norm, and that people that come here need to be encouraged that they could have a wonderful, symptomless life.
Ron
Check out what it says about antithyroid meds on Steve Lim’s Graves Page – and I know he has the research to back it up. There IS some suppression of the anti-bodies, they just don’t know how the ATMs do it. I’ve also read that on other medical sites on the web, so I don’t agree with Bobbi that it does not say it anywhere. Something mystical does happen, while ATMs suppress the thyroid from using iodine, some of those antibodies are stopped in their tracks.
Thanks, Jeannette, for the kind words. It has been a bit of an ordeal, if only from the psychological standpoint. I have not been as sick with this level of hyper as I was before RAI, but the yo-yoing between feeling terrific and feeling weak and shakey, has been a bit hard to take. The good news right now, however, is that I feel terrific again. And how nice it is that it is timed for the holidays! ; )
Glynis: Thanks for that reference. I had not seen that before. I would caution you, though, about the rest of what Steve Lim says. While he does say that while you are under treatment with the ATDs that the “circulating concentrations of autoantibodies TR Ab(TSI)” are “reduced”, he also says that “The effect” of the ATDs “is only operative as long as the drugs are being used. It does not prevent relapse at some subsequent period.” I am trying to track down which autoantibodies these are. They aren’t listed in the index of the immunology text I’ve got, so I’ve got some reading ahead of me. I think we may have two sets of autoantibodies in Graves (my bloodwork was done for at least two), so maybe — and after the holidays — I have some homework. Do you know more about these?
Joan: Your comment about Hashimotos antibodies only causing destruction of the thyroid may be just a question of semantics between the two of us. Here is an example of the type of information I have used to make my own comments. This is from Steve Lim’s page, but I’ve seen it elsewhere, as well. “Do not be mistaken that hypothyroidism is caused only by over-treatment of Graves’. Even in long-standing disease, progressive thyroid failure occurs because of chronic inflammation. The reserves of the gland are reduced giving rise to hypothyroidism.” . Whatever terms we use, we all need to be aware that hypothyroidism could be a result for us, whatever treatment option we choose. In my endocrinology text, it cautions (the training doctors, obviously) to check, on a regular basis, their Graves patients for the development of hypothyroidism.
Wishing all a sense of calm with the upcoming holidays,
Bobbi
The two antibodies are the ones that stimulate the thyroid “thyriod stimulating immunobodies” (hence the “TSI”) and the ones that cause the eye problems.
Good Luck
Ron
Ron, I don’t think your post about the two kinds of autoantibodies is accurate. The two they tested me for were Thyroglobulin antibodies and Microsomal (perioxidase) antibodies. My lab report shows thyroglobulin antibodies in the normal range, but microsomal antibodies 30.0 (0.0-1.0).
Bobbi, let us know when you find out more about this–you seem to have some great resources, and I really appreciate your taking the trouble to give us factual information with references, rather than giving treatment advice and personal conjecture, a function best left to those medical personnel who are trained to give it.
Dianne
Graves’ Disease is defined as being the overstimulation of the thyroid
gland because of the involvement of an antibody to the TSH receptor.
There is NO destruction of thyroid tissue involved. However, GD
could be accompanied by Hashimoto’s antibodies which do destroy the
thyroid tissue through inflammation. I’ve even read about identical twins
where one had GD and one Hashimoto’s.
I had a long discussion with Dr Robert Volpe about this during our
our first annual meeting in California. That’s what he told me.
He’s on our medical board also head of Thyroid Foundation of Canada.
I guess it’s okay to quote him since he spoke in public at this meeting.
By the way, I have no evidence of Hashimoto’s antibodies in tests taken
several years ago and I have no thyroid activity. So why, I don’t know.
Could have been because of the ATD’s at age 10 – 12, the RAI at age 12,
or the thyroidectomies at ages 12 and 22. (Note that after all three
treatments, it still returned 10 years later.) At any rate, I agree with
you that there is destruction of the gland, but medical science is not
defining things this way.
Dr. Volpe said there is no destruction from GD, if you have no working
thyroid tissue, it’s from Hashimoto’s. But no proof of that with me.
Anyway, let’s not argue since medical experts cannot seem to agree.
45 years into this I DON’T FEEL GOOD!
The GOOD news is, when I was 12 no one thought I was going to survive and
I just had my 55th birthday. SO there!Thyroglobulin antibodies from what I have read are the precursors to the thyroid stimulating antibodies. They can also become other thyroid antibodies that cause other diseases or protect from other thyroid disease. The antibodies that cause grave’s are called thyroid stimulating antibodies (TSI).
I did a lot of research into the antibodies last winter, and I found a lot of conflicting information, even at very reputable web sites, so make sure you double check when searching for antibody information. What I finally concluded was this:
Antithyroglobulins – I found no info on these at all
Antiperoxidase aka antimicrosomal – Found in almost all cases of Hashimoto’s, and in about 50% of Graves
TSab aka TSI – Thyroid stimulating antibodies, specific for Graves
TRab – TSH receptor antibodies, specific for Graves, I think these buggers latch onto the TSH receptor sites and fool the thyroid into thinking they are TSH
I also found a reference for one other antibody which was specific for Graves, but I can’t remember what it was called, and there was no information on it, except that it was rarely tested for.
Also, what I read indicated that antibody levels have to be pretty high to be considered active disease. For example, my lab may indicate that >2 is positive, but the medical sites I researched said that anything less than 80 could be a false positive, or possibly an indication of early stages of disease, but would not be considered active disease. Apparently there are many people with antibodies between 2 and 80 who do not have symptoms, and never develop the active disease.
I am not sure how these antibodies do their dirty work, and I have been wondering if any of them might be specific for Graves eye disease, but the info I found seemed focused on the thyroid problems.
If anyone has more info on the antibodies, I would be interested in hearing about it, or if anything I found is incorrect, I’d like to know that too! Please email me.All I know about this antibody stuff is that I was being tested for Lupus – it checks antibody levels in ones body and my thyroid antibodies were off the chart, that’s how they figured I had Graves. Also read that one way to check for Graves is to do an ANA test which is what I had and if graves is suspected, a very high anitbody result will be indicative of the disease.
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