-
AuthorPosts
-
Thyroid Eye Disease appears to have a completely separate disease course from Graves’ Thyroid Disease. Treatment for GD has no effect on the potential for having TED or having more severe TED. We do know a few things about TED, but there are a lot of things we do not know. At the last conference, there was some talk of the antibodies being closely related, but up until then the conventional wisdom was that the antibodies were separate. In other words, things are still being proven as far as that goes. Still, there appears to be no connection whatsoever between GD and TED other than that they commonly happen together. We know that smokers experience the worst symptoms of TED and the longer disease curves, but other than that, I’ve seen nothing that suggests any particular treatment or behavior can affect your chances of ending up with TED, no obvious commonalities between those with TED. I should actually say "severe TED," because they say that all of us, examined closely, will show some symptoms of TED.
My question probably doesn’t have a solid answer, but here goes. Is there something that triggers eye issues associated with GD? Some who have that problem (bulging eyes, can’t shut eyelids, sand in eyes feeling) seem to really suffer. Could it be that this happens if Graves goes undiagnosed a long time? Or could there be another factor?
My current TSH are 23 (range .25 – 5.00) but it took 8 months to get here. I just read about someone who was hypo 8 weeks after their RAI . I read about levels and am struck by how everyone is different with Grave’s. When I was hyper, the tremors, heart flutters, high BP, low tolerance for heat and depression were the worst. Never had eye muscle issues though.
I get that we are all going to experience this differently. The eye issues really have me curious though. Wonder why that one part some experience and others don’t? Just a difference from person to person and nothing more?Hi,
I would like a reply from either Bobbi or Ski. Thank You. My dosage of synthroid was changed from 88 to 75,
about two weeks ago. About one week after I started taking the new dose my one eye began to tear and then the
lid and under the eye began to become puffy. I’m wondering if this ever happed to anyone else, and if it did, did
it finally go back to normal. Or could it be that this dose is to low. My other eye is fine, and so far I feel fine.
I was wondering if my body just has to get used to the new dose. My eyes are not bulging , and my eyesight is
fine. At my last visit to the endo, which was two weeks ago, she checked my eyes and she said everything was
fine, but had not started the new dose of synthroid.Thank you,
SusanHi Susan,
Your dose of Synthroid doesn’t have the ability to affect what’s going on with your eyes. If you feel you may be seeing early symptoms of TED (bulging is not the only one), then find an ophthalmologist and have an examination to see what’s going on. It must be an ophthalmologist (not an optometrist or optician), because they are the only doctors with specific training related to TED. Even though GD and TED occur together, their progress and affect on us are unrelated. In other words, treatment for the thyroid disease does nothing to treat or prevent TED.
Hello All…it’s been quite some time since I’ve been on this site, but I’m currently 22 mos. into GD along with the TED. I went through 3 solumedtrol treatments as well as the radiation for the TED and was on tapazole for 20 mos. When my old endo dr. wanted me to have a thyroidectomy, I found another endo dr. that disagreed with him and took me off ALL my medicines!! Since he took me off all my meds, my vision has slightly improved (which is weird since the two are not related!) I’m thrilled, BUT, I’m scared too. My new endo dr. said that "if" I go back into hyperthyroidism, he will consult my TED dr. and consider giving me IODINE. I’ve ALWAYS READ that I should NEVER have IODINE b/c it could possibly make my TED worsen. Have you or anyone here heard of having IODINE for the GD when the patient has TED?? If so, was it a successful procedure and should I NOT worry or should I look for my third endocrinologist in the area?? Thanks so much for any insight into this since my dbl. vision is "tolerable" after 22 mos. into this monstrous disease.
Ski wrote:At the last conference, there was some talk of the antibodies being closely related, but up until then the conventional wisdom was that the antibodies were separate. In other words, things are still being proven as far as that goes. Still, there appears to be no connection whatsoever between GD and TED other than that they commonly happen together.Something to consider with TED ~ every person with TED goes through a defined disease curve ~ there is a period of activity, where the eyes change fairly rapidly and often (the ‘hot phase’). This is followed by a period of stability where nothing changes much, then a period of improvement, and finally, stability ~ whether your eyes have returned completely to normal or not. The degree of changes and improvements is different among all patients, but that is an absolutely certain list of steps, it happens to every patient, in that order. So it is possible that your TED symptoms would’ve stabilized without anything changing, without any extra meds, without going off the meds. It’s hard to correlate things precisely when it comes to TED. Some people have more than one "hot" phase, but that’s rare.
If you have indeed hit the "cold phase" of TED, then it’s unlikely that RAI could affect your eyes at all, but the bottom line is that the only evidence we have of some increase in TED symptoms following RAI is one small-ish study that has not been replicated since. Even those patients experienced no permanent change, just a "temporary worsening" of symptoms that resolved after a few months, and if the patient took a concurrent course of oral steroids, the incidence of this phenomenon fell to zero. So RAI is still a potential course of treatment for you, if you are interested. If not, I always say it ~ the choice of treatment is yours!
I got TED almost fifty years later. After I had a baby. I was very hyper, took tapazole, became hyper again, had a thyroid storm, then a subtotal thyroidectomy. After several decades, I became slightly hypo, no symptoms, take Synthroid now.
But the point of this email is to reflect what all the facilitators have said. TED is a separate entity. I spent one whole year being told that I needed new glasses, getting slight changes in my prescription. Finally, I realized that I had double vision, and was compensating for it by tipping my head back to see clearly. Even though I said I had to tip my head back so I did not see double, (quoted by me in the chart in 2003!) It was missed by the first eye doc who thought only of new glasses.If you have eye symptoms, photophobia (can’t stand bright light) double vision, dry eyes, red gritty eyes, bulging eyes, be sure to find an ophthamologist who hears what you are saying. It is wise to go to a neuro-opthamologist as well, to moniter your visual fields. In my case, I had optic nerve atrophy (loss in the visual fields, harder to see colors) and had to have an orbital decompression to save my vision, even though I was in the active phase.
I really hate TED, it has changed my social interractions with people (hard to look straight ahead or up.) I am finding that it is hard to tell if I am in the cold, or fibrotic stage. The doc who held up two fingers and five fingers said it all. He said to count on two years, as many as five surgeries, before I see the end of this. He is right. I have a couple strabismus surgeries (muscle surgeries, to move my muscles so I can look straight ahead and up at least 30 degrees) then eyelid surgery to accomodate my eyes. This is a very difficult experience, and I am most appreciative of the facilitators for their knowledge, and other participants who help me feel that I am not experiencing this hell by myself.Thanks ALL for your generous explanation, but, I have one question. I understand that RAI is still a "potential" treatment for me b/c the two diseases are independent, but "why" does everyone recommend that you DO NOT have IODINE contrast in the form of cat scans b/c of TED YET, it’s "okay" to have RAI which is "iodine" to destroy your thyroid? Isn’t "iodine’, "iodine"? This is "very confusing" for me.
I am not sure why an iodine contrast would be a problem for patients with TED, but some patients have allergic reactions to the contrast iodine and think they are allergic to iodine in general, which is not typically true. We need iodine, throughout our lives in order to have life. Iodine is the crucial ingredient in thyroid hormone, and without it the cells would cease to function. So, I guess to answer your question, it appears that the contrast form of iodine is somehow different from regular iodine. Is it because it is hugely concentrated? Or is it mixed with some other chemical? You would need to ask your doctors specifically what the problem is, and why you have been advised to stay away from it.
Thanks Bobbi, I will and will let you know when I find out the difference…there must be some sort of difference, I’m sure!! Appreciate your response.
Hi Sue – I have seen a few studies on RAI and eye disease that have been published through the 1990s and 2000s, and many do indicate there is at least some correlation between RAI and development and/or worsening of the eye disease. (The *worst* outcomes seem to occur with smokers who are treated with RAI.)
The most common study (which was discussed at last year’s conference) is the Bartalena et. al. study from 1998. This study compared eye outcomes of patients whose hyperthyroidism was treated with (a) RAI, or (b) RAI + prenisone or (c) methimazole.
About 15% of the RAI group experienced a worsening of eye symptoms. Of those patients, about 2/3 later improved, but the remaining required further treatment for their eye disease. About 4% of the methimazole group experienced a worsening of symptoms, and 0% of the RAI + Prednizone group experience a worsening of symptoms. (Of course, steroid therapy has its own risks, so this is not a decision to be taken lightly).
Keep in mind that the study does not prove that RAI *caused* the worsening – just that the eye disease is *observed* in somewhat greater numbers in patients who have had RAI. One study posed the theory that the eye disease is aggravated if the patient is allowed to go too hypO after RAI treatment. I’ve also heard a theory that the increased antibody activity that occurs after RAI is what triggers the worsening. There is so much that scientists still don’t understand.
If someone with existing eye disease chooses RAI, is it guaranteed that their eye issues will worsen? Absolutely not. But when making a treatment decision, this is a *risk* that needs to be taken into consideration, just like the risks that go along with ATDs or surgery. Best of luck!
-
AuthorPosts
- You must be logged in to reply to this topic.