Things are still very much the same for me, so not much has changed in that regard. I was just wondering though, if it's true what doctors say when they tell me that my Graves' should have no effect on me anymore, and that without a thyroid, I may as well not even have Graves'. I won't get into how strangely hurtful(?) it is to hear that, but it did get me wondering about how true that is. After all, it is an autoimmune disease, right? So, the thyroid is merely Graves' main victim and the typical symptoms associated are just the fallout from your thyroid being attacked. So, what do the antibodies do otherwise? Besides not being optimally medicated, am I, for all intents and purposes, "cured" of this disease?
Written by
lau99
To view profiles and participate in discussions please or .
No that is not wholly true. Hashimotos hypothyroidism autoimmune disease only attacks thyroid tissue so it's fluctuations stop when there is no thyroid tissue left to attack. The antibodies are the cleaners that mop up the mess left after the thyroid has been attacked.With Graves disease however the body turns on itself and attacks thyroid tissue and can attack tissue elsewhere that is similar. Generally that other tissue is around the eyes and this is TED thyroid eye disease. Removing the thyroid in Graves patients does not mean that TED will also stop though it may reduce the problem.
No as TED is independent of graves attacking the thyroid. Graves can attack the thyroid without affecting the eyes and it can attack the eyes without attacking the thyroid. The two things are caused by the same autoimmune condition but they are independent of each other. Just because your eyes are okay doesn't mean that Graves is in remission for your thyroid.
As far as i understand it ... thyroid eye disease can still happen, however it doesn't happen to everyone with graves. lots of people have graves hyperthyroid without ever getting the eye thing. And i think ? that once the thyroid is removed it may reduce the autoimmune activity , but not always.
Edit* i looked it up...... In a study of 35 patients - pubmed.ncbi.nlm.nih.gov/186... - "Conclusion: TT resulted in a significant reduction in TRAb levels with concomitant regression of recurrent GO (Graves Orbitopathy) in all patients."
pubmed.ncbi.nlm.nih.gov/146... "Recently, correlations between a high serum TRAb value and endocrine opthalmopathy were also suggested. Surgical resection of the thyroid is usually followed by a reduction of serum TRAb levels in variable degrees. The relation between the extent of the thyroidectomy and the degree of reduction is still controversial. In addition, the changes in the TRAb value after total thyroidectomy (TT) over a long period of time have never been studied. We studied the changes in serum TRAb values after TT and subtotal thyroidectomy (ST) for more than 7 years. Forty-one patients with Graves' disease underwent TT, and 99 patients underwent ST. The serum TRAb values and the ratio of the patients who achieved normal values among each group (normalization rates of TRAb) at 3 and 6 months, 1, 3, 5 and 7 years after surgery were compared between the TT group and ST group. The mean preoperative TRAb values were not significantly different between the TT and ST groups, and the mean TRAb values measured 3, 6 and 12 months after surgery were not significantly different between the groups. However, the TRAb values measured 3, 5 and 7 years after surgery were significantly (p<0.05) lower in the TT group than in the ST group . // The normalization rates of TRAb were not significantly different between the groups until 1 year after surgery. However, the normalization rates 3, 5 and 7 years after surgery were significantly higher in the TT group than in the ST group // TT is a treatment option for Graves' disease, especially in patients with a high TRAb value who wish to have children or who have Graves' opthalmopathy." End of Edit*
So i think ... the more relevant question is "what level are your TRab antibodies at now" rather than "do you still have a thyroid or not"
So if you know whether your TRab levels reduced after your thyroid was removed, that might possibly lead you to more research about risk's of developing eye disease in relation to TRab antibody levels. ..... Hopefully some one can point you to proper research , cos to be honest i've forgotten most of what i've read on the subject.
But.....
Telling you ' your graves should not affect you anymore' is rather like telling someone who had a full hysterectomy due to cancer that "the ovaries/womb are not there anymore, the cancer is all clear now , so she's better"... well she might be , and the cancer itself may never affect her anymore, but she's permanently changed because of it, and doesn't have her own hormones anymore.....with profound effects on her life from then on.
So if it helps (and i can understand why it would) i think you should continue to see yourself as someone who has Graves .....but don't get freaked out about developing eye disease.
Edited to add :-
In case it helps , i'll link you a very detailed paper i found on everything to do with thyroid antibodies... ncbi.nlm.nih.gov/pmc/articl...
Extra-thyroidal manifestation of Graves Disease ( GD ) include swelling of the orbital tissue and of the skin, termed as Graves’ orbitopathy (GO) and Graves’ dermopathy. The term ophthalmopathy is also being used, but orbitopathy is preferred because it describes the pathological alterations more correctly. GO affects about 25% of GD patients (113) and results in dysmobility of extraocular muscles and optic nerve compression. It represents also the only extra-thyroidal pathology where the role of anti-thyroid antibodies is relatively well known. ... //... Anti-TSHR antibody levels correlate with severity of GO and are predictive for the later development. By contrast, no correlation between severity of GO and hormone levels has been identified (116, 117). This finding highlights the role of TSHR antibodies as promoters of GO.
Graves’ dermopathy is an extra-thyroidal manifestation exclusively found in GD patients. Dermopathy develops in the presence of high TSHR antibody levels and is, with a frequency of 15%, a less common extra-thyroidal manifestation of GD (118). The main localization is pretibial and is associated with acropachy (digital clubbing, swelling of digits and toes, and periosteal reaction of extremity bones) in 20% of patients. TSHR is expressed in skin fibroblasts and abundant mucin deposition, possessing gel-like properties, separates the collagen fibers. Stimulation of fibroblasts by anti-TSHR antibodies along with mechanical factors and venous stasis causes accumulation of mucin. ...//...
In summary, anti-TSHR antibodies affect eye and skin as part of GD, and the mechanisms of anti-TSHR antibody action is relatively well known, while effects of anti-TPO antibodies are more varied and affect central nervous system, female reproductive organs, and female health. The underlying mechanisms are largely unknown. "
Thank you for this in-depth, informative (and very kind) response, tattybogle. I've just been re-reading some of my old posts and thought I should let you know how appreciative I am of this, although at the time when you wrote it I was too emotional to type out a proper reply to you. x Your mindset has certainly helped me get some closure.
Grave's disease is an autoimmune condition that most commonly affects young women under the age of forty. The hallmark about the disease is the presence of autoantibodies that exert TSH-like effects, called thyroid-stimulating antibodies (TSIs). TSIs stimulate TSH receptors on thyroid follicular cells leading to both hyperthyroidism and thyroid gland enlargement, hence a goiter. As T3/T4 levels increase, TSH goes down through negative feedback inhibition. In addition to the classical signs and symptoms of hyperthyroidism, Grave's disease also causes ophthalmopathy, which manifests as exophthalmos (bulging eyes), eye irritation, double vision, and possibly vision loss. Grave's ophthalmopathy most likely happens due to TSIs binding to receptors on the soft tissues and muscles behind the eyes. This initiates an inflammatory cascade that causes ocular symptoms to occur.[8]"
Which raises the interesting question .. where else in the body (apart from the thyroid and the soft tissues behind the eye) has TSH receptors ?
I don't know the answer to that question ......I've not heard about graves having other effect's apart from thyroid and eyes, but i'm sure i've read somewhere on here that lots of places have TSH receptors.
So presumably, TSI's could have an effect on any other sites with TSH receptors , but what that effect might be , i have no idea .. it wouldn't be stimulating the production of T4/3 cos that is the thyroid's job .. but IF there are TSH receptors , and IF here are still TSI's (TRab), then the TSI can still stimulate/attach to those receptors instead of TSH.
Then there is a much more comprehensive document. Which has two issues. First, it is sometimes a bit unclear as to which symptoms result simply from the excess of thyroid hormone. And which can manifest even if thyroid hormone levels are managed (e.g. by medicines).
Also, it reports a depressingly long list of sometimes severe issues.
Graves’ Disease and the Manifestations of Thyrotoxicosis
I have often wondered this myself. Surely the trigger for the condition remains and now there is no thyroid it will manifest itself some other way? Killing the thyroid is like using a hammer to crack a nut and driver for the autoimmunity remains? I don’t know the answer. Thankfully my eyes are ok. I have terrible eye bags but that’s all
I feel like I would be inclined to agree with you there...but it confuses me as that appears not to be what the science says? I just don't understand how I can simultaneously be "cured" of Graves' (if this is what being cured feels like, I don't want it) but then at the same time be told that I'll have Graves' for the rest of my life??
The main priority seems to be to switch people from what is deemed a " life threatening " disease if not treated to possibly a " life limiting " disease by thyroid disablement and rendering people with primary hypothyroidism.
Graves is an autoimmune disease that tends to wax and wane throughout one's life :
There is likely a genetic component and Graves can be triggered by a sudden shock to the system :
This happened to me, 4 months before my diagnosis having been physically threatened and verbally abused by a man I employed as my assistant manager, and then " soldiering on " through dismissal procedures and all that that can throw into a working relationship.
I didn't realise the significance of this until around 12 years later when I started reading up on Graves Disease, and also read of there being an increased proportion of people with Graves who were lefthanded and struggled with dyslexia - and I felt at home.
There was a very interesting post by Ling - a few weeks ago and from memory believe it spoke of a 4-11 year period from first diagnosis to Graves antibodies reducing enough in a cross section of patients to consider " finding remission off the AT drugs :
This time scale isn't in line with current thinking and NHS working guidelines.
I think the situation is compounded as currently the guidelines for treatment of primary hypothyroidism caused by a thyroidectomy or RAI ablation is T4 - Levothyroxine only.
There is no acknowledgement of patients without a thyroid having lost all their thyroid hormones which includes trace elements of T1.T2 and calcitonin plus a measure of T3 and a measure of T4. whilst there is a medication, for precisely this condition, widely available in other countries throughout the world.
Thank you for the insight, Penny. I think I recall reading the study that you mentioned, a couple of weeks ago. Somehow it just makes me sad that I didn't just wait it out on Carbimazole a little bit longer...a few more years of that versus a whole lifetime of this is a difficult tradeoff to come to terms with. Though, I might just be feeling extra gloomy since the two year anniversary of that horrible day (TT) is only a few days away...
It's strange and uncomfortable to think that I have Graves' disease, but I also don't have Graves' disease (anymore?) at the same time. It took so much away from me and caused me so much physical/emotional pain that still lingers on today (perhaps it's even a touch worse now?) yet I don't even get to claim that I have it/that it still affects me anymore. As though Graves' is supposed to just be a thing of my past, even though it somehow continues to torment me in my present.
(Sorry I always end up saying such depressing things to you!! I promise I'm much more fun to be around in person haha)
Content on HealthUnlocked does not replace the relationship between you and doctors or other healthcare professionals nor the advice you receive from them.
Never delay seeking advice or dialling emergency services because of something that you have read on HealthUnlocked.
True or false? 
Advice from Graves sufferers please
Blood results indicate Graves’ disease- what’s the likely treatment and will it help symptoms quickly?
Autoimmune thyroid disease and celiac disease - NICE guidelines.
Factitious thyrotoxicosis
