[NickyG]

#1183421

I was diagnosed with Graves in October of 2012. I got married in September 2012. I was really sick and had no idea what was going on with me until my primary doctor did blood work and referred me to an endo doctor. I was put on Methimazole and I am still one it. I usually pay attention to my body and get blood work to monitor my dosages of the pill since I have heard it can be damaging to the liver. Has anyone else heard of this? Well I am also confused by a low TSH and normal T3 and T4. I have been really sick the past few days and I got blood work today and my results are as follows

T3= 3.9 Standard Range 2.8 to 5.2
T4= 1.1 Standard Range 0.8 to 2.2
TSH= <0.015 Standard Range 0.300 to 5.000

Now my T3 and T4 seems normal but my TSH is really low. That is where I am confused. My doctor’s nurse is going to call me tomorrow to follow up. In the meantime I feel terrible, like I have a sore throat, chills, headache, pressure behind my eyes and temples. I also feel achy and I have a cough. I would like an opinion from others in this forum. Have they had these results before and what did you do, or what did your doctor suggest? This disease is so new to me and I would like to hear from experienced people who have dealt with the disease. I would appreciate any feedback, thanks.

[Kimberly]

#1183422

Hello – Yes, methimazole can cause liver issues, but this is much more common during the first 90 days of taking the meds. Many docs routinely test for liver issues, although the latest medical guidance favors testing only at the start of treatment and then if symptoms of liver problems occur. (These symptoms can include fever, loss of appetite, nausea, vomiting, tiredness, itchiness, dark colored urine, or yellowing of the skin or eyes).

We are fellow patients here, not docs, but the critical measurements in terms of dosing on the methimazole are Free T4 and T3. TSH can remain suppressed for quite some time, so is not a good benchmark for dosing.

I would call your doctor ASAP about the sore throat, as he/she might want to do a white blood cell count. There is a potential side effect of methimazole called agranulocytosis that is very serious and results in a severely depleted WBC count. Like the liver issues, this more commonly occurs in patients who are just starting the meds (and it could just be cold/flu, which is going around now), but best to err on the side of caution and let your doctor know what is going on.

[JEH]

#1183420

I don’t know if this helps but my endo has been very insistent that I use the branded ATD, Tapazole, rather than the generic methimazole. He has never said why but he diagnosed me with early optholmopathy when I first started treating with him in 1998. He recommended the Tapazole as the best treatment to minimize the eye problems.

I continued with the Tapazole until 2006 when I went into Graves remission and stopped all drugs. Last summer I started T4 supplementation again because the doc considered that I had become hypo.

I am sorry to hear your eyes are getting worse. Hopefully it is early enough in the inflammatory process to reverse it.

Jane

[bchick]

#1183423

I was diagnosed with Graves’ disease about three yrs ago. I have been able to keep my thyroid levels under control with methimazole but my eyes have continued to be an issue. My antibody levels remain high. The bulging has gradually continued and one eye is worse then the other which make me even more self conscious. My ophthalmologist does nothing but just monitor and tell me at each visit if my he thinks the bulging got worse or not. I live in the Philadelphia area and would love to find a doctor who might take a more proactive course of action. Right now I feel like u til my vision is affected it’s just wait and see and after three years of waiting and seeing I’ve had enough!

[Kimberly]

#1183424

@bchick – Hello and welcome! Doctors prefer to postpone any surgeries for TED until the disease has reached the inactive phase (also called the “cold” phase), where your symptoms are not getting better *or* worse. The reason for this is that if your eyes are still changing at the time surgery is done, you could have to go through the exact same surgery a second time. The one exception is if you have sight-threatening compression of the optic nerve, and in that case, emergency surgery is performed. A good test of whether you have optic nerve involvement is if colors are off – for example, something that you *know* is red starts looking more brown.

There are some other interventions that can be done prior to surgery, such as steroid therapy or radiotherapy, although both have risks and benefits. The International Thyroid Eye Disease Society has a nice page that discusses these options; from the link, highlight “What is TED” and then click on the specific section you want to look at.

(Note on links: if you click directly on the following links, you will need to use your browser’s “back” button to return to the boards after viewing, or you will have to log back in to the forum. As an alternative, you can right-click the link and open it in a new tab or new window).

http://thyroideyedisease.org/

If you think a second opinion would be helpful, you can check out our Physician Registry (located in the top right-hand corner of the screen when you visit gdatf.org) or you can visit http://www.asoprs.org – this is a society for eye surgeons, and they generally have good knowledge of Graves’. You can also check out the GDATF’s YouTube videos on TED, as we have presentations from a number of leading experts:

https://www.youtube.com/user/GravesAndThyroid/videos

Take care – and please keep us posted!

[Mforsberg21]

#1183425

Hello everyone. Just wanted to update. Here is what I have learned in the past year or so since finding out I had Graves.

So there are two types of TSI antibodies. One that stimulates the receptors on the thyroid causing hyperthyroidism, the other mimics TSH and stimulates the TSH receptors in the cells at the back of the eyes. Unfortunately there is no test to distinguish between the two. You are either positive for TSI or not.

However, if you are negative for Peroxidase, TRB Antibodies, Thyroglobulin Antibodies but positive for TSI, more than likely you have the mimicking antibodies. If you have a blood test done and like me you have subclinical hyperthyroidism, that is your TSH is suppressed but T3 and T4 normal, I would be insistent upon doing Antibody testing!!! Especially if your Endo wants to treat you with 40mg Methimazole or even worse RAI.

So I go to an Endo for low T. He does TSH reflex 4. My TSH is .005 but my free T4 is mid high range of normal. Probably because I was taking L-Tyrosine in a pre workout supplement for the past 3 years which I have read can raise T4 which would suppress TSH. He orders no antibody tests. He gives me 20 mg of Methimazole and says I’m going to feel much better. After 2-3 weeks my eyes start to bug out. I go back and he gives me 40 mg. My eyes continue to get much worse. Hmmm why you ask?

I am not a doctor just an idiot. Don’t listen to me. I probably don’t know what I’m talking about. There is the disclaimer.

So I have the TSI mimicking antibodies that mimick TSH. When I start the Methimizole my T4 starts to drop. My TSH rises quickly. The antibodies mimick TSH and stimulate, more like attack, the TSH receptors in the cells in the
back of the eye. As I continue the Methimazole my T4 goes to the bottom of the range I feel horrible. I taper off and my T4 goes back to mid range of normal and I am pretty much back where I started,however, maimed with 28mm in left eye and 25mm right eye. When will the stimulation stop? I don’t know. Could be several years.

Needless to say I no longer take the L-tyrosine supplement that clearly states, “Do not take this if you have Graves Disease”. I have read it can raise T4 and cause TSH suppression. Unfortunately I never knew I had TSI antibodies until I found another Endo who did and put me back on the right track. However, I will never be the same.

Forget about antibodies, I can’t find any research that suggests anti thyroid treatment improves quality of life for patients with subclinical hyperthyroidism in the first place.

Had I elected RAI my TSH would probably have shot up faster probably causing worse stimulation by the TSI mimicking antibodies. Then after my thyroid is dead I would take synthetic thyroid hormone for the rest of my life which would suppress my TSH again? Doesn’t make sense to me. But that’s what happend to my mom. Like I said I haven’t talked to her in years. Well I called her. I asked her when she got the eye problems from her Graves’ disease. She only remembered that she had been taking diet pills and lost a lot of weight. That was around 2000. She felt hyper and went to an Endo who diagnosed her with Graves and treated her with RAI. Her eyes are much worse than mine. Her doctor told her she has Iritis and continues to get immunosuppressive shots in her eye.

Now remember I’m an idiot. Don’t listen to me. But I would do lots of research before you go messing with your thyroid. For lots of people Methimizole and RAI are a lifesaver. Many people need these treatments. For me in my case not so much.

Think about it…. Ted and the hyperthyroidism from Graves run their separate courses. But you must treat the thyroid before you can treat the eye disease. Hmmmm. Why? Because the TSI mimicking antibodies mimick TSH and if you don’t stabilize your TSH the eye problems will continue. That’s how people can develop TED years after treating their thyroid. They kill the thyroid, start taking synthetic thyroid hormone and they’re TSH becomes suppressed. You get a bad batch of hormone or don’t take it consistently, your T4 drops and here comes your TSH. If you have developed the TSI mimicking antibody they mimic TSH and stimulate the eyes. You can also get the reverse. Just my story that’s all. I’m not a doctor. Just a patient.

I doubt any doctors will help me after I post this but if it helps someone it’s worth it.

[Kimberly]

#1183426

Hello – There are indeed multiple types of antibodies involved in Graves’ (stimulating, blocking, and neutral), although I have never seen any research indicating that there are two different kinds of *stimulating* antibodies, one that affects the eye and one the thyroid.

The decision to treat sublinical hyperthyroidism is a personal one between patient and physician. As with any aspect of this disease, it’s all about risks and benefits. Patients who are more likely to benefit from treatment of subclinical hyperthyroidism include those who are symptomatic and those who already have a predisposition to bone and heart issues. For other patients, a “watch and wait” approach is fine, with levels monitored at periodic intervals to see if the condition progresses to overt hyperthyroidism (T3/T4 out of range too high and TSH out of range too low).

Edit: And *anyone* on methimazole should have levels closely monitored (especially Free T4 and T3), as going hypo is a risk factor for thyroid eye disease.

[Mforsberg21]

#1183427

Hi Kimberly.

I haven’t seen any research that suggests Methimizole or thyroidectomy can trigger TED or make it worse. However, I see a lot of research that says RAI can trigger a TED flare up or make it worse. Why does RAI make TED worse? Is it the Radio Active Iodine itself or a sudden drop in T4 causing a sudden rise in TSH? I see lots of research that says RAI can make TED worse but not much research that says why?

[Kimberly]

#1183428

Hello – There are a couple of theories. One is that the spike in antibodies that occurs for 6+ months after RAI is responsible for the increased risk for new/worsening TED. Another is that the increased risk comes when doctors don’t start replacement hormone quickly enough after RAI and patients are allowed to go too hypO. I heard another theory at a recent conference that there is a specific substance shed during the breakdown of thyroid tissue following RAI that might be involved. (I need to find some additional info on that last one.)

[Mforsberg21]

#1183429

I was negative for all antithyroid antibodies including TRAB, Peroxidase, thyroglobulin, etc but positive for TSI. My TSH came back after 4months of Methimizole even though I reduced from 40mg to 5. I became hypo and quit. It seems some people develop TED shortly after starting Antithyroid treatment.

How can someone have normal T4 and T3 but TSH .005 and be negative for all antithyroid antibodies accept TSI? What is keeping T4 and T3 normal. How would treating someone in this condition with 20mg of Methimizole cause a severe TED flare up 2 to 3 weeks after starting? (I see Rasberrys reply on the first page) Also would bringing TSH to a normal level decrease TSI and help TED. I see some research that says restoring thyroid hormone levels to normal doesn’t necessarily help TED but I can’t find anything about restoring TSH. Thanks.

[Kimberly]

#1183430

A presenter at our 2010 conference noted that about 40% of patients experience thyroid and eye involvement at the same time, about 45% experience thyroid issues first, and the remaining 15% experience eye issues before having any thyroid involvement. So you have to consider the possibility that you would have developed eye symptoms even if you *hadn’t* started the methimazole. My own eye symptoms started about 10 months after diagnosis.

If your TSI was positive, you would expect TRAb to also be positive (since that test picks up both stimulating and blocking antibodies). However, antibody tests are extremely accurate, but not 100%.

The mechanisms just aren’t well understood. A presenter at the conference we attended in Florida noted that thyroid dysfunction and autoimmunity affect each other in a circular fashion. Thyroid dysfunction seems to fuel the autoimmunity – and the autoimmunity makes the thyroid dysfunction even worse.

[Mforsberg21]

#1183431

I wasn’t tested for TRab. It was TgAB from a different lab. One said Thyroglobulin and the other lab said TgAB. Getting my letters mixed up. I was positive for TSI but negative for all other anti thyroid test typically performed when Graves is expected. TPO or Thyroid Peroxidase antibody, TgAB or Thyroglobulin antibody were negative but TSI or Thyroid Stimulating Immunoglobulin positive.

[Kimberly]

#1183432

Hello – TSI is specific to Graves’, but TPOab and TGab are not. TPOab and TGab are “markers” for autoimmune thyroid disease and are very common in Hashimoto’s thyroiditis, which usually causes hypOthyroidism.

[Mforsberg21]

#1183433

How could my TSI be 480 and my T4 and T3 normal?

[Kimberly]

#1183434

Hello – That’s not the norm, but it *can* happen with patients who have thyroid eye disease. A presenter at a recent conference that we attended called the condition “Euthyroid Graves’ Orbitopathy”. The reasons that this can occur just aren’t well understood at this time.

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