- Natural Endocrine Solutions Dr. Eric Osansky, DC, IFMCP - https://www.naturalendocrinesolutions.com -

Hashitoxicosis vs. Graves’ Disease: How To Differentiate The Two

Posted By Dr. Eric On In Uncategorized | 24 Comments

Most cases of Graves’ disease and Hashimoto’s thyroiditis are relatively easy to distinguish from one another.  But every now and then it’s not clear as to which autoimmune thyroid condition someone has.  Of course there are also people with non-autoimmune thyroid conditions, but I’m not referring to these cases here.  Instead I’d like to focus on Hashitoxicosis, which sometimes can be mistaken for Graves’ disease, but is actually Hashimoto’s that involves transient hyperthyroidism.

Based on what I just said, if you are experiencing hyperthyroidism, then the next question you may have is “how do I know if my hyperthyroid condition is due to Hashitoxicosis or Graves’ disease?”  Well, let’s first go ahead and look at how Graves’ disease and Hashimoto’s thyroiditis are typically diagnosed, and then you should have a better understanding as to how Hashitoxicosis is diagnosed.

How Graves’ Disease is Diagnosed

Many reading this know that I was diagnosed with Graves’ disease in 2008.  Initially I was diagnosed with hyperthyroidism, which is characterized by a depressed (and usually undetectable) thyroid stimulating hormone (TSH), along with elevated T3 and T4 levels.  I also had many of the classic symptoms associated with hyperthyroidism, including an elevated resting pulse rate, heart palpitations, tremors, weight loss, an increased appetite, more frequent bowel movements, etc.

Upon visiting an endocrinologist I had my thyroid antibodies tested.  The thyroid stimulating immunoglobulins (TSI) are the most specific antibodies associated with Graves’ disease, and these were elevated, which confirmed my Graves’ disease diagnosis.  It’s also worth mentioning that TSI is a type of TSH receptor antibody (TRAB), and many times this is tested for instead of TSI, while sometimes both of these are tested by endocrinologists.

Endocrinologists also commonly recommend the radioactive iodine uptake test [1] as a way to determine that someone has Graves’ disease.  I didn’t have this test done, and to be honest, most people with Graves’ disease don’t need to have this test done.  If you have hyperthyroidism in the presence of elevated TSI levels then this confirms that you have Graves’ disease.  Some doctors will argue that the radioactive iodine uptake test can also reveal whether someone has hot or cold nodules, which is true, but of course a thyroid ultrasound [2] can also detect thyroid nodules, and the characteristics of an existing thyroid nodule on an ultrasound can give an idea as to whether a nodule is malignant or benign.  It’s not perfect, but neither is the radioactive iodine uptake test, and an ultrasound is much less invasive than the radioactive iodine uptake scan.

So let’s go ahead and summarize how Graves’ disease is diagnosed:

How Hashimoto’s Thyroiditis is Diagnosed

Hashimoto’s thyroiditis frequently takes longer to diagnose than Graves’ disease, and the main reason for this is because if someone is experiencing hyperthyroidism the person is more likely to seek immediate medical attention, whereas if someone is experiencing hypothyroid symptoms (i.e. fatigue, weight gain, cold hands and feet) they are less likely to take immediate action.  The reason why many people with these symptoms don’t consult with a doctor sooner than later is because many other factors can cause similar symptoms, and so it can be challenging to make the connection purely from a symptomatic standpoint.  On the other hand, the symptoms of hyperthyroidism are usually more alarming, as if someone has an elevated resting heart rate of 100+ BPM along with palpitations, tremors, weight loss, in some cases the symptoms of thyroid eye disease [3], etc., then they are much more likely to schedule an appointment with a doctor.

What also makes it challenging is that many people with Hashimoto’s don’t have overt hypothyroidism, but instead they have subclinical hypothyroidism [4].  This means that they have elevated thyroid stimulating hormone (TSH) levels, but their thyroid hormone levels look fine…at least from a lab reference range perspective.  Regarding Graves’ disease, some people with this condition do experience subclinical hyperthyroidism, but this is not as common as subclinical hypothyroidism.  In fact, it’s safe to say that just about everyone with Hashimoto’s will present with subclinical hypothyroidism prior to developing overt hypothyroidism.

I discussed this in a past blog post entitled “What Causes Thyroid Autoimmunity? [5]“, where I discussed the autoimmunity timeline.  With Hashimoto’s, the development of thyroid autoantibodies occurs first, and then over time the TSH usually becomes elevated.  After this it can take months or years before the thyroid hormone levels become out of range.  It’s important to mention that in many people the thyroid hormones will never become overtly depressed, but there is a good chance that eventually they will become less than optimal.  In other words, they might look fine on a blood test report, but be outside of the “functional reference range”.  But even in this situation it usually takes time for this to occur.

In any case, there are two thyroid autoantibodies commonly associated with Hashimoto’s.  These include thyroid peroxidase [6](TPO) and thyroglobulin antibodies.  If someone has an elevated TSH and at least one of these antibodies are elevated, then this is when they are typically diagnosed as having Hashimoto’s thyroiditis.  Once again, this can happen in the present of normal, depressed, or less than optimal thyroid hormone levels.  This is why some doctors don’t even bother to test the thyroid hormone levels, but will only look at the TSH (keep in mind that this isn’t something I recommend, as I feel it’s important to also measure the thyroid hormone levels).  It’s also worth mentioning that some sources will refer to those who have an elevated TSH, depressed thyroid hormone levels, and elevated TPO and/or thyroglobulin antibodies as having “Hashimoto’s hypothyroidism”.  For the sake of simplicity I always refer to this condition as “Hashimoto’s thyroiditis” in my blog posts.

So let’s go ahead and summarize how Hashimoto’s thyroiditis is diagnosed:

How Is Hashitoxicosis Diagnosed?

After reading this you now know that Graves’ disease is diagnosed when someone has a depressed TSH, elevated thyroid hormone levels, and elevated TSI levels (or an elevated radioactive iodine uptake test).  On the other hand, Hashimoto’s thyroiditis is diagnosed with an elevated TSH, along with elevated TPO and/or thyroglobulin antibodies.  As for how Hashitoxicosis is diagnosed, the person will present with hyperthyroidism (depressed TSH and elevated thyroid hormone levels), but unlike Graves’ disease, the TSI levels and radioactive iodine uptake test will both be negative.  However, at least one of the autoantibodies associated with Hashimoto’s (TPO and thyroglobulin antibodies) will be positive.

So let’s go ahead and summarize how Hashitoxicosis is diagnosed:

Why Do Some People With Hashimoto’s Have Hashitoxicosis?

So just as a reminder, Hashitoxicosis is a state of hyperthyroidism that occurs in some people with Hashimoto’s, but it’s differentiated from Graves’ disease in that people won’t have elevated TSI levels.  So essentially the person will have hyperthyroidism in the presence of Hashimoto’s antibodies.  But why do some people with Hashimoto’s thyroiditis also have Hashitoxicosis?  In other words, why would someone experience hyperthyroidism if they have Hashimoto’s antibodies (and not Graves’ disease antibodies)? The hyperthyroidism experienced in someone with Hashitoxicosis is caused by the release of preformed thyroid hormones caused by the destruction of the thyroid follicles (1) [7].

Having Antibodies For Both Graves’ Disease and Hashimoto’s

If for any reason you’re confused at this point, please go back and look at the summaries listed above.  And before wrapping up this blog post I’ll give a final summary below to further clarify everything.  But before doing this, I think it’s important to mention that it’s possible for someone to have thyroid antibodies for both Graves’ Disease and Hashimoto’s.  In fact, not only is it possible, but it is quite common.  This can occur in any of the following combination:

This may bring up another question…if someone has any combination of Graves’ disease antibodies (TSI) and Hashimoto’s antibodies (TPO, thyroglobulin), AND if they are presenting with hyperthyroidism, do they have Graves’ disease or Hashitoxicosis?  If someone has hyperthyroidism in the presence of elevated TSI levels, then this is diagnostic of Graves’ disease.  Now truth to be told, if someone has the antibodies for both Graves’ disease and Hashimoto’s and is presenting with hyperthyroidism, it’s very difficult to know for certain whether the hyperthyroidism is being caused by stimulation of the TSH receptor antibodies (typical of Graves’ disease), or by the release of thyroid hormone by the thyroid follicles (typical of Hashitoxicosis).  But to be honest, it doesn’t matter in this situation, as the treatment will be the same regardless.

In other words, from a symptom management perspective, a person with a depressed TSH, elevated thyroid hormone levels, and elevated TSI levels will want to do things to suppress the thyroid hormone levels, even in the presence of TPO and/or thyroglobulin antibodies.  And if someone has any type of thyroid autoantibody (TSI, TPO, and/or thyroglobulin antibodies), the goal should be to do whatever is necessary to reverse the autoimmune component and normalize the antibodies.  The challenge is that different types of autoantibodies can have different triggers.  For example, someone who has the antibodies for both Graves’ disease and Hashimoto’s might follow a natural treatment protocol and remove one or two triggers, thus causing normalization of one thyroid autoantibody, while another thyroid autoantibody remains elevated.  When this is the case, the goal should be to find the remaining triggers.

What’s The Best Treatment Approach For Hashitoxicosis?

Another challenge is that the hyperthyroidism associated with Graves’ disease usually will last longer than in someone who has Hashitoxicosis.  From a conventional medical standpoint, antithyroid medication [8] such as Methimazole or PTU is commonly recommended for those with Graves’ disease.  Some people with Hashitoxicosis are also prescribed antithyroid medication, but the concern here is that since the hyperthyroidism is usually transient, the person with Hashitoxicosis who takes antithyroid medication might become overtly hypothyroid sooner than later.  As a result, if Hashitoxicosis is diagnosed then the person might be prescribed a beta blocker [9] and not antithyroid medication.

The problem with only taking a beta blocker is that some people with Hashitoxicosis will experience hyperthyroidism for a few months.  And while a beta blocker can help to address the cardiac symptoms, elevated thyroid hormone levels shouldn’t be taken lightly, as they can have a negative effect on bone density [10].  In my practice I commonly recommend bugleweed to my Graves’ disease patients who aren’t taking antithyroid medication, and I have no problem recommending this herb on a temporary basis to people with Hashitoxicosis.  When this is the case it’s a good idea to do regular thyroid panels (i.e. every 2 to 4 weeks), and if someone starts experiencing hypothyroid symptoms then this is a good sign that the bugleweed needs to be reduced or stopped.

Low dose naltrexone [11] (LDN) is also something to consider in those with Hashitoxicosis.  The downside is that LDN doesn’t address the cause of the problem, and it doesn’t work in everyone, but the upside is that when it does work it modulates the immune system, and thus the person with Hashitoxicosis might not have to take either a beta blocker or antithyroid medication/herbs (which also don’t address the underlying cause).  So what ideally would happen is that someone with Hashitoxicosis would take LDN, and the immune system would no longer damage the thyroid follicles as I mentioned earlier, and thus the person wouldn’t be hyperthyroid.

Consider a Natural Treatment Approach for Hashitoxicosis

While some people with autoimmune conditions benefit from taking LDN, of course the long term goal of Hashitoxicosis should be to reverse the autoimmune component.  This is true with any autoimmune condition, and it’s no exception with Hashitoxicosis.  While it’s important to manage the hyperthyroid symptoms, at the same time you want to find and remove environmental triggers, heal the gut, etc.  I talk about this in greater detail in other articles and blog posts.

FINAL SUMMARY

If you understand the difference between Hashitoxicosis and Graves’ disease then you probably don’t need to read this “final summary”.  On the other hand, if you’re still confused I’ll try to clarify one last time…

You Probably Have Hashitoxicosis if You Have ALL of the following:

You Probably DON’T Have Hashitoxicosis if You Have ANY OF THE FOLLOWING:

By now it should be obvious that if you don’t have hyperthyroidism (depressed TSH and elevated thyroid hormones) then you don’t have Hashitoxicosis.  Similarly, if you don’t have elevated TPO and/or thyroglobulin antibodies then you probably also don’t have Hashitoxicosis.  If you’re still confused as to whether you have Graves’ disease, Hashimoto’s, or Hashitoxicosis then please feel free to post your thyroid panel and antibody results in the comments section below and I’ll briefly give you my feedback.  Just keep in mind that I can’t officially diagnose your condition, and I’ll also ask to please refrain from posting other lab values in the comments, as I’ll only be providing feedback to those who post their TSH, thyroid hormone levels, and thyroid antibodies.  And if anyone reading this has experienced Hashitoxicosis and would like to share their experience please feel free to post your comment as well.