>Hashitoxicosis -- A form of Graves disease that is easily misdiagnosed.
Hashitoxicosis is an autoimmune thyroid disorder, in which individuals with autoimmune hypothyrodism, usually Hashimoto's thyroiditis (HT), experience intermittent or sporadic periods where they also have symptoms of hyperthyrodism. In some ways, these patients can be described as having both HT and Graves' disease since the antibodies associated with both diseases are present.
The disease process in Hashitoxicosis focuses around the thyroid cell destruction seen in autoimmune hypothyroidism. Here, thyroid peroxidase and thyroglobulin antibodies cause thyroid cell inflammation and destruction. As thyroid cells die, their stored supplies of thyroid hormone are suddenly released into the blood circulation. These sudden bursts of thyroid hormone are responsible for the symptoms of hyperthyroidism. Often patients think that they need to have their medications adjusted and they suspect that their thyroid medication is too high. On other days, when they're dragging, depressed and experiencing weight gain, they suspect that their thyroid hormone replacement dose is too low.
Blocking TSH receptor antibodies in Hashitoxicosis can prevent the thyroid cell from absorbing thyroid hormone, worsening hypothyroidism. And stimulating TSH receptor antibodies can cause periods where excess thyroid hormone is produced. Depending on which antibodies predominate on a given day, symptoms can vary.
Furthermore, these sudden bursts of thyroid hormone affect laboratory results. If a patient experiences many recurring bursts of thyroid hormone, their blood thyroid hormone levels will be elevated. If this happens over a period of weeks, their TSH levels will drop. Depending on when they have their laboratory tests run, it can appear as if they're now hyperthyroid. If their medication is cut, they may soon be complaining of symptoms of hypothyroidism.
Patients with GD who have achieved remission after being on antithyroid drugs may also experience Hashitoxicosis. So can ablated patients who still have some remaining functional thyroid tissue. These patients worry that active Graves' disease has returned and ask to be put back on ATD's. Others who have had RAI end up having a second or third dose of RAI. A wait and see approach can prevent this from happening.
For patients who have symptoms of both hypothyroidism and hyperthyroidism but have never been diagnosed, diagnosis can be elusive. Often the periods of hypothyroidism and hyperthyroidism will balance each other out, causing normal thyroid hormone levels. Without a careful evaluation of symptoms, it will appear as if these patients are euthyroid. One clue is in the patient who shows signs of Graves' ophthalmopathy or thyroid eye disease.
If they have the proper antibody tests run, and are diagnosed with Hashitoxicosis, then they can be properly monitored and learn how to adjust their own thyroid meds depending on symptoms. A presumptive diagnosis can be made by biopsy, that is, fine needle aspiration. A lymphocytic (white blood cell) infiltration of the thyroid will be seen, and there will be certain cellular changes, particularly the presence of Hurthle cells. A probable diagnosis can also be made by thyroid antibody tests. In Hashitoxicosis, thyroid peroxidase, thyroglobulin, thyroid binding inhibiting immunoglobulins (TBII) and thyroid stimulating immunoglobulins (TSI or stimulating TSH receptor antibodies) will all be present.
Anyone who is genetically predisposed to autoimmune thyroid disease can develop Hashitoxicosis. It's not uncommon in one's lifetime to have HT, GD, primary myxedema and Hashitoxicosis at different times. According to some researchers, Hashitoxicosis is most likely to be encountered in the early stages of autoimmune hypothyroidism. Patients with GD who have achieved remission may actually be experiencing the early stages of spontaneous hypothyroidism when symptoms of Hashitoxicosis emerge.
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