This is part 1 in a series on anti bodies and auto immune thyreoditis. In this first part I will take a look at anti bodies in general and Anti-TPO in particular. I think you will be a little surprised at some of the findings. It’s maybe a little nerdy for some. But the main points are listed in the summary.
This is a complex topic, and there is a lot of research going on. I will probably revise these posts as I learn more.
Abstract
All anti bodies look the same, Y shaped. They differ only on the tips of the Y. That is where they bind onto specific anti genes. People without thyroid disease can also have low levels of anti bodies, particularly Anti-TPO and Anti-TG. But whether they GET a thyroid disease later, we don’t know. A study showed, that many women had anti bodies up to 7 years before they got symptoms (1).
All antibodies are produced within the thyroid itself by B lymphocytes. So if on has little or no thyroid, one does not have high levels of anti bodies.
TPO is an enzyme that takes part in the process where Iodide gets converted into Iodine. Iodine is the form the thyroid uses in it’s hormone production. TPO can get damaged by oxidative stress. Anti-TPO then gets produced against the damaged enzyme. Oxidative stress can start as a result of Iodine deficiency. The process has started.
Anti-TPO is not what causes the greatest damage to the thyroid. It’s B and T lymphocytes that do that. Plus a form of the TRAb anti body, the cleavage TRAb. That can cause cell death as well. I will write about that in part 3.
One can have high levels of Anti-TPO without the thyroid decreasing in size. We call everything Hashimotos, but that is not correct. Hashimotos is the AIDT that starts with a goiter. The thyroid gets infiltrated by B and T lymphocytes, and cannot function as it should. But it doesn’t atrophy. Whereas Ord’s does not start with a goiter, and the thyroid atrophies. I will write more about that in a later part in the series.
