I saw that on my test result, I have TPO antibodies of 9, which means I don't have Hashimoto's (since lab ranges says it needs to be >36 to have Hashi).
But what I don't understand is: if you have some level of TPO anti, isn't your body already attacking the thyroid then?
Why does it have to be 36?
Laura221,
Most people have some thyroid antibodies. The seepage of some thyroid peroxidase into the blood from an injury to the thyroid could cause antibodies to form. Once antibodies are over what is considered to be a normal range it is accepted that the antibodies are due to autoimmune thyroiditis (Hashimoto's).
Many healthy people have a small number of antibodies in their blood. 36 isn't a fixed number - each laboratory establishes or validates its own reference ranges, leading to differences in the numbers, which therefore vary from lab to lab. The numbers are arrived at based on what is typical for a particular group of people based on age, sex, and other characteristics, so in any generalisation there are outliers. Thyroid autoantibodies in healthy people increase with ageing although they are apparently rare in centenarians, often higher in women during their reproductive years, and also found in people with lupus - which apparently suggests a susceptibility gene shared by patients with SLE and autoimmune thyroid disease. But there's a lot still to learn about auto-aintibodies and the interconnectedness with difference diseases and role in good health.
BTW, to answer your question about is the thyroid already under attack, some believe that the reference range isn't too important/accurate a figure, which they believe is actually much higher. A recent study by Ehlers et al investigated the association between thyroid antibody levels and the risk for developing hypothyroidism. It was a retrospective study of 335 untreated AIT patients. Anti-thyroperoxidase (TPO) antibodies, anti-thyroglobulin (Tg) antibodies (Abs), and the TSH level were measured. Patients with TPO-Ab levels >500 IU/ml showed only a moderately increased risk of having elevated TSH levels [p=0.0023; relative risk (95% confidence interval): 1.343 (1.108-1.627)] compared to those below this 500 threshold. AIT patients with TPO- or Tg-Abs<100 IU/ml and between 100-500 IU/ml had NO significantly different TSH levels. Presence of Tg-Abs alone or in combination with TPO-Abs did not help to increase the sensitivity to identify patients at risk. Long term follow-up of AIT patients with high TPO-Abs level (>500 IU/ml) showed an increase of TSH levels (mean: 0.5 mIU/l; range: 2.52±2.73 to 3.02±3.05 mIU/l; p=0.0420). Still, these patients remained euthyroid. The data indicated largely elevated levels of TPO-Abs being associated with only a moderately increased risk of developing hypothyroidism.
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