Rationale: Autoimmunity

Updated 2018-07-09

A correct autoimmune diagnosis helps patients and doctors better understand the increased risk common diseases associated with autoimmune thyroid disease, such as type 1 diabetes, autoimmune gastritis, and celiac disease. [157, 158, 159, 160]

The two most common antibodies in Hashimoto’s thyroiditis, anti-thyroid peroxidase (TPO) and anti-thyroglobulin (TG), are diagnostic. High titres of TPO and TG antibodies are rare outside of Hashimoto’s, and their presence indicates that an autoimmune process is likely involved in progressive thyroid hormone deficiency as the follicular cells are destroyed.  Anti-thyroid antibodies participate to varying degrees in the process thyroid gland fibrosis, inflammation and/or atrophy. [44, 21]

An important thyroid antibody is currently overlooked in medical practice and guidelines: the TSH-receptor blocking antibody. In contrast, the stimulating variety of TSH receptor antibodies (TSAb) are very well understood as the cause of Graves’ disease, since TSAb directly stimulate the thyroid gland to continue producing excess hormone even in the absence of pituitary TSH.

The medical systems in Japan and Korea are more familiar with TSH receptor blocking antibodies (TBAb), and it is largely from their research that we have learned its extreme inflation of TSH pre-treatment, highly variable TSH while on therapy, the possibility of vacillating from hypo- to hyperthyroidism over 10 years, its associated health disorders, and sometimes an adverse response to L-T4 treatment. [161, 162, 163, 164]

All categories of autoimmune thyroid patients are susceptible to TSH blocking antibodies, and their rate of occurrence may vary across populations. According to a review of research 2017, TSH Blocking antibodies have been found in 10-75 % of atrophic thyroiditis patients, 25-75% of Graves’ disease patients, and 0-20% of Hashimoto’s patients. [44] A subsequent clinical study in Germany found TBAb in 4.2% (15 of 357) Graves’ disease patients and 9.3% (67 of 722) of Hashimoto’s patients. [162] Atrophic thyroiditis, formerly called Ord’s disease, has frequently been miscategorized as just one type of Hashimoto’s thyroiditis or “end-stage Hashimoto’s,” but it has a unique antibody and presentation and is genetically related to Graves’ disease. [21, 165]

Graves’ disease patients may have both the blocking and stimulating antibodies concurrently, and they may compete with each other over time. If TBAb supersede TSAb levels in a patient, the net effect will be to block, rather than stimulate, thyroid gland secretion of T4. Antibodies can also disappear and reappear. This has sometimes resulted in clinical confusion as patients alternate between hypothyroid and hyperthyroid states over many years or experience unexplained remission. [166, 167]

Extremely high TSH, such as values above 100, can be a telltale sign of the activity of TBAb in a hypothyroid patient. Theoretically, by means of blocking the TSH receptors on the pituitary gland itself (the ultrashort feedback loop), the pituitary cannot monitor its own TSH secretion as much, and it can become excessive. In high titres, this antibody can cut off or greatly reduce stimulation of the thyroid gland even in the presence of excess TSH secretion. Even after therapy is initiated, TBAb can exaggerate TSH secretion far past the expected level given the patient’s concentration of T4 in serum. These indicators of TSH blocking antibodies may suggest that either the gland is already atrophied, or very soon may become severely diminished in size. The antibodies can cause the thyroid gland to swiftly and permanently atrophy, whereas in contrast, follicular cell destruction triggered by TPO antibodies usually causes gland fibrosis.

Since standard North American TSH-antibody assays may not be capable of measuring the blocking variety, [166] an ultrasound can confirm the diagnosis by measurable proof that these antibodies have been active in a patient. [21]

Once the gland has atrophied, the patient usually remans hypothyroid, but antibodies may continue to interfere with TSH levels. Doctors who do not understand may assume the patient has been noncompliant in taking their L-T4 medication because their TSH is too high given their T4 lab test result. [168]

 

References

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