Autoimmune thyroiditis (Hashimoto’s disease)

Autoimmune thyroiditis is very different from other diseases that we will touch on in this book. Firstly, such patients are observed by endocrinologists, not rheumatologists. Secondly, in this disease, drugs that suppress the aggression of the immune system (prednisone and immunosuppressants) are not used at all. However, Hashimoto’s disease is the most common autoimmune disease in the world, and among other autoimmune (and immune-mediated) diseases, we see it especially often.

That is why we decided to tell our readers about this pathology.

What is this disease and why does it occur?

Autoimmune thyroiditis (chronic lymphocytic thyroiditis or Hashimoto’s disease) is an autoimmune disease of the thyroid gland, in which chronic aggression of the immune system gradually destroys this organ, which leads to a decrease in its function (hormone production decreases). According to the most conservative estimates, 1-2% of the world’s population suffer from this disease. Women get sick 5-10 times more often than men. You can get autoimmune thyroiditis at any age, but more often we see this disease in middle-aged people. The exact causes of this disease, like most autoimmune diseases, are unknown. Hashimoto’s disease is often found together with other autoimmune diseases, such as rheumatoid arthritis.

What are the manifestations of autoimmune thyroiditis?

All patients with this disease can be divided into three groups.

  1. Asymptomatic course of the disease. In most cases, Hashimoto’s disease proceeds completely unnoticed and for many years patients do not even realize that they have autoimmune thyroiditis.
  2. The development of hypothyroidism. Hypothyroidism is a condition of reduced thyroid function (see Table 1 “Thyroid function”). At the same time, general weakness, drowsiness, increased fatigue, apathy, decreased concentration and memory impairment, weight gain, increased fragility of nails, hair loss, dry skin, cold intolerance, constipation, swollen face, enlarged tongue, joint discomfort and muscle weakness may occur.
  3. The development of “Hashitoxicosis”. This is a short-term state of hyperthyroidism (see Table 1 “Thyroid function”), in which, due to an active immune attack, damaged thyroid tissues release their hormones into the blood. There may be palpitations, a feeling of heart failure, increased anxiety and anxiety.

In some patients with autoimmune thyroiditis, there may be an increase in the thyroid gland (goiter is formed), often this is recorded only according to ultrasound data. Pain in the anterior region of the neck or soreness during palpation (palpation) in such patients is extremely rare.

In other patients with this disease, the thyroid gland only atrophies (shrinks) as a result of chronic inflammation.

Also, postpartum thyroiditis is singled out separately, when the attack (usually “soft”) of the immune system on the thyroid gland occurs precisely in the period after childbirth.

How is autoimmune thyroiditis diagnosed?

In the blood of patients with Hashimoto’s disease, two main types of autoantibodies directed to the structural components of the thyroid gland are detected: antibodies to thyroid peroxidase (AT-TPO) and antibodies to thyroglobulin (AT-TG). Currently, it is considered that the titer (concentration or level) of antibodies has no clinical significance, i.e. in a simple way: there is no connection between their level and the activity of autoimmune thyroiditis or the rate of formation of hypothyroidism. That is why it is simply pointless to repeatedly retake these tests to track the dynamics of their blood levels, they are only needed to diagnose the disease.

A fundamentally important point for all patients with autoimmune thyroiditis is to determine the functional state of the thyroid gland. It can be evaluated by only two blood parameters: thyroid-stimulating hormone (TSH) and T4 free. Depending on their levels, three main conditions are identified: normal, or euthyroidism; decreased function, or hypothyroidism; increased function, or hyperthyroidism. In addition, there are two more borderline conditions with normal function – subclinical hypothyroidism and subclinical hyperthyroidism. For more clarity, see Table 1 “Thyroid function”.

How is autoimmune thyroiditis treated?

If the function of the thyroid gland is preserved (normal values of TSH and T4 are free) and antibodies to thyroid peroxidase and/or thyroglobulin are present, then only observation is required. As a rule, such patients are recommended by endocrinologists to take a blood test for TSH only once a year. There is NO NEED to treat this form of the disease! There is no need to take any anti-inflammatory drugs, including those of plant origin. We’re just watching!

With a decrease in the function of the thyroid gland and the development of hypothyroidism, the endocrinologist will recommend one of the hormonal drugs levothyroxine, which will compensate for the lack of its own thyroid hormones. Levothyroxine is one of the most prescribed medications in the whole world, and the word “hormonal” should not frighten you, because, in fact, we are only making up for the lack of our own hormones. At the beginning of treatment, the doctor, depending on the severity of the initial hypothyroidism, prescribes the starting dosage of levothyroxine, usually a small dose, in the range of 12.5–50 mcg per day. Subsequently, TSH monitoring is performed every 6-8 weeks (if necessary, free T4) to decide how to adjust the dose of levothyroxine. In most cases, the increase in the dosage of levothyroxine occurs slowly by 12.5-25 mcg every 6-8 weeks (or even less often!). In particular, this drug is slowly increased in the elderly and patients with heart rhythm disorders. With proper treatment, the initially elevated TSH level returns to normal, and the reduced free T4, on the contrary, increases and should also normalize. The closer TSH (and T4 free) approaches the norm, the less often tests are given.

When the dosage of levothyroxine is selected and TSH returns to normal, then it is taken no more than once a year.

Levothyroxine is taken in the morning, strictly on an empty stomach (30 minutes before meals), this medicine should be washed down only with water, preferably without combining it with other medications. Levothyroxine has a very good safety profile with the correct selection of dosages, and if you have any unpleasant sensations when taking it – you need to update the tests for TSH (and T4 free) and consult your doctor unscheduled.

A more complex treatment is required for the formation of” Hashitoxicosis”, that is, a temporary state of hyperthyroidism or hyperthyroidism. Perhaps, during this period, the endocrinologist will recommend taking drugs that suppress the function of the thyroid gland (for example, thiamosol). I would like to emphasize once again that hyperthyroidism in Hashimoto’s disease is a temporary phenomenon, and eventually the function of the thyroid gland will still decrease and may require treatment with levothyroxine.

In the past years, the possibility of adding food supplements containing selenium to patients with autoimmune thyroiditis was often discussed. Due to their use, a decrease in the level of antibodies to thyroid peroxidase and even an improvement in the ultrasound picture of the thyroid gland were noted. Nevertheless, further scientific studies have shown that selenium has no effect on the incidence of hypothyroidism, and this is the most important thing for Hashimoto’s disease. That is why selenium-containing additives are currently not widely used in academic (scientific) medicine.

What does autoimmune thyroiditis threaten me with?

Fortunately, Hashimoto’s disease has a favorable prognosis and, as it was written earlier, the main outcome of the disease is a decrease in the function of the thyroid gland, which is easy to restore with the help of drug therapy. Sometimes a significant increase in the size of the thyroid gland (goiter) as a result of long-term autoimmune thyroiditis requires surgical intervention.

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