Types and forms of hyperthyroidism

Types and forms of hyperthyroidism can be very diverse. If we talk about primary hyperthyroidism, then it mainly appears as a result of diffuse toxic goiter or so-called Graves' disease.

Graves' disease is an autoimmune disorder of unknown etiology. Many newly diagnosed patients report having a family history of the disease. This likely suggests that Graves' disease may be caused by a hereditary factor.

This disease causes the thyroid gland to become enlarged and hyperactive, producing an increased amount of thyroid hormones. This occurs because the immune system produces abnormal antibodies, thereby stimulating the thyroid gland.

Congenital hyperthyroidism

This disease occurs because thyroid-stimulating immunoglobulins undergo transplacental transfer. A high concentration of these substances in the blood of the expectant mother during pregnancy will most likely lead to the development of hyperthyroidism in the newborn.

Congenital hyperthyroidism is mostly transient and disappears after 3 months, sometimes lasting up to several years. Both boys and girls can suffer from it.

Quite a few babies are born prematurely, and many of them have an enlarged thyroid gland. Such children are very restless, hyperactive, and easily excitable. Their eyes are wide open and look bulging. There may be sharp accelerations in breathing and increased pulsation, high temperature. There is an increased T4 level in the blood serum. Symptoms such as bulging of the large fontanelle, rapidly ossifying skeleton, and synostosis of the sutures on the skull may also occur. Craniosynostosis may cause a delay in mental development. In such children, even though they actively suckle, body weight increases very slowly.

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Primary hyperthyroidism

There are 3 other causes of primary hyperthyroidism, although they are not as common. These are:

1. multinodular toxic goiter;
2. adenoma;
3. subacute thyroiditis.

But all of them together do not exceed 20% of all cases of hyperthyroidism.

Basically, the hyperthyroid phase is replaced by the hypothyroid phase. The course of treatment in such cases can last for a very long time - for many months.

Secondary hyperthyroidism

Secondary hyperthyroidism is called hyperfunction of the thyroid gland, as well as an increase in its production of T3 and T4 hormones. This occurs due to the pituitary gland, which has a stimulating effect on it.

Sometimes the disease can occur due to a pituitary tumor that produces an excess of thyroid-stimulating hormone, but this is rare. This hormone itself stimulates the thyroid gland to produce a large number of hormones. Another rare cause of hyperthyroidism can be the pituitary gland's resistance to the thyroid hormones it produces. Because of this, it will produce an excess of thyroid-stimulating hormone, despite the presence of thyroid hormones.

A woman may develop the disease due to a hydatidiform mole, because then the thyroid gland receives excessive amounts of chorionic gonadotropin. If the cause – the hydatidiform mole – is removed, hyperthyroidism will disappear.

Diagnosis is made based on the results of laboratory tests:

• The concentration of thyroid hormones in the blood is calculated - it will be elevated if the patient suffers from hyperthyroidism;
• The concentration of the pituitary thyroid-stimulating hormone is calculated, which also increases in the presence of secondary hyperthyroidism.

Drug-induced hyperthyroidism

The drug-induced type is caused by an excess of triiodothyronine and thyroxine in the body, introduced into it along with medications. The cause may also be hormone replacement therapy, which is used to cure hypothyroidism, suppressive therapy to get rid of thyroid cancer and benign nodes in it, an overdose of thyroid hormone medications, which are taken to control body weight.

Drug-induced hyperthyroidism can have the following types, which differ in severity:

• Mild form, including symptoms - no atrial fibrillation, heart rate 80-120/min., slight decrease in performance, no sudden weight loss, mild hand tremors;
• The average form, which includes increased heart rate, weight loss of 10 kg, heart rate of 100-120 beats/min, no atrial fibrillation, decreased performance;
• A severe form, in which the following are observed: atrial fibrillation, heart rate of 120+/min., sharp weight loss, thyrotoxic psychosis, loss of ability to work, parenchymal organs undergo degenerative changes.

There is also a slightly different classification of the degrees of problematic nature of the disease:

• Mild subclinical hyperthyroidism, which is diagnosed mainly based on the results of hormonal analysis, when the clinical picture is erased;
• Moderate manifest hyperthyroidism, in which the clinical picture of the disease is clearly visible;
• Severe complicated hyperthyroidism, which is characterized by heart failure, psychosis, atrial fibrillation, thyrogenic adrenal insufficiency, severe weight loss, and dystrophic changes in parenchymal organs.

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Autoimmune hyperthyroidism

Hyperthyroidism of the thyroid gland is often autoimmune in nature, and diseases of this kind usually appear due to a viral infection. The cell wall is infected, after which the immune system begins to reject it - as a result, instead of protecting the body, the immune system, on the contrary, destroys it.

Viral diseases in humans occur very often, and it takes quite a long time for the autoimmune process to develop, so it is often quite difficult to determine what infection caused autoimmune hyperthyroidism. It is also impossible to understand why autoantibodies produced by immune cells affect one organ or another. It is possible that the matter here is in some genetic defects that cause the development of certain diseases.

Antibodies stimulate the thyroid cells, as do thyroid-stimulating hormones. Their effect causes the thyroid tissue to grow, resulting in excess production of T4 and T3 hormones.

It should be noted that this disease most often affects women – 5 times more often than men.

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Toxic hyperthyroidism

It develops due to excess secretion of hormones by the diffuse tissue of the thyroid gland, which results in poisoning of the body with these hormones.

This disease can develop due to infection, poisoning with toxins, genetic factors, mental trauma.

Toxic hyperthyroidism develops in this way - immune surveillance is disrupted, due to which autoantibodies are formed against thyroid cells. They promote stimulation of the thyroid gland, which increases its functioning and enlarges the gland, since its tissue grows due to this. It is also important that the tissues change their sensitivity to thyroid hormones, which destroys their metabolic process.

To cure the disease, antithyroid drugs are used, which suppress the rate of hormone production and remove their excess from the body - this helps to calm the thyroid gland and reduce its size. These drugs also remove excess vitamins C and B, help improve metabolism, calm and support the functional activity of the adrenal glands.

Subclinical hyperthyroidism

Subclinical hyperthyroidism is a condition in which the concentration of TSH in the blood serum is low, while the thyroid hormone levels remain within the normal range. In these cases, there are also no obvious clinical signs that the patient has hyperthyroidism.

This disease mainly occurs as a result of long-term presence of multinodular goiter or in patients with a history of thyrotoxicosis who have also been treated with antithyroid drugs. Such patients should be checked periodically for thyroid hormone levels, as well as TSH, even if there are no signs of hyperthyroidism.

The risk of possible progression of subclinical hyperthyroidism to manifest form in clinical and biochemical cases was also studied. The studies were conducted with a small volume of selected cases, and the observation period was a time interval of 1-10 years. Observations showed that in the time interval of 1-4 years, the progress was approximately 1-5% per year, in addition, it was found that the probability of clinical manifestation will be higher in those patients who have a TSH level in the blood serum less than 0.1 mIU / L.

Artificial hyperthyroidism

In this case, thyroid hormone levels exceed their normal levels, which occurs due to the intake of a large number of hormonal medications for the thyroid gland.

The thyroid gland produces hormones T4 and T3, and in the case of hyperthyroidism, it begins to independently produce an excess of these substances. If a similar picture is observed as a result of taking hormonal drugs, the disease is called artificial hyperthyroidism.

The disease can also occur if the patient intentionally takes too much thyroid hormone. Sometimes, factitious hyperthyroidism can occur due to abnormal thyroid tissue.

To get rid of the disease, you need to stop taking the hormonal drug, and if medical indicators show that there is no need for it, you should reduce the dosage. In this case, you will need to be examined 1-2 times a month to make sure that the symptoms of the disease are decreasing or have disappeared altogether.

Patients who suffer from Munchausen syndrome need to undergo psychiatric observation and treatment in this area.

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Hyperthyroidism after childbirth

Often this type of hyperthyroidism occurs 2-4 months after childbirth, when a relapse of thyrotoxicosis begins, for the treatment of which antithyroid drugs are needed. Basically, this period is enough to carry out safe breastfeeding, but even during lactation, small doses of PTU (daily norm is about 100 mg) will not harm the child.

But sometimes the disease is so severe that it is necessary to stop lactation with the help of dopamine mimetics and take antithyroid drugs in large doses - as is done during periods outside of breastfeeding and pregnancy.

Postpartum thyroiditis, as well as autoimmune Graves' disease, can result in postpartum hyperthyroidism. While postpartum thyroiditis is considered a more common cause of short-term hyperthyroidism, the onset of Graves' disease should not be overlooked.

Among the main differences in these diseases is that in hyperthyroidism due to postpartum thyroiditis the thyroid gland does not enlarge much, there is no Graves' ophthalmopathy at all. In Graves' disease everything is the opposite, and, in addition, the concentration of thyroid hormones in the blood serum increases.

Borderline hyperthyroidism

Thanks to the thyroid-stimulating hormone, which acts on the thyroid gland, balanced circulation of T4 and T3 hormones, as well as iodothyronines, is ensured. The level of this hormone is controlled by the hypothalamic hormone TRH, and also has an inverse relationship with the production of hormones of the T3 type.

For example, in the primary stage, thyroid hormone production decreases, but TSH levels are generally quite high. But in the 2nd or 3rd forms of the disease, when the decrease in thyroid hormone production occurs due to problems with the functioning of the hypothalamus and pituitary gland, TSH levels are quite low.

Indications for primary testing in the differential diagnosis of thyroid pathology and monitoring the appropriateness of hormone replacement therapy should have the following expected values:

• Euthyroid status: from 0.4 to 4 μIU/ml;
• Hyperthyroid status: less than 0.01 μIU/ml.

If the TSH values are in the range of 0.01-0.4 μIU/ml, it is necessary to measure them again in the future, because this may be a symptom of borderline hyperthyroidism or some serious disease unrelated to the thyroid gland. Another reason for such values may be too aggressive treatment with drugs.

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Transient hyperthyroidism

This physiological variation mainly occurs before the 16th week of pregnancy and is quite easy to explain – it is necessary to cover the need for hormones in the volumes that are necessary for both mother and baby.

Signs of the disease include a slight increase in temperature, mood swings, and difficulty staying in hot climates. Some pregnant women may experience weight loss at the beginning of pregnancy, which will not be associated with toxicosis.

These symptoms are of course quite difficult to identify at the initial stage of pregnancy, since they are not very different from the usual behavior of the body in this position. But in such cases, all pregnant women are prescribed a series of laboratory tests to determine the level of hormones. This is done because such signs may indicate the presence of a serious pathology, such as, for example, diffuse thyrotoxic goiter.

If laboratory tests have shown the presence of transient hyperthyroidism, it does not need to be treated, although there is a need for constant monitoring of the body so as not to miss the moment of possible appearance of signs of more serious thyroid diseases. They are dangerous because they can be a threat to the baby.