Assessment of thyroid hormonal status

Evaluation of the hormonal status of the thyroid gland allows us to identify three of its functional states: hyperfunction, hypofunction, and euthyroid state. Determination of thyroid-stimulating hormone together with cT4 _is one of the leading "strategic" markers in assessing the hormonal status of the thyroid gland.

Thyroid-stimulating hormone is considered the most sensitive indicator of thyroid function. An increase in its content in the blood serum is a marker of primary hypothyroidism, and a decrease or complete absence is the most significant indicator of primary hyperthyroidism. Determination of _CT4 is most informative in patients with suspected abnormalities of binding proteins and allows one to estimate the true content of T4 _in the body. The combined determination of thyrotropic hormone and CT4 _is important for selecting adequate therapy for the detected thyroid dysfunction. The dose of thyroid hormone preparations used in the treatment of hypothyroidism is selected in accordance with the concentration of thyrotropic hormone in the blood (adequate treatment is accompanied by its normalization).

Determination of cT4 _is especially important for monitoring therapy for hyperthyroidism, since it may take 4-6 months for pituitary function to recover. During this stage of recovery, the concentration of thyroid-stimulating hormone in the blood may be reduced, despite the fact that the cT4 content is _normal or reduced and the treatment of hyperthyroidism is adequate.

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Hypothyroidism

Hypothyroidism is observed relatively often - approximately in 2-3% of the entire population, it is caused by a decrease in the content of one or both thyroid hormones in the circulating blood. Hypothyroidism can be associated with primary damage to the thyroid gland itself (primary hypothyroidism), a violation of the regulation of its function by the hypothalamic-pituitary system (tertiary and secondary hypothyroidism), as well as due to a violation of the transport, metabolism and action of hormones (peripheral). In the overwhelming majority of cases (90-95%), hypothyroidism is caused by a pathological process in the thyroid gland, disrupting the production of hormones (primary hypothyroidism).

Determination of cT4 _and thyroid-stimulating hormone in the blood serum is the best combination of tests for the diagnosis of hypothyroidism. In hypothyroidism, the basal level of thyroid-stimulating hormone is elevated due to primary thyroid gland damage (primary hypothyroidism) and is decreased in primary pituitary insufficiency (secondary, central hypothyroidism) or hypothalamus (tertiary, central hypothalamic hypothyroidism), in which thyroid dysfunction is secondary.

A characteristic feature of secondary hypothyroidism is a low concentration of thyroid-stimulating hormone in the blood against the background of reduced concentrations of CT4 _, T4 _, T3 _. In tertiary hypothyroidism, the concentrations of thyroid-stimulating hormone, CT4 _, T4 _, T3 _in the blood are also reduced. The content of TRH in the blood in tertiary hypothyroidism, in contrast to secondary hypothyroidism, is reduced.

An increase in the concentration of thyroid-stimulating hormone against the background of normal levels of thyroid hormones (cT3 _, cT4 ₎ in the blood is called subclinical hypothyroidism. There are 3 degrees (stages) of development of subclinical hypothyroidism.

• Stage I - minimal thyroid insufficiency (subclinical hypothyroidism, hypothyroidism with thyroid-stimulating hormone at the upper limit of normal, compensated variant of subclinical hypothyroidism) - the mildest form, which is characterized by the absence of symptoms in patients, the concentration of thyroid-stimulating hormone within the reference values (2-5 mIU/l) or slightly elevated (but less than 6 mIU/l) and a hyperergic response of thyroid-stimulating hormone to TRH stimulation.
• Stage II is similar to stage I, but the increase in the basal concentration of thyroid-stimulating hormone in the blood progresses (6-12 mIU/L); the likelihood of clinical manifestation of hypothyroidism increases significantly.
• Stage III is characterized by values of the concentration of thyroid-stimulating hormone in the blood above 12 mIU/l, the appearance of an erased clinical picture of hypothyroidism, which progresses in parallel with the hyperproduction of thyroid-stimulating hormone, as well as a high risk of developing overt hypothyroidism, usually within the next 10-20 years.

Hyperthyroidism (thyrotoxicosis)

Hyperthyroidism develops with excessive production of thyroid hormones (T3 _and T4 ₎. Currently, three forms of thyrotoxicosis are distinguished: diffuse toxic goiter (Graves' disease, Basedow's disease), toxic nodular goiter and autonomous thyroid adenoma.

In diffuse toxic goiter in patients who have not received antithyroid treatment, the concentration of T4, cT4, thyroglobulin in the blood is increased _, the _{concentration} of Hyperthyroidism is decreased. In these patients, the TRH test is negative, which indicates a sharp suppression of the thyrotropic function and the absence of reserves Hyperthyroidism in this disease.

In (multinodal) toxic goiter, T3 _- toxicosis is observed in 50% of patients (in diffuse toxic goiter - in 15%), therefore, an increase in the concentration of T3 is often detected in the blood _. One of the reasons for the violation of the ratio of T4 _and T3 _in the thyroid gland may be a lack of iodine, leading to compensatory synthesis of the most active hormone. Another reason for an isolated increase in the T3 level _may be an accelerated transition of T4 _to T3 _in peripheral tissues. Almost all patients with a pronounced clinical picture of the disease have an increase in the concentration of _cT4.

Thyrotropin-secreting pituitary tumors

TSH-secreting pituitary adenoma develops very rarely. The pituitary adenoma secretes excessive amounts of thyroid-stimulating hormone, which stimulates the thyroid gland. As a result, the concentration of cT4, T4, T3 in the blood increases _and symptoms _of hyperthyroidism _develop. The main signs of a thyrotropin-secreting pituitary tumor are a sharp increase in the concentration of thyroid-stimulating hormone in the blood (50-100 times or more compared to the norm) and the absence of a reaction of thyroid-stimulating hormone to TRH.

Thyroiditis

Subacute de Quervain's thyroiditis, or granulomatous thyroiditis, is one of the most common forms of the disease. Etiological factors of de Quervain's thyroiditis include measles viruses, infectious mumps, adenovirus infection, and influenza. Thyroiditis develops 3-6 weeks after viral infections.

During the course of subacute thyroiditis, 4 stages are distinguished.

• Stage I - thyrotoxic: inflammatory destruction of thyroid follicular cells results in the release of excess T4 _and T3 _into the blood, which can cause thyrotoxicosis.
• Stage II is an intermediate period (1-2 weeks) of euthyroidism, which occurs after the removal of excess T ₄ from the body.
• Stage III - hypothyroid, develops in severe cases of the disease.
• Stage IV - recovery (euthyroid state).

In subacute thyroiditis, the concentration of thyroid-stimulating hormone in the blood is normal or decreased, T ₄ and T ₃ are high or above normal, then they normalize. Changes in the level of thyroid hormones in the blood in de Quervain's thyroiditis depend on the stage of the disease. Thus, in stage I (duration 1-1.5 months), an increase in the concentration of cT ₄ (T ₄ and T ₃ ) in the blood and a normal or decreased level of thyroid-stimulating hormone are observed. Symptoms of thyrotoxicosis are clinically observed. These changes are due to excessive entry into the blood of previously synthesized hormones and thyroglobulin, due to increased vascular permeability against the background of inflammation. After 4-5 weeks, disruption of hormone synthesis in the inflamed thyroid gland leads to normalization of their content in the blood, and then to a decrease (3-4 months of the disease). A decrease in the formation of T ₄ and T ₃ activates the release of thyroid-stimulating hormone by the pituitary gland, its concentration in the blood increases and can be elevated for 4-6 months. Approximately by the end of the 10th month from the onset of the disease, the concentrations of thyroid-stimulating hormone, T ₄ and T ₃ in the blood are normalized. The content of thyroglobulin in the blood is elevated for a long time. The disease is prone to relapses, which requires long-term monitoring of the thyroid gland function. With the development of a relapse, the concentration of thyroglobulin in the blood increases again.

Chronic lymphocytic thyroiditis (Hashimoto's thyroiditis) is a disease caused by a genetic defect of immunocompetent cells (T-suppressors), leading to infiltration of the thyroid gland by macrophages, lymphocytes, and plasma cells. As a result of these processes, antibodies to thyroglobulin, thyroid peroxidase, and thyroid-stimulating hormone receptors are formed in the thyroid gland. The interaction of antibodies with the antigen leads to the appearance of immune complexes, the release of biologically active substances, which ultimately causes destructive changes in thyrocytes and leads to a decrease in thyroid function.

In the process of development of chronic autoimmune thyroiditis, thyroid function undergoes stage changes with an almost obligatory outcome in hypothyroidism. As the gland's insufficiency progresses, the concentrations of T4 and then T3 in the blood _decrease, _{and the content of thyroid-stimulating hormone gradually increases. Hypothyroidism with characteristic laboratory manifestations develops later. In some patients with autoimmune thyroiditis, signs of hyperthyroidism (a decrease in the concentration of thyroid-stimulating hormone and an increase incT4} ) are possible at the onset of the disease, which is caused by the processes of destruction of thyroid tissue.

Thyroid cancer

Papillary carcinoma accounts for 60% of all thyroid cancer cases and affects the youngest people (50% of patients are under 40 years of age). The tumor consists of cylindrical cells and tends to grow slowly.

Follicular carcinoma accounts for 15-30% of all thyroid cancers and histologically resembles normal thyroid tissue. The tumor often functions as normal thyroid tissue, taking up iodine in a TSH-dependent manner. Follicular carcinoma is more malignant than papillary cancer and often metastasizes to bone, lung, and liver.

Undifferentiated carcinoma accounts for 10% of thyroid cancer, affects patients over 50 years of age and is extremely malignant. It is characterized by rapid tumor growth with extensive metastases, which leads to death within a few months.

In most cases of thyroid cancer, the concentration of thyroid-stimulating hormone and thyroid hormones (T4 _, T3 ₎ remains within normal limits. However, with metastases of thyroid cancer that produce thyroid hormones, their content in the blood may be increased, and the concentration of thyroid-stimulating hormone decreased, while clinical signs of hyperthyroidism develop. The concentration of thyroglobulin in the blood is increased. In thyroid cancer, there is a direct relationship between the concentration of thyroglobulin in the blood and the risk of metastasis (the higher the level of thyroglobulin, the higher the probability of metastasis).

After surgical removal of a thyroid tumor and treatment with radioactive iodine, patients with follicular or papillary cancer are prescribed lifelong treatment with high doses of sodium levothyroxine to suppress the secretion of thyroid-stimulating hormone. The goal of suppressive therapy is to reduce the concentration of thyroid-stimulating hormone in the blood to a level of less than 0.1 mIU/L. In the presence of metastases, the dosage of the drug is not reduced; the concentration of thyroid-stimulating hormone should remain within 0.01-0.1 mIU/L.

Determination of thyroglobulin concentration in dynamics allows to evaluate the efficiency of surgical treatment of thyroid gland tumors. Persistent and steady decrease of thyroglobulin in blood in the postoperative period indicates radicalism of surgical treatment. Temporary decrease of thyroglobulin concentration in blood in the postoperative period and increase of concentration in the future indicates non-radicalism of tumor removal or presence of metastases. Determination of thyroglobulin concentration in blood in the postoperative period should be carried out every 4-6 weeks. Its study replaces usual radionuclide scanning in such patients.

Medullary carcinoma accounts for 5-10% of thyroid cancers. The tumor arises from parafollicular cells (C cells) that secrete calcitonin.

When conducting a provocative test with intravenous calcium administration, an increase in both basal (above 500 pg/ml) and stimulated serum calcitonin concentrations is determined. A strong correlation is observed between the degree of increase in blood calcitonin concentration after calcium administration and tumor size.

The only treatment for medullary carcinoma is surgical removal of the entire thyroid gland. Persistent elevated blood levels of calcitonin after tumor removal in patients with medullary thyroid cancer may indicate that the surgery was not radical or that there are distant metastases. A decrease and then a rapid increase in calcitonin levels after surgery indicate a relapse of the disease. After surgery, calcitonin should be tested in all patients at least once a year, and relatives (including children aged 2 years and older) should be examined for early diagnosis of a possible familial form of thyroid cancer.