Estimation of the hormonal status of the thyroid gland
Last reviewed: 23.04.2024
All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Estimation of hormonal status of the thyroid gland allows revealing its three functional statuses: hyperfunction, hypofunction and euthyroid status. The definition of a thyroid-stimulating hormone in conjunction with cT 4 is one of the leading "strategic" markers in assessing the hormonal status of the thyroid gland. Thyrotropic hormone is considered the most sensitive indicator of thyroid function. An increase in its content in the serum is a marker of primary hypothyroidism, while a decrease or total absence is the most significant indicator of primary hyperthyroidism. The definition of cT 4 is most informative in patients with suspected anomalies of binding proteins and allows one to assess the true T 4 content in the body. The joint determination of the thyroid-stimulating hormone and cT 4 is important for the selection of adequate therapy for the revealed thyroid dysfunction. The dose of thyroid hormone drugs that are used in the treatment of hypothyroidism, respectively, selects the concentration of thyroid-stimulating hormone in the blood (adequate treatment is accompanied by its normalization). Determination of PT 4 is especially important for monitoring the treatment of hyperthyroidism, because the recovery of pituitary function may require 4-6 months. At this stage of recovery, the concentration of thyroid-stimulating hormone in the blood can be reduced, even though the content of cT 4 is normal or decreased and the treatment of hyperthyroidism is adequate.
Hypothyroidism
Hypothyroidism is observed relatively often - in about 2-3% of the total population, it is due to a decrease in the content of circulating blood of one or both thyroid hormones. Hypothyroidism can be associated with a primary lesion of 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 disruption of transport, metabolism and hormone action (peripheral). In the vast majority of cases (90-95%), hypothyroidism is caused by a pathological process in the thyroid gland, which violates the production of hormones (primary hypothyroidism).
The determination of cT 4 and thyroid-stimulating hormone in serum is the best combination of tests for the diagnosis of hypothyroidism. In hypothyroidism, the basal level of thyroid-stimulating hormone is increased due to primary thyroid damage (primary hypothyroidism) and decreased in primary pituitary insufficiency (secondary, central hypothyroidism) or hypothalamus (tertiary, central hypothalamic hypothyroidism) in which thyroid dysfunctions are secondary.
A characteristic feature of secondary hypothyroidism is a low concentration of thyroid-stimulating hormone in the blood against a background of reduced concentrations of T 4, T 4, T 3. In tertiary hypothyroidism, the thyroid-stimulating hormone concentrations, cT 4, T 4, T 3 in the blood are also reduced. The blood content of TRH in tertiary hypothyroidism, in contrast to the secondary, is reduced.
An increase in the concentration of thyroid-stimulating hormone against the background of the normal content of thyroid hormones (cT 3, cT 4 ) in the blood is called subclinical hypothyroidism. There are 3 degrees (stages) of development of subclinical hypothyroidism.
- I degree - minimal thyroid insufficiency (subclinical hypothyroidism, hypothyroidism with thyroid-stimulating hormone at the upper border of the norm, compensated variant of subclinical hypothyroidism) is the easiest 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 the hyperergic response of the thyroid-stimulating hormone to stimulation of TGH.
- II degree is similar to I, but the increase in the basal concentration of thyroid-stimulating hormone in the blood progresses (6-12 mIU / L); The likelihood of a clinical manifestation of hypothyroidism is significantly increased.
- The third degree is characterized by the values of the thyroid-stimulating hormone concentration in the blood above 12 mIU / l, the appearance of the erased clinical picture of hypothyroidism, which progresses in parallel to the hyperproduction of the thyroid-stimulating hormone, and also the high risk of development of sheer hypothyroidism, usually within the next 10-20 years.
Hyperthyroidism (thyrotoxicosis)
Hyperthyroidism develops in excess of the formation of thyroid hormones (T 3 and T 4 ). Currently, there are three forms of thyrotoxicosis: diffuse toxic goiter (Graves 'disease, Graves' disease), toxic nodular goiter and autonomic adenoma of the thyroid gland.
With diffuse toxic goiter in patients who did not receive antithyroid treatment, the concentration of T 4, cT 4, thyroglobulin was increased in the blood , the concentration of Hyperthyroidism was reduced. In these patients, the test with TRH is negative, which indicates a sharp suppression of thyrotropic function and the absence of reserves of hyperthyroidism in this disease.
When the (many) nodal toxic goiter T 3 -toksikoz observed in 50% of patients (with diffuse toxic goiter - 15%), however in the blood often show increased concentration of T 3. One of the reasons for the violation of the ratio of T 4 and T 3 in the thyroid gland may be a deficiency of iodine, leading to compensatory synthesis of the most active hormone. Another reason for an isolated increase in T 3 level may be an accelerated transition of T 4 to T 3 in peripheral tissues. Almost all patients with a severe clinical picture of the disease show an increase in the concentration of cT 4.
Thyrotropin-secreting tumors of the pituitary gland
TTG-producing adenoma of the pituitary gland develops very rarely. Pituitary adenoma secrete excess amounts of thyroid-stimulating hormone, which stimulates the thyroid gland. This increases the concentration of PT in blood 4, T 4, T 3 and develop symptoms of hyperthyroidism. The main signs of a thyrotropin-secreting tumor of the pituitary gland are a sharp increase in the concentration of thyroid-stimulating hormone in the blood (50-100 times and more in comparison with the norm) and the absence of a thyrotropic hormone response to TRH.
Thyroiditis
Subacute thyroiditis of de Kerven, or granulomatous thyroiditis, is one of the most common forms of the disease. Etiological factors of thyroiditis of de Kerven include measles virus, infectious mumps, adenovirus infection, influenza. Thyroiditis develops in 3-6 weeks after the transferred viral infections.
During subacute thyroiditis, 4 stages are distinguished.
- Stage I - thyrotoxic: inflammatory destruction of follicular cells of the thyroid leads to the release of excess amounts of T 4 and T 3 into the blood, which can cause thyrotoxicosis.
- Stage II - intermediate period (1-2 weeks) euthyrosis, occurs after removing excess amount of T 4 from the body.
- Stage III - hypothyroid, develops in severe cases of the disease.
- Stage IV - recovery (euthyroid status).
With subacute thyroid concentration in the blood of thyroid-stimulating hormone is normal or decreased, T 4 and T 3 - high or above normal, then they are normalized. The change in the level of thyroid hormones in the blood with thyroiditis depends on the stage of the disease. Thus, in step I (duration 1-1.5 months) experienced higher concentration Ct 4 (T 4 and T 3 ) in blood and normal or reduced levels of thyroid stimulating hormone. Clinically observed symptoms of thyrotoxicosis. These changes are due to the excessive intake of previously synthesized hormones and thyroglobulin into the blood, due to increased vascular permeability against inflammation. After 4-5 weeks, a violation of the synthesis of hormones in the inflamed thyroid gland leads to a normalization of their content in the blood, and then to a decrease (3-4 months of the disease). Reducing 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 increased 4-6 months. Approximately to the end of the 10th month from the moment of the disease the concentrations of the thyroid-stimulating hormone, T 4 and T 3 in the blood are normalized. The content of thyroglobulin in the blood is increased for a long time. The disease is prone to relapse, which requires long-term monitoring of thyroid function. With the development of relapse the concentration of thyroglobulin in the blood increases again.
Chronic lymphocytic thyroiditis (Hashimoto's thyroiditis) is a disease caused by the 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, the formation of antibodies to thyreoglobulin, thyroid peroxidase, thyroid-stimulating hormone receptors occurs in the thyroid gland. Interaction of antibodies with antigen leads to the appearance of immune complexes, the release of biologically active substances, which ultimately causes destructive changes in thyroid cells and leads to a decrease in thyroid function.
In the development of chronic autoimmune thyroiditis, the thyroid gland function undergoes stage changes with a virtually mandatory outcome in hypothyroidism. As the gland failure progresses, the blood concentrations of T 4 and then T 3 decrease, and the thyroid-stimulating hormone gradually increases. In the future, hypothyroidism develops with characteristic laboratory manifestations. In some patients with autoimmune thyroiditis in the opening are possible signs of hyperthyroidism disease (thyroid-stimulating hormone concentration decrease and increase in Ct 4 ) due to degradation processes thyroid tissue.
Thyroid cancer
Papillary carcinoma accounts for 60% of all cases of thyroid cancer and affects the youngest people (50% of patients younger than 40 years). Neoplasm consists of cylindrical cells and tends to grow slowly.
Follicular carcinoma accounts for 15-30% of all cases of thyroid cancer, histologically resembling normal thyroid tissue. The tumor often functions as normal tissue of the thyroid gland, capturing iodine in a TTG-dependent type. Follicular carcinoma is more malignant than papillary cancer, it often gives metastases to the bones, lungs and liver.
Undifferentiated carcinoma accounts for 10% of thyroid cancer, affects patients older than 50 years, and is extremely malignant. A rapid growth of a tumor with extensive metastases is characteristic, which leads to death within a few months.
In most cases of thyroid cancer, the concentration of thyroid-stimulating hormone and thyroid hormones (T 4, T 3 ) remains within normal limits. However, with metastases of thyroid cancer producing thyroid hormones, their content in the blood can be increased, and the concentration of thyroid-stimulating hormone is reduced, with the development of clinical signs of hyperthyroidism. The blood concentration of thyroglobulin is increased. In thyroid cancer, there is a direct relationship between the concentration of thyroglobulin in the blood and the risk of metastasis (the greater the thyroglobulin level, the higher the probability of having metastases).
After surgical removal of the thyroid tumor and treatment with radioactive iodine, patients with follicular or papillary cancer are prescribed lifelong treatment with high doses of levothyroxine sodium to suppress the secretion of thyroid-stimulating hormone. The task of suppressive therapy is to reduce the concentration of thyroid-stimulating hormone in the blood to less than 0.1 mIU / l. In the presence of metastases, the dosage of the drug is not reduced, the thyroid-stimulating hormone concentration should remain within 0.01-0.1 mIU / l.
Determination of thyroglobulin concentration in dynamics allows to evaluate the effectiveness of surgical treatment of thyroid tumors. A persistent and steady decline in thyroglobulin in the blood during the postoperative period indicates a radical surgical treatment. The temporary decrease in thyroglobulin concentration in the blood in the postoperative period and the increase in concentration subsequently indicates a non-selectivity of tumor removal or the presence of metastases. Determining the concentration of thyroglobulin in the blood in the postoperative period should be done every 4-6 weeks. His research replaces conventional radionuclide scanning in such patients.
Medullary carcinoma accounts for 5-10% of cases of thyroid cancer. The tumor arises from parafollicular cells (C-cells) secreting calcitonin.
When conducting a provocative test with intravenous calcium intake, the increase in both basal (above 500 pg / ml) and stimulated serum calcitonin concentration is determined. There is a strong correlation between the degree of increase in calcitonin concentration in the blood after the administration of calcium and the size of the tumor.
The only method for treating medullary carcinoma is the operative removal of the entire thyroid gland. The persistent high content of calcitonin in the blood after removal of the tumor in patients with medullary thyroid cancer may indicate a non-surgical operation or the presence of distant metastases. Reduction, and then a rapid rise in the level of calcitonin after surgery, indicate a relapse of the disease. After surgical treatment, calcitonin should be examined in all patients at least once a year, and also to conduct a survey of relatives (including children from 2 years) for early diagnosis of a possible family form of thyroid cancer.