Diagnosis of hypothyroidism

Diagnosis of severe hypothyroidism, especially in those who underwent thyroid surgery, who received treatment with radioactive iodine, which caused autoimmune diseases, does not cause any special difficulties. It is more difficult to identify light forms with scanty, not always typical clinical symptoms, especially in elderly patients, where it is easy to suspect cardiovascular failure, kidney disease, etc. In young and middle-aged women, a number of symptoms similar to hypothyroidism are observed in the syndrome of idiopathic edema .

The diagnosis of primary hypothyroidism is specified by a number of diagnostic laboratory tests. Functional insufficiency of the thyroid gland is characterized by a decrease in the blood level of iodine bound to the protein - SBC, butanol extractable iodine and the degree of absorption of ¹³¹ I by the thyroid gland, mainly after 24-72 h (at a rate of 25-50% of the administered dose). However, these indicators are not always adequate to clinical symptoms and do not have absolute informativity. The use of the ¹³¹ I absorption test by the thyroid is almost more appropriate for the detection of hyper-, not hypothyroidism.

In recent years, it has become possible to determine directly in the blood TSH, as well as T ₃ and T ₄ radioimmunoassay using commercial kits.

The greatest diagnostic value for hypothyroidism has the definition of TSH, the level of which significantly (sometimes tens of times) increases, and the calculation of the index of free thyroxin.

Thyreoliberin TRH was the first isolated from the hypothalamus, and then synthesized by the releasing hormone. Intravenous injection of 200 μg of the drug in healthy individuals gives the maximum increase in blood TSH concentration in 15-30 minutes, thyroid hormones after 90-120 minutes. The most reliable increase in all values occurs after 24 hours. The increase in the concentration of TSH after 15-30 minutes after the administration of 200 μg of TRH in excess of 25 μmed / ml indicates a hyperergic reaction, which is noted when a hidden "preclinical" hypothyroidism is detected. In primary hypothyroidism, especially in the Van Vika-Henness-Ross syndrome, prolactin levels in the blood also increase, which leads to a differentiated diagnosis with Chiari-Fromm syndrome (occurs after birth) and Forbes-Albright (due to pituitary adenoma).

With secondary hypothyroidism, the SBS content and ¹³¹ I uptake are reduced, however, the results of a sample with intramuscular injection of TSH show that, unlike the primary hypothyroidism, they increase. The initial content of TSH is reduced, and in patients with pituitary thyroid disease the effect is not observed. In hypothalamic forms, when the decrease in TSH is a consequence of the inadequacy of endogenous thyreoliberin (tertiary hypothyroidism), the administration of exogenous thyroidiborin may increase the concentration of TSH in the blood, but to a lesser extent than with primary hypothyroidism.

The basal level of prolactin in pituitary forms of secondary hypothyroidism can be normal or decreased, and in response to the administration of thyroidiborin, its changes are insignificant. In hypothalamic forms, the basal level of prolactin and its reaction to thyreoliberin are within normal limits. The content of thyroid hormones in the blood is reduced, and in response to stimulation by exogenous TSH, thyroidiberin - is increased. A significant increase in T ₃ and T ₄ is observed 2-4 hours after intravenous administration of TRH.

For practical purposes, additional methods are used, such as determining the time of the Achilles reflex, cholesterol and beta-lipoproteins of the blood, electrocardiography.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11]