Adrenocorticotropic hormone in the blood

Reference values of concentration of ACTH in blood serum: at 8.00 - less than 26 pmol / l, at 22.00 - less than 19 pmol / l.

Adrenocorticotropic hormone is a peptide consisting of 39 amino acid residues with a molecular mass of approximately 4500. The secretion of ACTH into the blood is subject to circadian rhythms, the concentration is maximal at 6 o'clock in the morning, and the minimum is about 22 hours. Strong ACTH stimulator is stress. The half-life in the blood is 3-8 minutes.

Itenko-Cushing's disease is one of the most difficult and complex neuroendocrine diseases of the hypothalamic-pituitary genesis, followed by involvement of the adrenal glands and the formation of a syndrome of total hypercorticism and the associated violation of all types of metabolism. The pathogenetic basis of the Itenko-Cushing disease is a disruption in the feedback in the functional system of the hypothalamus → pituitary gland → adrenal cortex, characterized by constantly increased pituitary activity and hyperplasia of corticotrophs or, more often, the development of ACTH-producing pituitary adenomas and hyperplasia of the cortex of both adrenals. In most cases, Itenko-Cushing's diseases show adenomas of the pituitary gland (macroadenomas in 5%, microadenomas in 80% of patients).

For Isenko-Cushing's disease, a simultaneous increase in blood levels of ACTH and cortisol is characteristic, as well as an increased daily excretion in the urine of free cortisol and 17-ACS. The determination of ACTH in the blood is necessary for differential diagnosis of the disease and various forms of the Itenko-Cushing syndrome. The secretion of ACTH is significantly reduced in patients with corticosteroid and adrenal cortex cancer (Isenko-Cushing syndrome). In persons with Isenko-Cushing's disease and ectopic ACTH syndrome (pathological secretion of ACTH by a tumor of non-hypophyseal origin, most often by bronchial cancer or thymoma), the concentration of ACTH in the blood is increased. For differential diagnosis between the last two diseases, a KRG test is used. With the Itenko-Cushing's disease, the secretion of ACTH after CRH administration is significantly increased. ACTH-producing tumor cells of non-hypophyseal localization have no CRH receptors, so the concentration of ACTH at this sample does not change significantly.

Syndrome of ectopic secretion ACTH most often develops with lung cancer, carcinoid and bronchial cancer, malignant thymomas, primary carcinoids of the thymus and other mediastinal tumors. Less often, the syndrome accompanies tumors of the parotid glands, urinary and gallbladder, esophagus, stomach, colon, melanoma, and lymphosarcoma. Ectopic production of ACTH is also found in tumors of endocrine glands: cancer cells of the islets of Langerhans, medullary thyroid carcinoma, pheochromocytoma, neuroblastoma, ovarian cancer, testicles, prostate gland. Due to the prolonged high concentration of ACTH, hyperplasia of the adrenal cortex develops in the blood and the secretion of cortisol increases.

The concentration of ACTH in the blood can range from 22 to 220 pmol / l and more. In the diagnostic plan, in the syndrome of ectopic ACTH production, concentrations of ACTH in the blood above 44 pmol / L are considered clinically significant.

The best method for distinguishing the pituitary and ectopic sources of ACTH is a simultaneous bilateral study of blood from the lower cavernous sinuses for ACTH. If the concentration of ACTH in the cavernous sinuses is significantly higher than in the peripheral blood, then the hypothyroid is the source of hypersecretion of ACTH. If the gradient between ACTH content in cavernous sinuses and peripheral blood is not traced, the source of increased hormone formation is most likely a carcinoid tumor of another localization.

Primary insufficiency of the adrenal cortex (Addison's disease). With primary adrenal insufficiency, as a result of destructive processes in the adrenal cortex, the production of HA, mineralocorticoids and androgens decreases, which leads to disruption of all types of metabolism in the body.

The most frequent laboratory signs of primary adrenal insufficiency are hyponatremia and hyperkalemia.

With the primary failure of the adrenal cortex, the concentration of ACTH in the blood is significantly increased - by 2-3 times or more. Violation of the rhythm of secretion - the content of ACTH in the blood in both morning and evening is increased. With secondary adrenal insufficiency, the concentration of ACTH in the blood decreases. To assess the residual reserve of ACTH, a test with CRH is performed. If the pituitary gland is deficient, there is no reaction to CRH. When the process is localized in the hypothalamus (absence of CRH), the test can be positive, but the response of ACTH and cortisol to CRH administration is delayed. Primary adrenal insufficiency is characterized by a decrease in the concentration of aldosterone in the blood.

Secondary and tertiary adrenal insufficiency arise as a result of brain damage with subsequent decrease in ACTH production and development of secondary hypoplasia or atrophy of the adrenal cortex. Usually, secondary adrenal insufficiency develops simultaneously with panhypopituitarism, but sometimes an isolated insufficiency of ACTH congenital or autoimmune is also possible. The most common cause of tertiary adrenal insufficiency is the long-term use of glucocorticosteroids in high doses (treatment of inflammatory or rheumatic diseases). Suppressing the secretion of CRH with the subsequent development of adrenal insufficiency is a paradoxical consequence of the successful treatment of the Itenko-Cushing syndrome.

Nelson's syndrome develops after the total removal of the adrenal glands during the Itenko-Cushing disease; characterized by chronic adrenal insufficiency, hyperpigmentation of the skin, mucous membranes and the presence of a pituitary tumor. Nelson's syndrome is characterized by an increase in the concentration of ACTH in the blood. When conducting differential diagnosis between Nelson's syndrome and ectopic secretion of ACTH, it is necessary to conduct a simultaneous two-sided study of blood from the lower cavernous sinuses for ACTH, which allows us to clarify the localization of the process.

After surgical treatment (transsphenoidal operation with the removal of corticotropin), the determination of the concentration of ACTH in the blood plasma allows one to assess the radical nature of the operation.

In pregnant women, the concentration of ACTH in the blood can be increased.

Diseases and conditions in which the concentration of ACTH in blood serum can change

Increase in concentration	Reduction in concentration
Disease of Itenko-Cushing Paraneoplastic syndrome Adison's disease Post-traumatic and post-operative conditions Nelson's syndrome Adrenal virilism Application of ACTH, insulin, vasopressin Ectopic production of ACTH	Hypofunction of the adrenal cortex Tumor of the adrenal cortex Tumor releasing cortisol The use of glucocorticosteroids

[1], [2], [3]