Back

Cortisol in the blood (chromatography)

Glucocorticoid hormones are a steroid class synthesised from progesterone and its active form 17-hydroxyprogesterone in the bundle layer of the adrenal cortex. They demonstrate a pronounced anti-inflammatory effect, activate the breakdown of protein structures, actively affecting carbohydrate metabolism and contributing to the increase in blood glucose concentration. Glucocorticoids stimulate the formation of glucose from non-carbohydrate precursors (gluconeogenesis) and the breakdown of fat stores (lipolysis), which can lead to redistribution of body fat mass, especially in the abdominal region under chronic stress.

Cortisol is a key adrenal hormone that performs a protective function and a regulatory effect on blood pressure. It is actively involved in the metabolic processes of protein, fat and carbohydrate metabolism. Cortisol production is controlled by adrenocorticotropic hormone (ACTH) produced by the pituitary gland, a small gland in the brain.

The mechanism of regulation of ACTH and cortisol is carried out through feedback: lowering the level of cortisol provokes an increase in the synthesis of ACTH, which in turn restores the normal level of the hormone.

Elevated or decreased cortisol levels may be the result of disorders both at the level of the adrenal glands and in the pituitary gland - especially in the presence of tumor processes. Deficiency of the hormone is manifested by general symptoms: weight loss, weakness, loss of strength, decreased blood pressure and abdominal pain; a critical condition may require emergency medical attention.

Excessive cortisol leads to increased blood sugar, high blood pressure, and obesity with a characteristic abdominal type of adipose tissue distribution. Thinning of the skin and the appearance of purple striae on the sides of the abdomen are also observed.

Elevated levels are observed in:

  • Icenko-Cushing's syndrome; 
  • Itsenko-Cushing's disease; 
  • pituitary dysfunction and insufficient secretion of ACTH (ectopic ACTH syndrome); 
  • neoplasms of the adrenal glands; 
  • hyperthyroidism; 
  • polycystic ovary syndrome; 
  • obesity 
  • hypoglycemia; 
  • cirrhosis of the liver;
  • uncompensated diabetes mellitus; 
  • stress, prolonged depression; 
  • administration of atropine, ACTH, corticotropin-releasing hormone, cortisone, synthetic glucocorticoids, estrogens, glucagon, inserlin, interferons (a -2, b, g), interleukin-6, opiates, oral contraceptives, vasopressin, opiates. 

A decrease in the level is observed when:

  • congenital insufficiency of the adrenal cortex; 
  • adrenogenital syndrome with adrenal hyperplasia; 
  • pituitary dysfunction (hypopituitarism); 
  • Addison's disease; 
  • Nelson's syndrome; 
  • hypothyroidism; 
  • systemic diseases and pathologies of the liver (hepatitis, cirrhosis) and the biliary tract; 
  • administration of barbiturates, beclomethasone, clonidine, dexamethasone, deoxycorticosterone, dextroamphetamine, ephedrine, etomidate, ketoconazole, levodopa, magnesium sulphate, midazolam, methylprednisolone, morphine, nitric oxide, lithium preparations, triamcinolone (in long-term treatment).