What Are the Effects of Too Much Cortisol?

Cortisol, also known as hydrocortisone, also known as cortisol or compound F (compound F), is extracted from the adrenal cortex and has the strongest effect on carbohydrate metabolism. One.

Plasma: 8-9 am: 210-342 nmol / L; 3-4 am: 77-181 nmol / L.

RIA method: Blood F has obvious diurnal changes, so its plasma concentration also has corresponding diurnal fluctuations. The content is highest in the morning from 6 to 8 and gradually decreases in the future, and it is the lowest at 12 to 2 in the evening. At 8 am, it is 140-630 nmol / L; at 4 pm, it is 80-410 nmol / L; at 8 pm, it is less than 50% of that at 8 am.

The disease is due to hypothalamus-pituitary dysfunction or pituitary adenoma caused by adrenal hyperplasia or

Cortisol can be divided into the following four types according to its etiology and pathological changes of the pituitary and adrenal glands:

Iatrogenic cortisol

The long-term heavy use of glucocorticoids for the treatment of certain diseases can lead to clinical manifestations of cortisol, which is very common clinically. This is caused by exogenous hormones and can gradually recover after stopping the drug. However, long-term large-scale application of glucocorticoids can feedback inhibit the ACTH secretion of the pituitary gland and cause atrophy of the adrenal cortex. Once the drug is abruptly stopped, it can lead to a series of manifestations of inadequate cortical function and even crisis, so it should be paid attention to. Cortisol can also occur with long-term use of ACTH.

2. Pituitary bilateral adrenal hyperplasia

Bilateral adrenal hyperplasia is caused by excessive pituitary secretion of ACTH. The reasons: pituitary tumor. Almost basophilic tumors can also be seen in chromocytoma; There is no obvious tumor in the pituitary gland, but ACTH secretion increases. It is generally believed to be caused by the excessive secretion of corticotropin-releasing factor (CRF) by the hypothalamus. Only about 10% of the pituitary tumors can be detected clinically. In such cases, pituitary secretion of ACTH has reached an abnormally high level, and the increase in plasma cortisol is not sufficient to cause normal feedback inhibition, but oral high-dose flumetasone may still have an inhibitory effect.

3. Bilateral adrenal hyperplasia caused by external pituitary lesions

Bronchial lung cancer (especially oat cell carcinoma), thyroid cancer, thymic cancer, nasopharyngeal cancer, and tumors originating from neural crest tissue can sometimes secrete an ACTH-like substance with biological effects similar to ACTH, which can cause bilateral adrenal cortex Hyperplasia, so called heterologous ACTH syndrome. These patients also often have significant muscle atrophy and hypokalemia. The lesion secretes ACTHs autonomously, and high-dose oral flumesonone has no inhibitory effect. After the lesion is removed or cured, the symptoms gradually subside.

4. Adrenal cortical tumors

Most are benign adrenal adenomas, and a few are malignant adenocarcinomas. Tumor growth and adrenocortical hormone secretion are autonomous and not controlled by ACTH. Because the tumor secretes a large amount of corticosteroids, feedback inhibits the secretory function of the pituitary gland, reducing the plasma ACTH concentration, thereby causing the normal adrenal cortex of the non-tumor part to shrink significantly. Cortisol secretion does not change in such patients, whether they are given ACTH excitement or high-dose flumesonone inhibition. Adrenocortical tumors, especially malignant tumors, often have a significant increase in 17 ketones in the urine. ^[2]