In our time, the timely diagnosis of Cushing's syndrome is associated with some difficulties. In the absence of pathognomonic signs, hypercortisolism can proceed under the guise of other diseases for a long time, misleading even experienced clinicians.
Therefore, physicians of any specialty should be alert for Cushing's syndrome in patients with obesity, depression, cognitive decline, osteoporosis.
For more information on what may be the cause of Cushing's syndrome, as well as approaches to the diagnosis and treatment of hypercortisolism, read on estet-portal.com in this article.
Cushing's Syndrome: Causes of Development and Pathogenesis of Hypercorticism
Cushing's syndrome is a pathological condition that occurs against the background of prolonged exposure to the body of an excessive amount of hormones of the adrenal cortex.
The most common cause of Cushing's syndrome is the presence of hormone-producing neoplasms of the adrenal cortex.
There are also isolated cases of primary nodular adrenocortical hypertrophy of the adrenal cortex, contributing to the development of hypercortisolism. It is worth distinguishing between the concepts of "Cushing's syndrome" and "Cushing's disease".
Cushing's syndrome is a condition of primary hypercortisolism caused by hyperfunction of the adrenal cortex, while the cause of Cushing's disease is hyperproduction of ACTH (adrenocorticotropic hormone) by the pituitary gland.
Chronic exposure to excessive amounts of hormones, in particular cortisol, leads to catabolism of protein structures, pathological stimulation of gluconeogenesis and glycogenolysis, and changes in the distribution of adipose tissue in the body. All this leads to the characteristic clinical changes in Cushing's syndrome, described later in the article.
What are the clinical signs that indicate the presence of Cushing's syndrome
Cushing's syndrome often occurs under the guise of other pathologies: cardiovascular disease, osteoporosis, cognitive and behavioral disorders. The severity of the condition in Cushing's syndrome can vary from subclinical hypercortisolism to rapidly progressive endocrine pathology. Very characteristic of Cushing's syndrome are crimson striae with predominant localization on the abdomen, thighs, buttocks.
Patients often have a moon-shaped face, with excessive deposition of adipose tissue between the shoulders ("bull's hump"). Most of them are overweight or obese, as well as signs of proximal myopathy, which are subjectively expressed in a feeling of muscle weakness. Exposure to an excessive amount of hormones of the adrenal cortex leads to hypertension, hirsutism, osteoporosis.
Approximately 40% of patients with Cushing's syndrome have impaired glucose tolerance. They also often have mood disturbances with a tendency to depression, memory impairment, and sleep disturbances. Cases of psychosis have been described in patients with Cushing's syndrome.
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Modern methods for diagnosing hypercortisolism in Cushing's syndrome
The small dexamethasone test is used to diagnose hypercortisolism in Cushing's syndrome.
The procedure for performing the small dexamethasone test, also known as the small Liddle test, is as follows: after determining the initial level of blood cortisol, the patient should take the drug at 24:00 dexamethasone at a dose of 1.5 mg. Subsequently, the level of cortisol in the blood is again determined.
Normally, according to the feedback mechanism due to exogenous intake of steroid hormone, the cortisol level should drop to 50 nmol / l (positive test). If this does not happen (negative test), then the patient is confirmed to have endogenous hypercortisolism.
False positive results of the test can be caused by the use of drugs such as phenytoin, carbamazepine, barbiturates, rifampicin, nifedipine, pioglitazone, estrogen, so the latter should be excluded 24 hours before the test. In addition, false-positive results can occur against the background of endogenous depression, generalized anxiety disorder and alcoholism.
In addition to the small dexamethasone test, 24-hour urine cortisol excretion can also be used to confirm endogenous hypercortisolism in Cushing's syndrome. An increase in the latter over 400 nmol confirms the presence of pathology. It should be borne in mind that drugs such as spironolactone, ranitidine, aspirin, furosemide and estrogens can contribute to an increase in cortisol levels in daily urine.
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Treatment of Cushing's Syndrome: Surgical and Pharmacological Measures
In most cases, the treatment of Cushing's syndrome – surgical. An exception is iatrogenic episodes of pathology that occur during long-term treatment with glucocorticoids, for example, in patients with dermatomyositis, systemic lupus erythematosus, rheumatoid arthritis. In such cases, it is necessary to gradually cancel this group of drugs and prescribe other basic drugs.
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Surgical treatment consists in removing neoplasms of the adrenal glands or lungs, depending on the cause of hypercortisolism. If this operation is impossible, an adrenalectomy is performed.
After surgical treatment of Cushing's syndrome, temporary administration of hydrocortisone is necessary as replacement therapy against the background of postoperative hypocorticism.
In cases where surgical treatment of Cushing's syndrome is not possible, pharmacological correction of hypercortisolism should be applied. The following groups of drugs can be used for this: steroidogenesis inhibitors, dopamine agonists and somatostatin receptor agonists.
Thank you for staying with estet-portal.com. Read other interesting articles in the "Endocrinology" section. You may also be interested in What are the manifestations of Cushing's syndrome in corticosteroma.
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