It is a rare disease caused by chronic exposure to cortisol excess due to endogenous (pituitary or extrahypophyseal tumors) and exogenous (chronic corticosteroid treatment) causes. All endogenous forms are characterized by increased cortisol production by the adrenals and can be distinguished into ACTH-dependent and ACTH-independent forms (Table 1). Cushing’s disease is the most common among the ACTH-dependent forms. Cushing’s disease is characterized by an increased secretion of ACTH, which in 90% of cases is due to a pituitary adenoma and only in 10% of cases to hyperplasia of ACTH-secreting cells; the latter may be the consequence of alterations in the central nervous system leading to excessive hypothalamic production of CRH or CRH-secreting intrasellar gangliocytomas.

Table1. Endogenous causes of Cushing’s syndrome

ACTH-dependent forms are rarely due to ectopic secretion of ACTH or CRH from non-pituitary tumors; among these, the most common are small cell lung carcinoma or thymic, pancreatic, or ovarian carcinoid tumors, medullary thyroid carcinoma or bronchial adenomas. Endogenous ACTH-independent forms are, instead, due to adrenal neoplasms, usually unilateral and, in about half of the cases, malignant. Bilateral adrenal hyperplasias are characterized by a nodule with a diameter >1 cm (macronodular) or <1 cm (micronodular) and may be due to a hereditary disease (micronodular pigmented dysplasia) or to the stimulation of cortisol secretion by gastric inhibitory peptide (GIP) or luteinizing hormone, associated with the expression of specific receptors for these hormones in the adrenal cortex.

The most common cause of Cushing’s syndrome is the administration of exogenous corticosteroids or ACTH for therapeutic purposes.

The clinical signs of Cushing’s syndrome are variable due to the amount and duration of excess cortisol. In severe cases of hypercortisolism, the signs and symptoms are unmistakable. They include muscle weakness and easy fatigability due to hypotrophy of the skeletal musculature, striae rubrae, especially in the abdomen, facial plethora, and centripetal obesity due to deposition of fatty tissue in the upper part of the face leading to the appearance of the typical full moon face, in the interscapular region with buffalo hump, in the supraclavicular area, and the abdomen. Other non-specific symptoms of Cushing’s syndrome are osteoporosis, hirsutism, acne, hypertension, complicated in some cases by edema and heart failure, amenorrhea in women, and impotence in men. In addition, patients often present with emotional disturbances or psychosis (irritation, difficulty in concentrating, memory loss, and depression). It should be remembered that there are cyclical forms of the disease in which hormone overproduction occurs only periodically.

This is because many conditions such as obesity, chronic alcoholism, pregnancy, chronic exercise, anorexia nervosa, and depression can clinically mimic Cushing’s syndrome with increased cortisolemia. This condition can be treated by correcting the underlying pathology.

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مواضيع ذات صلة

marijuana (THC) test (Cannabinoid or cannabis testing, Tetrahydrocannabinol [THC] testing)

lung cancer molecular testing (AKT1, ALK, BRAF, Epidermal growth factor [EGFR], HER2, KRAS, MEK1, MET, NRAS, PIK3CA, RET, and ROS1)

kidney stone analysis (Urinary stone analysis, Renal calculus analysis)

Variability and Standardization of CSF Examination

Lab Diagnosis of Yellow fever

hexosaminidase (Hexosaminidase A, Hex A, Total hexosaminidase, Hexosaminidase A and B)

hemoglobin electrophoresis (Hgb electrophoresis)

growth hormone stimulation test (GH provocation test, Insulin tolerance test [ITT], Arginine test, Glucagon Stimulation test)

Markers of Bone Resorption: Amino and Carboxy-Terminal Telopeptides of Collagen Type I

Markers of Bone Resorption: Collagen Cross-Links

Bone Formation Markers : Osteocalcin

Diagnosis of Prion Disease