In this regard, impaired adrenocortical function is likely induced by atrophy of the residual adrenal tissue as a result of chronic suppression by the low ACTH levels of the hypercortisolism state.
The neurosurgical resection of her 2 mm adrenocorticotropic hormone (ACTH) secreting pituitary microadenoma resulted in a successful resolution of the patient's hypercortisolism and a significant recovery of her neurocognitive function.
A mono-centric and longitudinal study was conducted on 19 consecutive patients who underwent SBA for ACTH-dependent hypercortisolism between December 2003 and December 2017.
Cushing's disease (CD) is a rare condition caused by adrenocorticotropic hormone (ACTH)-producing adenomas of the pituitary, which lead to hypercortisolism that is associated with high morbidity and mortality.
A retrospective analysis of ten consecutive patients with ACTH-independent hypercortisolism who underwent AVS at our institution between 2009 and 2017.
Adrenal functional autonomy has been described in a subset of patients with CD, leading to the hypothesis of transition from ACTH-dependent to ACTH-independent hypercortisolism.
It has been thought that inhibition of a glucocorticoid positive-feedback loop is associated with remission of hypercortisolism in ACTH-dependent cyclic Cushing syndrome.
Elevated serum cortisol level of 95.7 µg/dL (8.7-22.4 µg/dL) and markedly elevated 24-hour urinary cortisol level of 6962.3 µg/24 hours (4.0-50.0 µg/24 hours) with concurrent adrenocorticotropic hormone (ACTH) level of 171 pg/mL (6-58 pg/mL) were suggestive of an ACTH-dependent source of hypercortisolism.
A glucocorticoid-driven positive-feedback regulation in this ectopic ACTH-secreting pheochromocytoma created a vicious cycle with rapid exacerbation of both hypercortisolemia and hypercatecholaminemia with extremely elevated plasma ACTH level.
The aim of the study is to detect these receptors in two patients with ACTH-independent hypercortisolism by means of the application of a screening protocol.
There were significantly fewer patients with hypercortisolism in the higher ACTH group; midnight serum cortisol levels were associated with hypercortisolism only in the lower ACTH group.
The participation of aberrant receptors and intra-adrenal ACTH in hyperplastic tissue are considered mechanisms that regulate hypercortisolism in PMAH.
Biochemical testing confirmed hypercortisolism with extremely elevated levels of plasma adrenocorticotropin, urinary cortisol and multiple steroids of a plasma panel that were all normal at previous testing.
OBJECTIVE Cushing disease is caused by a pituitary micro- or macroadenoma that hypersecretes adrenocorticotropic hormone (ACTH), resulting in hypercortisolemia.
Cushing's disease results from corticotroph adenomas of the pituitary that hypersecrete adrenocorticotropin (ACTH), leading to excess glucocorticoid and hypercortisolism.
Effect of hypercortisolism on bone mineral density and bone metabolism: A potential protective effect of adrenocorticotropic hormone in patients with Cushing's disease.
Most of these patients shared the following features of CS: skin thinning, severe hypercortisolemia (24-hour urinary free cortisol ≥10 times the upper limit of normal), ectopic secretion of ACTH, and severe hypokalemia.