Introduction to Cortisol Excess

Moreover, we emphasize the importance of evaluating psycho-behavioral factors in professional settings, because these modifiable variables can be addressed with tailored psychological interventions to ameliorate poor job satisfaction, reduce work-related distress, and avoid chronic cortisol excess experienced by shift workers.

In addition, MSI2 overexpression was associated with characteristics of unfavorable prognosis, such as cortisol excess (p =.

Cushing’s syndrome is a rare disorder of cortisol excess and is associated with significant morbidity and mortality.

Cushing’s disease (CD) is the most common cause of endogenous cortisol excess.

We compared the results of normal individuals, of patients with adrenal adenomas and normal hormone profiles and with subclinical autonomous glucocorticoid hypersecretion, as well as overt cortisol excess.

Endogenous Cushing’s syndrome (CS) is a rare, serious disorder caused by chronic cortisol excess.

METHODS A prospective database identified 108 patients who underwent UA for mild autonomous cortisol excess (MACE) (n=47), overt hypercortisolism (OH) (n=27), PA (n=22), and concurrent PA/HC (n=12) from 9/2014-10/2020; all underwent preoperative evaluation for HC.

Primary bilateral macronodular adrenal hyperplasia (PBMAH), characterized by bilateral benign adrenal macronodules (>1 cm) potentially responsible for variable levels of cortisol excess, is a rare and heterogeneous disease.

We present a case of a giant SCA which pre-operatively didn’t exhibit any clinical signs of cortisol excess but showed signs of early recurrence on follow up imaging.

Background: Cushing’s disease is a challenging endocrine disorder caused by non-physiological cortisol excess from adrenocorticotropic hormone (ACTH) secreting pituitary adenoma.

Recent clinical trials revealed therapeutic potential of both all-trans and 9-cis retinoic acid in patients with cortisol excess due to a pituitary ACTH-secreting adenoma and indicated that retinoids might act also on the adrenal.

If Cushing syndrome was due to bilateral adrenal hyperplasia independent of the patient’s pheochromocytoma, cortisol excess would not have resolved after unilateral adrenalectomy.

Some conditions, such as adrenal insufficiency and cortisol excess, may be risk factors of worse clinical progression once the infection has occurred.

Given the recent advancement of imaging, omics research, and computational approach, it is important to summarize the most updated evidence to disentangle the potential impact of cortisol excess in primary aldosteronism and whether the ACTH stimulation test needs to be considered during the diagnostic process of primary aldosteronism.

Chronic cortisol excess induces several alterations on protein, lipid and carbohydrate metabolism resembling those found in the metabolic syndrome.

We here describe the design of the Cardiovascular Status in Endogenous Cortisol Excess Study (CV-CORT-EX), a study aiming to comprehensively investigate the health status of patients with endogenous CS (with a particular focus on CV phenotypes, biochemical aspects, quality of life, and psychosocial status).

Methods: We conducted a cross-sectional analysis as part of an ongoing cohort study in patients with MACS compared to age and sex-matched referent subjects without cortisol excess.

To identify glucocorticoid‐responsive proteins measurable in human serum that may have clinical utility in therapeutic drug monitoring and the diagnosis of cortisol excess or deficiency.

The patient had no clinical features of cortisol excess.

Conclusion: We describe a case of bilateral adrenal hyperplasia with elevated ACTH and non-suppressed cortisol on LDDST suggestive of ACTH-driven cortisol excess.

OBJECTIVE To expand our understanding of the prevalence of somatic mutations in CPA from patients with overt Cushing syndrome (OCS) and "subclinical" mild autonomous cortisol excess (MACE), with an immunohistochemistry (IHC)‒guided targeted amplicon sequencing approach using formalin-fixed paraffin-embedded (FFPE) tissue.

A history of corticosteroid usage sometimes prevents us from the timely detection of endogenous cortisol excess.

Introduction: About 20–40% of patients with Cushing’s syndrome present with cyclic Cushing’s Syndrome characterized by episodes of cortisol excess interspersed with periods of normal cortisol secretion.

7mcg/dL on 1mg ONDST suggestive of autonomous cortisol excess and workup for primary hyperaldosteronism was negative.

While these results are potentially explained by different degrees of cortisol excess, the majority of patients received suboptimal hormone evaluation, suggesting a knowledge gap in the workup of adrenal adenomas in the broader medical community.

In situ cortisol excess was previously reported to promote cellular senescence, a cell response to stress, in cortisol-producing adenomas (CPA).

Context: Cushing Syndrome (CS) is characterized by cortisol excess, impaired glucose tolerance, and obesity.

Clinicians should be aware that recurrent fracture of trabecular bones may indicate Cushing’s disease even though other clinical features of cortisol excess are minimal or absent.

Cushing Syndrome (CS) is characterized by cortisol excess that leads to impaired glucose tolerance and obesity.

She was notably hyperglycaemic with clinical features of cortisol excess.

Methods: We conducted a cross-sectional analysis as part of an ongoing cohort study in patients with MACS compared to age and sex-matched referent subjects without cortisol excess.

The initial dissection was difficult given the extent of adipose tissue within the retroperitoneum and friability of the tissues as a result of the cortisol excess.

Cushing's syndrome (CS) is associated with skeletal muscle structural and functional impairment which may persist long‐term despite surgical removal of the source of cortisol excess.

Cushing disease (CD) is a rare endocrine disorder caused by ACTH secretion leading to cortisol excess [1].

Progression to mild autonomous cortisol excess (MACE) was observed in 15 (22 %) patients, with 14 of them having post overnight dexamethasone suppression test (ODST) cortisol between 50 and138 nmol/L and only one > 138 nmol/L.

11β-HSD1 is the major determinant of cortisol excess, and its inhibition alleviates metabolic abnormalities.

To understand the intratumoral steroid biosynthesis, we quantified 19 steroids by mass spectrometry in optimal cutting temperature compound (OCT)-embedded 24 CPA tissue from patients with overt CS (OCS, n = 10) and mild adrenal cortisol excess (MACE, n = 14).

Because the presence and extent of cortisol excess in prodromal Alzheimer’s disease predicts the onset of cognitive symptoms we hypothesised that corticosteroids would exacerbate the inhibition of hippocampal synaptic long-term potentiation in a rat model of Alzheimer’s disease amyloidosis.

It may, therefore, be of interest to test specific treatments targeting cortisol excess in selected hypertensive patients.

A 22-year-old woman who displayed classic signs of cortisol excess – excessive weight gain, difficultly losing weight and abdominal striae – was found to have a 10 cm mature teratoma cyst.

In most of the cases the resulting cortisol excess is insufficient to produce a typical Cushing phenotype but may have clinical consequences, such as hypertension, diabetes, obesity, dyslipidemia and osteoporosis.

The incidental identification of an increasing number of cases has shifted its clinical expression from the rarely encountered severe forms, regarding both cortisol excess and adrenal enlargement, to mild forms of asymptomatic or oligosymptomatic cases with less impressive imaging phenotypes.

Cushing syndrome is a severe endocrine disorder of cortisol excess associated with major metabolic and cardiovascular sequelae.

We should not exclude the possibility of PA in patients without suppressed plasma renin activity, especially who had a cortisol excess.

Statistical modeling of the transcriptomic changes in hearts at 130 and 140 days suggested that maternal cortisol excess disrupts cardiac metabolism.

It means changes of hypothalamic pituitary adrenal axis without classic clinically prominent signs of cortisol excess such as proximal myopathy, stretch marks, body fat redistribution and other metabolic changes related to cortisol.

OBJECTIVE To investigate if in subjects without overt or mild hypercortisolism the degree of GCS, GC sensitivity and peripheral activation are associated with hypertension (Hy) and with the number of the possible consequences of cortisol excess among T2D, fragility FX and Hy.

BACKGROUND: Adrenal incidentalomas (AI) are frequently associated with mild autonomous cortisol excess (MACE).

Here we demonstrated that the application of an experimental paradigm, which simulates prenatal stress by exposing embryos to cortisol excess, produced an alteration of gene expression pattern.

A rate of patients with subclinical cortisol excess was 13% in I group and 14% in non-I group in BMAH, whereas that in I group (50%) was higher than that in non-I group (23%) in ACC.

Subclinical Cushing′s syndrome(SCS) is a state of hypercortisolism in the absence of typical signs of overt cortisol excess.

The expressions of the peripheral clock genes in the patients were markedly reduced, which was thought to be caused by a remarkable cortisol excess.

Most adrenal incidentalomas (AI) are benign and frequently cause low-grade cortisol excess that may portend adverse clinical consequences.

Understanding the pathophysiology of Cushing’s syndrome has also led to the identification of potential targets that may decrease adrenocorticotrophic hormone and/or cortisol excess, and/or decrease tumor cell proliferation, and induce senescence or apoptosis.

In principle, this subclinical condition of mild cortisol excess may represent a preliminary stage of overt Cushing syndrome.

A frequent finding in patients with adrenal incidentalomas is failure to suppress cortisol sufficiently after dexamethasone administration in the absence of typical clinical signs of cortisol excess (3), a condition often called subclinical Cushing syndrome or, as recently coined, mild autonomous cortisol excess (MACE).

ACTH levels were high and cortisol levels were supranormal with the lack of clinical findings of cortisol excess or deficiency.

Introduction: Cyclic Cushing’s syndrome is defined as cortisol excess which fluctuates with periods of normal cortisol secretion, usually associated with Cushing’s disease (CD).

Recent data show that even mild cortisol excess is associated with adverse outcomes.

Severity of cortisol excess was inversely associated with BTM values; for CS vs MACS vs NFAT: Osteocalcin (median 10 [2.

The aim of the present study was to test the association between cortisol and these parameters in hypertensive patients without cortisol excess.

CONTEXT Cyclic Cushing syndrome is a rare variant of Cushing syndrome that demonstrates periodic cortisol excess.

SummaryAnalyses using the largest Korean cohort of adrenal incidentaloma (AI) revealed that subtle cortisol excess in premenopausal women and reduced dehydroepiandrosterone-sulfate (DHEA-S) in postmenopausal women and men are associated with bone mineral density (BMD) reduction in Asian patients with subclinical hypercortisolism (SH).

Background: Adrenal incidentalomas are mostly non-functioning adrenal tumors (NFAT) or adenomas with mild autonomous cortisol excess (MACE), of which the natural history is unclear.

In a phase 2 study, treatment with relacorilant showed improvement in glycemic and hypertension endpoints as well as other manifestations of cortisol excess in patients with endogenous Cushing syndrome (CS).