Nycthemeral rhythm of plasma cortisol levels in the Cushing's syndrome associated with hyperplasia of adrenal cortex, before and after treatment of hypophyseal suppression with ultrasonic technique

1967 ◽  
Vol 30 (1-4) ◽  
pp. 129-135
Author(s):  
G. Giusti ◽  
R. Toccafondi ◽  
B. Tarquini
Keyword(s):  
Adrenal Cortex ◽  
Cushing’S Syndrome ◽  
Plasma Cortisol ◽  
Cushing's Syndrome ◽  
Ultrasonic Technique ◽  
Before And After ◽  
Cortisol Levels

scholarly journals Association between posttest dexamethasone and cortisol concentrations in the 1 mg overnight dexamethasone suppression test

2012 ◽  
Vol 1 (2) ◽  
pp. 62-67 ◽  
Author(s):  
Bjørn O Åsvold ◽  
Valdemar Grill ◽  
Ketil Thorstensen ◽  
Marit R Bjørgaas
Keyword(s):  
Cushing’S Syndrome ◽  
Plasma Cortisol ◽  
Polynomial Regression ◽  
Regression Line ◽  
Cushing's Syndrome ◽  
Dexamethasone Suppression Test ◽  
Strong Negative Association ◽  
Suppression Test ◽  
Cortisol Levels ◽  
Dexamethasone Suppression

It has been suggested that comparison of posttest dexamethasone and cortisol concentrations may improve the evaluation of the dexamethasone suppression test (DST) for Cushing's syndrome. In particular, this would be reasonable if posttest cortisol differs by dexamethasone levels within the range that is usually attained in the DST. Using fractional polynomial regression, we therefore studied the association between posttest 0800 h dexamethasone and cortisol levels in 53 subjects without Cushing's syndrome who were tested with the 1 mg overnight DST. Plasma dexamethasone was associated with plasma cortisol (P<0.001), and the regression line suggested a strong negative association related to dexamethasone levels <5 nmol/l. However, among the 94% of subjects with plasma dexamethasone >5.0 nmol/l, there was no association between dexamethasone and cortisol levels (P=0.55). In conclusion, subjects tested with the 1 mg overnight DST usually attain an 0800 h plasma dexamethasone >5 nmol/l, and plasma cortisol does not differ by plasma dexamethasone in these subjects. This suggests that routine comparison of dexamethasone and cortisol levels may not be a useful approach to improve the performance of the 1 mg DST. However, dexamethasone measurements may identify subjects with inadequately low plasma dexamethasone and may therefore be of value when retesting subjects with possibly false-positive DST results.

scholarly journals Aberrant Membrane Hormone Receptors in Incidentally Discovered Bilateral Macronodular Adrenal Hyperplasia with Subclinical Cushing’s Syndrome

2001 ◽  
Vol 86 (11) ◽  
pp. 5534-5540 ◽  
Author(s):  
Isabelle Bourdeau ◽  
Pierre D’Amour ◽  
Pavel Hamet ◽  
Jean-Marie Boutin ◽  
André Lacroix
Keyword(s):  
Cushing’S Syndrome ◽  
Plasma Cortisol ◽  
Hormone Receptors ◽  
Gastric Inhibitory Polypeptide ◽  
Urinary Free Cortisol ◽  
Cushing's Syndrome ◽  
Cortisol Secretion ◽  
Adrenal Hyperplasia ◽  
Free Cortisol ◽  
Cortisol Levels

Cortisol secretion in adrenal Cushing’s syndrome can be regulated by the aberrant adrenal expression of receptors for gastric inhibitory polypeptide, vasopressin, catecholamines, LH/human CG (LH/hCG), or serotonin. Four patients with incidentally discovered bilateral macronodular adrenal hyperplasia without clinical Cushing’s syndrome were evaluated for the possible presence of aberrant adrenocortical hormone receptors. Urinary free cortisol levels were within normal limits, but plasma cortisol levels were slightly elevated at nighttime and suppressed incompletely after dexamethasone administration. Plasma ACTH was partially suppressed basally but increased after administration of ovine CRH. A 51-yr-old woman had ACTH-independent increases of plasma cortisol after 10 IU AVP im (292%), 100 μg GnRH iv (184%), or 10 mg cisapride orally (310%); cortisol also increased after administration of NaCl (3%), hCG, human LH, and metoclopramide. In a 61-yr-old man, cortisol was increased by AVP (349%), GnRH (155%), hCG (252%), and metoclopramide (191%). Another 53-yr-old male increased plasma cortisol after AVP (171%) and cisapride (142%). Cortisol secretion was also stimulated by vasopressin in a 54-yr-old female. This study demonstrates that subclinical secretion of cortisol can be regulated via the aberrant function of at least V1-vasopressin, LH/hCG, or 5-HT4 receptors in incidentally identified bilateral macronodular adrenal hyperplasia.

A New Perioperative Glucocorticosteroid Replacement Therapy for Cushing's Syndrome

2020 ◽  
Author(s):  
Liang Wang ◽  
Lin Yang ◽  
Yuanxing Yang ◽  
Zhe Cui ◽  
Liming Li
Keyword(s):  
Replacement Therapy ◽  
Intravenous Injection ◽  
Cushing’S Syndrome ◽  
Plasma Cortisol ◽  
Clinical Symptoms ◽  
Adrenal Adenoma ◽  
Cushing's Syndrome ◽  
Simple Method ◽  
Urine Cortisol ◽  
Cortisol Levels

Abstract Background: To evaluate the safety and effects of a new perioperative glucocorticosteroid replacement therapy for Cushing,s syndrome.Methods: A simple method of glucocorticosteroid replacement therapy as follow was adopted for 83 cases of Cushing's syndrome patient which were diagnosed before the operation: No glucocorticosteroid was used before operation, but during adrenal adenoma resection 100 mg hydrocortisone was given by intravenous injection，and another 200 mg hydrocortisone was given on the day of surgery. On day 1 and day 2 postoperative, 100 mg/12h and 100 mg/24h hydrocortisone were given by intravenous injection respectively. Prednisone(10mg/8h) was given from the day 2 postoperative by oral administration, then 5mg was reduced once a week until a maintenance dosage (5mg) was reached. Clinical symptoms were observed, plasma cortisol and 24h urine cortisol levels were intermittently measured post-operation to evaluate the safety and the curative effect of this new glucocorticosteroid replacement therapy.Results: Adrenal insufficiency and steroid withdrawal syndrome did not occur with all patients. Compared with the concentration of urine cortisol preoperation, it was significantly decreased on the day 7 postoperative. Plasma cortisol concentration was significantly decreased on day 6 postoperative compared with preoperative. All the patients were followed up to 6 months, plasma cortisol and 24h urine cortisol levels were all normal.Conclusions: This new glucocorticosteroid replacement therapy was safe, simple, and effective.

scholarly journals Decreased ligand affinity rather than glucocorticoid receptor down-regulation in patients with endogenous Cushing's syndrome

2000 ◽  
pp. 472-476 ◽  
Author(s):  
NA Huizenga ◽  
WW De Herder ◽  
JW Koper ◽  
P de Lange ◽  
D AJ v Lely ◽  
...  
Keyword(s):  
Glucocorticoid Receptor ◽  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
The Body ◽  
The Other ◽  
Down Regulation ◽  
Ligand Affinity ◽  
Other Hand ◽  
Receptor Number ◽  
Cortisol Levels

OBJECTIVE: Glucocorticoids (GCs) serve a variety of important functions throughout the body. The synthesis and secretion of GCs are under the strict influence of the hypothalamo-pituitary-adrenal axis. The mechanisms of action of GCs are mediated by the intracellular glucocorticoid receptor (GR). Over the years, many studies have been performed concerning the regulation of GR expression by GC concentrations. METHODS: In the present study, we determined the characteristics of the GR in peripheral mononuclear blood leukocytes (PBML) from thirteen patients with endogenous Cushing's syndrome and fifteen control subjects, using a whole cell dexamethasone binding assay. Furthermore, cortisol concentrations were determined in order to investigate a possible relationship between serum cortisol levels and receptor characteristics. RESULTS: There were no differences in mean receptor number between patients and controls. On the other hand, a significantly lower ligand affinity was identified in cells from patients with Cushing's syndrome compared with controls. A complete normalisation of the ligand affinity was observed after treatment in the only patient tested in this respect, whereas the receptor number was not affected. In patients, there was a statistically significant negative correlation between cortisol concentrations and ligand affinity, which was not found in controls. CONCLUSION: Receptor down-regulation does not occur in PBML from patients with endogenous Cushing's syndrome. On the other hand, there seems to be a diminished ligand affinity which possibly reflects receptor modification in response to exposure to the continuously high cortisol levels in patients with Cushing's syndrome. This assumption is substantiated by the fact that in one patient a normalisation of the ligand affinity after complete remission of the disease was seen.

scholarly journals The role of bilateral inferior petrosal sinus sampling in the diagnosis of Cushing's syndrome

2007 ◽  
Vol 51 (8) ◽  
pp. 1329-1338 ◽  
Author(s):  
Andrea Utz ◽  
Beverly M.K. Biller
Keyword(s):  
Cushing’S Syndrome ◽  
Venous Drainage ◽  
Cushing's Syndrome ◽  
Blood Levels ◽  
Inferior Petrosal Sinus ◽  
Ectopic Acth ◽  
Inferior Petrosal Sinus Sampling ◽  
Neoplastic Lesion ◽  
Before And After ◽  
Acth Secreting

Adrenocorticotropin hormone (ACTH)-dependent Cushing's syndrome is most often due to a pituitary corticotroph adenoma, with ectopic ACTH-secreting tumors representing approximately 15% of cases. Biochemical and radiological techniques have been established to help distinguish between these two entities, and thus aid in the localization of the neoplastic lesion for surgical resection. The test that offers the highest sensitivity and specificity is bilateral inferior petrosal sinus sampling (BIPSS). BIPSS is an interventional radiology procedure in which ACTH levels obtained from venous drainage very near the pituitary gland are compared to peripheral blood levels before and after corticotropin hormone (CRH) stimulation. A gradient between these two locations indicates pituitary Cushing's, whereas the absence of a gradient suggests ectopic Cushing's. Accurate BIPSS results require hypercortisolemia to suppress normal corticotroph ACTH production and hypercortisolemia at the time of the BIPSS to assure excessive ACTH secretion. In some cases, intrapituitary gradients from side-to-side can be helpful to localize small corticotroph adenomas within the sella. BIPSS has rare complications and is considered safe when performed at centers with experience in this specialized technique.

scholarly journals Circulating microRNA Expression in Cushing’s Syndrome

2021 ◽  
Vol 12 ◽  
Author(s):  
Sharmilee Vetrivel ◽  
Ru Zhang ◽  
Mareen Engel ◽  
Barbara Altieri ◽  
Leah Braun ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Validation Cohort ◽  
Cushing's Syndrome ◽  
Circulating Microrna ◽  
High Morbidity ◽  
Discovery Cohort ◽  
Serum Samples ◽  
Curative Surgery ◽  
Before And After ◽  
Diagnosis And Classification

ContextCushing’s syndrome (CS) is a rare disease of endogenous hypercortisolism associated with high morbidity and mortality. Diagnosis and classification of CS is still challenging.ObjectiveCirculating microRNAs (miRNAs) are minimally invasive diagnostic markers. Our aim was to characterize the circulating miRNA profiles of CS patients and to identify distinct profiles between the two major CS subtypes.MethodsWe included three groups of patients from the German Cushing’s registry: ACTH-independent CS (Cortisol-Producing-Adenoma; CPA), ACTH-dependent pituitary CS (Cushing’s Disease; CD), and patients in whom CS had been ruled out (controls). Profiling of miRNAs was performed by next-generation-sequencing (NGS) in serum samples of 15 CS patients (each before and after curative surgery) and 10 controls. Significant miRNAs were first validated by qPCR in the discovery cohort and then in an independent validation cohort of 20 CS patients and 11 controls.ResultsNGS identified 411 circulating miRNAs. Differential expression of 14 miRNAs were found in the pre- and postoperative groups. qPCR in the discovery cohort validated 5 of the significant miRNAs from the preoperative group analyses. Only, miR-182-5p was found to be significantly upregulated in the CD group of the validation cohort. Comparing all CS samples as a group with the controls did not reveal any significant differences in expression.OutcomeIn conclusion, our study identified miR-182-5p as a possible biomarker for CD, which has to be validated in a prospective cohort. Furthermore, our results suggest that presence or absence of ACTH might be at least as relevant for miRNA expression as hypercortisolism itself.

Cyclic Cushing's syndrome combined with cortisol suppressible, dexamethasone non-suppressible ACTH secretion: a new variant of Cushing's syndrome

1985 ◽  
Vol 110 (3) ◽  
pp. 289-295 ◽  
Author(s):  
Hans-Udo Schweikert ◽  
Horst Lorenz Fehm ◽  
Rudolf Fahlbusch ◽  
Rainer Martin ◽  
Rainer Kolloch ◽  
...  
Keyword(s):  
Cushing’S Syndrome ◽  
Normal Tissue ◽  
Plasma Cortisol ◽  
Cushing's Syndrome ◽  
Cortisol Secretion ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Normal Response ◽  
New Variant ◽  
Marked Suppression

Abstract. A 55 year old woman with an unusual form of Cushing's disease was studied. During several periods (periods lasting up to 84 days) evidence of cortisol hypersecretion with cycles occurring every 6 days was found. Suppression of plasma cortisol through orally administered dexamethasone (up to 32 mg per day) could not be achieved either during periods of cyclic cortisol hypersecretion or during apparent remission with normal cortisol secretion. Marked suppression of plasma ACTH was measured in response to an iv infusion of 50 mg cortisol over a period of 55 min whereas a similar test with 2 mg dexamethasone (iv bolus) did not suppress ACTH secretion. Transsphenoidal exploration of the sella revealed a tumour surrounding the anterior pituitary. Examination of the pituitary showed a few tiny tumour structures embedded in normal tissue which could not be removed, when the tumour was resected selectively under preservation of normal appearing tissue. Post-operatively, clinical and chemical remission (normal response to 1 mg dexamethasone) was observed for about 4 months. Thereafter, cortisol hypersecretion occurred again necessitating bilateral adrenalectomy. Our results are compatible with the assumption that normal hypothalamic-pituitary-adrenal suppressibility with cortisol, but not with dexamethasone, was caused by the loss of feedback receptors for dexamethasone in the presence of cortisol receptors in the cells which secrete ACTH or CRF. The combination of cyclic hypercortisolism with dexamethasone non-suppressible Cushing's syndrome has not been reported before and thus represents a new variant of Cushing's syndrome.

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