scholarly journals The Assessment of Patients with Cushing's Syndrome before and after Pituitary Implantation

1967 ◽  
Vol 60 (9) ◽  
pp. 911-911
Author(s):  
M Hartog ◽  
G F Joplin ◽  
K Fotherby ◽  
D Mattingly ◽  
T Russell Fraser
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing's Syndrome ◽  
Before And After

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.

scholarly journals The Hypothalamic-Pituitary-Thyroid Axis in Cushing Syndrome before and after Curative Surgery

2020 ◽  
Author(s):  
Skand Shekhar ◽  
Raven McGlotten ◽  
Sunyoung Auh ◽  
Kristina I Rother ◽  
Lynnette K Nieman
Keyword(s):  
Thyroid Function ◽  
Cushing’S Syndrome ◽  
Cushing Syndrome ◽  
Cushing's Syndrome ◽  
Curative Surgery ◽  
Central Hypothyroidism ◽  
Duration Of Symptoms ◽  
Before And After ◽  
Pituitary Thyroid Axis ◽  
Thyroid Axis

Abstract Background We do not fully understand how hypercortisolism causes central hypothyroidism or what factors influence recovery of the hypothalamic-pituitary-thyroid axis. We evaluated thyroid function during and after cure of Cushing’s syndrome (CS). Methods We performed a retrospective cohort study of adult patients with CS seen from 2005 – 2018 (cohort 1, c1, n=68) or 1985 – 1994 (cohort 2, c2, n=55) at a clinical research center. Urine (UFC) and diurnal serum cortisol (F: ~8AM and ~midnight (PM)), morning triiodothyronine (T3), free thyroxine (FT4) and thyroid stimulating hormone (TSH) (c1) or hourly TSH from 1500-1900h (day) and 2400-04000h (night) (c2), were measured before and after curative surgery. Results While hypercortisolemic, 53% of c1 had central hypothyroidism (low/low normal fT4 + unelevated TSH). Of those followed long-term, 31% and 44% had initially subnormal FT4 and T3, respectively, which normalized 6—12 months after cure. Hypogonadism was more frequent in hypothyroid (69%) compared to euthyroid (13%) patients. Duration of symptoms, AM and PM F, ACTH, and UFC were inversely related to TSH, FT4 and/or T3 levels (r -0.24 to -0.52, P <0.0001 to 0.02). In c2, the nocturnal surge of TSH (mIU/L) was subnormal before (day 1.00±0.04 vs night 1.08±0.05, p=0.3) and normal at a mean of 8 months after cure (day 1.30±0.14 vs night 2.17±0.27, p=0.01). UFC >1000 μg /day was an independent adverse prognostic marker of time to thyroid hormone recovery. Conclusions Abnormal thyroid function, likely mediated by subnormal nocturnal TSH, is prevalent in Cushing’s syndrome and is reversible after cure.

scholarly journals TXNIP is highly regulated in bone biopsies from patients with endogenous Cushing's syndrome and related to bone turnover

2012 ◽  
Vol 166 (6) ◽  
pp. 1039-1048 ◽  
Author(s):  
Tove Lekva ◽  
Thor Ueland ◽  
Hege Bøyum ◽  
Johan Arild Evang ◽  
Kristin Godang ◽  
...  
Keyword(s):  
Surgical Treatment ◽  
Cushing’S Syndrome ◽  
Bone Cells ◽  
Cushing's Syndrome ◽  
Gene Encoding ◽  
Osteoclast Activity ◽  
Bone Biopsies ◽  
Before And After

ObjectivePatients with endogenous Cushing's Syndrome (CS), as long-time treated patients with exogenous glucocorticoids (GCs), have severe systemic manifestations including secondary osteoporosis and low-energy fractures. The aim of the present study was to investigate the functional role ofTXNIPin bone with focus on osteoblast (OB) differentiation and OB-mediated osteoclast activity and functionin vitro.Design and methodsNine bone biopsies from CS before and after surgical treatment were screened for expressional candidate genes. Microarray analyses revealed that the gene encodingTXNIPranked among the most upregulated genes. Subsequentin vitroandin vivostudies were performed.ResultsWe found thatTXNIPgene in bone is downregulated in CS following surgical treatment. Furthermore, ourin vivodata indicate novel associations between thioredoxin andTXNIP. Ourin vitrostudies showed that silencingTXNIPin OBs was followed by increased differentiation and expression and secretion of osteocalcin as well as enhanced activity of alkaline phosphatase. Moreover, treating osteoclasts with silenced TXNIP OB media showed an increased osteoclast activity.ConclusionsTXNIPexpression in bone is highly regulated during the treatment of active CS, and by GC in bone cellsin vitro. Our data indicate that TXNIP may mediate some of the detrimental effects of GC on OB function as well as modulate OB-mediated osteoclastogenesis by regulating the OPG/RANKL ratio.

scholarly journals Endogenous and exogenous glucocorticoids decrease plasma ghrelin in humans

2004 ◽  
pp. 113-117 ◽  
Author(s):  
B Otto ◽  
M Tschop ◽  
W Heldwein ◽  
AF Pfeiffer ◽  
S Diederich
Keyword(s):  
Cushing’S Syndrome ◽  
Peptide Hormone ◽  
Cushing's Syndrome ◽  
Healthy Controls ◽  
Strong Negative Correlation ◽  
Before And After ◽  
Composition Characteristic ◽  
Exogenous Origin ◽  
Ghrelin Secretion ◽  
First Time

OBJECTIVE: The orexigenic and adipogenic peptide hormone ghrelin is predominantly produced and secreted by the stomach and seems to transduce changes in food intake to specific neuronal circuits in the brain. The activity of ghrelin also includes stimulatory effects on the corticotropic system. However, little is known about the influence of glucocorticoids on ghrelin levels. We therefore studied human plasma ghrelin levels in the presence and absence of elevated glucocorticoid levels of either endogenous or exogenous origin. METHODS: Plasma ghrelin levels were measured in five patients with chronic hypercortisolism (aged 29-58, median 46 years) due to Cushing's syndrome before and after successful surgery for the adenoma, and in eight healthy controls (aged 24-39, median 27.5 years) before and after 30 mg prednisolone (for 5 days) once a day in the morning (median body mass index (BMI) 22.7 kg/m(2)). Plasma ghrelin levels were measured with a commercially available radioimmunoassay. RESULTS: In patients with Cushing's syndrome, plasma ghrelin levels were low (median 363.2 pg/ml, range 161.9-525.7 pg/ml) and significantly increased by 26.6% (P=0.04) after successful surgery, while BMI decreased (median 26.2-24.0 kg/m(2), P=0.04). A strong negative correlation (r=-0.9, P=0.04) between changes in BMI and plasma ghrelin was observed. In healthy controls, plasma ghrelin levels (median 288.7 pg/ml, range 119.6-827.8 pg/ml) were significantly suppressed by 18.3% (P=0.04) after prednisolone treatment. CONCLUSIONS: We have shown for the first time that plasma ghrelin levels are decreased under endogenously or exogenously induced hypercortisolism, making ghrelin an unlikely candidate for causing the changes in energy balance or body composition characteristic of Cushing's disease. However, the reduced ghrelin secretion could reflect a compensation mechanism in reaction to the metabolic consequences of chronic hypercortisolism.

scholarly journals Improvement but no normalization of quality of life and cognitive functioning after treatment for Cushing’s syndrome

2019 ◽  
Author(s):  
Leonie H A Broersen ◽  
Cornelie D Andela ◽  
Olaf M Dekkers ◽  
Alberto M Pereira ◽  
Nienke R Biermasz
Keyword(s):  
Quality Of Life ◽  
Cognitive Functioning ◽  
Cushing’S Syndrome ◽  
Meta Analysis ◽  
Cushing's Syndrome ◽  
Treatment Quality ◽  
Cross Sectional ◽  
Effective Interventions ◽  
Before And After

Abstract Background Cushing’s syndrome is characterized by glucocorticoid excess, which induces physical and mental symptoms, impairments in functional status and perceived health, resulting in impaired quality of life. Biochemical remission is urgently required; however, quality of life and cognitive function may remain impaired. Objective To perform a systematic review and meta-analysis evaluating changes in health-related quality of life and cognitive functioning in patients with Cushing’s syndrome after treatment. Methods Eight electronic databases were searched in March 2017, and PubMed again in May 2018, to identify potentially relevant articles. Eligible studies were (randomized controlled) trials, cohort studies, and cross-sectional studies assessing quality of life or cognitive functioning in patients treated for Cushing’s syndrome. Differences were expressed as standardized mean difference, and reported with 95% confidence intervals. We compared patients before and after treatment (improvement), and patients after treatment and healthy controls (normalization). Results We included 47 articles with 2,643 patients. Most patients had Cushing’s disease and were in remission after treatment. Quality of life and cognitive functioning improved after treatment in all studied domains. Compared to a healthy control population, quality of life did not normalize. Cognitive functioning normalized in part, but not all, of the studied domains. Conclusions Treatment of Cushing’s syndrome improves quality of life and cognitive functioning. As normalization was not achieved in quality of life and in some aspects of cognitive functioning, special and continuous attention should be given to these aspects for patients after treatment. Effective interventions for further improvement and possibly normalization are urgently needed.

CORTICOSTEROIDS IN HUMAN BLOOD

1969 ◽  
Vol 60 (1) ◽  
pp. 13-35 ◽  
Author(s):  
Ludwig Kornel
Keyword(s):  
Essential Hypertension ◽  
Cushing’S Syndrome ◽  
Plasma Levels ◽  
Normal Subjects ◽  
Cushing's Syndrome ◽  
Normal Range ◽  
Upper Limit ◽  
Before And After ◽  
Intensive Work ◽  
Kinetics Of

ABSTRACT As an extension of our study on corticosteroid metabolism in essential hypertension, plasma levels of »free«, »polar free«, glucuronide and sulfate conjugated 17-hydroxycorticosteroids (17-OHCS), as well as »total conjugated« 17-OHCS, have been determined in 13 patients with Cushing's syndrome and 56 healthy people, before and after administration of corticotrophin (ACTH). Levels of these steroid fractions were also compared in normal subjects during rest and after intensive work. Furthermore, kinetics of the formation and disposal of each of these steroid fractions were investigated in vivo in 3 normal subjects and 3 patients with Cushing's syndrome, by means of radioisotopic tracer techniques. The results obtained indicated the following: (1) although mean levels of each of the estimated 17-OHCS fractions, both before and after ACTH, were in Cushing's syndrome statistically significantly higher than in normal subjects (exception: 17-OHCS-sulfates after ACTH), many individual values for steroid concentrations in Cushing patients were well below the upper limit of the normal range; (2) levels of conjugated and »polar free« 17-OHCS in these patients were much more often increased above the normal range than those of »free« steroids usually measured; moreover, levels of these steroids in the control specimens constituted a much better index of adrenocortical hyperactivity than those after ACTH administration; (3) arithmetical formulae were construed, taking into account both an absolute increase in steroid levels and a relative increase in levels of conjugated and »polar free« steroids above those of »free« 17-OHCS, which permitted a clear-cut separation of all patients with Cushing's syndrome from normal subjects; (4) in the sulfate conjugated 17-OHCS fraction in Cushing patients, the increase in levels of more polar steroids (extractable with ethyl acetate following solvolysis and removal of less polar steroids with dichloromethane) was statistically significantly greater than that of less polar steroids (extractable with dichloromethane), thus, patients with Cushing's syndrome resembled from this angle patients with essential hypertension; (5) when steroid levels in normal subjects were compared during rest and during intensive work, a proportional increase in all steroid fractions during work was noted; this points to a perfect homeostatic mechanism involving enzyme systems metabolizing cortisol under »normal« stressful conditions; (6) however, after ACTH administration, the increase in the levels of conjugated steroids in normal subjects considerably exceeded that of »free« 17-OHCS; in contrast, in Cushing patients the increase in the conjugated 17-OHCS after ACTH administration was relatively smaller than that of »free« 17-OHCS; this, it is believed, indicates that the level of activity of enzymes metabolizing cortisol is in patients with Cushing's syndrome closer to the upper limit of these enzymes' capacity than in normal subjects, possibly due to a chronic saturation with higher steroid concentrations; (7) the results of the radioisotopic tracer study of the kinetics of formation and disposal of various free and conjugated plasma corticosteroid fractions demonstrated that, under basal conditions: (a) biological halflife of cortisol in Cushing patients is shorter than in normal subjects, (b) rates of formation of conjugated and polar free metabolites are much faster in Cushing patients than in normal subjects; this indicates that patients with Cushing's syndrome develop adaptive mechanisms to metabolize chronically increased loads of cortisol, and explains why plasma levels of »polar free« and conjugated 17-OHCS are a better index of adrenocortical hyperactivity than those of the »free« steroids, usually measured.

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