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Glucocorticoid Excess sentence examples within Chronic Glucocorticoid Excess

Chronic Glucocorticoid Excess

CONCLUSION Our findings suggest that chronic glucocorticoid excess and accompanying secondary hormonal imbalances followed by eucortisolemia have detrimental effects on cognitive function in the developing brain; younger age and pubertal stage are risk factors for increased vulnerability, while older adolescents have cognitive vulnerabilities like that of adult patients affected with CD.

Younger age and early puberty are associated with cognitive function decline in children with Cushing disease.

Chronic Glucocorticoid Excess

However, chronic glucocorticoid excess, highlighted in Cushing’s syndrome, is established as being associated with increased cardiovascular disease (CVD) risk.

Glucocorticoids: Fuelling the Fire of Atherosclerosis or Therapeutic Extinguishers?

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10.1055/a-1539-6442

In particular, patients with adrenal non-producing adenomas already showed signs of glucocorticoid excess, including relative lymphocytopenia, lowered DHEAS, and ACTH concentrations than control individuals.

DHEAS and Differential Blood Counts as Indirect Signs of Glucocorticoid Excess in Adrenal Non-Producing Adenomas.

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10.1530/EC-20-0490

Moreover, NASH may also be found in many other endocrine diseases such as polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or glucocorticoid excess, for example.

Pathophysiology of NASH in endocrine diseases

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10.1530/EDM-20-0207

Learning points Unexplained osteoporosis requires thorough investigation and the workup for secondary causes is not complete without excluding glucocorticoid excess.

Metastatic medullary thyroid carcinoma presenting as ectopic Cushing’s syndrome

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10.1007/s11914-020-00645-9

Purpose of Review The goal of this review is to provide an overview of the impact and underlying mechanism of oxidative stress on connexin channel function, and their roles in skeletal aging, estrogen deficiency, and glucocorticoid excess associated bone loss.

Connexin Gap Junctions and Hemichannels Link Oxidative Stress to Skeletal Physiology and Pathology

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10.1210/jendso/bvab048.1561

In the clinical setting, menstrual abnormality, amenorrhea and hypermenorrhea can be shown in patients with glucocorticoid excess.

Involvement of BMP-15 in Glucocorticoid Actions on Ovarian Steroidogenesis by Rat Granulosa Cells

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10.1210/jendso/bvab048.444

Conclusion: Glucocorticoid excess predominantly affects trabecular bones (pelvis, ribs, lumbar spine) as compared to cortical bones.

Recurrent Atraumatic Pelvic Fractures in a Patient With Cushing’s Disease - Is DEXA Scan Really Useful to Predict the Future Fracture Risk?

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10.1111/cen.14603

PATIENTS One hundred and ninety-five consecutive subjects who underwent the low dose (1 μg) ACTH test, in whom decreased cortisol reserve was suspected due to former/present glucocorticoid excess, pituitary disease or/and unexplained weakness.

Impaired aldosterone response to ACTH without hypoaldosteronism: An unrecognized secretory pattern in search of clinical implications.

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10.2478/cipms-2021-0011

Most forms of exposure include maternal nutrient deprivation, nutrient excess, exogenous glucocorticoid excess and endogenous glucocorticoid due to maternal stress.

Effect of perinatal administration of flavonoid-rich extract from Hibiscus sabdariffa to feed-restricted rats, on offspring postnatal growth and reproductive development

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10.1111/cen.14611

CONCLUSION Our findings suggest that chronic glucocorticoid excess and accompanying secondary hormonal imbalances followed by eucortisolemia have detrimental effects on cognitive function in the developing brain; younger age and pubertal stage are risk factors for increased vulnerability, while older adolescents have cognitive vulnerabilities like that of adult patients affected with CD.

Younger age and early puberty are associated with cognitive function decline in children with Cushing disease.

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10.1530/JME-20-0236

Glucocorticoid excess often causes variety of cardiovascular complications, including hypertension, atherosclerosis, and cardiac hypertrophy.

Omentin-1 attenuates glucocorticoid-induced cardiac injury by phosphorylating GSK3β.

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10.3390/ijms22147622

However, chronic glucocorticoid excess, highlighted in Cushing’s syndrome, is established as being associated with increased cardiovascular disease (CVD) risk.

Glucocorticoids: Fuelling the Fire of Atherosclerosis or Therapeutic Extinguishers?

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10.1016/j.mehy.2021.110516

Although the clinical studies are in their infancy, the opinion is that genistein and daidzein have therapeutic potential for the safe treatment of ageing-caused androgen deprivation and glucocorticoid excess with related metabolic/hemodynamic issues in males.

Soy isoflavone-caused shunting of the corticosteroidogenesis pathways in andropausal subjects: Top-down impulse for the optimal supplementation design.

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10.1016/j.metabol.2018.12.003

METHODS We tested this hypothesis in the adipose specific 11β-hydroxysteroid dehydrogenase-1 (HSD11B1) transgenic mouse, an established model of adipose glucocorticoid excess.

Ectopic lipid deposition mediates insulin resistance in adipose specific 11β-hydroxysteroid dehydrogenase type 1 transgenic mice.

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10.1007/s40278-019-63033-4

A low-dose overnight dexamethasone suppression test (DST) was performed during liraglutide therapy to rule out chronic glucocorticoid excessinduced obesity, hypertension and diabetes.

Exenatide/liraglutide/dexamethasone interaction

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10.1007/s12020-019-02034-4

Purpose The evaluation of skeletal fragility in Cushing’s syndrome (CS) is a clinical challenge, since dual-energy X-ray absorptiometry (DXA) does not capture abnormalities in bone microstructure induced by glucocorticoid excess.

High bone marrow fat in patients with Cushing’s syndrome and vertebral fractures

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10.1113/EP087332

What is the central question of this study? Does glucocorticoid excess disrupt brown adipose tissue (BAT) phenotype and function? What is the main finding and its importance? Glucocorticoid excess induced an extensive remodelling of interscapular BAT, resulting in a white‐like phenotype in association with metabolic disturbances.

Brown adipose tissue remodelling induced by corticosterone in male Wistar rats

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10.1007/978-3-319-96364-8_16

Cushing’s syndrome is the name given to a group of symptoms resulting from glucocorticoid excess.

Cushing’s Syndrome

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10.1024/1661-8157/a003263

Sellar masses may present with an impairment of pituitary function (hypopituitarism), hormone hypersecretion (prolactinoma, acromegaly, glucocorticoid excess) or neurological symptoms (visual impairment, headache).

[Interdisciplinary Management of Sellar Masses].

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10.14341/PROBL10036

This fact is of particular importance in light of recent studies that have shown that PA is often associated with glucocorticoid excess.

[Aldosterone- and cortisol-co-secreting adrenal tumors: an uneasy sum of well-known parts (review)].

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10.1016/j.jsbmb.2019.105468

Because steroid-induced diabetes is the most common form of drug-induced hyperglycemia, we investigated mechanisms underlying the recognized phenotypes associated with glucocorticoid excess.

One week of continuous corticosterone exposure impairs hepatic metabolic flexibility, promotes islet β-cell proliferation, and reduces physical activity in male C57BL/6 J mice

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10.1007/s12192-019-01017-8

Glucocorticoid excess is one of those conditions that underlie the prenatal stress and can lead to many pathological disorders later in life.

Expression pattern dysregulation of stress- and neuronal activity-related genes in response to prenatal stress paradigm in zebrafish larvae

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10.1530/EJE-19-0305

OBJECTIVE Glucocorticoid treatment of inflammatory disorders is associated with significant adverse effects related to glucocorticoid excess as well as adrenal insufficiency.

Fifteen-year nationwide trends in systemic glucocorticoid drug use in Denmark.

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10.5603/EP.a2019.0022

Currently, the clinical importance TBS was verified in terms of disorders of the growth hormone/insulin-like growth factor 1 (GH/IGF-I) axis, glucocorticoid excess, thyroid and parathyroid disease, as well as in diabetes mellitus type 1 and 2.

Trabecular bone score (TBS) as a noninvasive and complementary tool for clinical diagnosis of bone structure in endocrine disorders.

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10.1097/PAS.0000000000001185

The morphologic and proliferative features of these 2 tumor types represent 2 ends of a spectrum; their function also can result in divergent clinical manifestations, one characterized by reduced urine output and the other by the more insidious features of glucocorticoid excess.

Hypothalamic Vasopressin-Producing Tumors: Often Inappropriate Diuresis But Occasionally Cushing Disease

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10.2478/inmed-2019-0058

Cushing’s syndrome (CS) is a clinical condition resulting from chronic exposure to glucocorticoid excess.

The Cardiovascular Risk in Cushing’s Syndrome

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10.31871/WJRR.8.2.16

Normally pregnancy is a state of hypercortisolemia (glucocorticoid excess) particularly in the latter stages and testing of HPA axis (hypothalamic-pituitary-adrenal axis) using validated stimulation or confirmation test during pregnancy are lacking.

An Unusual Case of Transient Cortisol Deficiency and Profound Hyponatremia in a Pregnant Female with Pre-Eclampsia

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10.1186/s12902-019-0401-4

The long term adverse effects of severe hypercortisolaemia on brain function and the pathophysiological mechanisms responsible for the structural and functional changes in brain anatomy due to glucocorticoid excess are reviewed.

Improvement in cognitive impairment following the successful treatment of endogenous Cushing’s syndrome-a case report and literature review

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10.3390/ijms20205141

Glucocorticoid excess escalates osteoclastic resorption, accelerating bone mass loss and microarchitecture damage, which ramps up osteoporosis development.

MicroRNA-29a Counteracts Glucocorticoid Induction of Bone Loss through Repressing TNFSF13b Modulation of Osteoclastogenesis

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10.1016/j.psyneuen.2019.104436

Their degradation is likely involved in long-term biases towards habit-based behaviors following glucocorticoid excess in adolescence.

Glucocorticoid-sensitive ventral hippocampal-orbitofrontal cortical connections support goal-directed action – Curt Richter Award Paper 2019

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10.1016/j.ajpath.2018.12.007

Intriguingly, the critical manifestation of Sost deficiency combined with glucocorticoid excess was sporadic, sudden, unprovoked, and nonconvulsive death.

Sost Haploinsufficiency Provokes Peracute Lethal Cardiac Tamponade without Rescuing the Osteopenia in a Mouse Model of Excess Glucocorticoids

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10.1007/s00431-019-03336-5

As glucocorticoid excess is not associated with such disproportion, our findings raise the possibility of an intrinsic disorder of growth in DMD.

Skeletal disproportion in glucocorticoid-treated boys with Duchenne muscular dystrophy

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10.1002/jcp.27655

Previous studies suggest that PAI‐1 is involved in the pathogenesis of osteoporosis induced by ovariectomy, diabetes, and glucocorticoid excess in mice.

Plasminogen activator inhibitor‐1 deficiency suppresses osteoblastic differentiation of mesenchymal stem cells in mice

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10.1530/EJE-19-0215

The causal approach of removing the mineralocorticoid excess, as well as the often-accompanying glucocorticoid excess, might provide one biologically plausible explanation for the observation of slightly better outcomes with surgical therapy.

THERAPY OF ENDOCRINE DISEASE: Medical treatment of primary aldosteronism.

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10.1016/J.COEMR.2019.08.008

Beside the long-term effects of hypertension itself, mineralocorticoid and glucocorticoid excess pose additional, independent risks of end-stage renal disease and cardiovascular morbidity and mortality.

Primary aldosteronism long-term outcome: Medical versus surgical therapy

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10.1159/000501640

Thus clinicians should be aware of the potential for development of adrenal insufficiency or symptoms of glucocorticoid excess in these patients receiving prednisone so that appropriate modifications in glucocorticoid dosing can be instituted without any delay.

Recognition and Treatment of Adrenal Insufficiency Secondary to Abiraterone: A Case Report and Literature Review

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10.3389/fendo.2019.00054

Glucocorticoid excess seen in the elderly population can have serious consequences in both the structural and functional integrity of various key areas in the brain, including the hippocampus, amygdala, prefrontal cortex, with consequent impairment in normal memory, cognitive function, and sleep cycles.

Adrenal Aging and Its Implications on Stress Responsiveness in Humans

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10.1016/j.diabet.2019.02.003

Also, recent findings of the coexistence of glucocorticoid excess in many cases of PA highlight the need for further studies to examine the presumed link between high aldosterone levels and various metabolic parameters.

Links between aldosterone excess and metabolic complications: A comprehensive review.

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Glucocorticoid Excess
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What is/are Glucocorticoid Excess?

Glucocorticoid Excess - In particular, patients with adrenal non-producing adenomas already showed signs of glucocorticoid excess, including relative lymphocytopenia, lowered DHEAS, and ACTH concentrations than control individuals. [1] Moreover, NASH may also be found in many other endocrine diseases such as polycystic ovary syndrome, hypothyroidism, male hypogonadism, growth hormone deficiency or glucocorticoid excess, for example. [2] Learning points Unexplained osteoporosis requires thorough investigation and the workup for secondary causes is not complete without excluding glucocorticoid excess. [3] Purpose of Review The goal of this review is to provide an overview of the impact and underlying mechanism of oxidative stress on connexin channel function, and their roles in skeletal aging, estrogen deficiency, and glucocorticoid excess associated bone loss. [4] In the clinical setting, menstrual abnormality, amenorrhea and hypermenorrhea can be shown in patients with glucocorticoid excess. [5] Conclusion: Glucocorticoid excess predominantly affects trabecular bones (pelvis, ribs, lumbar spine) as compared to cortical bones. [6] PATIENTS One hundred and ninety-five consecutive subjects who underwent the low dose (1 μg) ACTH test, in whom decreased cortisol reserve was suspected due to former/present glucocorticoid excess, pituitary disease or/and unexplained weakness. [7] Most forms of exposure include maternal nutrient deprivation, nutrient excess, exogenous glucocorticoid excess and endogenous glucocorticoid due to maternal stress. [8] CONCLUSION Our findings suggest that chronic glucocorticoid excess and accompanying secondary hormonal imbalances followed by eucortisolemia have detrimental effects on cognitive function in the developing brain; younger age and pubertal stage are risk factors for increased vulnerability, while older adolescents have cognitive vulnerabilities like that of adult patients affected with CD. [9] Glucocorticoid excess often causes variety of cardiovascular complications, including hypertension, atherosclerosis, and cardiac hypertrophy. [10] However, chronic glucocorticoid excess, highlighted in Cushing’s syndrome, is established as being associated with increased cardiovascular disease (CVD) risk. [11] Although the clinical studies are in their infancy, the opinion is that genistein and daidzein have therapeutic potential for the safe treatment of ageing-caused androgen deprivation and glucocorticoid excess with related metabolic/hemodynamic issues in males. [12] METHODS We tested this hypothesis in the adipose specific 11β-hydroxysteroid dehydrogenase-1 (HSD11B1) transgenic mouse, an established model of adipose glucocorticoid excess. [13] A low-dose overnight dexamethasone suppression test (DST) was performed during liraglutide therapy to rule out chronic glucocorticoid excessinduced obesity, hypertension and diabetes. [14] Purpose The evaluation of skeletal fragility in Cushing’s syndrome (CS) is a clinical challenge, since dual-energy X-ray absorptiometry (DXA) does not capture abnormalities in bone microstructure induced by glucocorticoid excess. [15] What is the central question of this study? Does glucocorticoid excess disrupt brown adipose tissue (BAT) phenotype and function? What is the main finding and its importance? Glucocorticoid excess induced an extensive remodelling of interscapular BAT, resulting in a white‐like phenotype in association with metabolic disturbances. [16] Cushing’s syndrome is the name given to a group of symptoms resulting from glucocorticoid excess. [17] Sellar masses may present with an impairment of pituitary function (hypopituitarism), hormone hypersecretion (prolactinoma, acromegaly, glucocorticoid excess) or neurological symptoms (visual impairment, headache). [18] This fact is of particular importance in light of recent studies that have shown that PA is often associated with glucocorticoid excess. [19] Because steroid-induced diabetes is the most common form of drug-induced hyperglycemia, we investigated mechanisms underlying the recognized phenotypes associated with glucocorticoid excess. [20] Glucocorticoid excess is one of those conditions that underlie the prenatal stress and can lead to many pathological disorders later in life. [21] OBJECTIVE Glucocorticoid treatment of inflammatory disorders is associated with significant adverse effects related to glucocorticoid excess as well as adrenal insufficiency. [22] Currently, the clinical importance TBS was verified in terms of disorders of the growth hormone/insulin-like growth factor 1 (GH/IGF-I) axis, glucocorticoid excess, thyroid and parathyroid disease, as well as in diabetes mellitus type 1 and 2. [23] The morphologic and proliferative features of these 2 tumor types represent 2 ends of a spectrum; their function also can result in divergent clinical manifestations, one characterized by reduced urine output and the other by the more insidious features of glucocorticoid excess. [24] Cushing’s syndrome (CS) is a clinical condition resulting from chronic exposure to glucocorticoid excess. [25] Normally pregnancy is a state of hypercortisolemia (glucocorticoid excess) particularly in the latter stages and testing of HPA axis (hypothalamic-pituitary-adrenal axis) using validated stimulation or confirmation test during pregnancy are lacking. [26] The long term adverse effects of severe hypercortisolaemia on brain function and the pathophysiological mechanisms responsible for the structural and functional changes in brain anatomy due to glucocorticoid excess are reviewed. [27] Glucocorticoid excess escalates osteoclastic resorption, accelerating bone mass loss and microarchitecture damage, which ramps up osteoporosis development. [28] Their degradation is likely involved in long-term biases towards habit-based behaviors following glucocorticoid excess in adolescence. [29] Intriguingly, the critical manifestation of Sost deficiency combined with glucocorticoid excess was sporadic, sudden, unprovoked, and nonconvulsive death. [30] As glucocorticoid excess is not associated with such disproportion, our findings raise the possibility of an intrinsic disorder of growth in DMD. [31] Previous studies suggest that PAI‐1 is involved in the pathogenesis of osteoporosis induced by ovariectomy, diabetes, and glucocorticoid excess in mice. [32] The causal approach of removing the mineralocorticoid excess, as well as the often-accompanying glucocorticoid excess, might provide one biologically plausible explanation for the observation of slightly better outcomes with surgical therapy. [33] Beside the long-term effects of hypertension itself, mineralocorticoid and glucocorticoid excess pose additional, independent risks of end-stage renal disease and cardiovascular morbidity and mortality. [34] Thus clinicians should be aware of the potential for development of adrenal insufficiency or symptoms of glucocorticoid excess in these patients receiving prednisone so that appropriate modifications in glucocorticoid dosing can be instituted without any delay. [35] Glucocorticoid excess seen in the elderly population can have serious consequences in both the structural and functional integrity of various key areas in the brain, including the hippocampus, amygdala, prefrontal cortex, with consequent impairment in normal memory, cognitive function, and sleep cycles. [36] Also, recent findings of the coexistence of glucocorticoid excess in many cases of PA highlight the need for further studies to examine the presumed link between high aldosterone levels and various metabolic parameters. [37]

Chronic Glucocorticoid Excess

CONCLUSION Our findings suggest that chronic glucocorticoid excess and accompanying secondary hormonal imbalances followed by eucortisolemia have detrimental effects on cognitive function in the developing brain; younger age and pubertal stage are risk factors for increased vulnerability, while older adolescents have cognitive vulnerabilities like that of adult patients affected with CD. [1] However, chronic glucocorticoid excess, highlighted in Cushing’s syndrome, is established as being associated with increased cardiovascular disease (CVD) risk. [2] A low-dose overnight dexamethasone suppression test (DST) was performed during liraglutide therapy to rule out chronic glucocorticoid excessinduced obesity, hypertension and diabetes. [3]