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Pituitary emergencies:
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Jessica Perini, Nadia Barghouthi, Gayatri Jaiswal
Necrosis of the corticotrophs of the pituitary will impair secretion of ACTH, which stimulates the production of cortisol by the adrenal glands. If the ACTH deficiency is severe and acute, adrenal insufficiency will rapidly develop and, if not identified and treated quickly, may progress to a potentially fatal adrenal crisis with severe hypotension, hypoglycemia, hyponatremia, and shock.If the corticotrophs are only mildly damaged, the deficiency of ACTH may not be immediately obvious and longer-term symptoms of adrenal insufficiency such as lethargy, loss of appetite, weight loss, and diarrhea may occur gradually.
Endocrine and Neuroendocrine Tumors
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2020
Natasha Shrikrishnapalasuriyar, P.N. Plowman, Márta Korbonits, Ashley B. Grossman
Silent corticotroph tumors and gonadotrophin-secreting and thyroid-stimulating hormone (TSH)-secreting tumors should be treated as functionless tumors. Some silent corticotroph tumors may progress to clinical Cushing’s disease and should be treated particularly vigorously. TSH-secreting tumors present with clinical and biochemical thyrotoxicosis with inappropriately non-suppressed TSH levels; they are usually macroadenomas, and are generally sensitive to somatostatin analogues, which may be given as a therapeutic trial; gonadotrophinomas may occasionally respond to gonadotrophin-releasing hormone (GnRH) antagonists (and, infrequently, to GnRH agonists), but most often require surgery.32
Vasoactive Intestinal Peptide: A Neural Modulator of Endocrine Function
Published in Craig A. Johnston, Charles D. Barnes, Brain-Gut Peptides and Reproductive Function, 2020
Willis K. Samson, Marc E. Freeman
The original descriptions of the PRF activity (Kato et al., 1978; Ruberg et al., 1978) of VIP have been confirmed by many laboratories (Samson et al., 1980; Enjalbert et al., 1980; Rotsztejn et al., 1980; Nicosia et al., 1982). In partially purified populations of lactotrophs (Rotsztejn et al., 1980), VIP, in doses ranging from 0.1–100 nM, significantly and in a dose-related fashion stimulated PRL release with an ED50 of 2 nM. VIP has not been demonstrated to synergize with other PRFs and it tends to reverse the inhibitory effect of dopamine, although this action is not mediated via an interaction with the dopamine receptor (Enjalbert et al., 1980). The effect is specific for PRL since the release of luteinizing hormone (LH), follicle stimulating hormone, growth hormone and thyroid stimulating hormone were not affected by the peptide (Samson et al., 1980, Nicosia et al., 1982). There is some controversy over possible direct effects of VIP on corticotrophs since, in dispersed cells, Rotsztejn et al. (1980) failed to observe any effect; however, others (Nicosia et al., 1982) have observed significant stimulation of ACTH release from human pituitary adenomas. We have seen some effect of VIP on ACTH release from dispersed cells in vitro (Samson, unpublished observations), but the dose required exceeds that of corticotropin releasing factor (CRF) by four to five orders of magnitude.
Subclinical hemorrhagic nonfunctionning pituitary adenoma: pituitary gland function status, endoscopic endonasal transsphenoidal surgery, and outcomes
Published in British Journal of Neurosurgery, 2023
Ming Wang, Yugang Jiang, Yang Cai, Huixuan Wu, Yong Peng
The following tests were used for assessing the pituitary hormonal status on admission in all patients: serum levels of thyroid-stimulating hormone (TSH) and free thyroxine for the thyrotroph axis; morning plasma adrenocorticotropic hormone (ACTH) and serum cortisol levels for the corticotroph axis; serum levels of prolactin (PRL) for hyperprolactinemia, follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone or estradiol for the gonadotroph axis; growth hormone (GH), insulin-like growth factor 1 (IGF-1) for the somatotroph axis. For a better assessment of the pituitary functions, some patients underwent a pituitary stimulation testing, including ACTH stimulation test for the corticotroph axis; Gonadotropin-releasing hormone stimulation tests for the gonadotroph axis; insulin hypoglycemia tests or arginine-loading tests for the somatotroph axis. The diagnoses of pituitary function pre- and postoperative were made by endocrinologists. Patients’ preoperatively pituitary dysfunction were categorized according to each identified pituitary hormonal abnormality, including hypoadrenalism, hypothyroidism, hypogonadism, ‘stalk compression’ hyperprolactinemia (non-prolactinoma), and diabetes insipidus (DI). Diabetes insipidus was diagnosed on the basis of urine specific gravity 1.005 and urine volume was great than 200 mL/h for at least three consecutive hours. If there were three or more kinds of hormonal deficiency, the condition was classified as panhypopituitarism.
Expression of Rasd1 in mouse endocrine pituitary cells and its response to dexamethasone
Published in Stress, 2021
Chad D. Foradori, Laci Mackay, Chen-Che J. Huang, Robert J. Kemppainen
All organisms strive to maintain a state of homeostasis, which is constantly challenged by a variety of internal and external stressors. Physiological systems have evolved to counterbalance the disruptions caused by stressors (Herman et al., 2016). The cells of the pituitary are crucially integrated into the regulation of both basal activity and the response to stress. One of the central stress-related mechanisms is the release of adrenocorticotropic hormone (ACTH) from corticotrophs of the pituitary upon the perception of a stressor through the activation of the hypothalamus-pituitary-adrenal (HPA) axis. Release of ACTH leads to adrenocortical activation and a subsequent rise in glucocorticoid concentrations. Glucocorticoids target cells throughout the body, and make immediate energy available to the organism to overcome acutely stressful situations and to restore homeostasis. It is extremely maladaptive for an organism if pituitary cells fail to respond to stimulation initiated by a stressor or fail to restore homeostasis after the stress response has been initiated. A failure to maintain homeostasis results in excessive or inadequate basal activity and responsiveness to stress associated with a wide variety of health consequences including stress-related mental conditions such as major depressive disorder (Chrousos, 2009).
CyberKnife for the management of Cushing’s disease: our institutional experience and review of literature
Published in British Journal of Neurosurgery, 2021
Ashraf Abdali, Pavel L. Kalinin, Yuriy Y. Trunin, Ludmila E. Astaf’Eva, Alexey N. Shkarubo, Gennady E. Chmutin, Vishal Chavda, Andrey Golanov, Badshazar Abdali, Ilya V. Chernov, Atul Vats, Bipin Chaurasia
Cushing`s disease is most commonly caused by corticotroph adenomas resulting in hypersecretion of adrenocorticotropin (ACTH) hormone which subsequently induces hypercortisolism through adrenal cortices and is eventually associated with significant morbidity.1 Trans-sphenoidal (TS) resection is the gold standard treatment with higher remission rates ranging between 59% and 97%.2,3 Despite efficient initial results after TS surgery in up to 50% of cases, recurrence has been noticed as late as 30 years after surgical resection.4,5 The use of radiation to target residual/recurring tumour as an adjuvant therapy is considered the next best treatment option available.5 The use of radiation therapy to treat CD has a long history. Harvey Cushing was the first who treated Cushing disease by conventional radiation therapy.6 Following him Alfred Pattison implanted radon seeds in the pituitary fossa to radiate and treat these lesions.7