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Neuroendocrine Factors
Published in Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan, Strength and Conditioning in Sports, 2023
Michael H. Stone, Timothy J. Suchomel, W. Guy Hornsby, John P. Wagle, Aaron J. Cunanan
Cortisol (C) is a steroid hormone secreted by the zona reticularis and zona fasciculata of the adrenal cortex. Production and secretion are stimulated by adrenocorticotropic hormone (ACTH), which is released by the anterior pituitary and regulated by hypothalamic-pituitary feedback mechanisms (100, 108). Cortisol is the primary stress hormone and is involved in a number of physiological actions including fuel substrate mobilization, gluconeogenesis, and immune system suppression. Cortisol generally has anti-anabolic and catabolic effects (108, 147). These effects are mediated by gene derepression and RNA synthesis (176). The primary functions of cortisol are described in the following paragraphs.
The patient with acute endocrine problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
The anterior pituitary is under the control of the hypothalamus, but also acts independently. The hormones most likely to be related to a medical emergency are: Adrenocorticotrophic hormone (ACTH).Thyroid stimulating hormone (TSH).
Integrated Cardiovascular Responses
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The endocrine response to shock also stimulates the pituitary gland. Adrenocorticotrophic hormone (ACTH) is released from the anterior pituitary, stimulating the adrenal cortex to increase the synthesis of glucocorticoids and aldosterone. High circulating glucocorticoid levels increase the responsiveness of vascular smooth muscles to catecholamines. Growth hormone released from the anterior pituitary increases blood glucose and free fatty acid levels. Dynorphins and endorphins are also released from the anterior pituitary. ADH released from the posterior pituitary acts principally on the renal collecting ducts to conserve water. It is also a vasoconstrictor.
Pharmacological Treatment of Generalised Anxiety Disorder: Current Practice and Future Directions
Published in Expert Review of Neurotherapeutics, 2023
Harry A. Fagan, David S. Baldwin
Corticotropin-releasing factor/hormone (CRF/CRH) is a peptide hormone secreted by the hypothalamus in response to stress. It stimulates secretion of adrenocorticotropic hormone (ACTH) by the anterior pituitary and is a component of the hypothalamic-pituitary-adrenal (HPA) axis. CRF binds two different GPCR (CRF1 and CRF2 receptors) which are expressed in the hypothalamus and other brain regions [117]. An anxiogenic (and pro-depressive) role of CRF1 receptors was identified in animal studies, leading to the development of several CRF1 receptor antagonists [117,118]. However, clinical studies of CRF1 receptor antagonists have not shown promise in anxiety disorders [118]. To date, only one RCT has been published in GAD, which showed that the CRF1 receptor antagonist pexacerfont did not differentiate from placebo treatment after 8 weeks of treatment [119].
How do nuclear factor kappa B (NF-κB)1 and NF-κB2 defects lead to the incidence of clinical and immunological manifestations of inborn errors of immunity?
Published in Expert Review of Clinical Immunology, 2023
Nazanin Fathi, Hanieh Mojtahedi, Marzieh Nasiri, Hassan Abolhassani, Mahsa Yousefpour Marzbali, Marzie Esmaeili, Fereshte Salami, Furozan Biglari, Nima Rezaei
Patients with clinically affected by NF-κB2 deficiency principally presented manifestations of recurrent sinopulmonary infections, alopecia, and endocrinopathies such as central adrenal insufficiency. Most NF-κB2 defective patients experience severe disease and early-onset IEI symptoms comprise clinical features of T cell dysfunction, such as chronic viral or opportunistic infections. Patients frequently experience autoimmune symptoms that are mostly T-cell mediated, including alopecia, lymphocytic organ infiltration, arthritis, diarrhea, and autoimmune cytopenia. Therefore, lymphoproliferation or auto-antibodies were not usual clinical markers, in contrast to typical CVID. Adrenocorticotropic hormone (ACTH) deficiency, deficient anterior pituitary with variable immune deficiency (DAVID) syndrome, growth hormone deficiency, ectodermal dysplasia, ITP, otitis, and gastrointestinal complications are also reported in some cases [13–16].
What’s new on the front-line of gout pharmacotherapy?
Published in Expert Opinion on Pharmacotherapy, 2022
Kurt E. G. Blake, Jordan L. Saag, Kenneth G Saag
Adrenocorticotropic hormone (ACTH) is an endogenous compound that can be used for the treatment of acute gout. ACTH acts by releasing steroids from the adrenal glands and as a natural inhibitor to inflammatory responses [26]. Among 181 patients with an acute gout flare that were treated with ACTH as a front line agent, a response was seen in 78% [27]. A metanalysis of 30 RCTs found that the use of intramuscular ACTH has a quicker pain resolution compared to indomethacin (p < 0.0001) and had a high degree of safety and efficacy in general [28]. There have not been any new developments in the use of ACTH for gout, it is more costly than a number of other therapies, does not have regulatory approval for this indication, and ACR guidelines do not support its routine use in this setting [19].