Adrenocortical Disease
T.M. Craft, P.M. Upton in Key Topics In Anaesthesia, 2021
The adrenal cortex produces glucocorticoid, mineralocorticoid and sex hormones (mainly testosterone). Cortisol, the principal glucocorticoid, modulates stress and inflammatory responses. It is a potent stimulator of gluconeogenesis and antagonizes insulin. Aldosterone is the principal mineralocorticoid. It causes increased sodium reabsorption, and potassium and hydrogen ion loss at the distal renal tubule. Adrenal androgen production increases markedly at puberty, declining with age thereafter. Androstenedione is converted by the liver to testosterone in the male and oestrogen in the female. Cortisol and androgen production are under diurnal pituitary control (adrenocorticotrophic hormone — ACTH). Aldosterone is released in response to angiotensin II, produced following renal renin release and subsequent pulmonary angiotensin I conversion.
Radionuclide scanning in the diagnosis and treatment of endocrine disorders
Philip E. Harris, Pierre-Marc G. Bouloux in Endocrinology in Clinical Practice, 2014
The adrenal cortex produces glucocorticoids, mineralo-corticoids, and small amounts of sex hormones. Benign tumors of the cortex are called adrenal cortical adenomas, whereas malignant tumors are called adrenal cortical carcinomas. All the aforementioned steroid hormones are synthesized from cholesterol. At present, two cholesterol analogs are used for imaging of the adrenal cortex: 131I-6ß-iodomethyl-19-norcholestrol (NP59) and 75Se-6ß-selenomethyl-19-norcholesterol.45 Overall, scintigraphy achieves a high sensitivity (71%–100%) with varying specificity (50%–100%) for the differentiation of malignant from benign adrenal masses.45 The disadvantage of these tracers is the high radiation dose to the adrenals. Currently, the clinical indications for adrenal cortex scintigraphy are very limited because of the development of CT, MRI, and highly sensitive biochemical assays.
Our strained relations with environmental agents
Richard Lawson, Jonathon Porritt in Bills of Health, 2018
The physiological purpose of stress or anxiety, as every schoolchild knows, is to prepare us for ‘fight or flight’. Adrenaline and noradrenaline are released by the adrenal medulla as a short-term response, and the steroid cortisol released from the adrenal cortex controls longer term reactions. In nature, the energy generated by adrenaline is dissipated in physical activity. Modern life, although stressful, does not offer much scope for physical activity. It is thought that the effects of the stress hormones are therefore expressed in increased muscle tension, increased blood pressure and emotional irritability. There is also an effect on the immune system. There is an intimate connection between the nervous system and the immune system. The autonomic nervous system, which controls the internal organs, including heart and blood vessels, also innervates the spleen and bone marrow, tissues that are home to the immune system. Some of the T-lymphocytes are derived from the ‘neural crest’, the same embryonic tissues that give rise to the brain and nervous system. These T-lymphocyte cells have neurotransmitter receptors just like nerve cells, and produce peptides called cytokines (production of which can be influenced by cortisol from the adrenal gland). These cells can be seen as the conscious controllers of our body's defences, the interface between mind and body. It is now understandable how periods of mental stress can result in physical illness.
Adrenocortical carcinoma arising from the colonic mesentery
Published in Baylor University Medical Center Proceedings, 2022
Samuel Z. See, Sinan Ali Bana, Nuvaira Ather, Amy Haberman
Primary ACC is a malignant tumor arising from the adrenal gland, specifically the adrenal cortex. The two primary components of the adrenal gland, the adrenal cortex and adrenal medulla, are formed by separate embryologic origins. The cortex is derived from the urogenital ridge and celomic epithelium, while the medulla is derived from neural crest cells.2,3 The urogenital ridge is a structure within the embryologic mesoderm that also gives rise to the gonads, kidneys, and reproductive tract while the celomic epithelium produces the lining of the abdominal organs and surface of the body wall.3,4 This embryologic phenomenon is thought to explain the observation of ectopic adrenocortical tissue. However, these cases are rarely observed in adults because ectopic adrenal tissue typically atrophies during infancy.4 Reported sites of ectopy include the testes, ovaries, kidneys, bowel, pancreas, liver, lungs, and mesentery.1 To our knowledge, fewer than five cases of ectopic ACCs have been reported to arise from the mesentery, which was the case in our patient.5–7
A patent review of anticancer glucocorticoid receptor modulators (2014-present)
Published in Expert Opinion on Therapeutic Patents, 2020
Marianna Lucafò, Martina Franzin, Giuliana Decorti, Gabriele Stocco
Cortisol is the main natural steroid hormone in humans, and is produced, starting from its precursor, cholesterol, by the zona fasciculata of the adrenal cortex, under the control of the hypothalamic-pituitary-adrenal axis. Under basal conditions, secretion follows a circadian rhythm, with peak levels in the morning that correspond to the active period in humans; in addition, the activity of the hypothalamic-pituitary-adrenal axis, and hence cortisol secretion, is increased upon stress [17]. A number of synthetic glucocorticoids have been developed (Figure 1), with optimized characteristics in terms of pharmacokinetics, of selectivity for binding to the glucocorticoid in comparison to the mineralocorticoid receptor and with higher potency [18,19]. Natural and synthetic glucocorticoids have a number of important physiological effects, such as regulation of metabolic homeostasis [20], maintenance of fluid and electrolyte balance [21], control of the immune response [22], growth and bone mineralization [23], cardiovascular function [24], reproduction and development [25]. In addition, these hormones are essential to allow the body to respond to stressful situations such as infections and traumas [26]. The use of glucocorticoids in the clinics is however burdened with numerous side effects, that can be extremely serious, such as osteoporosis, metabolic complications, and many others, that are often dose-dependent and related to the duration of therapy [27].
Drug design strategies for Cushing’s syndrome
Published in Expert Opinion on Drug Discovery, 2019
S. A. Usanov, A. V. Kliuchenovich, N. V. Strushkevich
Cushing’s syndrome (CS) denotes a set of clinical signs that evolve due to pathological exposure to cortisol as a consequence of its endogenous overproduction or corticosteroid treatment. ACTH-dependent endogenous cortisol excess due to a pituitary adenoma is called Cushing disease and account for ~70% of cases [1]. The disease was first described by Harvey Cushing in 1932 [2] and the treatment is still challenging for endocrinologists worldwide due to diverse etiologies, leading to hypercortisolism. ACTH-independent autonomous adrenal overproduction of cortisol caused by an adrenal cancer or by an adrenal adenoma leads to CS. Cortisol is a steroid hormone of the glucocorticoid class produced by the adrenal cortex. It is released in response to stress and low blood-glucose concentration and regulates metabolism and immune response. As a result, CS is associated with hypertension, weight gain, truncal adiposity, impaired glucose tolerance or diabetes, insomnia, cognitive impairment, mood changes ranging from anxiety and depression to psychosis, infections, and fractures [3,4]. Uncontrolled CS and severe hypercortisolism could lead to life-threating conditions, including mortality mainly due to cardiovascular disease [5,6].
Related Knowledge Centers
- Aldosterone Synthase
- Blood Pressure
- Mineralocorticoid
- Zona Fasciculata
- Zona Glomerulosa
- Zona Reticularis
- Androgen
- Adrenal Gland
- Aldosterone
- Renin–Angiotensin System