Erschienen in:
01.11.2015 | Editorial
Assessment of the HPA Axis: Another New Test?
verfasst von:
Ashley Grossman
Erschienen in:
Endocrine
|
Ausgabe 2/2015
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Excerpt
As the pituitary fails, each axis appears to show defects and then ultimately fails in a generally predictable order, with a sense that the least important hormones decrease first with the most critical hormonal axes only being lost when pituitary damage is at a maximum. There are exceptions, as in lymphocytic hypophysitis, but this is the exception which proves the rule. Thus, it is uncommon for pituitary disease to cause failure of the hypothalamo–pituitary–adrenal (HPA) axis, but when it does fail, it can be catastrophic. Pituitary ACTH, under the joint control of hypothalamic CRH and vasopressin, causes the release of adrenal corticosteroids, specifically and most critically corticosterone in rodents and cortisol in the human, while mineralocorticoids such as aldosterone are principally regulated by the renin–angiotensin system. Cortisol in humans is secreted in a circadian rhythm with maximum circulating levels at 7–9 a.m. and a nadir around midnight. However, most importantly, cortisol is a stress hormone which is stimulated by severe cardiovascular, infectious, and—to some extent—psychological stress. An absent or poor glucocorticoid response to stress causes cardiovascular collapse and may be lethal. Thus, any form of severe pituitary damage, most usually pituitary tumors but including hypothalamic disease, radiotherapy, and surgical intervention, may cause a failure of HPA responsiveness to severe stress (such as trauma, severe infection, or surgery) leading to cardiovascular collapse and death: hence, assessment of the HPA axis is crucial in monitoring patients with disorders of the pituitary and hypothalamus, and judging adequate replacement regimes [
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