Corticotropin [Neurosurgery Wiki]

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====== Corticotropin ======

AKA: [[Adrenocorticotropic hormone]] ([[ACTH]])
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A 39 amino acid trophic hormone synthesized from POMC. The first 13 amino acids at the amino-terminal of ACTH are identical to α-MSH. The active half-life is ≈ 10 minutes. Produces a diurnal peak in [[cortisol]] (the highest peak occurs in the early morning, with a second, lesser peak in the late afternoon) and also increases in response to [[stress]].
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The release of [[cortisol]] by the adrenal glands is stimulated by the adrenocorticotrophic hormone (ACTH) from the [[pituitary]] which in turn is stimulated by [[corticotropin-releasing hormone]] (CRH) from the [[hypothalamus]].
 
Adrenocorticotropic [[hormone]] stimulates the [[adrenal gland]]s to secrete [[steroid]] hormones, principally [[cortisol]].

It is a [[polypeptide]] tropic [[hormone]] produced and secreted by the anterior [[pituitary gland]]. It is an important component of the [[hypothalamic pituitary adrenal axis]] and is often produced in response to biological stress (along with its precursor [[corticotropin-releasing hormone]] from the [[hypothalamus]]). Its principal effects are increased production and release of [[corticosteroid]]s. 
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In secondary [[adrenal insufficiency]] caused by deficient corticotropin (ACTH) release by the pituitary, [[mineralocorticoid]] secretion is usually normal and only [[glucocorticoid]]s need to be replaced.
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[[Cushing’s disease]]

[[Nelson syndrome]] 

Primary adrenal insufficiency, also called [[Addison's disease]], occurs when adrenal gland production of [[cortisol]] is chronically deficient, resulting in chronically elevated [[ACTH]] levels.

When a [[pituitary tumor]] is the cause of elevated ACTH (from the anterior pituitary) this is known as [[Cushing's Disease]] and the constellation of signs and symptoms of the excess cortisol (hypercortisolism) is known as [[Cushing's syndrome]]. A deficiency of ACTH is a cause of secondary adrenal insufficiency. ACTH is also related to the circadian rhythm in many organisms.

[[Pituitary corticotroph adenoma]]s secrete inappropriate amounts of ACTH, which results in disorderly and excessive production of cortisol by the adrenal gland
((Aron DC, Findling JW, Tyrrell JB: Cushing's disease. Endocrinol Metab Clin North Am 16:705–730, 1987)).
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Abellán-Galiana et al. propose an ACTH value <15 pg/mL as a good long-term prognostic marker in the postoperative period of [[Cushing's Disease]]. Reaching the ACTH nadir in less time is associated to a lesser recurrence rate
((Abellán-Galiana P, Fajardo C, Riesgo-Suárez P, Pérez-Bermejo M, Ríos-Pérez C, 
Gómez-Vela J. Prognostic usefulness of ACTH in the postoperative period of
Cushing's disease. Endocr Connect. 2019 Aug 1. pii: EC-19-0297.R1. doi:
10.1530/EC-19-0297. [Epub ahead of print] PubMed PMID: 31394502.
)).

===== Adrenocorticotropic hormone deficiency =====
[[Adrenocorticotropic hormone deficiency]].

===== Assessment of postoperative ACTH (corticotropin) reserve =====

Simple assessment protocol for patients who go home on [[hydrocortisone]] and were not on it pre-op.

● taper hydrocortisone over 2–3 weeks down to 20 mg PO q AM and 10 mg q 4 PM (a little higher
than maintenance to provide for some stress coverage) for several days

● then hold the PM dose and check an 8 AM serum cortisol the next day

● to avoid adrenal insufficiency in patients with incompetent reserve: as soon as the blood is drawn
have the patient take their morning cortisol dose and resume regular dosing until the test results
are available

● if this 8 AM cortisol shows any significant adrenal function, then taper the patient off
[[hydrocortisone]].

===== Posttraumatic hypopituitarism =====
see [[Posttraumatic hypopituitarism]]