ACTH 1-39 25mg
ACTH 1-39 25mg Peptide
Product Name: ACTH (1-39),
Size: 10mg. Molecular Formula: C207H308N56O58S1
Molecular Weight: 4541.1
Sequence (One-Letter Code): SYSMEHFRWGKPVGKKRRPVKVYPNGAEDESAEAFPLEF
Sequence (Three-Letter Code): H-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-Gly-Lys-Lys-Arg-Arg-Pro-Val-Lys-Val-Tyr-Pro-Asn-Gly-Ala-Glu-Asp-Glu-Ser-Ala-Glu-Ala-Phe-Pro-Leu-Glu-Phe-OH
Adrenocorticotropic hormone, commonly referred to as ACTH and also known as corticotropin, is a polypeptide hormone produced in and secreted by the anterior pituitary gland. It is a key component in the hypothalamic-pituitary-adrenal axis, often produced in response to exogenous biological stress along with corticotropin-releasing hormone (which is also from the hypothalamus.) Its effects include increased production and release of corticosteroids and, as its name suggests, cortisol from the adrenal cortex.
ACTH acts through the stimulation of cell surface ACTH receptors, which are located primarily on adrenocortical cells of the adrenal cortex. This results in the synthesis and secretion of gluco- and mineralo-corticosteroids and androgenic steroids. The ACTH receptor is a seven-membrane-spanning G protein-coupled receptor. Upon ligand binding, the receptor undergoes conformation changes that stimulate the enzyme adenylyl cyclase, which leads to an increase in intracellular cAMP and subsequent activation of protein kinase A. This ultimately results in stimulation of steroidogenesis. Steroidogenesis. Steroidogenesis is the biological process by which steroids are generated from cholesterol and transformed into other steroids. The pathways of steroidogenesis differ between different species, but the pathways of human steroidogenesis are shown in the figure. Products of steroidogenesis include: androgens testosterone estrogens and progesterone corticoids cortisol aldosterone ACTH acts at several key steps to influence the steroidogenic pathway in the adrenal cortex: ACTH stimulates lipoprotein uptake into cortical cells. This increases the bio-availability of cholesterol in the cells of the adrenal cortex. ACTH increases the transport of cholesterol into the mitochondria and activates its hydrolysis. ACTH Stimulates cholesterol side-chain cleavage enzyme, which makes the rate-limiting step in steroidogenesis. This results in the production of pregnenolone.
ACTH deficiency is implicated in GHD (growth hormone deficiency) as part of a branch of a larger umbrella disorder referred to as hypothalamic pituitary axis disorder.
ACTH deficiency state can result from ACTH underproduction or tissue resistance; decreased production may be due to intrinsic pituitary disease (secondary) or may result from deficiency of CRH because of a hypothalamic disorder (tertiary). ACTH deficiency can be congenital or acquired, familial or sporadic, and partial or complete. It may occur as an isolated deficiency or as a part of a more global hypopituitarism.
Tseng et al highlight the complex nature of ACTH deficiency as part of a larger physiological issue:
SIADH-like hyponatremia as the presenting manifestation of ACTH deficiency is rare in childhood. Here we report a 14 year-old girl who, after 8 years of GH replacement and subsequent treatment for subclinical secondary hypothyroidism, presented with confusion and disorientation due to severe hyponatremia. When her pituitary axis was re-assessed, she was diagnosed as having ACTH deficiency associated with multiple pituitary hormone deficiencies (MPHD) (including GH, FSH, LH, and subclinical TSH deficiencies). She responded poorly to treatment with only hypertonic fluid, but improved after addition of hydrocortisone replacement. The purpose of this paper is to emphasize the importance of suspecting ACTH insufficiency in children with GH deficiency if hyponatremia develops.
ACTH deficiency is a concern when clinicians surgically treat Cushing’s syndrome, so much so that many now administer exogenous glucocorticoids pre-, peri-, and post-surgery: “The concern for ACTH deficiency has led many centers to advocate the use glucocorticoids before, during and after surgery.”
Alexandraki et al discuss ACTH-dependent Cushing’s syndrome, which accounts for roughly 20% of all cases of CS:
Ectopic Cushing’s syndrome usually relates to the ectopic ACTH syndrome (EAS) and represents approximately 20% of ACTH-dependent and approximately 10% of all types of Cushing’s syndrome (CS). Nearly any neuroendocrine or non-endocrine tumours may be associated with EAS, but the more prevalent tumours are bronchial carcinoids, small cell lung carcinomas, pancreatic carcinoids, thymic carcinoids, medullary carcinomas of the thyroid, and phaeochromocytomas. Occult tumours are highly represented in all the series (12-38%) and constitute the more challenging cases of EAS, requiring long term follow-up. The lack of any completely reliable diagnostic test procedure and imaging to clearly reveal the source of EAS suggests that we should adopt a step-by-step multidisciplinary approach for their diagnosis and therapeutic management. Clinical features are often similar in ACTH-dependent CS, but the rapid onset and progress may suggest an ectopic source. A combination of biochemical tests and imaging studies seems the most appropriate approach for the prompt identification of EAS, even if there are several pitfalls to be avoided along the way.
Positive administration of ACTH may be useful in treating osteonecrosis, or at least osteonecrosis caused by administration of glucocorticoids:
We report that adrenocorticotropic hormone (ACTH) protects against osteonecrosis of the femoral head induced by depot methylprednisolone acetate (depomedrol). This therapeutic response likely arises from enhanced osteoblastic support and the stimulation of VEGF by ACTH; the latter is largely responsible for maintaining the fine vascular network that surrounds highly remodeling bone. We suggest examining the efficacy of ACTH in preventing human osteonecrosis, a devastating complication of glucocorticoid therapy.
ACTH is sometimes indicated as part of an emergency treatment for sepsis, although:
Surviving Sepsis Campaign guidelines suggest that corticosteroid therapy should be considered for adult septic shock when hypotension responds poorly to adequate fluid resuscitation and vasopressors, regardless of any results of diagnostic tests. However, steroid treatment may be associated with an increase risk of infection…. Baseline cortisol level < or = 35 microg/dl is a useful diagnostic threshold for diagnosis of steroid responsiveness in Thai patients with septic shock and ACTH stimulation test should not be used.
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