Adrenocorticotropic hormone therapy

Chiyonobu T, Nakata S, Komori S, Katoh N, Ikegaya H, Nishimttra A, et al. Fatal varicella with multi-organ failure associated with low-dose adrenocorticotropic hormone therapy. Pediatr Int 2012 54(2) 305-6. 

Pharmacotherapy generally is reserved for patients (1) in whom the ectopic adrenocorticotropic hormone-secreting tumor cannot be localized (2) who are not surgical candidates (3) who have failed surgery (4) who have had a relapse after surgery or (5) in whom adjunctive therapy is required to achieve complete remission. 

Adrenocorticotropic hormone (ACTH) gel, 40 to 80 USP units, may be given intramuscularly every 6 to 8 hours for 2 to 3 days and then discontinued. Studies with ACTH are limited, and it should be reserved for patients with contraindications to first-line therapies (e.g., heart failure, chronic renal failure, history of GI bleeding). 

Whereas idiopathic OM often resolves, spontaneously or after administration of intravenous immunoglobuline or corticosteroids [58], the outcome of paraneoplastic OM is more variable and depends on the tumor response to therapy. Children with paraneoplastic OM frequently respond to chemotherapy, adrenocorticotropic hormone, or immunomodulation [223], The response to immune therapy in adults with paraneoplastic OM is very modest, but prompt tumor therapy, immunomodulation, and depletion of IgG may be of some benefit [62, 224], Without antineoplastic therapy, the prognosis is usually poor, and symptoms often progress, ultimately causing death [62],... 

One of the side effects of adrenocorticotropic hormone (ACTH) and corticoid therapy in humans is the development or reactivation of gastroduodenal ulcers. Daily subcutaneous administration of cortisol or A -cortisol to rats for 4 days results in the regular development of gastric ulcers (38). This procedure has been adapted to testing antiulcer activity (39). There are certain differences between steroid ulcers and "natural" ulcers in localization, rate of development, and severity (40). 

ACTH adrenocorticotropic hormone ADT alternate-day therapy APA aldosterone-producing adenoma BAH bilateraladrenalhyperplasia CBG corticosteroid-binding globuhn CRH corticotropin-releasing hormone CT computed tomography... 

Corticosteroids may be used to treat acute attacks of gouty arthritis, but they are reserved primarily for resistant cases or for patients with a contraindication to colchicine and NSAID therapy. Doses of 40 to 80 USP units of adrenocorticotropic hormone gel are given intramuscularly every 6 to 8 hours for 2 to 3 days, and then the doses are reduced in stepwise fashion and discontinued. Intra-articular administration of triamcinolone hexacetonide in a dose of 20 to 40 mg may be useful in treating acute gout limited to one or two joints. Prednisone may be administered orally in doses of 30 to 60 mg for 3 to 5 days in patients with multiple-joint involvement. Because rebound attacks may occur on steroid withdrawal, the dose should be tapered gradually by 5-mg decreases over 10 to 14 days and discontinued. 

An interesting clinical complication in the use of AG is that the decreased levels of cortisol cause increased secretion of adrenocorticotropic hormone (ACTH) by feedback stimulation of the pituitary gland, which will overcome the steroid synthesis inhibition of AG. This tendency must be overcome by coadministration of hydrocortisone. In spite of considerable clinical literature on the usefulness of AG in the treatment of advanced breast cancer and adrenocortical carcinoma, the only approved indication for AG in the United States (1990) is therapy for Cushing s syndrome. 

When administered in high doses or for prolonged therapy, hydrocortisone suppresses release of adrenocorticotropic hormone (ACTH) from the pituitary gland, and the adrenal cortex stops secreting endogenous corticosteroids. Because hydrocortisone suppresses immune response, patients should not be given live virus vaccines. 

Melatonin occurs in the pineal gland and is the biochemical clock in the brain (Bartsch 1994). Various forms of mental illness may respond to melatonin therapy Maurizi 1984) (Brown 1995). Melatonin blocks the actions of melanocyte-stimulating and adrenocorticotropic hormones (Axelrod). There are several synthetic methods used to produce melatonin (Szmuszkovicz 1959), Metabolism of melatonin see (Kopin 1961) (Kveder 1961). 

Sodium Excess. Most of the sodium ingested is excessive, and for the most part it is excreted by the kidneys in combination with bicarbonate or phosphate. However, under some circumstances sodium accumulates in the extracellular fluid and causes edema since the retention of sodium is accompanied by water retention. Such conditions include (1) cardiac or renal failure, (2) adrenal tumors which secrete excessive cortical hormones, and (3) adrenocorticotropic hormone (ACTH) or steroid hormone therapy. In these conditions, individuals benefit from sodium-restricted diets. 

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