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At least 145 records · Page 8Linked to original sources
PubMed1985

Concomitant suppression of plasma ACTH- and beta-endorphin-like immunoreactivity by cyproheptadine, naloxone, and somatostatin in the ectopic ACTH syndrome.

Release of plasma ACTH- and beta-endorphin (beta-EP)-like immunoreactivity (LI) was studied in vivo in a patient with an ectopic ACTH-producing malignant thymoma. Administration of lysin vasopressin stimulated concomitant release of plasma ACTH- and beta-EP-LI. Administration of cyproheptadine, naloxone, and somatostatin significantly suppressed plasma levels of ACTH- and beta-EP-LI, while saline infusion did not. Gel exclusion chromatography of the plasma extracts revealed that ACTH-LI consisted of two components, large and small molecular weight form, while beta-EP-LI consisted of three components, large molecular weight, beta-lipotropin-, and beta-EP-sized form; each of these components was incompletely suppressed by somatostatin infusion. It is suggested that certain tumors may have acquired aberrant multiple receptors during malignant transformation which may lead to the paradoxical hormone response as demonstrated in this case.

ACTH Syndrome, Ectopic↗
PubMed1994

ACTH-(11-24) antagonizes ACTH-(1-24)-induced behavioral syndrome.

The possible involvement of the ACTH-(11-24) fragment on the stretchings, yawnings and penile erections induced by the intracerebroventricular injection of ACTH-(1-24) in rats, was studied. The results indicate that this C-terminal fragment is devoid of any behavioral activity, but inhibits the behavioral syndrome induced by ACTH-(1-24). This suggests that the fragment-(11-24) of the ACTH molecule may contain or represent an address sequence for brain ACTH receptors and may be involved in the termination of the behavioral response to melanocortins.

Animals↗
PubMed1993

Seasonal changes in in vivo cortisol response to ACTH and in plasma and pituitary concentrations of ACTH in a desert rodent, the sand rat (Psammomys obesus).

1. During spring, decreased sensitivity of the adrenal cortex to adrenocorticotrophic hormone (ACTH) in the sand rat inhabiting the Béni-Abbès area (Algeria), results in a reduction in the production of cortisol. Thus the secretion of ACTH is enhanced, becoming maximal in June and presumably also during the following weeks. 2. Increase in ACTH secretion, together with a slightly increased adrenal sensitivity, is likely to stimulate corticosteroidogenesis throughout the summer. 3. In autumn, as levels of cortisol are high, the negative feedback increases leading to a reduction in ACTH production. 4. An increase in the adrenocortical sensitivity to ACTH allows a high production of cortisol until February.

Adrenal Glands↗
PubMed2005

Inherited ACTH insensitivity illuminates the mechanisms of ACTH action.

Adrenocorticotrophin (ACTH) insensitivity is a potentially lethal inherited disorder of ACTH signalling in the adrenal. Inactivating mutations of the ACTH receptor account for approximately 25% of these cases. A second genetic cause for this syndrome has recently been identified in the MRAP gene. The MRAP protein appears to function in the trafficking and cell surface expression of the ACTH receptor, and might indicate the existence of more widespread G-protein-coupled receptor trafficking mechanisms. Molecular defects underlying other causes of ACTH insensitivity syndromes will probably contribute further to our understanding of these pathways.

Adrenocorticotropic Hormone↗
PubMed1967

ACTH antibodies in patients receiving depot porcine ACTH to hasten recovery from pituitary-adrenal suppression.

Six patients who had experienced prolonged steroid-induced pituitary-adrenal suppression were treated with 100 U of depot procine ACTH every 2 to 4 days for several months. Such treatment did not hasten the recovery of normal pituitary-adrenal function compared with the rate of recovery of a group of similarly suppressed patients who received no depot ACTH. Eight of nine patients who received prolonged courses of depot porcine ACTH developed antibodies to ACTH that cross-reacted with endogenous ACTH, binding it in the circulation in inactive form and retarding its removal from the circulation. The presence of such antibodies did not in itself grossly alter pituitary-adrenal interrelationships.

17-Hydroxycorticosteroids↗
PubMed1982

Dynamics of adrenocorticotropin (ACTH) secretion in cyclic Cushing's syndrome: evidence for more than one abnormal ACTH biorhythm.

We have studied a 57-yr-old woman with cyclic Cushing's syndrome of apparent pituitary origin who had a predominant cycle of 2-6 days. The patient also demonstrated an abnormal circadian rhythm, with afternoon peaks of plasma ACTH and plasma cortisol. In addition to these abnormal biorhythms, Fourier analysis showed what appeared to be a separate 35-day cycle. After 35 days of consecutive urinary free cortisol measurement, the patient was given cyproheptadine. During therapy with this agent, the urinary free cortisol levels fell dramatically, but cyclic secretion continued, albeit with a diminished amplitude. During general anesthesia for a bilateral adrenalectomy, there was a striking increase in the plasma ACTH level, and the ACTH concentration remained high in both the immediate and late postoperative periods. These observations indicated that stress could overcome cyclic ACTH secretion and that cortisol exerted feedback suppression on ACTH secretion. Although this is the predictable response for classic pituitary-dependent Cushing's syndrome, it is of interest in cyclic Cushing's syndrome, since previous studies of this entity have implied that cortisol secretion is independent of stimulation or feedback.

Adrenalectomy↗
PubMed1984

The effect of intracerebroventricular infusions of CRF, sauvagine, ACTH (1-24) and ACTH (4-10) on blood pressure in sheep.

This study reviews the effects of intracerebroventricular (i.c.v.) infusion of corticotrophin releasing factor (CRF) and adrenocorticotrophic hormone (ACTH) (1-24) on blood pressure in conscious sheep. The effects of sauvagine, a peptide with 50% homology with CRF and ACTH (4-10) and other analogues of ACTH were studied. Intracerebroventricular infusion of CRF for 24 h at 10 and 100 micrograms/h increased blood pressure and heart rate. Sodium (Na) excretion also increased. Sauvagine at 10 micrograms/h also increased blood pressure. Both peptides raised body temperature and produced 'arousal' behaviour. ACTH (1-24) at 0.8 microgram/h for 48 h raised blood pressure and body temperature but had no significant effect on Na excretion or behavior. ACTH (4-10) and other related analogs (alpha-MSH, alpha gamma 1-MSH) at up to 10 micrograms/h for 48 h had no effects. These studies show that neuropeptides involved in the physiological response to 'stress' may have central effects on blood pressure.

Adrenocorticotropic Hormone↗
PubMedDate not supplied

[Lack of ACTH responsiveness in children and paroxysmal central nervous system manifestations. (Study of nine cases of isolated ACTH deficiency) (author's transl)].

Study of ACTH responsiveness to oral metyrapone and insulin hypoglycemia in children with repetitive nervous system manifestations (convulsions, coma, mental confusion apathy, tremor) has led to diagnosis of isolated ACTH deficiency in nine children within a three year period. Hypoglycemia was ascertained in five children; in four cases no hypoglycemia was proved, possibly because of promptly disappearance or because of other mechanisms accounting for clinical symptoms (occurrence of intracellular overhydratation associated with corticol deficiency is considered). The incidence of isolated ACTH deficiency in children is possibly undervalued. Reappraisal of isolated ACTH deficiency in childhood as to be considered in idiopathic spontaneous hypoglycemia and perhaps in some paroxysmal neurologic and/or digestive manifestations without proved hypoglycemia and so far poorly defined or held for epileptic fits. In order to disclose further additional tropic hormone deficiencies, and to differentiate permanent from transient impairment of ACTH responsiveness which often seems to be related to emotional deprivation syndrome, more protracted follow up studies are needed.

Adolescent↗
PubMed1993

[Value of basal cortisol and ACTH in the immediate postoperative period of hypophyseal surgery in non-ACTH secretory adenomas].

BACKGROUND: The aim of this study was to evaluate the usefulness of basal cortisol and ACTH in the immediate postoperative period of pituitary surgery as indicators of definitive adrenocorticotropin function. METHODS: Twenty-one patients with pituitary, non producers of ACTH, adenomas, three microadenomas and 18 macroadenomas treated by adenomectomy by a trans-sphenoidal route were respectively studied. The basal cortisol and ACTH were compared in the first week following surgery with the definitive results obtained after one month by dynamic tests (stimulation with ACTH or insulin hypoglycemia). RESULTS: The six patients with secondary adrenal failure (AF) in the definitive evaluation had lower basal cortisol in the immediate postoperative period than the patients with AF (135.3 +/- 225.3 nmol/l versus 473.6 +/- 147.2 nmol/l; p < 0.05). The values of ACTH were also lower (2.3 +/- 1.6 nmol/l versus 4.8 +/- 3.4; p < 0.05). In all the patients with definitive AF except one, the basal cortisol in the first week was lower than 130 nmol/l and in those who did not present AF it was greater than 220 nmol/l. CONCLUSIONS: In the immediate postoperative period after pituitary surgery cortisol is a good indicator of definitive adrenocorticotropin function. This parameter may identify the patients requiring posterior substitutive treatment.

Adenoma↗
PubMed1999

Marked increase in plasma ACTH with tumor reduction after chemotherapy in ectopic ACTH syndrome.

We report on a case of rapid and marked hormone release as a result of rapid tumor reduction due to chemotherapy in a 36-year-old woman with ectopic ACTH syndrome due to small cell lung cancer. Treatment of the cancer with cisplatin and etoposide resulted in an 80% reduction in tumor size on computed tomographic scan within two weeks. Concurrently, plasma ACTH exhibited an unexpected and astonishing increase from 373 pg/ml before treatment to more than 1200 pg/ml. There were no biochemical characteristics observed in tumor lysis syndrome of solid tumors such as azotemia, increased LDH and hyperkalemia. The present case indicates that anticancer chemotherapy instituted in patients with ectopic ACTH syndrome could result in an acute increase of plasma ACTH and exacerbation of hypercortisolism, similar to tumor lysis syndrome, which is a potentially fatal complication following anti-cancer chemotherapy.

ACTH Syndrome, Ectopic↗
PubMed1985

In vivo and in vitro ACTH response to ovine corticotropin-releasing factor in a bronchial carcinoid from a patient with ectopic ACTH syndrome.

ACTH response in vivo and in vitro to synthetic ovine corticotropin-releasing factor (o-CRF) was examined in a bronchial carcinoid from a patient with ectopic ACTH syndrome. o-CRF, 1 microgram/kg iv bolus, scarcely increased plasma ACTH or cortisol on one occasion, but they showed a low response on retesting. On the other hand, 10(-8) and 10(-7) M of o-CRF significantly stimulated ACTH release in cultured bronchial carcinoid cells.

ACTH Syndrome, Ectopic↗
PubMed1998

Genetic heterogeneity of adrenocorticotropin (ACTH) resistance syndromes: identification of a novel mutation of the ACTH receptor gene in hereditary glucocorticoid deficiency.

Hereditary primary adrenal insufficiency syndromes due to ACTH resistance include hereditary glucocorticoid deficiency (HGD) and Allgrove's syndrome (AS). Patients with both conditions present in childhood with failure to thrive, weakness, and fatigue or adrenal crisis; patients with AS in addition have alacrima and achalasia (triple A syndrome). We studied four kindreds with HGD and four kindreds with AS for abnormalities of the ACTH receptor (ACTHR) gene. The ACTHR coding sequence in all AS kindreds and two HGD kindreds was normal. Analysis of the ACTHR gene of the proband in one of the HGD kindreds showed him to be homozygous for the previously described G221T transition causing a Ser74Ile substitution of the protein, which has been shown to inactivate the ACTHR in signal transduction. The proband in another HGD kindred was found to be a compound heterozygote with the G221T transition in one allele and a novel C818A transition in the other allele of ACTHR. The C818A transition caused the substitution of the highly conserved Pro273 by His in the receptor protein. In vitro expression of the mutated ACTHR in mouse melanoma M3 cells showed that at a medium ACTH concentration of 3 nM, cells transfected with the wild-type ACTHR produced twofold and threefold, respectively, of the amount of intracellular cAMP when compared to cells transfected with the ACTHR carrying the Pro273His and the Ser74Ile mutation, respectively, confirming that HGD in this kindred is caused by loss-of-function mutations of the ACTHR. These results showed that the genetic cause of the ACTH-resistant syndromes is heterogeneous.

Adrenal Insufficiency↗
PubMed1984

Lack of ACTH lowering effect of sodium valproate in patients with ACTH hypersecretion.

The effect of an oral dose of 200 or 400 mg sodium valproate (DPA) on ACTH and cortisol secretion was assessed in 11 patients with Cushing's disease (3 bilaterally adrenalectomized), 3 patients with Nelson's syndrome and 6 patients with Addison's disease. In none of the patients examined DPA induced changes in ACTH (and cortisol) levels appreciably different from the fluctuations recorded after placebo administration. The effect of a long term administration of sodium valproate (600-1000 mg/day) was evaluated in 2 patients with active Cushing's disease and in 1 patient with Nelson's syndrome (3 weeks, 3, 9 months respectively); in the 2 patients with Cushing's disease ACTH and cortisol secretion, 17-hydroxy-corticosteroids (17-OHCS) urinary excretion did not change during DPA treatment. Similarly the cortisol response to hypoglycemia and the 17-OHCS urinary excretion after dexamethasone were not normalized. Long term DPA administration did not induce either clinical or hormonal modifications in the patient with Nelson's syndrome. These findings do not support the possibility that a deficiency of a GABAergic system plays a role in the pathogenesis of ACTH hypersecretion. DPA does not seem to be of therapeutical value in the medical management of Cushing's disease and Nelson's syndrome.

Addison Disease↗
PubMed1982

VIP stimulates ACTH release and adenylate cyclase in human ACTH-secreting pituitary adenomas.

The effect of vasoactive intestinal polypeptide (VIP) on in vitro ACTH release and adenylate cyclase activity was investigated in human ACTH-secreting pituitary adenomas from 4 patients with Cushing's disease and 2 patients with Nelson's syndrome. In all the tumors tested, VIP elicited a dose-dependent stimulation of hormone release from adenoma fragments (90-247% at 10-7 M VIP) and of cAMP formation in membrane preparations (75-140% at 3 X 10-6 M VIP). Therefore a role of VIP in the control of ACTH secretion in human ACTH-secreting adenomas is suggested; a cAMP-dependent mechanism of action can also be hypothesized.

Adenoma↗
PubMed2000

Effect of ACTH on renal excretion of purine bases in a patient with isolated ACTH deficiency.

We investigated the renal transport of purine bases (uric acid, hypoxanthine and xanthine) after rapid and continuous ACTH loading tests in a patient with isolated ACTH deficiency, a rare cause of secondary adrenocortical insufficiency. Plasma uric acid concentration and the urinary ratio of uric acid/creatinine did not change in the rapid ACTH test, which did not increase plasma cortisol concentration. In the continuous ACTH loading test, the plasma concentration of uric acid and oxypurines (hypoxanthine and xanthine) decreased, and the urinary excretion and fractional clearance of them increased as well as the plasma concentrations and urinary excretion of cortisol. These findings suggest that glucocorticoid directly affects the common renal transport pathway for uric acid, hypoxanthine, and xanthine.

Adrenal Cortex↗
PubMed1997

A suppressive effect of dexamethasone (DEX) on adrenocorticotropin (ACTH) response to vasoactive intestinal peptide (VIP) in Cushing's disease: a parallel modulation by DEX of ACTH responses to VIP and corticotropin-releasing hormone.

We have previously reported and confirmed that vasoactive intestinal peptide (VIP) is a significant stimulator of ACTH and cortisol secretion in at least some patients with Cushing's disease. We have also found that the hormonal responses to corticotropin-releasing hormone (CRH) in VIP-responsive patients with Cushing's disease were higher than those in VIP non-responders, which suggested a linkage between the actions of CRH and VIP in this disorder. Therefore, in the present study we examined whether this linkage also exists after glucocorticoid treatment by testing the effect of dexamethasone (DEX) pretreatment (1.0 mg, intravenous bolus, 60 min before) on ACTH and cortisol responses to CRH (100 microg, i.v. bolus) and VIP (100 microg, i.v. bolus) in 7 patients with Cushing's disease who were responsive to both neuropeptides while under no DEX pretreatment. The results were that in 5 patients, DEX was able to significantly suppress the ACTH and cortisol responses to both CRH and VIP, and in the remaining 2 patients, DEX did not significantly affect the action of either CRH or VIP. This study is the first to demonstrate the parallel inhibition by DEX of ACTH and cortisol responses to CRH and VIP in Cushing's disease. Although the possibility cannot be excluded that VIP may act on CRH receptors in corticotropinomas as a partial agonist, it seems more likely that specific receptors for CRH and VIP, respectively, may concurrently express in substantial quantity in those corticotropinomas that are responsive to both neuropeptides.

Adrenocorticotropic Hormone↗
PubMed1985

Similarity between the corticotropin (ACTH) receptor and a peptide encoded by an RNA that is complementary to ACTH mRNA.

An interesting pattern in the genetic code was recently observed: Codons for hydrophilic and hydrophobic amino acids on one strand of nucleic acid are complemented by codons for hydrophobic and hydrophilic amino acids on the other strand, respectively. The average tendency of codons for "uncharged" (slightly hydrophilic) amino acids is to be complemented by codons for "uncharged" (slightly hydrophilic) amino acids. We have postulated that this pattern can result in the binding of peptides that are encoded by complementary RNA strands and we have presented supporting evidence. In this report we demonstrate the specific and high-affinity binding of naturally occurring peptides [corticotropin (ACTH) and gamma-endorphin] to synthetically derived counterparts that were specified by RNA sequences complementary to the mRNA for ACTH and gamma-endorphin, respectively. That this binding might result from one peptide being an "internal image" of the other was strongly suggested by the observation that antibody to the peptide that was encoded by the complementary RNA for ACTH recognized the adrenal cell ACTH receptor. Based on these findings, a theory on the evolution of peptides and their receptors is suggested.

Adrenocorticotropic Hormone↗
PubMed1998

ACTH therapy for infantile spasms: a combination therapy with high-dose pyridoxal phosphate and low-dose ACTH.

Combination therapy consisting of high-dose pyridoxal phosphate (40-50 mg/kg/day) and low-dose synthetic ACTH (0.01 mg/kg/day) was prescribed in 28 children with infantile spasms. Monotherapy with pyridoxal phosphate provided excellent seizure control in 3 of the 28 (11%) patients. ACTH was subsequently added to the regimen of the remaining 25 patients. As of 1 month after discontinuing the ACTH treatment, 21 of the 25 (84%) patients had experienced no seizures. The mean interval until seizure control was achieved was 4.1 days after the start of treatment with ACTH. The 21 patients have been monitored for a mean of 34.9 months (range 2-81 months); 6 patients (29%) have had recurrences of infantile spasms, and 10 (48%) have experienced normal development. Fourteen of the 28 patients (50%) have had transient increases in liver enzymes, but none of the patients developed more serious side effects.

Age of Onset↗