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PubMed2002

[Cushing's disease and corticotroph adenoma: anterior pituitary function before and after trans-sphenoidal microsurgery].

BACKGROUND AND PURPOSE: Cushing's disease is characterized by an overproduction of ACTH inducing an hypersecretion of corticosteroids. We assessed the non-corticotrophic pituitary functions before and after microsurgical resection of the corticotrophic adenoma. METHODS: We reviewed retrospectively a series of 98 patients (19 males, 79 females) undergoing transsphenoidal surgery between 1974 and 2001. Prolactin levels, somatrotrophic, gonadotrophic and thyroidotrophic functions were assessed and compared before and after resection of the adenoma. RESULTS: Before surgery, we observed an elevation of prolactin and a reduction of the GH, TSH, LH and FSH levels. These modifications were not linked to the volume of the adenoma but depended on the systemic effect of the hypercorticism or on local paracrine mechanisms. Selective adenomectomy usually restored altered corticotrophic and also, unlike (partial or total) hypophysectomy, the non-corticotrophic functions. CONCLUSIONS: Non-corticotrophic functions are often altered in Cushing's disease but can be restored after selective adenomectomy.

Adenoma↗

PubMed1992

Cortisol inactivation overload: a mechanism of mineralocorticoid hypertension in the ectopic adrenocorticotropin syndrome.

The more severe mineralocorticoid manifestations in the ectopic ACTH syndrome compared to pituitary Cushing's disease have been attributed to hypersecretion of 11-deoxycorticosterone. Another difference between the two forms of ACTH-excess, however, is a more severe degree of hypercortisolism in the ectopic syndrome. Cortisol can become a potent mineralocorticoid if its peripheral metabolism is interfered with as occurs in the syndrome of apparent mineralocorticoid excess. This mechanism also occurs in an experimental model of the apparent mineralocorticoid excess syndrome induced by licorice derivatives. We have tested the hypothesis that cortisol is a major mineralocorticoid in the ectopic ACTH syndrome because of two factors, marked hypersecretion and incomplete peripheral metabolism of cortisol as a result of an overload of metabolizing enzymes. Two measures of the peripheral metabolism of cortisol were found to be markedly decreased in two patients with the ectopic ACTH syndrome. The cortisol turnover quotients were 17.2 and 19.6 (normal = 215 +/- 98) and the ring A reduction constants were 11.8 and 13.8 (normal = 101 +/- 23). These values were comparable to that found in the syndrome of apparent mineralocorticoid excess and consistent with the hypothesis that cortisol is a significant functioning mineralocorticoid in the ectopic ACTH syndrome.

ACTH Syndrome, Ectopic↗

PubMed1984

Differences in hypothalamo-pituitary-adrenocortical activity in the rat after acute and prolonged treatment with morphine.

The influence of opioid substances on the secretion in vivo and in vitro of corticosterone, corticotrophin (ACTH) and corticotrophin releasing factor (CRF) in the rat was studied. Rats given a single injection of morphine exhibited a marked hypersecretion of ACTH and an exaggeration of the hypothalamo-pituitary-adrenocortical (HPA) response to stress. In contrast, animals rendered tolerant to morphine failed to release ACTH or corticosterone in response either to a subsequent injection of the opiate or to stress. The development of the inhibitory effect paralleled the development of tolerance to the analgesic actions of the drug. The production of ACTH by pituitary segments removed from control animals was not affected by the addition of opioid substances to the incubation medium. However, morphine, met-enkephalin and leu-enkephalin stimulated the secretion of CRF by hypothalami and their effects were competitively antagonized by naloxone. The secretory activity of hypothalami removed from rats treated acutely with morphine was enhanced. In contrast hypothalami from morphine-tolerant rats failed to secrete CRF in response to morphine, met-enkephalin, acetylcholine or 5-hydroxytryptamine. Neither the density nor the affinity of 3H-naloxone binding sites in the hypothalamus was influenced by the morphine treatment. The results suggest the opioid peptides and their receptors play a major role in the regulation of HPA function.

Adrenal Cortex↗

PubMed1991

Cyclical Cushing's disease. A case report.

A 41-year-old man with clinical Cushing's syndrome and intermittent central ACTH hypersecretion for a period of 9 1/2 years follow-up is described. Episodes of biochemical and clinical remission alternated with periods of florid Cushing's disease, characterized by circadian hyperpulsatile ACTH and cortisol secretion. Responses to metyrapone and inhibition of ACTH and cortisol hypersecretion after high dose dexamethasone during active phases of the disease favored a central origin of ACTH hypersecretion, confirmed by simultaneous bilateral venous sampling of the sinus petrosus inferior. Prolonged clinical remission followed near total anterior hypophysectomy. However, on anatomopathological examination of the pituitary neither corticotroph cell hyperplasia nor a microadenoma could be documented. The possibility of a functional ACTH hypersecretion is discussed.

Adrenal Glands↗

PubMed1978

Pituitary hormones and ergot alkaloids.

From the data presented it appears that ergot drugs are both a useful tool for use in the study of neuroendocrine control of pituitary hormone secretion and a valid pharmacologic weapon for treatment of hyperprolactinemic states, GH and, probably, ACTH and MSH hypersecretion. In fact, they are capable of a long-lasting disruption of PRL secretion from a normal or tumoral pituitary gland, are unable to affect directly the somatotrophs of an intact AP, but inhibit GH and, possibly, ACTH secretion from a hyperplastic or tumoral gland. Ergolines also exert clear-cut PRL-lowering effects and are capable of suppressing GH secretion in acromegaly. The intimate mechanism(s) and hence site(s) of action of some of these compounds await clarification.

Acromegaly↗

PubMed2004

An aberrant ACTH-producing ectopic pituitary adenoma in the sphenoid sinus.

A 32-year-old woman with an ectopic adrenocorticotropic hormone (ACTH)-secreting pituitary adenoma (EAPA) is presented. She had rapidly gained weight and suffered recurrent facial acne for a few years but lacked the typical Cushingoid features. Endocrine examinations revealed that her plasma ACTH was markedly high (196 to 280 pg/ml) without showing normal circadian rhythm and failed to respond to corticotropin-releasing hormone stimulation. Her cortisol levels ranged from 22 to 30 microg/dl throughout observation but low doses (1 and 2 mg) of dexamethasone failed to suppress either ACTH or cortisol level. Magnetic resonance imaging study revealed a 3-cm mass occupying the sphenoidal sinus with partial enhancement by gadolinium, which was separated from the normal pituitary in the sella region. The tumor resected by transsphenoidal surgery was histologically diagnosed as an ACTH-producing pituitary adenoma. After surgery her weight gain and acne remitted in accordance with decreases in plasma ACTH. Analysis of patient plasma by gel filtration method revealed the existence of big ACTH molecules eluted with a peak of authentic 1-39 ACTH, suggesting that this biologically less-active ACTH might be the reason why overt features of Cushing's syndrome failed to develop in this case. Although EAPA is clinically rare in parasellar disorders, the presence of ectopic pituitary adenoma should be considered in such cases showing ACTH hypersecretion without typical Cushingoid features.

ACTH Syndrome, Ectopic↗

PubMed1994

Socioregulatory effects on squirrel monkey pituitary-adrenal activity: a longitudinal analysis of cortisol and ACTH.

Squirrel monkeys show unusually prolonged elevations in plasma cortisol when separated from like-sex social companions. To determine whether this hypersecretion of cortisol reflects a deficiency in feedback mechanisms that normally inhibit the prolonged activation of the pituitary-adrenal axis, we simultaneously measured plasma cortisol and corticotropin (ACTH) in 30 juvenile monkeys housed in established groups, individual cages, and newly formed groups. As found in recent longitudinal studies of adults, when juveniles were living without companions, mean cortisol titers were consistently higher than those observed when the same juveniles were living in like-sex social groups. When cortisol was elevated, however, ACTH titers were significantly and chronically reduced. These results suggest that elevated cortisol does inhibit ACTH synthesis or release, and that hypercortisolism in squirrel monkeys living without companions is not a consequence of chronic elevations in ACTH. Similar peculiarities in pituitary-adrenal activity are evident in a number of affective disorders in human beings.

Adrenocorticotropic Hormone↗

PubMed2004

Flavonoids of St. John's Wort reduce HPA axis function in the rat.

A common biological alteration in patients with major depression is the activation of the hypothalamic-pituitary-adrenal (HPA) axis, manifested as hypersecretion of adrenocorticotropic hormone (ACTH) and cortisol. The hyperactivity of the HPA axis in depressed patients can be corrected during clinically effective therapy with standard antidepressant drugs such as imipramine, indicating that the HPA axis may be an important target for antidepressant action. We previously showed that a methanolic extract of St. John's Wort (SJW) and hypericin, one of its active constituents, both have delayed effects on the expression of genes that are involved in the regulation of the hypothalamic-pituitary-adrenal (HPA) axis , whereas the phloroglucinol derivative hyperforin was inactive in the same model . Since flavonoids of SJW are also discussed as active constituents it was of interest to determine whether these compounds can modulate HPA axis function. Imipramine (15 mg/kg), hypericin (0.2 mg/kg), hyperoside (0.6 mg/kg), isoquercitrin (0.6 mg/kg) and miquelianin (0.6 mg/kg) given daily by gavage for two weeks significantly down-regulated circulating plasma levels of ACTH and corticosterone by 40 - 70 %. However, none of the compounds tested had an effect on plasma ACTH and corticosterone levels after chronic treatment (daily gavage for 8 weeks). Our data suggest that besides hypericin, flavonoids of SJW play an important role in the modulation of HPA axis function. Furthermore, the results support the hypothesis that flavonoids are involved in the antidepressant effects of SJW.

Administration, Oral↗

PubMed1982

Effects of a met-enkephalin analog on adrenocorticotropin (ACTH), growth hormone, and prolactin in patients with ACTH hypersecretion.

The effect of D-Ala2, MePhe4, Met-(0)enkephalinol (Sandoz FK 33-824; 0.5 mg, im) on pituitary hormone secretion was studied in 11 patients with Addison's disease and 11 patients with ACTH-dependent Cushing's disease. In patients with Addison's disease, a pronounced fall of plasma ACTH levels was observed (P less than 0.005). The ACTH response to FK 33--824 was partially reversed by naloxone (4 mg, iv). In patients with Cushing's disease, no unequivocal decrease in either ACTH or cortisol was seen. Moreover, FK 33--824 failed to influence the vasopressin-induced ACTH increase in 5 patients with Cushing's disease. In patients with cortisol deficiency due to either Addison's disease or bilateral adrenalectomy for Cushing's disease, FK 33--824 led to increases in PRL and GH similar to those described in normal subjects. However, in the presence of longstanding hypercortisolism, the PRL increase was significantly diminished, and the GH response to FK 33--824 was completely abolished. Our results suggest that in Addison's disease ACTH release is influenced by inhibitory opiate receptors. In patients with Cushing's disease, ACTH secretion is insensitive to FK 33-284, presumably because of an autonomous pituitary adenoma or hypothalamic derangement. The impairment of the PRL and GH responses to FK 33--824 in Cushing's syndrome seems to reflect a direct action of the elevated cortisol level, for it is not seen after bilateral adrenalectomy.

Addison Disease↗

PubMed1990

A novel biochemical model linking dysfunctions in brain melatonin, proopiomelanocortin peptides, and serotonin in autism.

A novel biochemical model for autism is presented, which proposes that a subgroup of autistic individuals may have a hypersecretion of pineal melatonin that produces a cascade of biochemical effects including a corresponding hyposecretion of pituitary proopiomelanocortin (POMC) peptides and a hypersecretion of hypothalamic opioid peptides and serotonin (5-HT). The model is reviewed, and supporting animal and clinical research, is summarized. The first arm of the model suggests that increases in pineal melatonin results in hypersecretion of 5-HT in hypothalamus and blood. The second arm of the model indicates that hypersecretion of melatonin also inhibits the release of hypothalamic corticotrophin-releasing hormone (CRH). Hyposecretion of CRH may result in decreased release of both pituitary B-endorphin (B-E) and adrenocorticotrophin hormone (ACTH); this, in turn, may result in decreased plasma concentrations of B-E, ACTH, and cortisol. In autism, a genetically determined hypersecretion of hypothalamic B-E may further contribute to an inhibition of pituitary B-E because of negative feedback inhibition. Therefore, autism may reflect a dysfunction in the pineal-hypothalamic-pituitary-adrenal axis which, modulates POMC and 5-HT systems of the brain. This model is consistent with numerous clinical investigations implicating hypersecretion of brain 5-HT and opioid peptides in autism. The model may have heuristic importance in guiding future research in the biochemistry of autism.

Autistic Disorder↗

PubMed2003

Neuroendocrine aspects of hypercortisolism in major depression.

A consistent finding in biological psychiatry is that hypothalamic-pituitary-adrenal (HPA) axis physiology is altered in humans with major depression. These findings include hypersecretion of cortisol at baseline and on the dexamethasone suppression test. In this review, we present a process-oriented model for HPA axis regulation in major depression. Specifically, we suggest that acute depressions are characterized by hypersecretion of hypothalamic corticotropin-releasing factor, pituitary adrenocorticotropic hormone (ACTH), and adrenal cortisol. In chronic depressions, however, enhanced adrenal responsiveness to ACTH and glucocorticoid negative feedback work in complementary fashion so that cortisol levels remain elevated while ACTH levels are reduced. In considering the evidence for hypercortisolism in humans, studies of nonhuman primates are presented and their utility and limitations as comparative models of human depression are discussed.

Adrenocorticotropic Hormone↗

PubMed2002

Macroprolactinoma associated with Cushing's disease, successfully treated with cabergoline.

Multiple pituitary hormone hypersecretions have already been described, but the co-occurrence of PRL and ACTH excess is very rare. To our knowledge, medical treatment with cabergoline only, avoiding pituitary surgery and radiotherapy in this type of tumor has never been reported before. This case report deals with a 31-yr-old man affected with a macroprolactinoma associated with a florid clinical image of Cushing's disease. Normalization of the prolactin levels and the disappearance of clinical and biochemical features of Cushing's disease were obtained after administration of medical treatment only.

Adrenocorticotropic Hormone↗

PubMed1991

A case of pituitary adenoma producing both growth hormone (GH) and adrenocorticotropic hormone (ACTH).

The authors report a very rare case of pituitary adenoma producing both GH and ACTH. A 29-year-old female was admitted with obesity, amenorrhea, acromegaly, hirsutism, excessive pigmentation, acne, and diabetes mellitus. Computed tomography revealed an intrasellar tumor 16 mm in height, with a destroyed sellar floor. The blood concentrations of GH, ACTH and cortisol were increased (GH: 92 ng/ml, ACTH: 94 pg/ml, cortisol: 18.3 micrograms/dl). No diurnal variation in the amount of cortisol was observed. The urinary 17-OHCS was suppressed by 8 mg but not by 2 mg of dexamethasone. A subtotal adenomectomy was then performed through the transsphenoidal approach, which led to a sufficient reduction of both blood GH and ACTH (cortisol). Histologically the tumor was an acidophilic pituitary adenoma. Immunoperoxidase staining showed diffuse GH and sporadic ACTH producing cells, but failed to show any cells producing both hormones. The electron micrograms of neoplastic cells showed the ultrastructural characteristics of respective GH and ACTH cells. Another increase in both GH and cortisol, which occurred 19 months after the operation, has been controlled by bromocriptine administration. This case may be the first reported case of a pituitary adenoma producing both GH and ACTH, not accompanied by prolactin (PRL) hypersecretion, which has been fully confirmed endocrinologically and histopathologically.

Adenoma↗

PubMed1995

The effect of desipramine on basal and naloxone-stimulated cortisol secretion in humans: interaction of two drugs acting on noradrenergic control of adrenocorticotropin secretion.

Desipramine (DMI), a tricyclic antidepressant and norepinephrine (NE) reuptake blocker, is reported to induce ACTH and cortisol release acutely in humans, probably by facilitating central NE neurotransmission. Tricyclic antidepressant therapy, including DMI, normalizes the ACTH and cortisol hypersecretion that often accompanies depression. The mechanism of hypothalamic-pituitary-adrenal (HPA) axis inhibition by DMI in humans is unknown. In rats, DMI reduces the activity of the locus ceruleus, a major source of NE innervation of the hypothalamic paraventricular nucleus, the site of CRH neurons. Naloxone induces ACTH and cortisol release in humans through a noradrenergic-mediated mechanism and a probable consequent stimulation of hypothalamic CRH release. To study the interaction of these drugs on NE neurotransmission and, hence, HPA axis activity in humans, we administered DMI alone and with naloxone in a randomized, double blind, placebo-controlled protocol in eight healthy male volunteers. DMI (75 mg, orally) was given 180 min before naloxone (125 micrograms/kg BW, i.v.). Plasma ACTH and cortisol were measured at frequent intervals from 60 min before to 120 min after naloxone treatment. Plasma cortisol levels were 77% higher 180 min after DMI compared to those after placebo treatment (287 +/- 17 vs. 162 +/- 14 nmol/L; P = 0.000005). DMI reduced the naloxone-induced rise in cortisol (P = 0.02), but there was no change in the integrated cortisol response. The increase in basal plasma ACTH levels after DMI treatment did not reach statistical significance. DMI significantly increased systolic blood pressure and heart rate consistent with an effect on the noradrenergic control of the cardiovascular system. In summary, DMI increased basal cortisol levels consistent with facilitation of NE neurotransmission and, hence, hypothalamic CRH release. However, DMI had no enhancing effect on naloxone-induced cortisol release. This contrasts with the synergy observed when non-antidepressant agents that increase NE neurotransmission are given with naloxone to humans. DMI increases glucocorticoid feedback sensitivity in the rat HPA axis after several weeks through up-regulation of central corticosteroid receptors. However, this slowly developing effect is unlikely to occur during these acute studies. The effect of DMI on naloxone-induced cortisol release is consistent with an inhibitory effect on central noradrenergic control of ACTH release, perhaps at the locus ceruleus. This is the first human study to suggest an inhibitory effect of DMI on central noradrenergic control of ACTH release.

Adrenocorticotropic Hormone↗

PubMedDate not supplied

Long term bromocriptine therapy in Cushing's disease.

Recently, bromocriptine has been successfully introduced as medical therapy for the pituitary hypersecreting syndromes of hyperprolactinemia and acromegaly. Subsequently, an inhibitory effect on ACTH secretion was reported using bromocriptine in Cushing's disease. While most studies have focused on the acute response to bromocriptine, few have investigated the response to chronic therapy with this agent. In this report, we describe a patient with Cushing's disease in whom an acute inhibition of ACTH and cortisol was demonstrated following bromocriptine and in whom the long term administration of bromocriptine as the sole therapy produced a transient beneficial response. Further pharmacologic testing suggested this inhibitory effect on the hypothalamic-pituitary-adrenal axis was mediated through dopaminergic stimulation.

Adrenocorticotropic Hormone↗

PubMed1982

Bioactive and immunoreactive adrenocorticotropin in normal equine pituitary and in pituitary tumors of horses with Cushing's disease.

Equine Cushing's disease is caused by hypersecretion of ACTH by hyperplasia or adenomas of pars intermedia (PI) cells, in contrast to human Cushing's disease, which is caused by hyperplasia or adenomas of pars distalis (PD) ACTH-secreting cells. We assayed both bioactive and immunoreactive (IR) ACTH in two normal equine pituitary glands and in the PD, PI, and pars nervosa of four such glands, as well as in the PI adenomas of five horses with Cushing's disease. In normal horse pituitaries, as in those of other species, most of the bioactive and IR-ACTH was found in PD, much less in PI, and only traces in pars nervosa. In PI adenomas of horses with Cushing's disease, bioactive ACTH concentrations were similar to those in normal PI, but the total tumor content of bioactive ACTH exceeded that of normal whole pituitary. IR-ACTH concentrations were even higher in PI tumors, suggesting that some of the tumor ACTH was biologically inactive. Plasma IR-ACTH, which, like the PI adenoma tissue, presumably included a major fraction of bioactive ACTH, was greatly elevated in five horses with Cushing's disease and would account for the adrenal hyperplasia and hyperfunction observed in these animals.

Adrenocorticotropic Hormone↗

PubMed1987

[Anterior pituitary hypersecretion syndromes].

Anterior pituitary hypersecretion can be due to abnormal hypothalamic regulation, decreased peripheral hormone feedback or pituitary tumor. In some cases hypersecretion gives rise to a typical clinical syndrome involving acromegaly, hyperprolactinemia, and excess corticotropin (ACTH). The etiology of acromegaly is a growth hormone (GH)-secreting pituitary tumor in the vast majority of cases. Hyperprolactinemia and excess cortisol, however, may be due to many causes among which prolactin (PRL)- and ACTH-secreting pituitary tumors are not frequent. Glycoprotein-secreting pituitary tumors, especially gonadotropin (LH and FSH) and free subunits usually do not cause a typical excess hormone syndrome. Perhaps for this reason they are seldom recognized clinically, although histopathological studies are increasingly disclosing the gonadotrope nature of many pituitary tumors. Mixed hormonal secretions are common. When pituitary hormone secretion can be selectively suppressed by medical therapy, a significant reduction of tumor size is by no means rare. In other cases, pituitary irradiation or surgery, or even treatment aimed at a peripheral target gland, may be necessary.

Acromegaly↗

PubMed1988

Detection of mRNA of prolactin and ACTH in clinically nonfunctioning pituitary adenomas.

Clinically nonfunctioning pituitary adenomas have been thought to synthesize some pituitary hormones as shown by studies involving cell culture, immunocytochemistry, or measurement of hormone levels in tumor homogenates. Nevertheless, they are not associated with hypersecretion of pituitary hormones. To further clarify hormone synthesis in such pituitary adenomas, the presence of messenger ribonucleic acid (mRNA) of prolactin (PRL) growth hormone, and adrenocorticotropic hormone (ACTH) in the cytoplasm of 16 nonfunctioning adenomas was determined by means of a hybridization technique, and compared to the immunocytochemical findings. In three adenomas (19%) PRL mRNA was detected and in one case (6%) ACTH mRNA was detected. The hybridization technique appears to be more sensitive than immunohistochemistry for detection of specific mRNA's in assigning the hormone synthesis potential to clinically nonfunctioning tumors. The results suggest that PRL and ACTH are synthesized in some cases of clinically nonfunctioning pituitary adenomas and that hybridization techniques are useful to investigate hormone synthesis in pituitary adenomas. The ability to demonstrate PRL mRNA in tumor tissues allowed differentiation between hyperprolactinemia caused by synthesis of PRL in the tumor and that due to hypersecretion from the adjacent normal pituitary.

Adenoma↗