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A cat that was suspected some insulin resistance was diagnosed as pituitary dependent hyperadrenocorticism from an adrenocorticotropic hormone (ACTH) stimulation test, dexamethasone suppression test and measure of endogenous plasma ACTH concentration. Histopathological examination revealed chromophobe adenoma in pituitary gland and hyperplasia in adrenal cortex.
The hypothalamic-pituitary-adrenal (HPA) axis is integrated in the human stress system and controls the metabolism of many cell systems in the body. Therefore, hypofunction or hyperfunction of the HPA axis potentially threatens the life of the whole organism. Noncontrolled overproduction of its key regulators, CRH and ACTH, causes dysfunction of the stress system. Ectopic secretion of these compounds may be part of extraadrenal paraneoplastic syndromes caused by various benign or malignant tumors. However, ectopic ACTH and CRH may originate from the adrenal itself. A local CRH/ACTH system exists in the normal human adrenal medulla. Overproduction of CRH and ACTH has been documented in pheochromocytomas causing Cushing's syndrome. Finally, ectopic production of ACTH causing Cushing's syndrome has also been demonstrated in adrenocortical cells. This suggests a marked plasticity within the HPA axis and the neuroendocrine cell system.
Chronically elevated luteinizing hormone (LH) induces significant pathology in the LHbetaCTP transgenic mouse model, which uses the bovine gonadotropin alpha (alpha)-subunit promoter to direct transgene expression specifically to gonadotropes in the anterior pituitary. Previously, it was shown that female LHbetaCTP mice are infertile due to anovulation, develop granulosa cell tumors, and undergo precocious puberty from elevated LH and steroid hormones that fail to completely repress the alpha-subunit promoter. This chapter will discuss recent studies that further elucidate the impact of chronically elevated LH on diverse physiological systems. Granulosa cell tumors induced by elevated LH are strain dependent and prevented when transgenics are treated with human chorionic gonadotropin (hCG) surges. A granulosa cell tumor-associated transcriptome is generated, revealing several possible gene candidates for ovarian granulosa cell tumorigenesis. Primordial follicles in LHbetaCTP transgenics become depleted and oocytes exhibit increased rates of meiotic segregation defects, although meiotic competency is acquired normally. Anovulation can be rescued in transgenics by superovulation, though pregnancy fails at midgestation due to maternal factors. Uterine receptivity defects prevent implantation of normal embryos following induction of pseuodpregnancy. Transgenics develop Cushing-like adrenocortical hyperfunction with increased corticosterone production following induction of adrenal LH receptor expression. Elevated LH acts as a tumor promoter in the gonads and the adrenal gland, when expressed in conjunction with the inhibin-alpha SV40 transgene. Finally, chronic elevated LH promotes mammary tumorigenesis. The understanding of multiple clinical pathologies--including ovarian cancer, perimenopausal reproductive aging, premature ovarian failure, polycystic ovarian syndrome, Cushing's syndrome, and breast cancer--may be enhanced through further study of this useful transgenic mouse model.
The actions and interactions of the pituitary gland and the nervous system constitute a regulatory system whereby the physiologic activity of the thyroid, adrenals, and gonads is controlled. Damage to or interference with the pituitary gland may cause hyper- or hypofunctional states resulting in devastating changes in a person's body and life. This article limits its discussion to several of the more frequently encountered pathological states, their diagnostic work-up, evaluation, and treatment.
AIM: To study clinical and laboratory manifestations of hormonal activity in hypertensive patients with undifferentiated adrenal tumors. MATERIAL AND METHODS: 40 patients (19 males and 21 females aged 16-60 years) with undifferentiated adrenal tumors were examined. They were treated surgically. The results of the examination were compared with histological evidence on the resected adrenals. Clinical and laboratory signs of hormonal activity of the tumor were ascertained. RESULTS: Clinical symptoms in patients with adrenal tumors differed from those of typical symptoms of Icenko-Cushing, Cohn syndromes, pheochromocytoma. Hypertension in patients with cortical tumor may arise because of high synthesis of hydrocortisone, in patients with medullary tumor--of catecholamines. However, the level of hormones was not high enough for development of classic syndromes. That's why these tumors were named undifferentiated. CONCLUSION: Adrenal cortical tumors have signs of mixed androgeno-mineral-glucocorticoid activity. In medullary adrenal tumors hypersecretion of catecholamines is associated with cortical hyperfunction.
On the basis of this review and others, adrenal imaging using MRI requires functional biochemical data, such as scintigraphy (NP-59 and MIBG), for cortical adrenal assessment. For medullary hyperfunction such as intra-adrenal pheochromocytomas and neuroblastomas, MRI provides excellent staging and localization. Computed tomography is preferred for biochemically established hyperfunction such as Cushing's and Conn's syndromes.
The concentration of testosterone and estradiol in the blood plasma and the binding capacity of testosterone-estradiol binding globulin (TEBG) were studied in 30 women and 6 men with Icenko-Cushing's disease in the active phase and in 24 women with hormonally active adrenal tumors. In hypercorticism against a background of unchanged of lowered concentration of plasma estradiol there was a decrease in the concentration of testosterone and an increase in the testosterone-estradiol binding capacity (TEBC) in men and an increase in the concentration of testosterone and a decrease in TEBC in women. The authors have assumed that the testosterone/TEBC ratio reflects more accurately change in the dynamics of androgens than isolated concentrations of testosterone and TEBG, and recommended its determination for the assessment of the body androgenic saturation in disturbed function of the adrenal or sex glands.
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Leu-enkephalin, a potent, endogenous, opiate-like regulatory peptide, is present in a subpopulation of normal adrenal medullary cells and in a spectrum of proliferative lesions of adrenal and extra-adrenal chromaffin cell origin. The presence, extent, and intensity of leu-enkephalin-like immunoreactivity is variable in normal and pathological states. While areas of diffuse medullary hyperplasia consistently exhibited leu-enkephalin-like immunoreactivity, approximately 50% of hyperplastic medullary nodules, pheochromocytomas, and paragangliomas were positively stained. Tumors of neuroblastic origin, on the other hand, did not contain leu-enkephalin-like immunoreactivity. Variations in leu-enkephalin-like immunoreactivity may be related to aberrations of feedback mechanisms, multicentric origins of lesions from chromaffin cells with or without the capacity for leu-enkephalin synthesis, or to a variety of other mechanisms, including defective innervation of hyperplastic and neoplastic chromaffin cells. The results of these studies indicate that leu-enkephalin-like immunoreactivity is a useful tissue marker for the demonstration of chromaffin cell hyperplasia and neoplasia and may also prove to be an important clinical marker for the assessment of chromaffin cell hyperfunction.
Ectasia of a left adrenal vein in a 64-year-old man is described. The "cyst" thus formed contained 500 ml of blood. Its wall had three layers and was lined with endothelium. The structure of the adrenal was unimpaired. The morphology was indicative of malformation of the vein wall rather than neoplasia. The interest of the case lies in the fact that removal of this rare abnormality resulted in the cure of stable arterial hypertension. The literature reveals other cases of adrenal "cysts" of various kinds associated with continuous or paroxysmal hypertension or adrenal hyperfunction, followed by regression after asportation on all occasions. A morphogenetic classification of adrenal cysts is proposed with notes on each form.
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Two low-dose dexamethasone suppression test protocols were evaluated in 18 dogs with hyperadrenocorticism (14 dogs with pituitary-dependent hyperadrenocorticism [PDH] and 4 dogs with adrenocortical tumor) and in 5 healthy control dogs. Blood was obtained immediately before and 2, 4, 6, and 8 hours after IV administration of either 0.01 mg of dexamethasone sodium phosphate/kg of body weight or 0.015 mg of dexamethasone polyethylene glycol/kg. At 8 hours after dexamethasone administration, 18 of 18 (100%) dogs with hyperadrenocorticism given the sodium phosphate preparation and 16 of 18 (89%) affected dogs given the polyethylene glycol preparation failed to have suppression of plasma cortisol concentration (less than 1.4 micrograms/dl). Plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl at 2, 4, and/or 6 hours after administration of either dexamethasone preparation in 5 of 14 dogs with PDH and to less than 50% of baseline cortisol concentration in 10 of 14 dogs with PDH. Suppression, as identified by these 2 criteria, was not observed at 2, 4, 6, or 8 hours after administration of either dexamethasone preparation in dogs with adrenocortical tumor. For both protocols, the 8-hour plasma cortisol concentration was suppressed to less than 1.4 micrograms/dl and to less than 50% of baseline in the 5 control dogs. Both protocols were comparable for use as screening tests in establishing a diagnosis of hyperadrenocorticism. Suppression of plasma cortisol concentration to less than 50% of baseline (or less than 1.4 micrograms/dl) during the test was consistent with diagnosis of PDH. Failure to have such suppression, however, was observed in dogs with PDH as well as in those with adrenocortical tumor.
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Small in size but powerful in influence, the adrenal glands and their hormones are necessary to sustain life and maintain homeostasis. If not detected in a timely fashion, adrenal disorders can have fatal consequences. This articles reviews the anatomy and physiology of the adrenal glands and, with the use of case studies, considers many disorders of the adrenal glands, including Cushing's disease, aldosteronism, hyperaldosteronism, and Addison's disease.
Widespread use of contemporary imaging techniques (ultrasound, computerized axial tomography, and magnetic resonance imaging scans) have led to the incidental discovery of asymptomatic adrenal neoplasms with increasing frequency. Patients with such adrenal "incidentalomas" typically have no clinical manifestations of adrenal cortical hyperfunction at the time of discovery. We have studied 122 patients with asymptomatic adrenal masses ranging in size from 2 to 7 cm in diameter from 1978 to 1988. Selected patients, after adrenal metastases, pheochromocytoma, myelolipomas, and cysts were ruled out, were further evaluated for adrenal cortical hyperfunction by measuring urinary 17-hydroxysteroids, 17-ketosteroids, and free cortisol, serum A.M., P.M. cortisol, and plasma ACTH levels. These values were also measured before and after dexamethasone suppression. NP-59 adrenal scintiscans were performed on all patients. Six patients were identified with sub-clinical Cushing's syndrome. Baseline cortisol levels were normal in each of these patients. Loss of diurnal rhythm appeared to be the most sensitive indicator of abnormal adrenal cortical function. When adrenalectomy is performed in such patients, especially when contralateral adrenal gland suppression is evidenced by NP-59 scanning or other biochemical assessment, perioperative steroids should be administered in a manner similar to that used for patients with symptomatic Cushing's syndrome. Unilateral adrenalectomy in a patient with an asymptomatic adrenal adenoma, insufficiently studied, may result in Addisonian crisis.