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PubMed1980

Evolution of the surgical management of primary aldosteronism.

During the past two decades 50 patients were operated on for primary aldosteronism. Diagnosis was based on high aldosterone excretion or secretion during a high sodium intake and, more recently, low stimulated plasma renin activity. Computed tomography and adrenal venography with selective adrenal vein catheterization for determination of aldosterone/cortisol ratios were helpful in the distinction between adenoma and bilateral hyperplasia. As a result of preoperative localization, unilateral posterior or flank approach to the adrenal has replaced transabdominal as the approach of choice. Overall in-hospital mortality in this series was 10% and occurred exclusively with a transabdominal approach in the early part of the series. Adrenalectomy has been curative in 66% of patients with adenoma and in 38% of patients with hyperplasia which includes patients with adenomatous (dominant macroscopic adenoma, 1 cm or greater) hyperplasia when the cure rate was 75%. Currently, only patients who have unilateral adrenal hyperfunction, who respond to spironolactone with a fall in blood pressure, and who are a good operative risk are considered for operation by posterior or flank approach. These guidelines for the management of primary aldosteronism, used since 1974, have been associated with an excellent response (92%), zero mortality and reduced morbidity.

Adenoma↗

PubMed1998

Incidentally discovered adrenal tumors: endocrine and scintigraphic correlates.

Hormonal and morphological data were investigated in 202 consecutive patients with adrenal incidentalomas (171 unilateral and 31 bilateral) in an attempt to assess subclinical hyperfunction or malignancy. In addition to the classical evaluation, scintiscan was carried out in a large number of these patients. In unilateral incidentalomas, 83% showed normal hormonal function, whereas 17% had biochemical signs of adrenal overactivity (hyperaldosteronism in 3, hypercortisolism in 17, medullary hyperfunction in 9). [75Se]Methylnorcholesterol scintigraphy depicted malignant, space-occupying lesions as decreased or absent radiotracer uptake by the mass, and cortical adenomas as increased or normal uptake. In cortical adenomas a relationship between radiocholesterol uptake and degree of functional autonomy was demonstrated. [123I]Metaiodobenzilguanidine scintiscan visualized 7 of 8 pheochromocytomas. In bilateral incidentalomas, abnormal adrenal function was more frequent, accounting for 29% of cases (hyperaldosteronism in 3, hypercortisolism in 3, adrenal insufficiency in 2, and congenital adrenal hyperplasia in 1). Malignant lesions were not scintigraphically visualized. [75Se]Methylnorcholesterol scan also provided functional information in the case of a cortisol-secreting adenoma and an aldosteronoma with a concomitant contralateral nonhypersecreting adenoma, showing the greatest uptake in the hyperfunctioning adenomas. In both unilateral and bilateral lesions, endocrine testing failed to differentiate benign from malignant tumors. Although hormonal assessment is mandatory to clarify the functional patterns, only morphofunctional examination by scintiscan seems to provide more data about the likelihood of malignancy.

17-alpha-Hydroxyprogesterone↗

PubMed1960

Intranasal injection of corticosteroids.

Intranasal injections into the inferior turbinates of a slightly form of prednisolone TBA (Hydeltra(R) TBA) into persons with complaint of nasal obstruction gave considerable relief in 78 per cent of cases. Nasal hyperfunction due to seasonal allergic rhinitis, vasomotor rhinitis and secondary nasal edema from sinusitis was the indication for use. No local or general reactions other than a small amount of bleeding at the time of injection was noted. This method allows full utilization of the anti-inflammatory activity of corticosteroids at the local tissue level without producing a systemic effect.

Administration, Intranasal↗

PubMed1979

The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review.

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.

Adrenocortical Hyperfunction↗

PubMedDate not supplied

Ultrasonographic characteristics of the adrenal glands in dogs with pituitary-dependent hyperadrenocorticism: comparison with normal dogs.

Ultrasonographic evaluation of the adrenal glands was performed in 10 dogs with pituitary-dependent hyperadrenocorticism (PDH) and in 10 age- and weight-matched healthy control dogs. Thickness, shape, and echogenicity were determined for each adrenal gland. Adrenal thickness in dogs with PDH (median, 10 mm-left; 8.5 mm-right) was significantly greater than thickness in control dogs (median, 6 mm-left; 6 mm-right). Other ultrasonographic characteristics associated with PDH included bilaterally symmetrical adrenomegaly and maintenance of normal adrenal shape. Adrenal echogenicity was homogeneous and less than that of the adjacent renal cortex in 8 of 10 dogs with PDH and in 10 of 10 control dogs. Heterogenous echogenicity was present in 2 of 10 dogs with PDH, and was associated with nodular cortical hyperplasia in one of those dogs. Results of this study confirm the difference in sonographic appearance between PDH-induced bilateral cortical hyperplasia and functional adrenocortical neoplasia, and show a difference in sonographically determined adrenal size between healthy dogs and dogs with PDH.

Adrenal Glands↗

PubMed2001

[Steroids, cognitive processes and aging].

Adrenal steroids, besides acting on the pituitary and the hypothalamus to exert classical feedback activity, can also have endocrine and extra-endocrine actions at the level of sub-cortical areas, as the hippocampus and the amygdala, involved in cognition and effectiveness. Acting on the hippocampus, an area particularly equipped with specific receptor sites, adrenal steroids exert either a feedback inhibition on their own secretion or a morphological and functional age-related deterioration of this target area. Loss of hippocampal neurons and corticosteroid receptors with ageing endangers the feedback inhibitory action of the steroids, and induces an over-exposition of the hippocampus to their detrimental action, enhancing the vulnerability of the neuronal cells to metabolic stimuli (hypoxia, hypoglycemia). Hence, either in the physiological ageing of the brain as well as in age-related neurological diseases or psychiatric diseases, harboring a primary neuro-anatomical-functional alteration of the hippocampus, or when the hippocampus is over-exposed to adrenal steroids, a cohort of cognitive and behavioral alterations may be partly due to adrenal gland hyperfunction. Gonadal steroids exert effects on the CNS which go far beyond regulation of gonadotropin secretion and sexual function, though their action is opposite to that of adrenal steroids. Estrogens stimulate hippocampal synaptogenesis, enhance cholinergic neurotransmission, possess anti-oxidative and anti-amiloidogenic properties, dilate cerebral vessels and have platelet anti-aggregating activity. One is led to postulate that the dramatic decrease of estrogen secretion at menopause should increase the vulnerability of the CNS by the many factors contributing to neurodegeneration associated to brain ageing or Alzheimer disease.

Adrenal Cortex Hormones↗

PubMedDate not supplied

Plasma renin activity (PRA) and plasma aldosterone in the adrenal cortex hyperactivity. Studies on 50 hypertensive patients.

The authors have studied on 50 patients hospitalized in the Adrenal Pathology unit of the Institute of Endocrinology, the etiopathogeny of arterial hypertension (AH) in hypercorticism and the therapeutic implications, arriving at the conclusion that in 20% of the cases AH was probably due to an increased activity of renin-angiotensin and in 47% to elevated levels of aldosterone. The authors hypothesize that AH in the remaining 30% of the hypercorticism cases in this study is due to other mineralocorticoids in excess and suggest that the treatment should be pathogenic and strictly individualized.

Adrenocortical Hyperfunction↗

PubMed2001

In vitro release of aldosterone and cortisol in human adrenal adenomas correlates to mRNA expression of steroidogenic enzymes for genes CYP11B2 and CYP17.

Adenomas of the adrenal cortex cause different disorders depending on the main steroid synthesized and released. The aim of this research is to increase our understanding of the pathophysiology of steroidogenesis in adrenocortical disorders by comparing the release of steroids from adrenocortical adenomas in vitro with the messenger RNA (mRNA) expression of steroid synthesizing enzymes. Fourteen patients with adrenal tumors were included in the present study; nine were diagnosed with primary aldosteronism and three with Cushing's syndrome. Two patients had an adrenal tumor discovered on computed tomography (CT) during workup for an unrelated disease. Serum cortisol, plasma aldosterone, and urinary catecholamines were normal. Tissue was taken for in vitro steroid release, and aldosterone and cortisol in the medium after a 1-hour incubation were determined. Oligonucleotide probes with sequences complementary to mRNAs encoding for the steroid synthesizing enzymes 11 beta-hydroxylase (CYP11B1), 18-hydroxylase (CYP11B2), 17 alpha-hydroxylase (CYP17), and 21-hydroxylase (CYP21) were synthesized (Genset, Paris, France) and in situ hybridization was performed. Moderate expression of CYP11B2 and low expression of CYP11B1 were seen in the zona glomerulosa. The zona fasciculata of the control adrenals expressed a high signal of CYP11B1, whereas the expression of CYP11B2 was very low. There was considerable variation in aldosterone release from the aldosteronomas, whereas the tumors from the Cushing patients showed no detectable release of aldosterone. In contrast, tumors from patients with primary aldosteronism, Cushing's syndrome, and no hyperfunction all had the ability to synthesize and release cortisol in vitro. The highest cortisol release was found in tumors from patients with Cushing's syndrome, but also the nonhyperfunctioning tumors and some of the aldosteronomas released significant amounts of cortisol. The two patients with highest release of aldosterone in vitro showed the highest expression of CYP11B2 and the lowest expression of CYP11B1 and CYP17. The remaining aldosteronomas had low expression of CYP11B2, similar to the two other groups. Expression of CYP11B1 was high as expected in the Cushing adenomas, but also the two nonhyperfunctioning tumors and some of the aldosteronomas showed a moderate expression. Adenomas from Cushing's syndrome, nonhyperfunctioning adenomas, and some of the aldosterone-producing adenomas had moderate to high expression of CYP17. This paper presents new means for functional characterization of adrenocortical tumors. Diagnosis of an aldosteronoma is often difficult, and with the advent of these methods it is possible to determine the functional capacity of a tumor, once it is removed. This is of special interest if the patient remains hypertensive postoperatively, and it is not clear whether the patient indeed had a functioning tumor.

Adrenal Cortex Neoplasms↗

PubMedDate not supplied

[Energy metabolism during stressful exposures (ionizing radiation), its self-regulation and correction].

Normal hormonal regulation of energy metabolism is mainly realized by glucocorticoids and insulin, their physiological antagonist. Under the effect of different extremal factors (including ionizing radiation) there arises non-specific stress, a syndrome the main component of which is the hyperfunction of glucocorticoids--the intermediate hormonal link in the stress reaction. Stimulation of hypercorticism by administering hydrocortisone to intact animals as well as its stimulation by administering this preparation to irradiated animals causes development and intensification of inhibition and uncoupling of the oxidative phosphorylation as well as disturbance in adenylic nucleotides metabolism. The administered insulin, softening the reaction of hypercorticism and changing the ratio of the hormone levels in favour of insulin, weakens essentially the stress (ray) disturbances in the energy metabolism.

Adrenal Cortex↗

PubMed2001

Scintigraphic patterns of adrenocortical carcinoma: morpho-functional correlates.

OBJECTIVE: Adrenocortical scintigraphy has demonstrated clinical utility in the morpho-functional characterization of adrenal tumors. The aim of this study was to identify possible relationships between the scintigraphic pattern and endocrine and/or morphological data in a series of adrenocortical carcinomas. DESIGN AND METHODS: Twenty-one patients with adrenocortical carcinoma (11 nonfunctioning and 10 hormone-secreting) were investigated with 75Se-methyl-nor-cholesterol scintigraphy. Clinical, hormonal, radiological, and pathological data were analyzed. RESULTS: The adrenal mass showed no radiocholesterol uptake in 18 cases (11 nonfunctioning and 7 functioning lesions). Contralateral normal adrenal gland was visualized in all patients with nonfunctioning tumors, whereas classic bilateral nonvisualization was observed in the 7 cases with hyperfunctioning masses. Three patients with cortisol-producing carcinomas showed radiotracer uptake by the mass, without visualization of the contralateral gland. At histology, the tumors were shown to be undifferentiated adrenocortical carcinomas; they had an aggressive clinical behavior. CONCLUSIONS: Radiocholesterol scintigraphy has an important role in diagnosing adrenocortical carcinomas, which typically are not visualized. However, 30% of hypersecreting adrenocortical carcinomas show an atypical increased tracer uptake, not predictive of the biochemical and histological features of the tumor.

Adolescent↗

PubMed1979

Uptake of 131I-19-cholesterol by normal and spontaneously hyperfunctioning canine adrenals.

In six normal dogs the adrenals could be visualized as separate areas of radioactivity at 7--10 days after injection of 20--40 muCi 131I-iodocholesterol per kg of body weight. Image analysis revealed uptake values of 0.15--0.3% of the injected dose. In five dogs with pituitary-dependent hyperadrenocorticism the adrenals became visible at 3--5 days after injection of the radiopharmaceutical, with uptake values of 0.38--2.2%. In six dogs with hyperadrenocorticism due to adrenocortical tumor the scintigraphy contributed to the diagnosis and the presurgical localization. The uptake values were within the normal range; the tumor could be observed at 3--10 days after injection. Additional findings on adrenal asymmetry and a case of fluctuating pituitary-dependent hyperadrenocorticism are discussed.

19-Iodocholesterol↗

PubMed1992

Treatment of Behçet's disease.

Behçet's disease is a systemic inflammatory disorder capable of inducing thrombophlebitis. Clinicopathologically, it is characterized by neutrophil and platelet hyperfunction. Lesions are formed presumably because neutrophils infiltrating the affected tissue release active oxygen and lysosomal enzymes in large amounts. The mechanism of neutrophil hyperfunction was obscure, but in recent years attention has focused on the effects of cytokines released by mononuclear cells. As more has been learned about the etiopathogenesis of Behçet's disease, novel anti-inflammatory drugs, immunosuppressants, anti-thrombotic agents, and anticoagulants have helped to achieve remarkable progress in treatment. Particularly notable is the effect on severe uveitis of cyclosporine, which is more effective than colchicine and conventional immunosuppressants. With the advent of cyclosporine, the number of patients with Behçet's disease who lose their eyesight has clearly decreased.

Adrenal Cortex Hormones↗

PubMed1998

p53 protein and its messenger ribonucleic acid in human adrenal tumors.

The role of p53 tumor suppressor gene in the pathomechanism of adrenal tumors was investigated by measuring p53 protein and its messenger ribonucleic acid (mRNA) in 12 normal human adrenals as well as in 56 adrenal tumors (7 aldosterone-producing adenomas, 5 adrenocortical adenomas causing Cushing's syndrome, 19 non-hyperfunctioning adrenocortical adenomas, 5 adrenocortical carcinomas, 12 pheochromocytomas, 3 myelolipomas, 4 ganglioneuromas and 1 hemangioma). The p53 protein concentration was significantly increased in aldosterone-producing adenomas (394+/-36 pg/mg cytosolic protein, mean+/-SE, vs 266+/-18 in normal human adrenals), whereas the concentration of this protein in Cushing's adenomas, non-hyperfunctioning adrenocortical adenomas, pheochromocytomas, and in all but one adrenocortical carcinomas was similar to that measured in normal human adrenal tissues. One adrenocortical carcinoma tissue showed very high p53 protein content (3000 pg/mg cytosolic protein). By contrast, myelolipomas (23+/-20) ganglioneuromas (43+/-15) and a hemangioma (11 pg/mg cytosolic protein) had very low p53 protein content. Northern blot analysis revealed the presence of p53 mRNA in each adrenal tissue examined with highest levels in aldosterone-producing and Cushing's adenomas. It is possible that the differences in p53 protein and/or mRNA contents reflect corresponding differences in the pathogenetic importance of p53 alterations in these types of adrenal tumors.

Adenoma↗

PubMed2003

[Adrenocortical tumours].

Adrenocortical tumours have to be differentiated from cortical hyperplasias, medullary tumours and extra-adrenal tumours or metastases. These diagnoses are mostly possible using routine paraffin sections. In some cases, immunostaining for differing cortical and medullary tumours and metastases are necessary. Adrenal hyperplasias can be congenital or acquired. They are diffuse, micronodular or macronodular and may be inactive or induce a cortical hyperfunction. Very rarely, macronodular hyperplasias may transform into autonomous adenomas. Primary, pigmented adrenocortical disease is a rare, special type of primary adrenal Cushing's syndrome, showing many small tumours with pleomorphic cells and an atrophic surrounding cortical tissue. Adrenal adenomas are mostly unilateral and solitary tumours weighing less than 50 g. Adrenal cortical carcinomas are mostly larger. Like the adenomas, they may be inactive and may induce a hypercortisolism, a hyperandrogenism or (very rarely in carcinomas) a hyperaldosteronism. Differentiating cortical adenomas and carcinomas is difficult in some cases but is possible using a diagnostic algorithm. Myelolipomas are benign, inactive tumours composed of mature fat cells and bone marrow cells. They have to be differentiated from adenomas with myelolipomatous metaplasia. Further, rare primary cortical tumours are mentioned.

Adenoma↗

PubMed1995

Lysine vasopressin stimulation of cortisol secretion in patients with adrenocorticotropin-independent macronodular adrenal hyperplasia.

We present two patients with Cushing's syndrome due to ACTH-independent macronodular adrenal hyperplasia who showed marked plasma cortisol response to lysine-8-vasopressin (LVP) injection (from 930 and 731 pmol/L to 2177 and 1920 pmol/L, respectively), while plasma ACTH levels remained undetectable. The ACTH independence of cortisol secretion in the two patients was determined from the following endocrinological findings. Plasma cortisol levels were not increased by corticotropin-releasing hormone injections and were not suppressed by high dose (16 mg) dexamethasone administrations. The plasma ACTH levels, measured by two independent sensitive immunoassays, were persistently undetectable even after corticotropin-releasing hormone injection, metyrapone administration, and bilateral adrenalectomy. The particular pathological finding of the two cases, atrophic lesions in nonnodular parts of the adrenal cortexes, also indicated ACTH independence of the macronodular hyperplasia. In vitro examination revealed a direct effect of LVP on cortisol secretion from the adrenal cells of the macronodules. We also examined seven patients with Cushing's syndrome caused by adrenal adenoma and found a statistically significant plasma cortisol response to LVP injection. The direct effect of LVP was also demonstrated in cultured adenoma cells. In conclusion, we discovered a direct adrenal effect of LVP on cortisol secretion in patients with ACTH-independent macronodular hyperplasia and, to a lesser extent, in patients with cortisol-producing adrenal adenoma. The cortisol response to LVP may serve to facilitate their diagnosis and choice of therapy.

17-Hydroxycorticosteroids↗

PubMed1991

[Adrenocortical scintigraphy to evaluate incidental adrenal mass (incidentaloma) discovered on computed tomography].

To assess the nature of adrenal mass incidentally discovered on computed tomography, adrenocortical scintigraphy with I-131-6 beta-iodomethyl-19-norcholest-5(10)-en-3 beta-ol (I-131 Adosterol) in 29 patients was retrospectively reviewed. All patients had no clinical symptoms and biochemical evidence of adrenal hyperfunction. Six of them had extra-adrenal malignancy. Increased tracer uptake on the side of adrenal mass was observed in 13 patients (concordant group): cortical adenoma in 8, macronodular hyperplasia in 1, no growing tumor in 1, and no further examination in the remaining 3 patients. No cancer patients were included in the concordant group. Symmetric uptake was seen in 9 patients (symmetric group): 1 cortical adenoma and 1 ganglioneuroma, 6 no growing tumor (two of them had malignancy), and no further examination in 1 patient. Decreased uptake were shown in 7 patients (dis-concordant group): metastasis in 4, adrenal cyst in 2, and no growing tumor in 1. Adrenocortical scintigraphy was helpful in distinguishing benign functioning adrenal masses from non-functioning adrenal masses such as metastatic tumor and cyst.

Adenoma↗

PubMed1998

Anesthetic implications for surgical patients with endocrine tumors.

The preoperative evaluation and safe anesthetic treatment of patients with endocrine gland tumors mandate an understanding of the physiologic dysfunctions attributable to these tumors. Some patients will exhibit various signs and symptoms characteristic of the MEN syndromes. In the patient with acromegaly, a fiberoptic-guided intubation of the trachea to secure the airway before induction of general anesthesia must be anticipated. Anesthetic treatment of the patient with hyperadrenocorticism requires knowledge of the physiologic effect of excess cortisol. In the patient with severe hyperparathyroidism, we attempt to correct the markedly elevated plasma calcium levels and maintain adequate hydration and urine output perioperatively. Following thyroidectomy for MCT, 2 potential problems of concern are upper airway obstruction and aspiration resulting from injury (unilateral or bilateral) to the recurrent laryngeal nerve and the superior laryngeal nerve, respectively. The major focus during excision of an insulinoma is prevention of wide swings in blood glucose concentrations. In the gastrinoma patient, the anesthesiologist not only must correct any intravascular fluid volume deficit or electrolyte imbalance but must also consider the patient to have a full stomach at the time of anesthetic induction. Correction of hypokalemia and control of hypertension may be required in the preoperative preparation of the patient with an adrenal cortex tumor. Preoperative alpha-adrenergic blockade must be initiated in the patient with a pheochromocytoma to prevent dangerous elevations in blood pressure during anesthesia and surgery for the tumor's removal. Vasodilators with rapid onset and short duration are used to treat intraoperative hypertension. After ligation of the tumor's blood supply, falls in blood pressure may require treatment with fluids and vasopressors. Carcinoid syndrome patients should be treated with somatostatin to prevent stimuli such as anxiety, abdominal scrubbing, or tumor manipulation from precipitating severe hypotension, hypertension, bronchospasm, or tachycardia. In both pheochromocytoma and carcinoid patients, a smooth anesthetic induction and tracheal intubation plus avoidance of drugs that release histamine or activate the sympathetic nervous system may also prevent intraoperative crises.

Acromegaly↗

PubMed2003

Ectopic adrenocorticotropin (ACTH) and corticotropin-releasing hormone (CRH) production in the adrenal gland: basic and clinical aspects.

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.

Adrenal Cortex Neoplasms↗