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PubMed1989

[Bile excretion system in endogenous hypercorticism syndrome].

Bile excretion and biochemical properties of bile were investigated in 86 patients with the endogenic hypercorticism syndrome, 78 patients with the Itsenko-Cushing disease and in 8 patients with corticosteroma. A considerable incidence of functional and organic biliary disorders was demonstrated. Changes in cholecyst contractility were recorded in 54.6% of the patients, with hypermotor dyskinesia (36.4%) prevailing. An excess of endogenic corticosteroids was frequently accompanied by a hypotonus of Oddi's sphincter (65.6%) or Lutkens' sphincter (67.2%). Chronic (stoneless) cholecystitis was diagnosed in 70.9% of the patients, cholelithiasis, in 16.3%, and cholecyst cholesterosis, in 3.5%. Adrenocortical hyperfunction was associated with natural changes in biochemical composition of the bile, such as excessive cholesterol and a relative deficiency of cholic acid and phospholipids which might be conducive to cholelithiasis. High incidence of biliary disturbances and their pattern should be taken into account in the treatment of patients with hypercorticism.

Adolescent↗
PubMed1990

[Immunoreactive trypsin in the blood of patients with functional disorders of the adrenal cortex].

Blood serum trypsin was radioimmunoassayed in 46 patients with adrenocortical hyperfunction and in 24 ones with its hypofunction. The findings evidence that excess of endogenous adrenal steroids leads to elevation of radioimmune trypsin (RIT) concentration. The presence of chronic pancreatitis in hypercorticism did not essentially influence the value of the examined parameter, nor did the development of diabetes mellitus. Corticosteroid deficit in the body was not associated with changes in the blood serum RIT concentration. Systematic glucocorticoid therapy resulted in elevation of RIT level. The serum enzyme concentration was also increased in hypoadrenocorticism patients not administered glucocorticoids, suffering from concomitant chronic pancreatitis. Therefore the test was not informative for the diagnosis of chronic pancreatitis in the patients with the endogenous hyperadrenocorticism syndrome but may be helpful in the recognition of the condition in the patients with chronic adrenal insufficiency; interpretation of this test results in hypoadrenocorticism patients treated with glucocorticoids should be performed by efficient specialists.

Adolescent↗
PubMed1979

Gastrinoma associated with common bile duct obstruction and the ectopic production of ACTH.

A case of adrenocortical hyperfunction due to ectopic production of ACTH by a gastrin-producing tumor of the pancreas is described. Cushing's syndrome preceded the appearance of the overt Zollinger-Ellison syndrome by 2 years and was treated by bilateral adrenalectomy. The Zollinger-Ellison syndrome was initially treated with cimetidine, which successfully reduced the secretion of gastric acid. Because the pancreatic gastrinoma continued to grow, causing obstruction of the common bile duct, biliary diversion and total gastrectomy were performed. There is evidence that the pancreatic gastrinoma was the source of the ectopic production of ACTH and possibly secretion. The role of Histamine-2 blocking agents as therapy in the Zollinger-Ellison syndrome is discussed.

Adrenocorticotropic Hormone↗
PubMed1988

Diseases of the adrenal cortex.

The adrenal cortex is functionally a three-dimensional gland that secretes glucocorticoids, mineralocorticoids, and sex steroids. Of these three classes of steroids only the gluco- and mineralocorticoid hormones are necessary to sustain life. The availability of sensitive and specific radioimmunoassays has permitted accurate measurement of practically every steroid hormone secreted by the adrenal cortex. As in other endocrinopathies, suppression studies are employed when hyperfunction is suspected, while provocative tests are used to detect hypofunction. These dynamic studies enable the clinician to evaluate the functional status of the adrenal cortex. The anatomic configuration of the adrenal cortices is delineated by high-resolution computed tomography (and magnetic resonance imaging), obviating the need for invasive procedures such as venography or arteriography. The disorders of the adrenal cortex can be viewed from the dual perspectives of hyperfunction and hypofunction. Clinical expressions of hyperfunctional adrenocortical syndromes include Cushing's syndrome, primary hyperaldosteronism, and the adrenogenital syndrome. The expressions of hypofunctional syndromes include Addison's disease and selective hypoaldosteronism. The diagnosis and treatment of these disorders are outlined in this issue.

Addison Disease↗
PubMed1992

Clinical features of depressed patients who do and do not improve with placebo.

The substantial placebo response in depression confounds treatment decisions and the assessment of new therapies. Improvement with placebo occurs infrequently in patients with chronic depression and in those with pituitary-adrenocortical hyperfunction, but other consistent predictors of placebo response have not been detected. We divided 241 moderately to severely depressed patients who had received placebo on a double-blind basis for 3 to 6 weeks into responders (greater than or equal to 50% improvement in Hamilton depression score, final Hamilton depression score less than or equal to 10), extreme nonresponders (less than 25% improvement), and partial responders (all others). Improvement with placebo was associated with a relatively short illness, a precipitating event, depression of only moderate global severity, and a good response to previous antidepressant treatment. These observations suggest that depressed patients who do and do not recover with placebo have different conditions that have not yet been fully characterized.

Adult↗
PubMed1989

Scintigraphic studies in adrenal hypertension.

Endocrine hypertension secondary to disorders of the adrenal glands is uncommon, but by no means rare. The importance of correct biochemical diagnosis and subsequent localization of the responsible lesion(s) lie in the fact that many of these syndromes occur in younger patients, may exhibit familial patterns of inheritance and are frequently amenable to surgical cure. The radiopharmaceuticals (131)1-6 beta-iodomethyl-19-norcholesterol (NP-59), a marker of adrenocortical cholesterol uptake, and (131)1- and (123)1-metaiodobenzylguanidine (MIBG), a norepinephrine (NE) analog and marker of energy-dependent NE storage vesicle accumulation, can be shown to accurately localize adrenal cortex and sympathoadrenal dysfunction, respectively. In Cushing's syndrome (CS) not only does the pattern of NP-59 uptake depict the adrenal dysfunction and its pathophysiologic basis, but the level of NP-59 accumulation reflects the degree of adrenocortical hyperfunction. Adrenocorticotrophin-independent CS is uniformly and accurately localized, especially in bilateral cortical nodular hyperplasia where even high resolution computed tomography (CT) may fail to depict the often subtle, asymmetric anatomic abnormalities. Dexamethasone suppression NP-59 adrenal scintigraphy has been shown to be highly sensitive and specific, and exceeds the efficacy of CT in the differentiation of adenoma and bilateral hyperplasia in primary aldosteronism. MIBG is useful as a sympathoadrenal imaging agent whose clinical utility has been demonstrated in the localization of pheochromocytoma, especially as a modality to screen the body for multiple and extraadrenal, recurrent, or metastatic lesions. Moreover, the extent of metastatic involvement from neuroblastoma can also be accurately depicted using MIBG. In this review we will examine the role of adrenal scintigraphy in the characterization of hypersecretory disorders of the adrenal cortex, medulla, and related conditions that produce hypertension as part of their symptom(s) complex. This approach, which is complementary to other anatomical modalities of imaging, can be used to advantage in the localization of functioning cortical and medulla adrenal diseases and other neoplasms of adrenergic origin.

3-Iodobenzylguanidine↗
PubMed1975

The effect of carbenoxolone sodium on the plasma 11 hydroxycorticoid levels in chronic gastric ulceration.

The mineralcorticoid effects of carbenoxolone sodium are well established and seem related to the ulcer healing of the drug. In the present study the plasma 11 hydroxycorticoid responses were assessed in 12 patients undergoing treatment with carbenoxolone for chronic gastric ulceration. After treatment with carbenoxolone for one month the plasma 11 hydroxycoticoid levels rose significantly, suppression by dexamethosone was less marked and the normal diurnal periodicity was abolished. Carbenoxolone therapy influences the results of tests designed to assess the function of the pituitaryadrenal axis and may lead to sub-clinical adrenocortical hyperfunction.

Adult↗
PubMed1979

Effects of the obese (ob/ob) genotype on spleen cell immune function.

Spleen cells from mice homozygous for the obese (ob) mutation killed DBA/2 mastocytoma target cells less well than spleen cells from lean littermates or unrelated age-and sex-matched controls of the same strain. Killing was impaired only when the attacker cells were primed in vivo, not following in vitro priming. Hence the effect of the ob/ob genotype is not to produce an irreversible functional change in the lymphocyte, but rather to produce an environment in which lymphocytes are less able to react to priming antigen. Not only were the spleen cells of in vivo primed obese mice less active than those of lean controls, but also their number per spleen was significantly decreased. Such a quantitive difference was no longer found in adrenalectomised animals, but the qualitative difference in spleen cell cytotoxic activity still occurred. This suggests that adrenocortical hyperfunction may affect immune function in obese mice, without necessarily being the only factor in the in vivo environment of obese mouse spleen cells capable of depressing cellular immune reactivity.

Adrenalectomy↗
PubMed1988

Hypercortisolism and the resistance to dexamethasone suppression during gestation.

Maternal adrenocortical function was studied by measuring plasma cortisol and urinary free cortisol during gestation. Changes in suppressibility of pituitary-adrenocortical function were determined by dexamethasone administration. Urinary free cortisol as well as plasma cortisol increased during the course of gestation. The suppressibility by dexamethasone became less effective as pregnancy advanced. These results suggest that pregnant women have pituitary-adrenocortical hyperfunction and tissue refractoriness to glucocorticoid which increases during the course of gestation.

Adrenal Cortex↗
PubMed1989

Radiochemical diagnosis of adrenal disease.

The adrenal gland consists of cortical and medullary components, both of which may be functionally imaged using radiopharmaceuticals designed to take advantage of the specialized physiology of each tissue. Radiolabeled cholesterol derivatives are taken up by normal and abnormal adrenal cortex and provide an in vitro map of adrenocortical function in Cushing's Syndrome, hyperaldosteronism, and hyperadrenogenism. Quantification of uptake shows strong correlation with biochemical parameters of adrenocortical hyperfunction. In the case of incidentally discovered euadrenal masses scintigraphy may help to distinguish between benign, nonfunctional cortical adenomas, and destructive, potentially malignant lesions. Radiolabeled metaiodobenzylguanidine (MIBG) is a tracer of type I uptake and intracellular storage capacity for catecholamines in sympathomedullary tissues and tumors derived from this system. This permits the location of pheochromocytomas of all types (benign and malignant, intra- and extra-adrenal, sporadic and familial) as well as neuroblastomas in all stages. Other neuroendocrine tumors with type I uptake capacity may also be imaged. In suitable cases preliminary data suggests the administration of large doses of MIBG may permit internal radiotherapy of otherwise untreatable neuroendocrine tumors.

Adrenal Gland Diseases↗
PubMed1978

Adrenal function testing.

Glucocorticoid stimulation and suppression tests are essential to the definitive diagnosis of diseases of the hypothalamic-pituitary-adrenal axis, because they document abnormal physiologic control of hormonal secretion. Similarly, diseases of the renin-angiotensin-aldosterone axis are diagnosed by mineralocorticoid stimulation and suppression testing. [Ed. Note: See Moore TJ, Williams GH: Adrenal causes of hypertension, in this issue.] Unlike tests of glucocorticoid function, testing of the renin-angiotension-aldosterone system is more complicated, because knowledge of posture and dietary sodium are necessary to interpret the results. However, measurement of the tropic hormone renin and plasma levels of aldosterone can be accurately made, allowing precise definition of this system. Errors are most commonly encountered when dynamic tests of cortisol output are performed in patients taking medications that may interfere with the assays or with the metabolism of the administered compounds, such as dexamethasone or metyrapone. Abnormal, spurious values may also be obtained in some individuals who do not have adrenocortical hyperfunction if they are very obese or if testing is performed in a setting of clinical stress. Careful attention to these pitfalls will avoid errors and allow the clinician to arrive at the correct diagnosis.

17-Hydroxycorticosteroids↗
PubMed1990

[Immunoreactive trypsin in the blood serum of patients with endogenous hypercorticism].

Radioimmunoassay (RIA) was used to measure the response of serum trypsin to intravenous secretin and pancreozymin in 16 subjects with adrenocortical hyperfunction (group I) versus 6 subjects with hypercorticism (group II). In group I the enzyme reaction to the peptides was active and long-term. A similar rise in trypsin level occurred equally in patients free of chronic pancreatitis often present in Itsenko++ -Cushing syndrome. In group II patients RIA trypsin values comply with normal levels. The data obtained suggest an affected pancreatic status in adrenal hyperfunction both in the presence and absence of chronic pancreatitis which minimizes the informative value of the test in identification of chronic pancreatitis in endogenic hypercorticism.

Adult↗
PubMed1986

Diagnosis and pathophysiology of Cushing's syndrome.

Cushing's syndrome is the consequence of a sustained overproduction of cortisol (hydrocortisone) by the adrenal cortex. This may be due to excessive secretion of cortisol by functioning adrenocortical tumors or to "nontumorous" adrenocortical hyperfunction. The latter may be a result of stimulation of the adrenal cortex by increased release of corticotropin (ACTH) from a small pituitary tumor or from nonpituitary nonadrenal tumor. Carcinoids or carcinomas of the lung or pancreas, and even pheochromocytomas have caused the syndrome of ectopic ACTH production. The problems involved in the diagnosis of Cushing's syndrome are establishing its presence and determining the underlying cause. Treatment is then dependent upon the underlying pathogenetic lesion.

Adenoma↗
PubMed1992

Changes in adrenocortical lipid fluidity of hyperfunctioning human adrenals.

Lipid droplets, the storage places of cholesterol in adrenocortical cells, exhibit a relatively uniform appearance studied by the electron microscope but they are heterogeneous in respect of their optical polarizing properties. Optical birefringency was studied in cryosections of normal and hyperfunctioning adrenal cortex by a polarizing microscope, equipped with a cold/hot stage working in the temperature range from -40 to 40 degrees C. The majority of lipid droplets in normal adrenal cortex were optically anisotropic in each cortical zone at room temperature (22 degrees C) indicating a long-range molecular order of the lipid components. The lipids of the zona glomerulosa, in the cases of Conn's and Bartter's syndromes, became anisotropic when the temperature was lowered below ambient. The birefringency of the lipids of the zona fasciculata in the case of Cushing's disease was observed at temperatures below -10 degrees C indicating ordered packing of the components of lipid droplets at this temperature. Thus the lipids were more fluid in the hyperfunctioning, hormone-producing cells--this may represent an optimal precondition for their mobilization and processing by the hydrolyzing enzyme system. The changes in fluidity of the intracellular lipids can be attributed to different functional states in the adrenal cortex. Study of the thermotropic phase transitions of the lipid droplets by polarizing microscopy may be a useful additional method for the diagnosis of some adrenocortical diseases.

Adrenal Cortex↗
PubMed1989

Nuclear bodies in the normal and hyperfunctional human adrenal cortex.

Adrenal pieces obtained from six female patients, three without increased adrenocortical function and three with Cushing's disease, showed, in all adrenal cortex zones, cells containing simple and complex nuclear bodies. The simple nuclear bodies were spherical or ovoid and had a filamentous structure surrounded by a clear halo. Complex nuclear bodies were more numerous and heterogeneous in patients with adrenal pathology, and they were spherical with a proteinaceous filamentous capsule surrounding a core; the core was granular, filamentous or a mixture of granular and filamentous material, sometimes with a reticular or concentric arrangement. Some bodies showed vacuolar or multilocular aspect, and others had a close relationship with the nucleolus or appeared near the interchromatin granules. The meaning of adrenal nuclear bodies is discussed as well as their relationship with ACTH stimulation.

Adolescent↗