[Effect of prednisone & prednisolone on adrenocortical androgenic hyperfunction].
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Adrenal Hyperplasia, Congenital↗
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Effects of chronic glucocorticoid excess in man on insulin binding to circulating cells: differences between endogenous and exogenous hypercorticism.
We measured [125I]insulin binding to circulating monocytes or erythrocytes from 16 patients with chronic glucocorticoid excess, 9 chronically treated with prednisone and 7 with adrenocortical hyperfunction. With monocytes, [125I]insulin binding was iincreased in all patients. Analysis of binding data indicated that increased binding in patients treated with prednisone was due to an ncrease in receptor concentration, whereas in patients with adrenocortical hyperfunction, it was due to an increase in receptor affinity. With erythrocytes from patients with adrenocortical hyperfunction there was an increase in receptor affinity and a decrease in receptor concentration, so that the binding of [125I]insulin was normal. The disparity of results between endogenous and exogenous hypercorticism, between the two cell types, and between the present studies and previous studies suggest that the effects of glucocorticoid excess on the insulin receptor are extremely complex and wide-ranging and that in this condition, extrapolations in humans from data with circulating cells to liver and muscle may not be appropriate.
Adolescent↗
The central mechanism of hypothalamic-pituitary-adrenocortical system hyperfunction in depressed patients.
While hypercortisolemia is commonly observed in depression, exactly where in the hypothalamic-pituitary-adrenocortical (H-P-A) axis this dysfunction arises remains undefined. In attempting to distinguish between central or peripheral locus of dysfunction, we studied in 12 patients (10 females, two males) with primary major depression and eight age-matched controls (six females, two males) in their adrenal cortisol response to infused adrenocorticotropic hormone (ACTH) (cosyntropin 0.05 microg/kg bodyweight) while endogenous ACTH was suppressed with 1 mg of dexamethasone. Compared with the control group, pre-dexamethasone plasma baseline cortisol level was significantly higher in depressed patients while ACTH level remained normal. Post-dexamethasone responses of both hormones were greatly non-suppressed in the depressed group. Exogenous cosyntropin-elicited rise in plasma cortisol was significantly lower in depressed patients while the ACTH response was not significantly different. These findings suggest that an adrenal cortisol response to ACTH was significantly decreased during depression as compared with normals in Chinese depressed patients. Therefore, the central mechanism of hyperfunctioning H-P-A axis causing hypercortisolemia should be emphasized.
Adolescent↗
Plasma and salivary 6beta-hydroxycortisol measurements for assessing adrenocortical activity in patients with adrenocortical adenomas.
The aim of this study was to examine and compare the potential usefulness of plasma and salivary 6beta-hydroxycortisol measurements for assessing adrenocortical activity in patients with adrenocortical adenomas. Plasma and salivary cortisol as well as 6beta-hydroxycortisol determinations were performed by radioimmunoassay after extraction with ethyl acetate followed by chromatographic separation using a modified paper chromatographic system. Samples were obtained from 36 control subjects and 37 patients with non-hyperfunctioning adrenocortical adenomas in the morning at 8 a.m. after a low-dose of dexamethasone and after stimulation with synthetic depot ACTH. Basal and post-dexamethasone hormone levels were also measured in plasma and salivary samples of 4 patients with Cushing's syndrome from adrenal adenomas. In the baseline state, patients with non-hyperfunctioning adrenocortical adenomas had significantly higher plasma and salivary 6beta-hydroxycortisol levels (mean+/-SE, 79.0+/-7 and 17.1+/-2.2 ng/dl, respectively) compared to those measured in controls (62.0+/-4 and 7.7+/-0.6 ng/dl, respectively), whereas baseline plasma and salivary cortisol levels (9.6+/-0.5 microg/dl and 342+/-39 ng/dl, respectively) were similar to those measured in the control group (9.9+/-0.4 microg/dl and 366+/-24 ng/dl, respectively). In all groups, the changes in plasma and salivary 6beta-hydroxycortisol concentrations after dexamethasone suppression and ACTH stimulation were similar to the changes in plasma and salivary cortisol levels, although the differing ratios of 6betaOHF to cortisol indicated potentially important variations in the induction of 6beta-hydroxylase activity between the three groups. In patients with Cushing's syndrome, baseline plasma and salivary 6beta-hydroxycortisol concentrations (754+/-444 and 104+/-88 ng/dl, respectively) were more markedly increased than plasma and salivary cortisol levels (24.8+/-6.7 microg/dl and 1100+/-184 ng/dl, respectively), and all remained non-suppressible after dexamethasone administration. These results suggests that plasma and salivary 6beta-hydroxycortisol determinations may precisely detect not only overt increases of cortisol secretion in patients with Cushing's syndrome but also mild glucocorticoid overproduction presumably present in patients with non-hyperfunctioning adrenocortical tumors.
Adrenal Cortex Neoplasms↗
Osmoregulation of systemic vasopressin release during long-term glucocorticoid excess: a study in dogs with hyperadrenocorticism.
In 9 dogs with pituitary-dependent hyperadrenocorticism and in 6 dogs with hyperfunctioning adrenocortical tumours, the osmoregulation of arginine vasopressin (AVP) release was investigated by iv infusion of 20% NaCl for 2 h at a rate of 0.03 ml per kg body weight. The responses were analysed in terms of sensitivity and threshold of the osmoregulation of AVP secretion. The sensitivity was normal in 6 dogs and lowered in 9. In 4 of the latter dogs there was complete absence of a response to hypertonicity. The osmotic threshold of AVP release was raised in 9 dogs and normal in 2 dogs, whereas in the four dogs without any response the term threshold was not applicable. The results were not different for dogs with pituitary-dependent hyperadrenocorticism and dogs with hyperfunctioning adrenocortical tumour. It is concluded that corticosteroid excess per se induces a marked impairment of the osmoregulation of AVP secretion. The loss of reactivity of the osmoreceptor system may contribute to the corticosteroid-induced polyuria, which is also the result of resistance to AVP in the kidney.
Adrenal Cortex↗
Magnetic resonance imaging of adrenocortical adenomas in childhood: correlation with computed tomography and ultrasound.
There are few descriptions of the magnetic resonance (MR) appearance of hyperfunctioning adrenocortical tumours, particularly those occurring in childhood. We studied five patients, two girls and three boys, aged 6-14.3 years, presenting with clinical syndromes of adrenocortical hyperfunction. The diagnoses were Cushing's syndrome (n = 2), virilisation (n = 2), and Conn's syndrome (n = 1). Biochemical features suggested an adrenal lesion in each case. MR and ultrasound were performed in all five cases, with CT in four. Each patient had a functional adrenal tumour secreting either cortisol, androgens or aldosterone alone, or a combination of cortisol, androgens and oestradiol. The histological diagnosis was adenoma in four cases and tumour of indeterminate nature in one case. MR clearly showed the tumours (diameter 1.0-7.5 cm), all the lesions being of high signal intensity relative to liver on T2-weighted sequences. CT revealed an adrenal mass in each of the four patients scanned, three of which enhanced after intravenous contrast medium injection. The multiplanar imaging of MR allowed better distinction from adjacent structures and also demonstrated an unenlarged contralateral adrenal gland. In the patient with a 1-cm Conn's adenoma the lesion was more easily seen on MR than CT. Ultrasound showed the four larger tumours but was unable to visualise the contralateral adrenal or the Conn's adenoma. In conclusion, the MR appearances of four adrenocortical adenomas and one indeterminate tumour in children are described. MR has been found to be at least equal to CT in the detection of these tumours, with some possible advantages. Both techniques are superior to ultrasound.
Adenoma↗
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↗
[Immunoreactive trypsin in the blood serum of patients with endogenous hypercorticism].
Basal immunoreactive serum trypsin (RIT) was determined in comparative study of 46 patients with adrenocortical hyperfunction and 24 patients with hypocorticism for specifying the potentialities of the diagnostic test. Excess of endogenous corticosteroids is accompanied by a marked increase in the RIT serum concentration, this increase is particularly pronounced in Itsenko-Cushing syndrome and in exacerbations of Itsenko-Cushing disease in comparison with its level in Itsenko-Cushing disease remission. The presence of steroid diabetes had no significant RIT changes in Itsenko-Cushing disease. Attendant chronic pancreatitis that developed in patients with adrenocortical hyperfunction had no influence on blood serum RIT content. In patients with adrenal steroid deficiency who did not take glucocorticoids the serum RIT concentration was lower than that in those who constantly used hormones. RIT is increased in cases of chronic pancreatitis combined with chronic adrenal insufficiency. Measurement of the basal serum RIT may contribute to the diagnosis of pancreatitis in patients with hypocorticism but provides no information on this pathology in patients with endogenous hypercorticism.
Adolescent↗
The prevalence of antibodies against Toxoplasma gondii among hospitalized animals and stray dogs.
Hospitalized animals and stray dogs were serologically tested for antibodies against Toxoplasma gondii. In addition, the data were examined for the possibility of toxoplasmosis infection being associated with the clinical diagnosis and with the discharge status (alive vs. dead). Among 1056 hospitalized animals, 17 (20%) of 86 cats, 112 (14%) of 804 dogs, 34 (26%) of 133 horses and 6 (18%) of 33 cattle had serological evidence of infection with T. gondii. Only 22 (6%) of 342 young (median age = one year) stray dogs were seropositive. The difference in antibody prevalence between hospitalized and stray dogs was thought to be due to age and dietary factors. Of 249 dogs grouped by clinical diagnosis, there was significantly (p less than 0.01) higher prevalence of seropositives among dogs with diseases of the kidney or with adrenocortical hyperfunction than among dogs hospitalized for other diseases. Of 19 dogs with diseases of the kidney and 12 with adrenocortical hyperfunction 37% and 42%, respectively, were seropositive.. There was higher risk of being discharged from the hospital dead among seropositive dogs, cattle and horses than among seronegative animals of the same species. The exception was cats, where of 69 seronegative cats 29% were dead at discharge and where of 17 seropositive cats 18% were dead at discharge. The possible effects of stress due to hospitalization need further research.
Animals↗
Elevated luteinizing hormone induces expression of its receptor and promotes steroidogenesis in the adrenal cortex.
Transgenic (TG) female mice expressing bLHbeta-CTP (a chimeric protein derived from the beta-subunit of bovine luteinizing hormone [LH] and a fragment of the beta-subunit of human chorionic gonadotropin [hCG]) exhibit elevated serum LH, infertility, polycystic ovaries, and ovarian tumors. In humans, increased LH secretion also occurs in infertility and polycystic ovarian syndrome, often concomitant with adrenocortical dysfunction. We therefore investigated adrenal function in LH overexpressing bLHbeta-CTP female mice. The size of their adrenals was increased by 80% with histological signs of cortical stimulation. Furthermore, adrenal steroid production was increased, with up to 14-fold elevated serum corticosterone. Primary adrenal cells from TG and control females responded similarly to ACTH stimulation, but, surprisingly, the TG adrenals responded to hCG with significantly increased cAMP, progesterone, and corticosterone production. LH receptor (LHR) expression and activity were also elevated in adrenals from female TG mice, but gonadectomized TG females showed no increase in corticosterone, suggesting that the dysfunctional ovaries of the intact TG females promote adrenocortical hyperfunction. We suggest that, in intact TG females, enhanced ovarian estrogen synthesis causes increased secretion of prolactin (PRL), which elevates LHR expression. Chronically elevated serum LH, augmented by enhanced PRL production, induces functional LHR expression in mouse adrenal cortex, leading to elevated, LH-dependent, corticosterone production. Thus, besides polycystic ovaries, the bLHbeta-CTP mice provide a useful model for studying human disorders related to elevated LH secretion and adrenocortical hyperfunction.
Adrenal Cortex↗
Evaluation of steroid laboratory tests and adrenal gland imaging with radiocholesterol in the aetiological diagnosis of Cushing's syndrome.
Basal values of the urinary excretion of 17-oxogenic steroids and serum levels of cortisol were not satisfactory in the differentiation of 'suspected' subjects from patients with true Cushing's syndrome. With an RIA method for serum cortisol determination, the overnight dexamethasone suppression test provided the most reliable single test in establishing adrenocortical hyperfunction. Thirty-five normal subjects, fifty-nine obese patients, thirteen 'suspected' patients, and thirteen patients with disease states other than Cushing's syndrome had suppressed values below 4.0 microgram/100 ml. None of the ten patients with Cushing's syndrome had a cortisol concentration less than 16.3 microgram/100 ml. Adrenal gland scintigraphy after radiocholesterol injection is a more valuable tool than the metyrapone test and the high-dose dexamethasone suppression test in the localization and differential diagnosis of adrenocortical lesions causing Cushing's syndrome. It obviates the need for angiographic procedure in the localization of adenomas. It is a reliable technique for identifying functioning adrenal remnants. We therefore propose a schedule for studying patients with suspected adrenocortical hyperfunction.
17-Ketosteroids↗
A model for later-life effects of perinatal drug exposure: maternal hormone mediation.
In the female rat chronic ethanol intake increased plasma levels of corticosterone; acute stress in the pregnant or lactating rat increased plasma levels of corticosterone in the fetuses or sucklings. In the lactating rat, corticosterone rapidly equilibrated between plasma and milk, so that variations in the mother's adrenocortical secretion could be promptly reflected in the suckling's body. The role of maternal adrenocortical hormone with regard to the development of pituitary-adrenocortical and behavioral activities was indicated by endocrine (plasma corticosterone), neurochemical (hippocampal corticosterone binding) and behavioral (avoidance performance) anomalies in the adult offspring of lactating rats with adrenocortical "hyperfunction" or "insufficiency." Further, the offspring of rats with adrenocortical "insufficiency" showed abnormalities in "in vitro" hypothalamus, pituitary and adrenocortex release of hormones. When searching for later effects in the offspring of drugs given to the mother in perinatal life one must be cognizant that, aside from their expected pharmacological action, drugs can produce variations in the mother pituitary-adrenocortical activity, sensed by the conceptus through the placenta or milk.
Adrenocortical Hyperfunction↗
Perianal adenomas and hypertestosteronemia in a spayed bitch with pituitary-dependent hyperadrenocorticism.
Hypertestosteronemia was diagnosed in a spayed bitch with pituitary-dependent hyperadrenocorticism and perianal adenomas. Serum concentrations of cortisol and testosterone decreased after treatment with mitotane was instituted. Excessive testosterone in this dog was thought to have been produced by the adrenal cortex, possibly in response to excessive ACTH concentrations. Development of androgen- or estrogen-responsive tumors in castrated dogs may be an early indication of adrenocortical hyperfunction.
Adenoma↗
Studies on ectopic ACTH-producing tumors. II. Clinical and biochemical features of 30 cases.
This report describes the clinical and biochemical features of 30 cases of ectopic ACTH-producing tumors diagnosed by the detection of ACTH in the tumor tissues. Several uncommon tumors, such as tumors of the esophagus, stomach, and larynx, were included in this series. None of the patients with bronchogenic carcinoma showed signs of classical Cushing's syndrome, whereas 7 of the remaining 13 patients with other tumors were Cushingoid in appearance. Adrenocortical hyperfunction was present in 61 percent at the first examination and developed during the course of the disease in 18 percent more. In the remaining patients (21 percent), adrenocortical function remained within normal limits. These results indicate that there exist ectopic ACTH-producing tumors without clinical and biochemical sequelae of excess hormone. In some of the tumor extracts studied, MSH and CRF-like activities and serotonin were detected. This suggests that multiple hormone production is not uncommon in ectopic ACTH-producing tumors.
Adrenocortical Hyperfunction↗
Defective cortisol binding globulin affinity in association with adrenal hyperfunction: a case report.
A patient with an apparent abnormality of cortisol binding globulin (CBG) is reported. Investigations showed that while the plasma CBG binding capacity (equivalent to the plasma CBG concentration) was normal, the binding affinity was reduced by a factor of four. The significance of this observation is discussed with regard to its possible role in the development of the adrenocortical hyperfunction also seen in this patient.
Adrenocortical Hyperfunction↗
[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↗
[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↗
Cushing's syndrome secondary to adrenocorticotropin-independent macronodular adrenocortical hyperplasia due to activating mutations of GNAS1 gene.
ACTH-independent macronodular adrenal hyperplasia (AIMAH) is an uncommon cause of Cushing's syndrome characterized by bilateral nodular adrenocortical hyperfunction in the presence of suppressed ACTH levels. We investigated whether activating mutations in the ACTH receptor (MC2-R) or G(s alpha) (GNAS1) genes might be involved in AIMAH genesis. Five women with Cushing's syndrome due to AIMAH, confirmed by histological studies, and no signs of McCune-Albright syndrome were selected for molecular analysis of these genes. The single exon of the MC2-R gene and exons 8 and 9 of the GNAS1 gene were amplified by PCR in genomic DNA from adrenal nodules and peripheral blood. Direct sequencing revealed only MC2-R wild-type sequences. GNAS1 PCR products at denaturing gradient gel electrophoresis revealed abnormal migration patterns in adrenal tissues of three patients. Automatic sequencing showed two different activating mutations at codon Arg(201) of GNAS1, a substitution by histidine in two cases and by serine in one case. In conclusion, we found two different gsp mutations in three patients with Cushing's syndrome due to AIMAH, and we speculate whether they belong to the spectrum of McCune-Albright syndrome or whether these are the first reported cases of AIMAH due to gsp mutations.
Adrenocortical Hyperfunction↗