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Results for “Adrenocortical Hyperfunction”

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At least 883 records · Page 49Linked to original sources
PubMed1978

The relationships between serum concentrations of 17OH-progesterone and other serum and urinary steroids in patients with congenital adrenal hyperplasia.

Simultaneous determinations of serum concentrations of 17OH-progesterone, testosterone, androstenedione, and progesterone, and of urinary excretion of 17-ketosteroids and pregnanetriol have been performed at intervals in 31 patients with the C21-hydroxylase form of congenital adrenal hyperplasia. In prepubertal patients there were highly significant correlations between levels of 17OH-progesterone and those of testosterone, androstenedione, and progesterone, respectively. Similar correlations were observed in adolescent girls. In adolescent boys rising 17OH-progesterone levels were reflected by increasing levels of androstenedione and progesterone, but there was no change in serum testosterone concentrations. Levels of serum 17OH-progesterone below 200 ng/dl were uniformly associated with normal serum concentrations of testosterone, androstenedione, and progesterone, and normal urinary 17-ketosteroid and pregnanetriol excretion. In contrast, levels above 1000 ng/dl were accompanied by increased levels of the other steroids except in adolescent males; in this group the finding of unchanging serum testosterone concentrations in spite of rising 17OH-progesterone levels presumably indicates that testosterone of adrenal origin causes suppression of testicular testosterone production, either through a direct effect upon Leydig cells or via suppression of LH release.

17-Ketosteroids↗
PubMed1978

Plasma aldosterone response to ACTH in primary aldosteronism and in patients with low renin hypertension.

ACTH alpha 1-24 was infused at incremental rates of 12.5-200 mIU/30 min in dexamethasone-suppressed hypertensive patients on a regular sodium diet. The plasma aldosterone response to this stimulus in 8 patients with hyperaldosteronism due to an adrenal aldenoma and 11 with adrenal hyperplasia was significantly greater at all infusion rates (P less than 0.05) when compared with the response in 6 normal subjects on a similar diet. This responsiveness to ACTH in the patients with primary hyperaldosteronism was similar to that of the normal subjects on a low sodium diet. Twelve patients with low renin and 6 patients with normal renin essential hypertension were similarly studied. There was no significant difference in the median aldosterone response between these 2 groups and the normal subjects on a normal diet, but the response was significantly lower compared with that in patients with primary hyperaldosteronism. These data show that patients with hyperaldosteronism from an adrenal adenoma or hyperplasia have a consistent and exaggerated response to ACTH. The hyper-responsiveness is not apparently shared by the majority of patients with low renin essential hypertension and does not support the concept that this group is an intermediate form of primary aldosteronism. Individual patients within this group, however, may have such a response and might be identified by this type of testing.

Adenoma↗
PubMed1979

The significance of elevated levels of plasma 18-hydroxycorticosterone in patients with primary aldosteronism.

Plasma 18-hydroxycorticosterone (180HB) concentration was measured in 23 patients with primary aldosteronism. After overnight recumbency, the levels were markedly elevated and were 6 times higher in patients with aldosterone-producing adenomas than in patients with hyperplasia. A value of 100 ng/dl or greater at 0800 h after overnight recumbency distinguished an adenoma from hyperplasia. There was no overlap of values, as was observed with plasma aldosterone concentration (PAC) at 0800 h and after 4 h of upright posture at 1200 h. There was a significant negative correlation between the ratio of 180HB to PAC and the potassium concentration in patients with primary aldosteronism due to hyperplasia. Potassium repletion with potassium chloride and/or spironolactone in patients with aldosterone-producing adenomas decreased the 180HB:PAC ratio by decreasing 180HB and increasing PAC. 180HB is an effective discriminator of an adenoma and may be a useful marker of the events in late aldosterone synthesis.

18-Hydroxycorticosterone↗
PubMed1979

An attenuated form of congenital virilizing adrenal hyperplasia.

The families of two patients with hirsutism and oligomenorrhea were studied with iv ACTH (Cortrosyn) stimulation. The parents responded with a combined incremental rise of progesterone and 17-hydroxyprogesterone greater than 6.5 ng/dl.min, a response seen in the heterozygote parents of patients with congenital virilizing adrenal hyperplasia (CVAH). One sibling in one family responded as do heterozygous subjects, while two other siblings responded normally. The abnormal response of the two pairs of parents and the sibling along with the pattern of steroid secretion observed in the propositi suggest that the so-called adult-onset CVAH is a mild form of the homozygous state of CVAH.

Adolescent↗
PubMed1980

Primary aldosteronism due to unilateral adrenal hyperplasia.

A 45-yr-old man with hypertension, hypokalemia, low plasma renin, and hyperaldosteronism was studied. Plasma and urine aldosterone were consistently above normal, remaining abnormally high even on a 300-meq sodium intake. Plasma aldosterone had a marked circadian rhythm, which was correlated with plasma cortisol. Aldosterone secretion was temporarily suppressed after dexamethasone administration and was stimulated by exogenous ACTH. The effect of posture was variable in the eight studies performed, possible due to episodic secretion of aldosterone observed near the sampling times of 0800 and 1200 h. Blood from the right adrenal vein contained 50--100 times more aldosterone than the left adrenal venous samples. The right adrenal gland was excised and found to contain many microscopic subcapsular nests of clear cells. Plasma aldosterone, renin, and potassium returned to normal after surgery, and blood pressure fell to 120/75 over the next 8 months. Three years later, the patient is normotensive without drugs.

Adrenalectomy↗
PubMed1982

The mean 1300-1600 h plasma cortisol concentration as a diagnostic test for hypercortisolism.

The 24-h mean plasma cortisol concentration was compared with the mean plasma cortisol concentrations during short subperiods of the day in 88 normal subjects and 223 patients with a very wide range of mean 24-h cortisol levels. The correlation between the 1300-1600 h mean plasma cortisol concentration and the mean 24-h plasma cortisol concentration was extremely high in all groups. Mean cortisol concentrations during this short subperiod powerfully discriminate cortisol hypersecretors (patients with Cushing's syndrome, anorexia nervosa, or prostate cancer) from normal controls. Hence, it is suggested that the mean or integrated 1300-1600 h plasma cortisol concentration can be used as a reliable afternoon cortisol test for the presence of hypercortisolism.

Adrenocortical Hyperfunction↗
PubMed1983

Primary cortisol resistance: a family study.

Primary cortisol resistance is an autosomal disease characterized by increased plasma cortisol concentration and high urinary free cortisol, resistance to adrenal suppression by dexamethasone, and the absence of clinical stigmata of Cushing's syndrome. The proband with the severe form had hypertension and hypokalemic alkalosis. In subjects with a less severe resistance to cortisol, there are no clinical abnormalities and the condition is revealed only by detailed examination of several parameters of cortisol secretion.

Adrenocortical Hyperfunction↗
PubMed1987

Cyclical edema and hypokalemia due to occult episodic hypercorticism.

Yearly episodes of edema, hypokalemia, anxiety, and depression were found to be due to cortisol and deoxycorticosterone surges secondary to a pituitary adenoma in a woman without any of the usual clinical features of Cushing's syndrome. During the long clinical remissions, she had no recognizable laboratory abnormality. She had two episodes in the year following incomplete transphenoidal pituitary tumor resection, but has had none in 2 yr since receiving radiotherapy. The episodes were caused by mineralocorticoid actions of large ACTH-induced increases in cortisol and deoxycorticosterone secretion. A history of episodic edema and hypokalemia, often attributed in women to surreptitious diuretic abuse, requires a careful search for hypercorticism even in the absence of clinical Cushing's syndrome.

Adenoma↗
PubMed1987

Decreased deoxyribonucleic acid binding of glucocorticoid-receptor complex in cultured skin fibroblasts from a patient with the glucocorticoid resistance syndrome.

A patient with the syndrome of glucocorticoid resistance was studied. A 27-yr-old woman initially was diagnosed as having Cushing's disease, based on the findings of high plasma ACTH and serum cortisol levels, increased urinary cortisol secretion, resistance to adrenal suppression with dexamethasone, and bilateral adrenal hyperplasia by computed tomography and scintigraphy of the adrenal glands. However, she had no signs or symptoms of Cushing's syndrome. During a 5-yr follow-up, no clinical abnormalities developed, although hypercortisolism persisted. End-organ resistance to cortisol was suspected. To explain the end-organ resistance to cortisol, the glucocorticoid receptors (GR) in peripheral mononuclear leukocytes and cultured skin fibroblasts from a forearm skin biopsy were characterized and compared with the results of similar studies in normal subjects. The patient's GR in whole cell assays had an increased dissociation constant (Kd). In the cytosol of cultured skin fibroblasts from the patient, there was also decreased binding capacity. The thermal stability and the sedimentation coefficient in a sucrose density gradient of the receptors in the cytosol of cultured skin fibroblasts from the patient and normal subjects were similar. GR complex activation, analyzed by DEAE-cellulose chromatography, was decreased in the patient. DNA binding of the GR complex after temperature-induced activation was lower in the patient than in normal subjects. Nuclear translocation of GR complexes from the patient was also slightly decreased. These results suggest that the patient's glucocorticoid resistance was due to a decrease in the affinity of the receptor for glucocorticoids and a decrease in the binding of the GR complex to DNA.

Adrenocortical Hyperfunction↗
PubMed1988

Hypercortisolism in patients with functional hypothalamic-amenorrhea.

Hypercortisolism was found in patients with functional hypothalamic amenorrhea (HA) in preliminary short term studies conducted during the morning hours (0800-1100 h). This observation prompted us to characterize the circadian and pulsatile patterns of serum cortisol and LH levels at 15-min intervals for 24 h in 10 women with functional HA and in 7 normal women during the early follicular phase of their cycles. The mean integrated 24-h serum cortisol levels (area under the curve) were significantly (P less than 0.01) higher in the HA patients than in normal women. The mean cortisol levels in the HA patients were elevated (P less than 0.005) compared to those in the normal women during the daytime hours (0800-1600 h), but not during the evening (1600-2400 h) and sleeping hours (2400-0800 h). This selective hypercortisolism during the waking period of the day was almost entirely related to increased duration and amplitude of secretory episodes (peak area) rather than a change in pulse frequency. The serum cortisol increments in response to a noon meal that occurred in normal women were markedly impaired (P less than 0.01) in the HA patients. Compared with that in the normal women, mean LH pulse frequency was reduced by 30% in the HA patients. The 24-h mean LH levels and mean LH pulse amplitude were not significantly different from those in the normal women. However, among the HA patients there were marked individual differences in LH pulse frequency and amplitude, with prolonged interpulse quiescent periods, indicative of dysfunction of the hypothalamic GnRH pulse generator. We conclude that neuroendocrine activation of the ACTH-adrenal axis and inhibition of the GnRH pulse generator in women are associated with HA. Further, spontaneous resumption of normal cyclicity occurred in the majority (8 of 10) of the HA patients with no medical treatment, suggesting that this syndrome is a reversible hypothalamic disorder of a functional nature.

Adrenocortical Hyperfunction↗