Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Hydroxycorticosteroids”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,153 records · Page 64Linked to original sources
PubMed1995

Exacerbation of rheumatoid arthritis after removal of adrenal adenoma in Cushing's syndrome.

A 46-year-old woman with rheumatoid arthritis had been on non-steroidal antiinflammatory agents for eighteen years until she developed cushingoid features and hypertension resistant to antihypertensive drugs. She had high plasma cortisol and 24 h urinary 17-hydroxycorticosteroids (17HCS) which were not suppressed by 8 mg dexamethasone per day for two days. The circadian rhythm of plasma cortisol was absent and plasma ACTH concentrations were suppressed before and after intravenous administration of CRH. Abdominal computed tomography demonstrated a tumor (3.0 x 3.0 x 2.3 cm) in the right adrenal gland and a 131I-6 beta-19-nor-methylcholesterol scan revealed marked uptake on the same side. The patient underwent a right adrenalectomy and the diagnosis of a cortisol secreting benign adenoma was histologically confirmed. Blood pressure declined and cushingoid features regressed, but three months after the operation and while the patient was on replacement, she complained of pain on motion, marked tenderness and swelling of fingers, wrists, elbows, knees and foot joints, and had very high rheumatoid factors. Treatment with immunosuppressive drugs and oral and intraarticular administration of glucocorticoids were necessary to relieve the clinical symptoms of rheumatoid arthritis. In summary, we report a patient with rheumatoid arthritis and Cushing's syndrome due to an adrenal adenoma, in whom rheumatoid arthritis was exacerbated after curing the Cushing's syndrome. This suggests that it is imperative to follow the development and/or course of autoimmune diseases after the treatment of Cushing's syndrome.

17-Hydroxycorticosteroids↗
PubMed1995

Young female patient with testosterone-producing adrenocortical adenoma also showing signs of subclinical Cushing's syndrome.

A 28-year old female patient with virilization due to left adrenocortical adenoma was studied. The patient had clinical features of hyperandrogenism such as hirsutism and a low pitched voice, but not of hypercorticoidism. Plasma testosterone and dehydroepiandrosterone-sulfate (DHEA-S) were high. Although the basal plasma cortisol concentration and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were within the normal range, the absence of diurnal variation in plasma cortisol and loss of suppressibility by dexamethasone suggested constitutive secretion of cortisol by the tumor. Inappropriate cortisol secretion was also supported by blunted ACTH response to provocative stimuli. After successful removal of the left adrenal tumor, such endocrinological abnormalities were all normalized. Immunohistochemical analysis revealed that tumor cells were positively stained for C21 hydroxylase cytochrome P-450 (P-450C21) and P-450(11) beta which convert 17-hydroxy (OH) progesterone to cortisol as well as P-450SCC, 3 beta-hydroxysteroid dehydrogenase and P-450(17) alpha which are involved in testosterone biosynthesis. These findings suggest that adrenocortical adenoma secretes predominantly testosterone and constitutively cortisol in a young woman patient with virilization.

17-Hydroxycorticosteroids↗
PubMed1995

Possible pre-Cushing's syndrome due to an adrenal adenoma incidentally discovered.

We demonstrated the functional evaluation of adrenal incidentaloma in 8 patients who had no abnormal finding associated with Cushing's syndrome. Adrenal tumors were incidentally discovered by abdominal echogram in 5 patients and by computed tomography (CT) in 3 patients. Serum cortisol levels and urinary excretion of 17-hydroxycorticosteroids (17-OHCS) were within normal limits in four of 8 patients. Urinary excretion of free cortisol was also within normal limits except for patient 8. Urinary excretion of 17-OHCS, however, was not suppressed by dexamethasone administration in five of 8 patients. Excretion of urinary 17-OHCS did not increase in response to metyrapone in 3 of 4 dexamethasone-insuppressible patients, but increased in 3 dexamethasone-suppressible ones. Serum cortisol increased in response to exogenous ACTH in all 6 patients examined. 131I-Adosterol accumulation was found in only the tumor side in 7 patients and bilaterally in one patient. Adrenalectomy was done in 7 patients, and microscopic findings showed adrenocortical adenoma. Serum cortisol was significantly suppressed in response to dexamethasone in the post-operative stage in all 7 patients examined. These results indicate that these adrenal incidentalomas seem to have a cortisol over-production which is dexamethasone-insuppressible and ACTH-dependent, and that they can be classified as "Pre-Cushing's Syndrome."

17-Hydroxycorticosteroids↗
PubMed1996

Incidentally discovered adrenocortical adenomas are not fully nonfunctioning: immunohistochemical and dispersed adrenocortical cell study.

To clarify the precise function of incidentally discovered adrenocortical adenoma, immunohistochemical and dispersed adrenal cell studies were performed. We have recently seen five patients with so-called nonfunctioning adrenocortical adenoma. Diurnal variation in plasma cortisol and suppression of plasma cortisol and urine 17-hydroxycorticosteroids in response to dexamethasone administration revealed adrenocortical function within normal limits in all cases, and no signs or symptoms of adrenal steroid hormone excess were evident. Since a high uptake of iodomethylnorcholesterol was recognized in each adrenal mass, it was supposed that these adrenal tumors produced steroid hormone to a certain extent, and each patient received unilateral adrenalectomy. P450c17, a key enzyme involved in cortisol production, was expressed in the tumor region in all cases in an immunohistochemical study. Upon in vitro steroidogenesis with dispersed adrenal cells in two cases, all steroid hormones measured except for aldosterone (progesterone, 17 alpha-hydroxyprogesterone, pregnenolone, 17 alpha-hydroxypregnenolone, 11-deoxycortisol, cortisol, 11-deoxycorticosterone, corticosterone, 18-hydroxydeoxycorticosterone, dehydroepiandrosterone and androstenedione) were produced in a culture medium. The results indicated that these tumors possessed the capacity for cortisol production, which was in agreement with the results of an iodomethyl-norcholesterol scintigraphy. All patients with mild hypertension or diabetes mellitus had no signs or symptoms of steroid hormone excess, but they could potentially develop a steroid excess syndrome such as Cushing's syndrome in the future.

17-Hydroxycorticosteroids↗
PubMed1997

ACTH-independent macronodular adrenocortical hyperplasia (AIMAH): report of two cases and the analysis of steroidogenic activity in adrenal nodules.

We report clinical findings and steroidogenic activities in adrenal tissues in 2 cases of AIMAH. Endocrine studies revealed an undetectable level of plasma ACTH and a diminished circadian rhythm of plasma cortisol. A significant increase in plasma cortisol levels in response to ACTH stimulation was observed in both cases. After the administration of metyrapone in one case, urinary excretion of 17-hydroxycorticosteroid (17-OHCS) significantly increased, although the plasma ACTH level did not respond. Computed tomography showed large masses in both adrenal glands, and bilateral uptake was identified on adrenal scintigraphy. The totals for the bilateral adrenal glands were 98 g and 105 g, respectively, and the left adrenal was larger than the right in both cases. Steroid content in the nodules measured by high performance liquid chromatography (HPLC) showed that the cortisol content was definitely lower than that in cortisol-producing adenoma (CPA) and even in normal adrenals. The activities of cytochrome P450c17, P450c21 and P450c11 were evaluated in one case, and all of them were reduced in the nodules. Especially that of P450c17 was remarkably reduced. These data suggest that cortisol production in AIMAH is inefficient, and that the cause of Cushing's syndrome may be related to the marked increase in the number of cells or bulk of the tumor.

17-Hydroxycorticosteroids↗
PubMed2001

Involvement of the cholinergic pathway in the pathogenesis of pituitary Cushing's syndrome.

Transsphenoidal adenomectomy is currently the first choice for treatment of patients with pituitary ACTH-dependent Cushing's syndrome. However, pharmacotherapy is prescribed for some patients, e.g., unsuccessful surgery. We treated a woman in whom pituitary Cushing's syndrome was improved while she was on antimuscarinic cholinergic agents, atropine sulphate and pirenzepine hydrochloride. The diminished effect of anticholinergics on ACTH and cortisol was incidentally identified in an inferior petrosal sinus sampling procedure. A single intramuscular injection of atropine significantly decreased both ACTH (43.9 pg/ml to less than 12.0; normal, 12.0-40.0 pg/ml) and cortisol (29.9 microg/dl to 13.6; normal, 7.6-23.6 microg/dl). An M1-muscarinic receptor specific antagonist, pirenzepine hydrochloride, also had a diminishing effect on these hormones and this inhibiting effect was partially blocked by the simultaneous administration of an anticholinesterase agent, pyridostigmine bromide. Chronic oral ingestion of these agents led to improvement in clinical symptoms, and urinary 17-hydroxycorticosteroid and 17-ketosteroid levels were at normal to upper-normal levels. This is the first documentation of involvement of the cholinergic system in the pathogenesis of pituitary Cushing's syndrome.

17-Hydroxycorticosteroids↗
PubMed1975

A case of acromegaly improved by pituitary apoplexy.

This report deals with a detailed course of one patient with acromegaly who had a pituitary apoplexy. The pituitary apoplexy occurred suddenly 5 days after administration of a oral hypoglycemic agent, buformin, during hospitalization. Immediately after the attack changes of the concentrations of several hormones such as serum growth-hormone, serum thyroid hormone and urinary 17-hydroxycorticosteroids were followed until the development to hypopituitary state. Simultaneously with the decrease of the concentrations of the above-mentioned hormones, a regression of the physical manifestations of acromegaly and a complete amelioration of diabetes mellitus were observed.

17-Hydroxycorticosteroids↗
PubMed1988

Phase-shifted diurnal rhythm of cortisol secretion in a patient with Cushing's syndrome due to adrenocortical adenoma.

A 21-year-old woman with Cushing's syndrome was found to have a marked diurnal variation in cortisol secretion. Serum cortisol concentrations and urinary excretion of 17-hydroxycorticosteroids were normal in the morning but clearly increased in the afternoon. The patient was cured by resection of an adrenocortical adenoma. ACTH and prostaglandin E1 stimulated cortisol release from incubated adenoma tissues in vitro. The cause of the abnormal diurnal rhythm of cortisol secretion is unknown.

17-Hydroxycorticosteroids↗
PubMed1989

Normotensive glucocorticoid-suppressible hyperaldosteronism in adult.

A 40 year-old man was admitted to our hospital for detailed examination of hypokalemia (2.7 mEq/l). His blood pressure was normal. Metabolic alkalosis, ACTH dependent hyperaldosteronism (18 ng/dl) and over-response to synthetic ACTH were observed. Plasma renin activity, on the other hand, was within the normal range (1.7 ng/ml/hr). Serum potassium was normalized to 4.1 mEq/l and the responsiveness of the renin-angiotensin-aldosterone system was recovered after the administration of dexamethasone. These results led us to suggest that this case might be normotensive glucocorticoid-suppressible hyperaldosteronism. The etiology which was not associated with hypertension and low plasma renin activity has not been clarified but may be related to the shortness of duration of this disease. Our case was also afflicted with mild hypercortisolemia and excessive excretion of urinary 17-hydroxycorticosteroid and 17-ketosteroid which was suppressed by the administration of dexamethasone (2 mg/day). These findings may be related to hypersensitivity of the fascicular zone of the adrenal gland to ACTH.

17-Hydroxycorticosteroids↗
PubMed1990

Combined reserpine and pituitary irradiation therapy for Cushing's disease patients following unsuccessful transsphenoidal microsurgery.

The effectiveness of treatment with reserpine and pituitary irradiation, and with reserpine alone was evaluated in three female patients with Cushing's disease whose transsphenoidal pituitary microsurgery (TPM) had been unsuccessful. In these patients, endocrinological examination after the surgery demonstrated a recurrence of the disease although the microadenomas had apparently been curetted out from the pituitary in all patients. The first patient therefore received 1.0-2.0 mg/day of reserpine with 60 Gy x-ray irradiation, and there was complete remission within 3 months and the patient remained asymptomatic even when reserpine was reduced to 0.1 mg/day 10 years later. The second case was treated with low dose x-ray (20 Gy) and reserpine (0.5-2.0 mg/day), which were also effective. However, 2 weeks discontinuation of the drug caused urinary 17-hydroxycorticosteroids (17-OHCS) and serum cortisol to increase abnormally again, but these were finally re-normalized by an additional administration of reserpine. The third case was given reserpine alone (1.0-2.0 mg/day). She also had a remission in 3 months and the treatment was continued for one year, requiring no further treatment. These results suggest that additional treatment with reserpine and pituitary irradiation or with reserpine alone after unsuccessful TPM may be an effective alternative for patients with Cushing's disease.

17-Hydroxycorticosteroids↗
PubMed1975

The excretion of individual adenocartical steroids during normal childhood and adolescence.

The excretion of 7 individual 17-oxosteroids and 7 individual corticosteroids in 24 h urine samples from 62 normal infants, children and adolescents, based on an accurate and specific paper chromatographic method for their separation and quantitation, is reported. The excretion of the 11-deoxy-17-oxosteroids gradually increases from 7 years of age and the increase becomes more rapid 2 or 3 years before the clinical signs of puberty appear. The rise continues throughout puberty and beyond it until the adult level is reached. The increase far exceeds that which would be accounted for by the growth of the individual. The increase in the excretion of the 11-oxy-17-oxosteroids with age is much more gradual. Androgens favour the formation of 5alpha metabolites and the 5alpha:5beta ratio of the total 5alpha 17-oxosteroids and the total 5beta 17-oxosteroids shows a statistically significant increase with age. In addition, a relatively high 5alpha:5beta ratio is noted in male infants, which is likely to be related to their relatively high plasma testosterone levels. The excretion of the 17-hydroxycorticosteroids and the alpha-ketolic metabolites of cortisol gradually rises with age and correlates with body weight. The alpha-ketolic metabolites of corticosterone are relatively high in infancy, but after the age of 4 years their excretion also correlates with body weight. An increase in the 5alpha:5beta ratio of allo-THF to THF is noted at puberty similar to that found with the 5alpha:5beta ratios of the 17-oxosteroids.

17-Hydroxycorticosteroids↗
PubMed1978

Circadian and circannual rhythms in plasma hormones and other variables of five healthy young human males.

Every other month (plasma) and every month (urine) circadian rhythms were documented during the course of 14 months. Annual changes were validated in the 24 h mean of: plasma FSH (annual crest time: February), LH (March), thyroxine (September), cortisol (February), renin activity (April), testosterone (October), urinary 17-hydroxycorticosteroids (March), aldosterone (March), potassium (May) as well as sexual activity (September) [self-recorded daily]. Plasma prolactin did not show an annual variation. In addition, annual changes in the circadian acrophase (crest time location in the 24 h scale) occurred for some of the documented variables: plasma thyroxine, cortisol, renin activity, testosterone, urinary aldosterone and potassium.

17-Hydroxycorticosteroids↗
PubMed1980

Investigation of the secretion and metabolism of cortisol during a 100 km race using [4-14C] and [11 alpha-3H] cortisol.

A mixture of [11 alpha-3H] and [4-14C] cortisol was administered orally to healthy men, following which urine was collected for 24 h. Four subjects acted as basal controls, going about their normal (sedentary) work; a further 3 resting subjects also received 100 mg cortisol orally (high cortisol controls) and 6 subjects competed in a 100 km race. Decreases in the carbon-14 specific activity of the cortisol metabolite excreted by the runners suggested that they secreted cortisol at 2-4 times the rate of the basal controls. This change was mirrored by the excretion of urine free cortisol but not by that of 17-hydroxycorticosteroids. The isotope ratio (3H:14C) of 11-hydroxy metabolites of cortisol from the runners was intermediate between those of the basal and high cortisol controls, from which we conclude that though the fractional oxidation of cortisol to cortisone is reduced by increasing the cortisol pool, it is not affected by exercise per se. This and other results show that although continuous running for 6-8 h, involving energy expenditure in excess of 25 megajoules, leads to a moderate increase in the rate of cortisol secretion, running per se does not appear to markedly affect the metabolism of cortisol.

17-Hydroxycorticosteroids↗
PubMed1983

Urinary free corticoids: an evaluation of their usefulness in the diagnosis of Cushing's syndrome.

We evaluated the usefulness of measurement of urinary free corticoids (UFC) in the diagnosis of hypercorticism. One hundred and thirty patients with features suggestive of Cushing's syndrome were examined. Twenty-six patients were proved to have Cushing's syndrome. The remaining 104 patients were considered not to have this disease on the basis of other investigations, and were designated as 'suspected patients'. UFC and 17-hydroxycorticosteroids were measured in all these patients in the basal state and on the 5th day of a low-dose-dexamethasone suppression test (3 mg/day for 5 days). UFC values of patients with Cushing's syndrome were well above 125 micrograms/24 h in the basal state and higher than 10 micrograms/24 h during the suppression test. UFC values of 'suspected patients' were between 20 and 125 micrograms/24 h in the basal state and below 10 micrograms/24 h during the suppression test. It can be concluded that the measurement of UFC in the basal state and on the 5th day of a suppression test is not only a very sensitive but also a specific method for the diagnosis of Cushing's syndrome.

17-Hydroxycorticosteroids↗
PubMed1984

Concomitant falls of plasma cortisol and ACTH levels in a case of Cushing's disease during treatment with trilostane.

A 72-year-old man with Cushing's disease was treated with trilostane, a competitive inhibitor of adrenal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSDH). The treatment with trilostane successfully lowered urinary excretion of 17-hydroxycorticosteroids (17-OHCS) and plasma levels of cortisol and elevated the plasma level of dehydroepiandrosterone. Unexpectedly, plasma ACTH fell from 109.7 +/- 45.0 to 42.7 +/- 27.3 pg/ml (P less than 0.01) in parallel with plasma cortisol. The hyperresponsiveness of plasma ACTH observed both in the metyrapone test and the lysine-vasopressin test was also ameliorated by treatment with trilostane. Then low dose of pituitary irradiation with cobalt-60 was added and his urinary excretion of 17-OHCS and plasma levels of cortisol decreased further. After treatment with trilostane was finally stopped, the plasma ACTH increased from 45.9 +/- 21.9 to 69.6 +/- 25.3 pg/ml (P less than 0.05) in parallel with plasma cortisol. Since then he has had no recurrence for 12 months. These observations suggest that trilostane, like other adrenal enzyme-inhibiting drugs, may induce unexpected improvement of the abnormality of the hypothalamic-pituitary axis present in Cushing's disease.

17-Hydroxycorticosteroids↗
PubMed1986

Single-dose metyrapone test at 06.00 h: an accurate method for assessment of pituitary-adrenal reserve.

One dose of metyrapone (1.5g) administered at 06.00 h, with subsequent measurement of 11-deoxycortisol and 17-hydroxycorticosteroid (17-OHCS) levels in plasma at 12.00 and 14.00 h, allowed accurate assessment of the pituitary-adrenal reserve. Normal response was defined as achieving a serum 17-OHCS level of more than 10.0 micrograms/100 ml and a 11-deoxycortisol level of more than 6.0 micrograms/100 ml at either 12.00 or 14.00 h. These criteria are based on a group of 18 persons with normal pituitary-adrenal axis, and 86 additional cases responded in this normal range. In this group of 104 subjects, 11-deoxycortisol levels rose to 9.2 +/- 3.5 micrograms/100 ml at noon and 17-OHCS levels to 15.4 +/- 4.7 micrograms/100 ml at 14.00 h. Post-metyrapone 17-OHCS levels were significantly higher than normal cortisol levels at these times (P less than 0.001) and than those observed at 08.00 h on the day of the test, demonstrating stimulation of adrenal corticoid production in addition to blockade of cortisol production by metyrapone. Thirty-one patients found to suffer from secondary adrenal failure showed impaired response. All these patients had limited pituitary-adrenal reserve, either proven by other pituitary-adrenal tests or implicated by severe pituitary disease.

17-Hydroxycorticosteroids↗
PubMed1995

A case of cyclical Cushing's disease associated with corticosteroid-binding globulin deficiency: a rare pitfall in the diagnosis of Cushing's disease.

We experienced an extremely unusual combination of Cushing's disease and corticosteroid-binding globulin (CBG) deficiency that has been reported in only one similar case to date. A 53-year-old woman presented at a medical clinic with clinical Cushing's disease. However, her plasma levels of adrenocorticotropin (ACTH) and cortisol were in the normal range. Six months later, during a second visit, a high urinary excretion of 17-hydroxycorticosteroids was found, but plasma ACTH and cortisol levels were normal again. Further investigation revealed a decreased CBG concentration. Free plasma cortisol levels were clearly elevated. Furthermore, the Cushing's disease of our patient was complicated by periodic secretion of ACTH and cortisol, with high or normal outputs of corticosteroids occurring alternately every 1-3 days, which explained the occasionally normal plasma ACTH and cortisol levels. A combination of a decreased serum CBG concentration and periodic secretion of ACTH can be an important pitfall in the diagnosis of Cushing's disease.

17-Hydroxycorticosteroids↗
PubMed1975

Studies on plasma corticosteroids in the rhesus monkey (Macaca mulatta).

The physiological regulation of the plasma corticosteroid concentration, measured by competitive protein-binding, was studied in female rhesus monkeys (M. mulatta) sedated with phencyclidine hydrochloride. Morning basal levels of plasma corticosteroids were found to be in the range 8-0-25-2 mug/100 ml, which is lower than that previously reported in this species. A circadian rhythm in plasma cortisol concentration was demonstrated. Prolonged sedation with phencyclidine was associated with a gradual increase in the plasma cortisol concentration. Synthetic alpha1-24 adrenocorticotrophic hormone given intravenously caused a rapid rise in plasma cortisol, the minimum effective dose was between 1 and 10 ng/kg body weight and the response was maximal after 1000 ng/kg. The administration of lysine-vasopressin and the induction of hypoglycaemia by insulin were both followed by an increase in the plasma corticosteroid concentration. Metyrapone caused a decline in plasma 11-hydroxycorticosteroids and a concomitant increase in total corticosteroids measured by competitive protein-binding. It is concluded that the hypothalamic-pituitary-adrenal system in the rhesus monkey functions in a manner which is qualitatively and quantitatively similar to that of man.

11-Hydroxycorticosteroids↗