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PubMed1974

Measurement of the dynamics of stimulation and inhibition of steroidogenesis in isolated rat adrenal cells by using column perfusion.

Isolated adrenal cells were perfused in a small column by using Bio-Gel polyacrylamide beads as an inert supporting matrix, and the time-course of the response to various stimuli was observed by measuring fluorogenic 11-hydroxycorticosteroids in the effluent. A small but significant response was observed 1 min after stimulation with physiological concentrations of ACTH (adrenocorticotrophin), but the response did not start to build up rapidly for 3-4min and eventually reached a plateau after 9-10min. A similar pattern of events was observed for the decay of the steroid output on removal of ACTH. ACTH analogues, including one with a long duration of action in vivo, were found to produce responses with similar kinetics. However, cyclic AMP caused a more rapid increase in steroidogenesis and its effects were more short-lived after withdrawal. If, as present evidence suggests, cyclic AMP is produced rapidly after ACTH stimulation the delayed build-up of the steroidogenic response to ACTH would indicate that cyclic AMP may not be the intracellular mediator. When inhibitors were applied during ACTH stimulation, aminoglutethimide, which blocks mitochondrial conversion of cholesterol into pregnenolone (3beta-hydroxypregn-5-en-20-one), caused a rapid fall in steroid output (1 min), whereas cycloheximide took longer to achieve its full effect. Nevertheless, the response had fallen by 50% in 2 min, indicating a much shorter half-life than that previously reported for the labile protein implicated in steroidogenesis. In addition the rapid response to cyclic AMP makes it unlikely that steroid production is induced as a result of initiation of protein synthesis. This suggests that the labile protein plays an obligatory but permissive role in the development of the response. Column perfusion has proved to be a simple technique which can readily yield accurate data on responses of cells to stimulants and inhibitors.

Acrylamides↗
PubMed2002

Effects of a 1 day fast on biohumoral variables associated with human circadian rhythmicity.

1. The aim of the present study was to investigate the effects of a short (1 day) fast by testing biohumoral variables associated with the human circadian rhythm. 2. Fifteen clinically healthy male volunteers (32 +/- 8 years old) participated in the study. Subjects were fed a control diet for 7 days. The last day was a control day and the following 8th day was the fasting day. Each subject was asked to collect urine seven times over a 24 h period. Chemical and hormonal variables were measured in each fractionated urine specimen. The time- qualified urinary excretion rates were biometrically analysed using conventional and chronobiological methods. 3. During fasting, significant incremental changes were detected in the urinary excretion rates of potassium, aldosterone, 17-hydroxycorticosteroids and adrenaline and significant decremental changes were detected in the excretion rates of sodium, chloride, creatinine, urea nitrogen, uric acid, 17-ketosteroids, noradrenaline and dopamine. The circadian rhythmicity of the variables was well preserved and remained almost stable throughout the fasting phase. 4. Fasting affected the mean oscillatory levels and oscillatory amplitudes of variables, suggesting that nutrients may have played roles as tonic and phasic modulators on the mechanisms that physiologically regulate ircadian rhythmicity.

Adult↗
PubMedDate not supplied

Skin manifestations of Cushing disease in children and adolescents before and after the resolution of hypercortisolemia.

Cushing disease (CD) is a common cause of endogenous hypercortisolism in childhood. Its skin manifestations include striae, facial acne, hirsutism, acanthosis nigricans, fungal infections, hyperpigmentation and easy bruisability. We followed 36 children and adolescents with CD (14 boys and 22 girls), to define the natural history of skin disease in endogenous hypercortisolism. Physical examination and 24 hour urinary free cortisol (UFC) and 17-hydroxycorticosteroid (17-OHS) excretion values were obtained preoperatively and quarterly for 18 months. Preoperatively our patients exhibited purple subcutaneous striae (77.7%), steroid-induced acne (58.3%), hirsutism (63.7% of the 22 girls), acanthosis nigricans (27.7%), ecchymoses (27.7%), hyperpigmentation (16.6%), and fungal infections (11.1%). The levels of UFC and 17-OHS preoperatively were 351.84+/-243.85 microg/m2/day (mean+/-SD) and 17.92+/-7.86 mg/g creatinine/day, respectively. No correlation was found between these levels and the severity of the lesions. All patients were cured. Symptoms decreased dramatically within the 3 postoperative months and progressively disappeared within the first year of the follow-up period with the exception of light-colored striae; they were present in 5.6% of the patients at 18 months postoperatively. No acanthosis nigricans or hyperpigmentation were observed at 3 months postoperatively. Hirsutism was not present at 9 months postoperatively. We conclude that in children with CD the skin is affected at multiple sites; however, the severity of the manifestations does not correlate with the biochemical indices of the disease. With the exception of striae, cutaneous effects of endogenous hypercortisolism completely heal within the first year after surgical cure of the disease.

Adolescent↗
PubMedDate not supplied

[Hormonal findings in obese children. A review].

Serum thyroid hormones in childhood obesity are not altered but caloric intake affects monoiodination of T4 to T3 and rT3. Plasma cortisol and urinary free cortisol concentrations are normal. Increase in cortisol production and secretion rate is reflected in increased values of urinary 17-hydroxycorticosteroids. Elevated urinary 17-ketosteroids are caused by increased androgen synthesis accounting for the increased height velocity in obese preadolescents and for the accelerated skeletal maturation. In both sexes earlier onset of puberty is noticed without remarkable alterations in gonadal steroids. Whether altered prolactin concentrations reflect neuroendocrine abnormalities remains unclear. Impairment of growth hormone release in face of normal or high somatomedins is not of clinical significance. Basal and stimulated insulin concentrations are high. Insulin resistance exists because glucose tolerance is simultaneously impaired. This is due to reduction in insulin receptor numbers and post-receptor defects in insulin action. Weight loss is effective in normalizing the above mentioned hormonal defects.

Adolescent↗
PubMed1995

Characterization of 11 beta-hydroxysteroid dehydrogenase activity in fetal and adult ovine tissues.

11 Beta-hydroxysteroid dehydrogenase (11 beta-HSD) converts 11-hydroxycorticosteroids to 11-oxocorticosteroids, thereby influencing the availability of bioactive cortisol or corticosterone in target tissues. The activity of this enzyme was investigated in sheep by: (1) measuring relative 11 beta-HSD activities in kidney, liver and placenta, and in various areas of the brain (hypothalamus, hippocampus, and brainstem); (2) characterizing the optimum pH of activities in the tested tissues; (3) investigating the possible effect of gonadal steroids on 11 beta-HSD activity in adult hypothalamus and kidney; and (4) investigating possible developmental changes in activities in the tested tissues. The optimum pH in liver and placenta was pH 9-10, whereas the optimum pH in kidney was pH 7-8. In tissues from adult ewes, 11 beta-HSD activity was highest in liver (84.6 +/- 3.8%) and kidney (49.8 +/- 11.6%), lower but measurable in pituitary (38.8 +/- 3.7%), and near the limit of detection in hypothalamus and hippocampus (2.7 +/- 0.9% and 3.2 +/- 0.8% respectively). Liver, kidney and pituitary from late-gestation fetal sheep contained activities which were similar to those in the adult (76.9 +/- 4.5%, 66.0 +/- 6.7% and 26.3 +/- 3.0% respectively). Activity in the pituitary was not related to fetal gestational age. Placenta also contained measureable 11 beta-HSD activity (21.4 +/- 4.7%). However, no activity was detected in hypothalamus (-1.7 +/- 0.2%), hippocampus (-0.2 +/- 0.6%) or brainstem (-1.0 +/- 0.6%) in late-gestation fetal or neonatal sheep. Enzyme activities in kidney and hypothalamus did not change significantly when the circulating concentrations of ovarian steroids were altered over a 1-3-week period. It is concluded that the ovine kidney, liver and placenta, but not hypothalamus or cerebral cortex, contain 11 beta-HSD activity. In addition, there is no change in 11 beta-HSD activity between late-gestation fetal life and adult life, and the relative activities are not altered by the ovarian steroid milieu.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMed1995

Ontogeny of 11 beta-hydroxysteroid dehydrogenase in ovine fetal kidney and lung.

Eleven-beta-hydroxysteroid dehydrogenase (11 beta-HSD) is an enzyme which degrades 11-hydroxycorticosteroids to biologically inactive 11-oxocorticosteroids (cortisone and 11-dehydrocorticosterone). In some tissues, the activity of this enzyme prevents binding of cortisol to mineralocorticoid receptors. The present experiments were designed to test the hypothesis that the fetal kidney contains 11 beta-HSD, that the activity of 11 beta-HSD in fetal kidney increases near term, and that the fetal lung does not contain significant 11 beta-HSD activity. In kidney and lung tissue from 23 fetal sheep ranging in age between 86 and 145 days' gestation, we measured 11 beta-HSD activity. We found significant activity in fetal kidney (14-85% conversion from cortisol to cortisone) but no measurable activity in fetal lung (0-9%). The activity of 11 beta-HSD was significantly related to fetal gestational age (r = 0.76, n = 14). We conclude that 11 beta-HSD activity in the fetal kidney develops as a function of fetal gestational age, and that activity cannot be demonstrated in fetal lung. We speculate 11 beta-HSD in the fetus might function to alter the sensitivity of target organs to glucocorticoids, as well as to mineralocorticoids, and that the absence of activity in the lung allows a high sensitivity of pulmonary tissue to cortisol at the end of gestation.

11-beta-Hydroxysteroid Dehydrogenases↗
PubMedDate not supplied

Endocrine and reproductive dysfunction in men associated with occupational inorganic lead intoxication.

In an attempt to define a postulated effect of lead on male endocrine function, seven men with symptomatic occupational lead intoxication (maximum whole blood lead levels 66-139 micrograms/dl) underwent in-patient endocrine evaluation at the time of diagnosis. Defects in thyroid function, probably of central origin, were present in three patients. Six patients had subnormal glucocorticoid production measured by 24-hr urinary 17-hydroxycorticosteroids and plasma cortisol responses to vasopressin- and/or insulin-induced hypoglycemia. Although serum testosterone concentration was normal in six patients, five had defects in spermatogenesis, including two with oligospermia and two with azoospermia. Repeat examinations after chelation therapy showed only partial improvement. It is concluded that heavy occupational exposure to lead, sufficient to cause clinical poisoning, may be associated with diffuse disturbances of endocrine and reproductive functions in men which are not rapidly reversible with standard treatment. Since men without overt poisoning have not been studied, these results cannot yet be included as sequelae of low-dose exposures.

Adrenal Cortex Function Tests↗
PubMed1962

Prevention of experimental allergic encephalomyelitis (EAE) by vitamin C deprivation.

Scorbutic guinea pigs injected with CNS and mycobacterium to induce experimental allergic encephalomyelitis (EAE) showed no clear-cut neurological signs and failed to show histological evidence of central nervous system damage. The degree of protection afforded by vitamin C deprivation was related directly to the duration of the scorbutogenic diet and inversely to the strength of the CNS challenge. Vitamin C deprivation also abolished tuberculin sensitivity as measured by the PPD skin reaction. Upon restoration of vitamin C, the animals recovered their sensitivity to PPD but did not develop EAE. It was further demonstrated that these effects of vitamin C deprivation were not related to inanition or to the endogenous levels of 17-hydroxycorticosteroids.

Animals↗
PubMed1981

Multiple sclerosis: a two-stage process?

The concept that the pathogenesis of multiple sclerosis (MS) is dependent on both an environmental factor and host factors associated with the puberty period was tested using the data for the Faroe Islands "outbreak." Although this "outbreak" affected only 25 individuals, its value may be unique since it is the only virgin outbreak described. The population affected demonstrated an age-associated bimodality. Incubation period for the older group, using 1942 (midpoint of British troop occupation) as onset time, was 5 years, while for the younger group, using puberty as onset time, a similar 5.7-year incubation period was demonstrated. Male and female incubation periods for both groups were similar, demonstrating an internal validity check. Although 10 cases were below the age of puberty at the time of the occupation, none of these developed disease prior to reaching puberty. The data suggest that onset of pathogensis of MS is dependent on passing or having passed through the puberty period. This would explain why MS is rarely seen below age 10, is unusual below age 15, why age 15 has been a "critical time" in migration studies and why females have an earlier onset than males. The data further indicate that susceptibility to MS may be acquired over a wide range of ages. The fact that many aging curves such as those for estrogen, testosterone or 17-hydroxycorticosteroid show striking similarity to the MS incidence curves raises the question whether infection is the entire explanation for the age distribution.

Adolescent↗
PubMedDate not supplied

Urinary free cortisol excretion in patients with metastatic cancer.

Many patients with metastatic carcinoma have an increase in urinary excretion of 17-hydroxycorticosteroids (17-OHCS), plasma concentrations of 17-OHCS, plasma total cortisol, plasma nonprotein-bound cortisol, or cortisol production rate. A small portion of circulating cortisol is excreted in the urine as unaltered or free cortisol. This urinary free cortisol, which is believed to reflect the average unbound plasma cortisol circulating during the day, is an excellent measure of adrenal cortical function. In this study, we compared the urinary free cortisol of 35 patients with metastastic cancer (10 small cell carcinomas of the lung, 8 other types of carcinoma of the lung, 8 breast carcinomas, and a miscellaneous carcinomas) with a group of 15 healthy age-matched volunteers. There were no significant changes in urinary free cortisol excretion in the patients with cancer.

Adrenocorticotropic Hormone↗
PubMed1989

Primary adrenal causes of Cushing's syndrome. Diagnosis and surgical management.

Cushing's syndrome is rare with only 20% of patients having a primary adrenal cause of hypercortisolism. We have developed a strategy to evaluate patients with suspected Cushing's syndrome and to localize the pathologic condition responsible for the hypercortisolism. This report reviews the last 11 consecutive patients who had a primary adrenal cause of hypercortisolism. Each patient had elevated 24-hour urine free cortisol and 17-hydroxycorticosteroid excretion consistent with hypercortisolism. All but one patient had undetectable plasma ACTH levels. No patient suppressed urinary steroid levels with high-dose dexamethasone and only one patient increased plasma ACTH or cortisol levels with oCRH, findings that were consistent with a pituitary-independent form of hypercortisolism. No patient had a pituitary tumor detected by computed tomography or magnetic resonance imaging, and eight patients had adrenal tumors accurately imaged. MRI of the adrenal glands correctly diagnosed adenoma in 5 of 6 patients with adenomas, carcinoma in 1 patient, and ACTH-producing pheochromocytoma in 1 patient. One tumor classified as carcinoma by MRI appeared on pathologic examination to be an adenoma. Three patients underwent petrosal sinus sampling for measurement of ACTH before and after oCRH administration, and each had petrosal sinus ACTH levels equal to peripheral levels, consistent with a primary adrenal cause of hypercortisolism. Two of these patients had typical bilateral pigmented micronodular adrenocortical disease and the third patient had macronodular adrenocortical hyperplasia. Each of the 11 patients was cured of hypercortisolism by unilateral or bilateral adrenalectomy and no patient has developed recurrent disease during the 7 to 29 month follow-up period. New modalities including the ovine CRH test, MRI, and petrosal sinus sampling have improved the evaluation of certain patients with Cushing's syndrome.

Adolescent↗
PubMed1979

Alcohol-induced Cushingoid syndrome.

A 35-year-old woman with alcoholic liver disease presented with physical stigmas and laboratory confirmation of Cushing's syndrome. With discontinuance of alcohol, her signs of Cushing's syndrome resolved and the urinary free cortisol and the urinary 17-hydroxycorticosteroid response to dexamethasone returned to normal. These findings broaden the spectrum of deranged glucocorticoid chemistry that can occur in alcohol-induced cushingoid syndrome.

Adult↗
PubMed1991

A case of cervical carcinoma of the uterus presenting with hyperosmolar non-ketotic coma as a manifestation of ectopic adrenocorticotropic hormone syndrome.

A case of advanced cervical carcinoma of the uterus with ectopic adrenocorticotrophic hormone (ACTH) syndrome is described. The patient was seen for general malaise 21 months after surgical treatment of the primary lesion whose histology was undifferentiated small cell carcinoma of the uterine cervix. She had extensive metastases in the liver and the abdominal wall. In addition to the typical clinical manifestations of Cushing's syndrome such as moon face, central obesity and acne vulgaris, hyperglycemia was so severe that she was in a hyperosmolar non-ketotic coma. Endocrinological examinations revealed elevated plasma ACTH and cortisol, and urinary excretion of 17-hydroxycorticosteroids and 17-ketosteroids, which were not suppressed by high-dose dexamethasone administration. Based on these clinical and laboratory findings, a diagnosis of ectopic ACTH syndrome was made. Among the results of other endocrinological examinations conducted to find the etiological cause of the hyperglycemic coma, which seemed to be unusual for ectopic ACTH syndrome, the plasma somatostatin level was abnormally high. Metastatic tumors in the liver obtained at the time of autopsy contained large amounts of both ACTH and somatostatin, and gel filtration studies revealed that the peptides produced by the tumor had the molecular sizes of the biologically active forms of the respective peptides. These observations suggest possible involvement of the somatostatin in deteriorating glucose intolerance to develop hyperglycemic hyperosmolar non-ketotic coma as a drastic disturbance of metabolism.

Adrenocorticotropic Hormone↗
PubMed1976

Hormonal variations in secondary amenorrhoea during the metyrapone test.

The occurrence of uterine bleeding following administration of Metyrapone in cases of secondary amenorrhoea and oligomenorrhoea led the authors to measure pituitary, gonadal and adrenal hormone levels, before and after the oral administration of this drug in sixteen patients, in an attempt to provide an interpretation of this phenomenon. There were expected changes in plasma ACTH and urinary 17-hydroxycorticosteroids, but no variations were noted in serum FSH and LH, plasma oestradiol and urinary oestrogens; the most important alterations occurred in plasma progesterone and urinary pregnanetriol levels. It is suggested that bleeding occurs because of the changes which are induced in plasma progesterone levels.

Adrenal Cortex Hormones↗
PubMed1983

Plasma calcitonin and ACTH responses to lysine vasopressin, calcium and pentagastrin in a patient with medullary thyroid carcinoma associated with Cushing's syndrome.

In a case study of medullary thyroid carcinoma (MTC) associated with Cushing's syndrome, elevated levels of urinary 17-hydroxycorticosteroids, plasma ACTH, cortisol, calcitonin (CT) and somatostatin (GHRIH) were documented. Lysine vasopressin administration further increased the levels of plasma ACTH, cortisol and CT, whereas the administration of calcium and pentagastrin increased only the level of plasma CT. Immunoreactive ACTH, CT and GHRIH were highly concentrated in the tumour tissues. Basal plasma ACTH levels were more progressively increased than plasma CT during the postoperative course when the patient was treated with o,p'-DDD, since the tumour was not completely resected. These findings suggest that the secretion of ACTH and CT from MTC were regulated in a different manner.

Adrenocorticotropic Hormone↗
PubMed1985

Congenital adrenal hyperplasia due to deficient cholesterol side-chain cleavage activity (20, 22-desmolase) in a patient treated for 18 years.

Two siblings, a 9-week-old female and an 18-year-old male pseudohermaphrodite are described with deficient cholesterol side-chain cleavage activity. The female died untreated in 1954; the second sibling, a phenotypically female infant with 46 XY karyotype, was diagnosed at age 5 weeks. Massive adrenal hyperplasia was revealed by intravenous pyelography showing downward displacement of the kidneys. Secretion rates of cortisol, aldosterone, deoxycorticosterone and corticosterone were unmeasurable. Urinary 17-hydroxycorticosteroids (17-OHCS), tetrahydrocortisol, 17-ketosteroids (17-KS), pregnanetriol, pregnanediol, and delta 5-3 beta-ol steroids were not detected during prolonged administration of ACTH. Plasma concentrations and urinary excretion of gonadotrophins were increased. Gonadal mitochondria did not convert radiolabelled cholesterol to pregnenolone. The gluccocorticoid and mineralocorticoid deficiencies have been controlled well by steroid replacement therapy. Plasma ACTH concentrations and plasma renin activity remained strikingly elevated even when supraphysiologic doses of glucocorticoids and mineralocorticoids were given. Oestrogen replacement alone induced a pubertal growth spurt. The differential diagnosis, the effects of long-term steroid replacement therapy, and comparison with previously reported findings are discussed.

Adolescent↗
PubMed2004

Case of combined adrenal cortical adenoma and myelolipoma.

We report a case of myelolipoma 10 mm in size within a functional cortical adenoma that was 33 x 22 x 17 mm in size. A 29-year-old woman was referred to hospital for transient hypertension. A right adrenal tumor was detected by computed tomography (CT) scan and magnetic resonance imaging (MRI). Her cortisol levels indicated a loss of the normal diurnal pattern, and urinary 17-hydroxycorticosteroids was elevated. She underwent a right adrenalectomy under the diagnosis of adrenal adenoma with Cushing's syndrome. The tumor was fairly well encapsulated by a thin layer of connective tissue. The major tumor portion was composed of two distinct cell types, clear cells and eosinophilic cells, arranged in an alveolar structure. These findings were representative of cortical adenoma. The adrenal cortical adenoma centrally included well-demarcated adipose tissue admixed with scattered islands of myelopoietic elements: erythroblasts, myeloid cell series and lymphocytic cells, which was eventually recognized as myelolipoma. Recently, adrenal myelolipoma has commonly been found because of the ease of detecting it as an incidentaloma by CT scan or MRI. However, the present adrenal myelolipoma case is uncommon because it is combined with a functioning cortical adenoma. Only six similar cases have previously been reported in English and Japanese publications. Furthermore, in the present case, the myelolipoma formed a tumor nodule, and to our knowledge, this is the first reported case of a radiographically recognizable tumor nodule. We discuss the etiology of myelolipoma and suggest that myelolipoma can develop in the course of endocrine hyperfunction.

Adenoma↗
PubMed1978

Hypertension due to 17alpha-hydroxylase deficiency.

A female patient with hypertension, hypogonadism and hypokalaemia due to 17alpha-hydroxylase deficiency is described, in whom the diagnosis was initially based on the finding of low urinary 17-ketosteroids and 17-hydroxycorticosteroids, in the presence of high plasma fluorometric 11-hydroxycorticoids. Later studies confirmed the diagnosis by demonstrating low circulating levels of 17alpha-hydroxyprogesterone and the steroids derived from this precursor: 11-deoxycortisol, cortisol, oestradiol and testosterone. Plasma progesterone, corticosterone and deoxycorticosterone (DOC) were greatly increased, but plasma and urine aldosterone were very low. The initial subnormal cortisol and 11-deoxycortisol levels responded to tetracosactrin administration, suggesting that the adrenal was not maximally stimulated by endogenous ACTH and indicating that the 17alpha-hydroxylase deficiency was incomplete. Plasma and urinary aldosterone levels were still suppressed after 12 months treatment with prednisone despite normalization of the previously suppressed renin levels. The findings indicate that this uncommon cause of medically-controllable juvenile hypertension can be identified without specific steroid assays.

Adolescent↗