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Results for “Adrenocortical Hyperfunction”

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At least 433 records · Page 24Linked to original sources
PubMed1977

Secretion of the adrenal androgen, dehydroepiandrosterone sulfate, during normal infancy, childhood, and adolescence, in sick infants, and in children with endocrinologic abnormalities.

Serum concentrations of the adrenal androgen, dehydroepiandrosterone sulfate, were measured by radioimmunoassay in normal infants and children, in sick premature and full-term newborn infants, and in patients undergoing evaluation of the hypothalamic-pituitary-gonadal and -adrenal systems. Premature infants had significantly greater (p less than 0.001) levels of DHAS (263 +/- 40)[SE]migrong/dl) than did full-term infants (58.9 +/- 5.2) during the first ten days of life; further increments occurred in stressed "sick" infants. A gradual age- and maturity-related rise in serum concentrations of DHAS was observed during childhood with the earliest increase occurring prior to the onset of pubertal production of gonadal steroids. Serum levels of DHAS rose following administration of ACTH and were increased in patients with congenital adrenal hyperplasia, in whom rapid decrements followed treatment with dexamethasone. hCG or LH-RH treatment did not alter DHAS concentrations. These data suggest that direct secretion of DHAS by the adrenal gland and/or peripheral sulfation of DHA, rather than gonadal secretion, accounts for the majority of DHAS production. The involvement of adrenal androgens in the pubertal maturation of the reproductive endocrine system thus may be evaluated by quantitation of serum DHAS.

Adolescent↗
PubMed1978

Plasma levels, half-life values, and correlation with physiologic assays for growth and immunity.

Plasma prednisolone levels have been measured hourly in children receiving a single dose of oral prednisone. Peak prednisolone levels occurred one to two hours after ingestion; half-life studies gave a mean value of 132 minutes in most children. Some children had marked variability in absorption and metabolism of prednisone. Somatomedin activity and cell-mediated immunity were inhibited by plasma prednisolone values which were achieved by single doses of prednisone of 0.5 mg/kg or higher. Monitoring prednisolone levels may be of value in identifying those children who accumulate excessively high levels on moderate dosage regimens.

Administration, Oral↗
PubMed1980

Periodic ACTH discharge.

A 9 1/2-year-old girl is presented who had cyclical attacks of abdominal pain, vomiting, emotional disturbance, and marked weight change for two years. Associated findings were facial plethora, hypertension, transient hyperglycemia and glycosuria, elevated plasma ACTH, cortisol, and urinary 17-OHCS excretion, and low plasma osmolality with hyponatremia. Urinary excretion of catecholamines and porphyrin metabolites was not increased. Between episodes, she showed no abnormal clinical signs or laboratory data. The attacks were effectively suppressed with the administration of chlorpromazine. The disorder appears to be due to the periodic release of excessive ACTH; the cause remains unknown.

Adrenocortical Hyperfunction↗
PubMed1984

The insulin receptor.

Cells are endowed with specific cognitive molecules that function as receptors for hormones, neurotransmitters, and other intercellular messengers. The receptor molecules may be present in the plasma membrane, cytoplasm, or nucleus. When occupied by the messenger, the receptor is coupled to the cellular machinery that responds to the message-bearing molecules. For some hormones the events following attachment of the messenger to the receptor are well known. An example is the generation of cAMP after combination of glucagon with its receptor and the series of steps culminating in activation of phosphorylase. In the case of many other messengers, including insulin, the nature of these coupling steps is not known. Receptors are subject to the regulatory processes of synthesis, degradation, and conformational change; alterations in receptor properties may have significant effects on the qualitative and quantitative responses of the cell to the extracellular messenger. The insulin receptor is located in the plasma membrane, is composed of two pairs of subunits, and has a molecular weight of about 350,000. It is located in cells such as adipocytes, hepatocytes, and skeletal muscle cells as well as in cells not considered to be typical target organ cells. Insulin receptors in nonfetal cells are downregulated by exposure of the cells to high concentrations of insulin. Other factors that regulate insulin binding include muscular exercise, diet, thyroid hormones, glucocorticoids, androgens, estrogens, and cyclic nucleotides. The fetus has high concentrations of insulin receptors in several tissues. These begin to appear early in fetal life and may outnumber those found in adult tissues. Fetal insulin receptors are unusual in that they may not undergo downregulation but may experience the opposite when exposed to insulin in high concentrations. Thus the offspring of a mother with poorly controlled diabetes may be placed in double jeopardy by fetal hyperinsulinemia and augmented insulin binding by the receptors. Many disorders in children and adults are associated with changes in the properties of the insulin receptor. In general, the alterations have been measured in receptor-bearing cells that are readily accessible, such as circulating monocytes and erythrocytes. The receptors on these cells generally reflect the status of receptors on the major target organs of insulin, although exceptions are known, and conclusions drawn from studies of receptors on circulating cells must be made with caution.(ABSTRACT TRUNCATED AT 400 WORDS)

Acanthosis Nigricans↗
PubMed2002

Hypercortisolemia in acute stroke is related to the inflammatory response.

Hypercortisolemia is thought to be a marker of the stress response following stroke. The aim of this study was to investigate the prevalence and prognostic significance of hypercortisolemia. The circadian variation of cortisol level and the relationship between serum cortisol levels and other stress, inflammatory, and haemostatic markers were also investigated. Seventy consecutive patients with their first ischemic stroke and 24 age- and sex-matched controls were included in the study. Serum cortisol levels (at 6:00 AM, 10:00 AM, 6:00 PM, and 10:00 PM), 24-h urine catecholamine excretion, beta-thromboglobulin levels, and other standard biochemical and haematological parameters were measured on the first day of hospitalisation and in control subjects. Outcome measures used the Barthel Index at Day 30, as well as 30- and 90-day mortality rates. Hypercortisolemia, defined as at least two of the four measurements above the normal range of serum cortisol levels (i.e. >618 nmol/l from the morning samples and >460 nmol/l from the evening samples) was found in 25 (35.7%) of the acute stroke patients and in 3 (12.5%) of the controls (p<0.05). Hypercortisolemia was associated with older age, greater severity of neurological deficit, larger ischemic lesions on CT, and worse prognoses (p<0.05). The study did not find a correlation between serum cortisol levels and other markers of the stress response such as catecholamines excretion and glucose levels. A significant correlation between serum cortisol levels and some markers of the inflammatory response, such as fever, fibrinogen level, white blood cell (WBC) count, and beta-thromboglobulin level, was established in stroke patients. Prognostic significance of hypercortisolemia in acute stroke patients seems to be related to the inflammatory response rather than to the stress response.

Acute Disease↗
PubMed1977

Testis tumors associated with congenital adrenal hyperplasia: a continuing diagnostic and therapeutic dilemma.

A 9-year-old boy with documented congenital adrenal hyperplasia owing to a deficiency in C21 hydroxylation is described. Precocious virilization and testicular asymmetry were noted when he was 5 years old. Both of these conditions persisted despite progressively larger doses of replacement steroid therapy. The right testis was 3 times larger than the left testis and serum testosterone was well within the adult male range. A right inguinal orchiectomy was performed. Pathologic diagnosis was interstitial cell tumor. A review of the literature emphasizes the continuing dilemma of separating interstitial cell tumors from hypertrophy of adrenal rest tissue in the presence of congenital adrenal hyperplasia. Possible methods of distinction are discussed.

Adrenal Hyperplasia, Congenital↗
PubMed1975

Pediatric nephrolithiasis.

The management of 78 children with upper urinary calculi is described. Boys outnumbered girls by a ratio of 2 to 1. Two-thirds of the patients had identifiable metabolic causes, while the remaining third had infected renal lithiasis. In this latter group, all patients had had multiple urologic procedures, urinary infection, and stasis with diversionary and indwelling drainage devices. Contrary to earlier views, idiopathic renal lithiasis with or without hypercalciuria was the most common metabolic form of nephrolithiasis in children. Sixty-seven patients (86 per cent) were followed for an average of 7 1/2 years. With appropriate therapy, stone disease became inactive in 70 per cent of the children. The remaining 30 per cent continued with active disease--5 died of renal failure and 1 has received a renal allograft. Stone formation may be regarded as a solitary complication or one of several manifestations of a large number of underlying disorders. Along with a thorough search for etiologic factors there must be an equally aggressive therapeutic effort. Because the disease is ofter sporadic, careful long-term followup of the patients with active as well as those with inactive stone disease is mandatory.

Acidosis, Renal Tubular↗
PubMed1986

Endocrine disorders of the pancreas and adrenal cortex in pediatric patients.

Hyperinsulinemia, a common cause of persistent hypoglycemia in infants and children, can result in permanent damage to the central nervous system. Thus, early diagnosis and treatment are important. The typical clinical manifestation of hyperinsulinemic hypoglycemia is symptomatic hypoglycemia that responds poorly to medical therapy. Affected infants may have tremors, jitteriness, apnea, cyanosis, or seizures. If initial medical therapy (frequent feedings, large amounts of intravenously administered glucose, diazoxide, and glucocorticoids) fails to stabilize plasma glucose levels, subtotal pancreatectomy is indicated. This surgical intervention does not completely correct the hypoglycemia in all patients, but it effectively reduces the severity of the condition. Surgical treatment of pediatric patients with Cushing's syndrome or aldosteronoma has also been effective. In our experience, survival of patients with adrenocortical adenomas has been 100%, whereas only five of nine children with adrenocortical carcinomas survived, and four of the five were younger than 10 years of age.

Adrenal Cortex Neoplasms↗