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Results for “Adrenocortical Hyperfunction”

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At least 217 records · Page 12Linked to original sources
PubMed1975

Primary aldosteronism. A study in contrasts.

Two patient with primary aldosteronism, one with a solitary adrenal adenoma and the other with bilateral nodular hyperplasia, are described. Both patients showed the classic features of primary aldosteronism in electrolyte and hormone patterns, but there were important differences in the biochemistry of their excised adrenal tissue. In addition, the injection of plasma from the patient with bilateral adrenal hyperplasia into the sheep's transplanted adrenal gland elicited a definite aldosterone secretory response, but there was no aldosterone response to the injection of plasma from the patient with a solitary adrenal adenoma. The findings support the hypothesis that an extra-adrenal stimulus may contribute to the pathogenesis of bilateral adrenal hyperplasia.

Adenoma↗
PubMed1978

Maternal and amniotic fluid 17 alpha-hydroxyprogesterone levels during pregnancy: diagnosis of congenital adrenal hyperplasia in utero.

17 alpha-Hdroxyprogesterone levels (17 alpha-OHP) were measured in 70 samples of amniotic fluid and 30 samples of maternal serum obtained at different stages of normal pregnancy and in samples of maternal serum and amniotic fluid from a pregnancy with the fetus affected with congenital adrenal hyperplasia. The mean level of 17 alpha-hydroxyprogesterone in the amniotic fluid from control pregnancies was 133.9 +/- 7.6 ng. per 100 ml. (range, 25.1 to 266.6 ng. per 100 ml). The levels were significantly higher in midpregnancy (157.4 +/- 8.4 ng. per 100 ml.) than in late pregnancy (79.2 +/- 6.8 ng. per 100 ml.) (p less than 0.01). Amniotic fluid 17 alpha-OHP levels in the affected pregnancy were significantly higher than the control levels. Mean maternal 17 alpha-OHP level during early pregnancy and midpregnancy was 259.5 +/- 22 ng. per 100 ml. and there was a two-to three-fold increase after 37 weeks (672.2 +/- 61 ng. per 100 ml.) The maternal 17 alpha-OHP levels in the affected pregnancy were significantly higher than the control levels after 34 weeks, but before 34 weeks, the level was within the range seen in control pregnancies. Measurement of 17 alpha-OHP levels in the amniotic fluid before 24 weeks and maternal serum after 34 weeks can be utilized for the prenatal diagnosis of congenital adrenal hyperplasia.

Adrenal Hyperplasia, Congenital↗
PubMed1979

Maternal and amniotic fluid steroids throughout human pregnancy.

Concentrations of testosterone, dihydrotestosterone, androstenedione, progesterone, 17 alpha-hydroxyprogesterone, and estradiol were measured by radioimmunoassay in the amniotic fluid and maternal peripheral blood obtained from normal pregnancies between 14 and 40 weeks of gestation. There was a sex difference in the levels of all the androgenic steroids in the amniotic fluid before 20 weeks with higher levels in pregnancies with male fetuses. Amniotic fluid 17 alpha-hydroxyprogesterone levels were significantly elevated in a pregnancy with the fetus affected with congenital adrenal hyperplasia. The levels of all the steroids in the amniotic fluid were significantly elevated in the pregnancy with molar degeneration of the placenta. There was a sex difference in the levels of dihydrotestosterone in the maternal peripheral blood before 20 weeks with higher levels in pregnancies with male fetuses. There was no correlation between the steroid levels in the maternal serum and amniotic fluid even though most of the samples of maternal serum were drawn at the same time as amniocentesis.

Adrenocortical Hyperfunction↗
PubMed1995

Effect of marginal ascorbic acid deficiency on saliva level of cortisol in the guinea pig.

Male guinea pigs subjected to prolonged marginal ascorbic acid deficiency developed moon facies and oedema, features of functional adrenal hypercorticism. Compared with age- and sex-matched controls fed an adequate diet for a similar period, ascorbate deficiency had no effect on submandibular gland weight but elicited a significant (p < 0.005) reduction in stimulated whole-saliva flow rate. Plasma cortisol concentration (nmol/L) was significantly increased (p < 0.005) in the deficient animals (998.21 +/- 57.19 compared to 254.66 +/- 15.62 for the controls). Associated with marked hypercortisolaemia in the deficient animals was a significant (p < 0.01) but less prominent increase in the whole-saliva cortisol level, resulting in a mean saliva/plasma cortisol ratio of 46% for this group compared to 72% for the controls. Increased corticosteroid levels suppress immunological and inflammatory responses, particularly neutrophil function, impair production of some cytokines, inhibit collagen synthesis, and impair wound healing and bone matrix formation. Numerous conditions such as ageing, stress, smoking, ionizing radiation, ingestion of drugs, protein malnutrition, diabetes, and several other pathological states, which are among the risk factors for xerostomia and periodontal/oral mucosal lesions, promote tissue depletion of ascorbate. This study suggests that increased salivary and blood levels of glucocorticoids in these conditions may be important in reducing the ability of the host to mount an effective immune response to oral pathogens.

Adrenocortical Hyperfunction↗
PubMed1987

Laboratory evaluation for Cushing's syndrome in psychiatric patients with cortisol nonsuppression following the overnight dexamethasone suppression test.

Laboratory tests used for the differential diagnosis of Cushing's syndrome have infrequently been employed in investigations of psychiatric patients who demonstrate hypothalamic-pituitary-adrenal (HPA) overactivity, and these laboratory procedures have not previously been applied for the specific purpose of further evaluating the endocrine function of psychiatric patients with serum cortisol nonsuppression following the standard 1-mg overnight Dexamethasone Suppression Test (DST). Low-dose (4 mg/48 hr) and high-dose (16 mg/48 hr) DSTs were administered to 10 psychiatric patients who exhibited cortisol nonsuppression after the overnight DST. Patients all had normal suppression to both the low-dose and high-dose tests. HPA overactivity in these patients was thus not sufficient to meet laboratory criteria for the diagnosis of Cushing's syndrome. Study results suggest that psychiatric patients with abnormal cortisol suppression following the 1-mg overnight DST are likely to have normal responses when assessed by standard laboratory protocols used for the diagnosis of Cushing's syndrome.

Adrenocortical Hyperfunction↗
PubMed1990

Hypercortisolism and its possible neural bases.

As is clear from the pages of this journal, biological psychiatrists remain fascinated by the phenomenon of dexamethasone (DEX) resistance and the hypercortisolism of various neuropsychiatric disorders. The mere existence of the endocrine abnormalities attests to the biological reality of these disorders. Furthermore, progress continues in using the occurrence of these endocrine defects as both diagnostic and prognostic markers of disease subtypes. Progress has also been made in understanding the mechanisms underlying the endocrine defects. The adrenocortical axis is vastly complex, involving multiple hypothalamic-releasing factors under CNS control, shifting pituitary and adrenal sensitivies to hormonal signals, and feedback regulation at all three levels. What defects within this system produce DEX resistance and hypercortisolism? In this paper, we review data suggesting that the endocrine problems is, at least in part, neural in nature. Drawing upon a rodent literature, we will also suggest some models by which this can occur. The hypercortisolism found in cases of affective disorders, anorexia nervosa, Alzheimer's disease, among the very aged or the chronically stressed, is not a uniform phenomenon. Basal cortisol concentrations can be elevated in all or part of the circadian cycle. Resistance to glucocorticoid (GC) feedback inhibition (as typically demonstrated by DEX resistance) can occur; the resistance can be complete, or occur as early escape from DEX suppression. Finally, elevated basal cortisol concentrations and DEX resistance can occur independently of each other. Until the end of this review, we will conveniently refer to these variants of adrenocortical hyperactivity as "hypercortisolism." In addition, rather than using the term "hypercortisolism" for the rat, we will use "hyperadrenocorticism" (as they secrete corticosterone, rather than cortisol).

Adrenocortical Hyperfunction↗
PubMed1976

[Determination of serum transcortin levels by electroimmunodiffusion (author's transl)].

The isolation of transcortin in a pure form made possible the preparation of a monospecific anti-human transcortin rabbit serum. Serum transcortin levels were measured by electroimmunodiffusion. Experimental results expressed as errors by the calculating of interserial reproducibility were 4.74 per 100. The mean value was significantly different for men (36 subjects: 39.7 +/- 3.6 mg/l) from women (36 subjects: 42.1 +/- 3.9 mg/l). The transcortin determination was performed in pregnancy serum and in serum of women during oestroprogestative treatment. Some studies were performed in pathological cases (hyper- and hyperthyroidism, hyper- and hypocorticism, Kahler disease, ascitic cirrhosis).

Adrenal Insufficiency↗
PubMed1976

Long-term effects of aminoglutethimide on steroid metabolism in congenital adrenal hyperplasia.

Five cases of congenital adrenal hyperplasia due to C21-hydroxylase defect were treated with a combination of aminoglutethimide and prednisolone. In the third year of treatment the urinary levels of 17-oxosteroids increased above normal values while the total 17-hydroxy-corticosteroids were normally low. Specifically, urinary pregnanetriol was normal in 3 cases. To determine the reasons for this disparity the adrenal metabolism of cholesterol, as judged by the urinary steroid metabolites, was studied. Fractionation of urinary steroid metabolites was by thin-layer chromatography (TLC) followed by gas-liquid chromatography (GLC). The results indicate that aminoglutethimide inhibits steroidogenesis less than prednisolone; that a pathway from cholesterol via 17 alpha, 20 alpha-dihydroxycholesterol to dehydroepiandrosterone is likely to operate after long-term aminoglutethimide therapy; that 11 beta-hydroxylase, at least for pregnenes may be inhibited by aminoglutethimide and that the metabolic breakdown of testosterone may be delayed by this drug.

17-Hydroxycorticosteroids↗
PubMed1976

Congenital adrenal hyperplasia caused by defect in steroid 21-hydroxylase. Establishment of definitive urinary steroid excretion pattern during first weeks of life.

The steroid excretion of two female infants with congenital adrenal hyperplasia due to 21-hydroxylase deficiency has been studied during the first weeks of life. The techniques used were gas chromatography on an open-tubular column and combined gas chromatography-mass spectrometry using selected ion recording. During the first days of life 3beta-hydroxy-5-ene steroids predominate and the levels found were considerably greater than those found in normal infants. Selected ion recording mass spectrometry permitted detection of pregnanetriol and 11-oxo-pregnanetriol several days before these steroids could be determined with accuracy by conventional gas chromatography. Pregnanetriol and 11-oxo-pregnanetriol were first detected on the third day of life. The results of this investigation demonstrate that 21-hydroxylase deficiency may be indicated during the first week of life by an increased 3beta-hydroxy-5-ene steroid excretion, but the definitive excretion pattern required for firm diagnosis may not develop for several days. The amounts of the definitive steroids excreted may not be sufficient to be detected by the more usual methods for several weeks.

Adrenocortical Hyperfunction↗
PubMed1977

Cholesterol side-chain cleavage enzyme activity and cytochrome P-450 content in adrenal mitochondria of a patient with congenital lipoid adrenal hyperplasia (Prader disease).

An autopsied case with congenital lipoid adrenal hyperplasia (Prader disease) was presented. The cholesterol side-chain cleavage (SCC) enzyme activity in adrenal mitochondria of this case was assayed with [3H]cholesterol as substrate, combined with purified bovine adrenodoxin and adrenodoxin reductase, by measuring the amount of [3H]pregnenolone formed. The cytochrome P-450 content was also measured by recording the difference absorption spectra of carbon monoxide-complexed P-450. The cholesterol SCC enzyme activity in adrenal mitochondria of Prader disease was 0.81 nmol pregnenolone/nmol P-450 per min, which was approximately 10% of that in normal tissue. The content of cytochrome P-450 was 0.074 nmol/mg protein, which was about half of that in controls. These results indicate that there is a cholesterol SCC enzyme deficiency in adrenal mitochondria in this disease.

Adrenal Glands↗
PubMed1979

A method for identification and follow-up of patients with a steroid-21-hydroxylase deficiency.

A method is described for the determination of 17 alpha-hydroxyprogesterone from blood samples obtained by heel prick and dried on filter paper. Discs (10 mm diameter) were cut from the filter paper and extracted in the assay tubes with 1 ml of a methanol/diethyl ether/ethyl acetate (50 :45 :5, v/v) solvent mixture. Antibody, tritium-labelled tracer and dextran-coated charcoal were added to assay tubes using a multichannel dispenser. The approach used permits one technician to analyze two series, each of 60 duplicate samples, within one working day. Thus the method is applicable for the centralized screening of suspected cases, while emergency samples may be analyzed at the same time within 4 h. Comparisons with a highly specific but more elaborate technique for the determination of blood 17 alpha-hydroxyprogesterone showed a correlation coefficient of 0.99, and the regression equation for the present method (y) against the established method (x) was y = 1.07x + 2.72. The calculated upper reference limit (mean +/- S.D.) for 17 alpha-hydroxyprogesterone in healthy infants from two days to eight years of age of 7.5 ng/ml of serum.

Adrenal Glands↗