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Results for “Adrenocortical Hyperfunction”

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At least 721 records · Page 40Linked to original sources
PubMed1979

C26 sterol in a human urine.

A new C26 sterol, 22-trans-27-norcholesta-5,22-dien-3 beta-ol, was found in the urine of a 6-year-old girl, with a clinical diagnosis of congenital adrenal hyperplasia of the salt losing type, accompanied by symptoms of mixed sex anatomy and skin pigmentation. The structure of the sterol was determined by comparison with the synthetic compound. The sterol was also detected in ther serum. This appears to be the first case in which a C26 sterol has occurred in mammalia.

Adrenocortical Hyperfunction↗
PubMed1976

Female phenotype in a male child due to 17-alpha-hydroxylase deficiency.

The discovery of testicles in a 3-year-old girl with XY karyotype led to a diagnosis of testicular feminization. Subsequently, however, hypokalaemia, hypertension, and severe prostration during a mild infection suggested adrenal involvement, and investigations showed a 17-alpha-hydroxylase deficiency. Diagnosis of testicular feminization should not be made without excluding a defect of testosterone synthesis.

Adrenocortical Hyperfunction↗
PubMed1977

Hypoglycaemia in congenital adrenal hyperplasia.

Two young children with salt-losing congenital adrenal hyperplasia developed profound hypoglycaemia. In one child hypoglycaemia occurred after a prolonged fast and in the other it was precipitated by infection. This complication may be more common than the literature suggests, and emergency treatment with glucose or hydrocortisone, given by injection, should be given to any child with the disorder who suddenly or unexpectedly collapses.

Adrenal Hyperplasia, Congenital↗
PubMed1978

Management of congenital adrenal hyperplasia. Urinary steroid estimations--review of their value.

A retrospective study was made of 16 children with 21-hydroxylase-deficient congenital adrenal hyperplasia of the salt-losing variety, who were treated with fludrocortisone and prednisone and were in good health during the period under review. The height velocity of the children was subnormal, height achievement was poor, and their bone ages retarded. Urinary 17-oxosteroid and pregnanetriol excretion were used to monitor the therapy of the children and these data have been related to growth velocities. In spite of urinary steroid figures in excess of those published as desirable for monitoring therapy, the children failed to grow properly, probably as a result of glucocorticoid overdosage. Published urinary steroid criteria are considered too strict and in order to achieve them one would need to give unnecessarily high doses of steroid. Regular measurement of height velocity and skeletal maturation rate are better indicators of therapeutic control and should lead to more satisfactory growth and ultimate height.

17-Ketosteroids↗
PubMed1978

Gonadotrophin release in untreated congenital virilising adrenal hyperplasia.

A 9.9-year-old boy and a 9.8-year-old girl with virilising congenital adrenal hyperplasia were subjected to an IV LH-RH (luteinising hormone-releasing hormone) test (so microgram/m2 before initition of therapy with corticosteroids. The pattern of response of LH and follicle-stimulating hormone to LH-RH was found to correspond to the stage of their precocious sexual development and advanced bone age, but not to their chronological age. This finding has implications with regard to the mechanism controlling gonadotrophin secretion at puberty.

Adrenocortical Hyperfunction↗
PubMed1979

Plasma 17OH-progesterone concentrations in newborn infants.

Plasma concentrations of 17OH-progesterone were determined in 60 normal newborn infants aged between 3 and 36 hours. Mean levels decreased rapidly during this time after removal of the placental contribution of this steroid. A further 70 normal infants, studied between ages 2 and 7 days, showed a mean plasma 17OH-progesterone concentration of 3.5 nmol/1 (1.2 ng/ml). By comparison, plasma concentrations in untreated infants with congenital adrenal hyperplasia were markedly raised. At 36 hours of age, there was an obvious difference between plasma levels of this steroid in normal and affected infants. Determination of plasma 17OH-progesterone concentrations are valuable in the evaluation of disorders of sexual differentiation and electrolyte balance in newborn infants, provided due care is given to the timing of sample collections.

Adrenal Hyperplasia, Congenital↗
PubMed1979

Continuing need for mineralocorticoid therapy in salt-losing congenital adrenal hyperplasia.

Four patients with salt-losing congenital adrenal hyperplasia (CAH) who had stopped mineralocorticoid therapy for several years, showed raised plasma concentrations of 17OH-progesterone and plasma renin activity, despite adequate glucoticoid therapy. One patient was able to reduce urinary sodium excretion when the sodium intake was restricted. Another patient who was a salt-loser, developed signs of an adrenal crisis when salt deprived. In comparison, one nonsalt-loser and 2 normal subjects decreased urinary sodium excretion in response to sodium restriction. The addition of fludrocortisone (100 micrograms) to usual maintenance doses of glucocorticoid, resulted in normal levels of plasma 17OH-progesterone and plasma renin activity in all 4 salt-losers. Two female salt-losers, with raised plasma testosterone concentrations, began menstruating when their plasma testosterone concentrations returned to normal after treatment with fludrocortisone. It is recommended that salt-losing CAH patients should be given mineralocorticoid, in addition to glucocorticoid therapy, at least until adult life.

Adolescent↗