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Results for “Adrenocortical Hyperfunction”

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PubMed1992

Regulation and dysregulation of the hypothalamic-pituitary-adrenal axis. The corticotropin-releasing hormone perspective.

This article is an up-to-date review of the impact that the discovery of corticotropin-releasing hormone (CRH) has had on basic science and clinical medicine. It discusses hypothalamic CRH, placental CRH, immune CRH, and hypothalamic and immune CRH. Clinical studies in normal and disease states and synthesis and future directions also are presented.

Adrenocortical Hyperfunction↗
PubMed1951

[Cushing's disease].

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Adrenocortical Hyperfunction↗
PubMedDate not supplied

Cushing's disease.

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Adrenocortical Hyperfunction↗
PubMedDate not supplied

[Effectiveness of correcting radiation injuries of the thymic endocrine function by T-activin in conditions of reduced postradiation hypercorticism reaction].

T-activin administered to rats after exposure to whole-body 1.5 Gy neutron- and 6 Gy X-radiation increases considerably the thymosin-like serum activity, accelerates cellularity restoration in the thymus and spleen, but does not influence the survival rate. Ionol administered prior to X-irradiation reduces the postirradiation hypercorticism reaction and the indirect effect of radiation on lymphoid organs which it is responsible for. The combined injection of ionol and T-activin increases the thymosin-like serum activity and spleen cellularity to the highest possible level and increases the survival rate of rats from 24 to 64 per cent and the lifespan up to 6 days.

Adjuvants, Immunologic↗
PubMed1978

Management of congenital adrenal hyperplasia using serum dehydroepiandrosterone sulfate and 17-hydroxyprogesterone concentrations.

Simultaneous serum concentrations of dehydroepiandrosterone sulfate (DHEA-S) and 17-hydroxyprogesterone (17-OHP) were compared with urinary 17-ketosteroid (17-KS) and pregnanetriol (PT) excretion during therapy in 18 prepubertal patients with the 21-hydroxylase deficiency form of congenital adrenal hyperplasia (CAH). Patients were classified into those in good, poor, or questionable control on the basis of clinical examination, skeletal age, and 17-KS and PT excretion. During therapy, use of serum steroid concentrations was found to be nearly as accurate in judging adequacy of control as use of urine steroid concentrations. Of 34 evaluations, a definite assessment of adequacy of control could be arrived at 25 times using urinary values and 22 times using both serum DHEA-S and 17-OHP concentrations. DHEA-S concentration responded sluggishly when treatment was not adequate, being greater than 100 microgram/dl only in patients significantly undertreated. It was never elevated in well-controlled patients. Mid-afternoon 17-OHP concentrations were less than 200 ng/dl in well-controlled patients but readily escaped suppression and could not be used to differentiate poor from borderline control or from temporary noncompliance. Therefore, an increases DHEA-S concentration indicated poor control and a suppressed 17-OHP concentration indicated good control. The combination of normal DHEA-S level with elevated 17-OHP level, however, did not permit exact evaluation of the degree of control. Of significance is that not all patients with CAH present with an elevated DHEA-S concentration, and only in those in whom an elevated level has been documented can DHEA-S level be used as an index of control during therapy.

17-Ketosteroids↗