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PubMed1994

Localization of steroidogenic enzymes in adrenal cortex and its disorders.

Immunolocalization and in situ hybridization analysis of steroidogenic enzymes demonstrated the localization of steroidogenesis in the adrenal cortex and its disorders. The findings obtained provided new insights into adrenocortical hormonal metabolism, especially through establishing endocrine-pathological correlation.

Adrenal Cortex↗
PubMed2006

Triple-A syndrome--the first Chinese patient with novel mutations in the AAAS gene.

We report on the first Chinese patient with triple-A syndrome, who presented at 22 months with status epilepticus secondary to hyponatraemia and hypoglycaemia. Subsequent endocrine investigations confirmed primary adrenal insufficiency and aldosterone deficiency. In the presence of achalasia and alacrima, this patient satisfies the diagnostic criteria of triple-A syndrome. Further molecular testing detected compound heterozygous mutations in the AAAS gene: a c.580C --> T transition in exon 7 and a c.771delG single nucleotide deletion in exon 8. Testing of parents and brother confirmed their heterozygous carrier status.

Adrenal Cortex Diseases↗
PubMed1982

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism.

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dogs was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

Adrenal Cortex↗
PubMed1990

An antioxidant drug, silibinin, modulates steroid secretion in human pathological adrenocortical cells.

Because human adrenocortical cells from different adrenal disorders exhibit pathologically altered corticosteroid synthesis, and free radical mechanisms may induce pathological changes in the activities of corticosteroid biosynthetic enzymes (cytochrome P-450), we examined the effect of an antioxidant, silibinin, on basal and ACTH-stimulated secretion of several corticosteroids in isolated adrenal cells from an aldosterone-producing adenoma, atrophied adrenal tissues surrounding the adenoma, and hyperplastic adrenals from Cushing's syndrome. In the presence of a high concentration (100 mumol/l) of silibinin, variably diminished secretion of basal aldosterone, corticosterone, cortisol, 18-OH-corticosterone and 11-deoxycorticosterone was found. In contrast, the addition of 0.01 mumol silibinin/l, which failed to produce a clear effect on basal corticosteroid secretion, resulted in a potentiation of ACTH-stimulated secretion of several corticosteroids in the adenomatous and hyperplastic adrenocortical cells. These results suggest that the dose-dependent dual effect of silibinin on corticosteroid secretion may be attributed to corresponding changes in the activities of cytochrome P-450 enzymes, and that stimulation of ACTH-induced corticosteroidogenesis by silibinin is presumably due to the antioxidant property of the drug.

18-Hydroxycorticosterone↗
PubMed1988

Adrenal localization in the adrenocorticotropic hormone-independent Cushing syndrome.

STUDY OBJECTIVE: To assess the efficacy of 131I-6-beta-iodomethylnorcholesterol scintigraphy in the adrenocorticotropic hormone-independent Cushing syndrome and to compare this with computed tomography. DESIGN: Retrospective analysis of case series from 1977 to 1987. SETTING: Referral to the Division of Nuclear Medicine at a tertiary-care university medical center. PATIENTS: Twenty-four patients with a pathologically-confirmed diagnosis of the adrenocorticotropic hormone-independent Cushing syndrome had 131I-6-beta-iodomethylnorcholesterol scintigraphy and, in most cases, computed tomography. MEASUREMENTS AND MAIN RESULTS: Using 131I-6-beta-iodomethylnorcholesterol scintigraphy, adenomas were accurately seen as focal, unilateral tracer uptake in 14 of 14 patients. In carcinoma, the classic scintigraphic pattern of bilateral nonvisualization was observed in 3 of 4 patients, with ipsilateral uptake of tracer in 1 patient with a histologically well-differentiated malignancy. Computed tomography done during the same interval depicted abnormal adrenals in all cases of adenoma and carcinoma. In cortical nodular hyperplasia, however, computed tomography identified abnormal pairs of adrenals in only one of four cases studied, whereas scintigraphy showed typical patterns of bilateral increased uptake in all of the cases. CONCLUSION: 131I-6-beta-iodomethylnorcholesterol scintigraphy accurately shows the location and nature of adrenal dysfunction in the adrenocorticotropic hormone-independent Cushing syndrome and may be particularly useful in identifying the bilateral adrenal involvement in cortical nodular hyperplasia.

19-Iodocholesterol↗
PubMed1975

[Chronic adrenal insufficiency in childhood: clinical features and hormonal diagnosis (author's transl)].

An investigation was carried out on 6 children with clinical symptoms of adrenal insufficiency. The diagnosis was verified biochemically in 4 cases, 1 child was found to have secondary adrenal insufficiency and 1 had normal adrenal function. These findings demonstrate 2 types of adrenal insufficiency with different clinical pictures: Type 1 is characterized by cortisol deficiency with hypoglycaemia, low corticoid levels and a low cortisol secretion rate; Type 2 shows aldosterone deficiency with prominent salt loss. The clinical picture is correlated in extenso to the biochemical data in respect of ketosteroids, corticosteroids, plasma corticoids, cortisol secretion rate and aldosterone determination in a constant ACTH stimulation test. The methods of determination of the plasma aldosterone level and the cortisol secretion rate were greatly modified and redeveloped in this laboratory.

Acidosis↗
PubMed2001

Diagnosis of adrenal cortical dysfunction by liquid chromatography-tandem mass spectrometry.

Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to measure 6 metabolic compounds of the adrenocorticosteroid pathway simultaneously on residual specimens from patients who had previously been previously diagnosed, on the basis of immunoassays, as having congenital adrenal hyperplasia (CAH), 11 beta-hydroxylase deficiency, 21-hydroxylase deficiency, or Addison disease (adrenal insufficiency). Two subjects with normal adrenal function had serum cortisol values of 13.6 and 8.9 micrograms/dL and serum cortisone values of 2.1 and 0.6 microgram/dL, but the rest of the compounds were undetectable. Two patients with 11 beta-hydroxylase deficiency had serum 11 beta-deoxycortisol values of 14.9 and 10.0 micrograms/dL and serum 11-deoxycorticosterone values of 3.9 and 1.0 microgram/dL, but their serum levels of cortisol and cortisone were diminished. A patient with 21-hydroxylase deficiency had a highly increased serum 17-hydroxyprogesterone concentration of 28.5 micrograms/dL (or 28,500 ng/dL, the traditional unit to report this assay) and a serum 21-deoxycortisol concentration of 6.9 ug/dL (this is a pathologic marker of 21-hydroxylase deficiency that is nondetectable in sera of healthy subjects). This patient also had diminished concentrations of serum cortisol and cortisone (0.9 and 0.3 microgram/dL, respectively). At 30 and 60 min after corticotropin (ACTH) stimulation, serum cortisol was the only compound that showed a dramatic increase in the normal subjects; the patient with 21-hydroxylase deficiency showed an increase of serum 17-hydroxyprogesterone level, but no increase of serum cortisol level; the patient with Addison disease showed no increase in the levels of serum cortisol or other compounds. Metyprapone, which blocks 11 beta-hydroxylase activity, increased the serum 11-deoxycorticosteroid levels and decreased the serum cortisol level. This pilot study demonstrates that it is feasible to use LC-MS/MS for the laboratory diagnosis of adrenal cortical dysfunction. The authors envision that LC-MS/MS may soon become an ideal analytical technique for the diagnosis of such endocrine diseases.

17-alpha-Hydroxyprogesterone↗
PubMed2003

[Current aspects of diagnosis and treatment of symptomatic arterial hypertension of adrenal genesis].

AIM: To analyse the experience in diagnosis and treatment of arterial hypertension (AH) of adrenal genesis. MATERIAL AND METHODS: A total of 243 patients with adrenal AH (mean age 46.3 +/- 3.2 years) were examined. 134 of them had endogenic adrenohypercorticism (EAH), 62--primary hyperaldosteronism (PHA), 47--chromaffin tissue tumors (CTT). Diurnal urinary excretion of adrenal hormones (epinephrine, norepinephrine, aldosteron, hydrocortisone) and peripheral blood hormones (aldosteron, renin, hydrocortisone, ACTH) were measured. Topic diagnosis was made with ultrasound, computed tomography, MR-imaging, angiography, adrenal venous sampling and 123I-MIBG scintigraphy. RESULTS: Adrenalectomy was made in 224 patients (predominantly with tumor lesions). 19 patients (idiopathic hyperaldosteronism, advanced adrenocortical carcinoma) were treated conservatively (calcium antagonists, ACE inhibitors, AT1-receptor blockers, spironolacton). Good results of the surgical treatment were achieved in 60% patients with aldosterone-producing adenoma and adrenal Cushing's syndrome as well as in 80.5% patients with pheochromocytoma. Long-term outcomes depend on hypertension duration, histologic type of the tumor, age and family hypertension history (risk of essential hypertension). CONCLUSION: Hypertension of adrenal origin occurs more frequently than it was supposed previously. Its late diagnosis may be due to lack of typical signs and symptoms, insufficient application of novel diagnostic techniques and poor alertness of physicians. It is recommended to include tests for adrenal hormones in urine and blood and ultrasound investigation of the adrenals in a complex of primary examination of patients with severe refractory hypertension.

Adrenal Cortex↗
PubMed1953

Virilism.

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Adrenal Cortex↗