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At least 487 records · Page 27Linked to original sources
PubMed1996

Evidence for heterogeneous etiologies of adrenal dysfunction in polycystic ovary syndrome.

OBJECTIVE: To examine the hypothesis that, in polycystic ovary syndrome (PCOS), ovarian steroids induce adrenal enzyme dysfunction or adrenal androgen hyperresponsiveness to ACTH. DESIGN: Prospective controlled clinical study. SETTING: Reproductive endocrinology unit of an academic medical center. PATIENTS: Twelve women with PCOS who had adrenal androgen excess were compared with five weight-matched ovulatory women. In half of the women with PCOS, prestudy screening was suggestive of mild 3 beta-hydroxysteroid dehydrogenase (HSD) deficiency. INTERVENTIONS: Basal and adrenal dynamic blood sampling before and after GnRH agonist (GnRH-a) administration for 6 months. MAIN OUTCOME MEASURES: Basal E2 and androgen levels as well as dexamethasone-suppressed, ACTH-stimulated 17 alpha-hydroxyprogesterone, 17 alpha-hydroxypregnenolone, and androgen levels before and after ovarian suppression. RESULTS: Although none of the subjects with PCOS proved to have mild 3 beta-HSD deficiency, the majority of them (58%) met the criteria for 17,20 lyase hyperactivity before and after GnRH-a therapy. As a group, the remaining subjects with PCOS exhibited an elevated DHEAS response to ACTH before GnRH-a treatment, which may have normalized after GnRH-a treatment. CONCLUSION: Adrenal androgen excess in PCOS may be heterogeneous in etiology, whereas 17,20 lyase hyperactivity appears to be an intrinsic adrenal disorder, adrenal androgen hyperresponsiveness to ACTH may be ovarian induced. Reliance on historical controls may lead to overdiagnosis of mild 3 beta-HSD deficiency.

17-alpha-Hydroxypregnenolone↗
PubMed1997

Comparison of results of adrenocorticotropic hormone stimulation and low-dose dexamethasone suppression tests with necropsy findings in dogs: 81 cases (1985-1995).

OBJECTIVE: Comparison of diagnostic accuracy of results of low-dose dexamethasone suppression (LDDS) and ACTH stimulation tests with necropsy findings in 81 dogs. DESIGN: Retrospective study. ANIMALS: 81 dogs that had undergone screening tests for hyperadrenocorticism and that had a complete necropsy report. PROCEDURE: Medical records were evaluated for results of CBC, serum biochemical analysis, urinalysis, endocrine testing, signalment, treatment, and necropsy findings. Each dog was definitively classified as having true-positive, true-negative, false-positive, or false-negative results. Statistical analyses included determination of prevalence, apparent prevalence, accuracy, number of dogs misclassified, sensitivity, specificity, and positive- and negative-predictive values. RESULTS: Of the 81 dogs that fit the criteria for selection, 40 (49%) were confirmed as having hyperadrenocorticism (30 had pituitary-dependent disease and 10 had adrenal gland tumors). Forty-one dogs had illnesses attributable to a cause other than disease of the adrenal glands. Sensitivity of ACTH stimulation and LDDS tests were 95 and 96%, respectively. Specificity for the ACTH stimulation test was higher (91%) than that of the LDDS test (70%). When prevalence of the disease in the study population was taken into consideration, the positive-predictive value for the ACTH stimulation test was 91%, compared with 76% for the LDDS test. CLINICAL IMPLICATIONS: The ACTH stimulation test was more specific than the LDDS test, although sensitivity was similar for both tests. The ACTH stimulation test also had a significantly higher positive-predictive value than the LDDS test when a prevalence of 25% was taken into consideration.

Adrenal Gland Neoplasms↗
PubMed1976

Gamma camera imaging of bilateral adrenocortical hyperplasia and adrenal tumors in the dog.

Gamma camera imaging of the adrenal glands was done in 8 dogs with hyperadrenocorticism and 4 normal dogs given intravenous injections of 131I-19-iodocholesterol. In normal dogs, both adrenal glands could be visualized separately, and there was no difficulty in distinguishing among the images of normal glands, hyperplastic glands, and functional adrenal tumors. In addition, gamma camera imaging enabled the correct surgical site to be selected for removal of adrenal tumors. Hyperadrenocorticism was diagnosed in 8 dogs by evaluation of urinary 17-hydroxycorticosteroid (OHCS) excretion rates, urinary 17-OHCS and plasma 11beta-OHCS RESPONSES TO DEXAMETHASONE SUPPRESSION OF ENDOGENOUS ADRENOCORTICOTROPIN (ACTH) secretion, and plasma 11beta-OHCS response to intravenous administration of ACTH. Base line 17-OHCS excretion increased in 5 of the 8 dogs. Plasma 11beta-OHCS concentrations were not decreased by dexamethasone administration in the 4 dogs subsequently found to have adrenal tumors; however, there was an exaggerated increase in plasma 11beta-OHCS concentration after administration of ACTH in 3 of the 4 dogs which had bilateral adrenocortical hyperplasia.

11-Hydroxycorticosteroids↗
PubMed1986

[The thyroid gland and adrenal cortex in the large fetus and their role in the development of macrosomia].

In a morphological study of thyroid glands and adrenal cortex of large fetuses compared to the controls the authors revealed a significant increase of the thyroid gland functional activity, as well as of glomerular and fascicular zones of adrenal cortex. The functional tension of the thyroid gland appeared to be reduced in large fetuses with obesity. Hyperfunction of all zones of the adrenal cortex was also revealed in them. In medium height fetuses with obesity hypofunction of the thyroid gland, as well as hyperfunction of the fascicular and fetal adrenal cortex zones were present. Correlation-regression analysis has revealed close interrelations between the functional state of the thyroid gland, adrenal cortex and fetal mass.

Adrenal Cortex↗
PubMed1989

[Crisis of arterial hypertension in patients with primary aldosteronism].

A clinical picture of the disease was analyzed in 55 patients with primary aldosteronism due to adrenal aldosteronoma. A crisis variant of the course in arterial hypertension was detected in 50% of the patients. Its comparison with morphological signs of the adrenals enabled the authors to reveal that the crisis of arterial hypertension was accompanied by adrenal medullary hyperplasia and hyperfunction.

Adrenal Cortex Neoplasms↗