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Results for “Adrenocortical Hyperfunction”

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PubMed1950

Adrenocortical tumors.

Hormonally active tumors of the adrenal cortex are either benign adenomas or adenocarcinomas. They may be located within the adrenal gland or as adrenal rests along the Wolffian tract. Hyperplastic cortical tissue without actual neoplastic formation is also capable of elaborating excessive cortical secretions.AT THE PRESENT STATE OF KNOWLEDGE, ANY ONE OR A COMBINATION OF THE FOLLOWING COMPOUNDS MAY BE ELABORATED IN A GIVEN CASE: the electrolytic, glucogenic, androgenic, or estrogenic corticosteroids. Whether or not Cushing's syndrome is primarily pituitary or adrenal in origin is still a matter of conjecture.

Adenoma↗
PubMed2004

Macronodular adrenocortical hyperplasia in a postmenopausal woman.

This case report describes the diagnosis of Cushing's syndrome due to macronodular adrenal hyperplasia in an elderly woman who presented with fatigue, muscle weakness and oedema, and recent excessive bruising. Long-standing disease and comorbidity precluded adrenalectomy. Despite treatment with metyrapone and diuretics, the patient died after two months hospitalisation. Postmortal examination revealed overexpression of luteinising hormone (LH) receptors in the adrenal glands, suggesting that the postmenopausal rise in LH may have a role in adrenal hyperplasia and hypercortisolism.

Adrenal Cortex↗
PubMed2004

[Endocrine obesity: bioelectric profiles (biotypes) detected in the body composition].

136 patients were selected (16 men and 120 women with non-specific menstrual disturbances) with a BMI (Body Mass Index) between 25 and 45 kg/m2, which were diagnosed with "disendocrinia" (GH deficit, hyperadrenocorticism, hypothyroidsm, hyperandrogenism, menstrual cycle disorders). The proposed approach, based on the visualization of the value distribution of the electric measures in different graphics, is able to immediately explain the bioelectric state of the individual's lean-mass. Subjects with hypothyroidism present, along with their overweight, less bio-conducting mass, with an altered fluid intra/extra-cellular distribution. Patients with hyperadrenocorticism show instead an hyperhydratation of the body mass, especially in the extracellular level. Patients with menstrual disorders (amenorrea, polycystic ovary syndrome, anovulatory cycle etc...) present a lean mass reduction (elevated Rs) and an increase of the intra-cellular compartment (elevated-Xc). Patients with hyper-androgenism (and hirsutism) show a characteristic bioelectric "pattern", with low Rs levels and high Xc levels. Subjects with GH deficit (men and women), has a trend of documenting bioelectric measures with lower lean mass and higher fat-mass. Different electric biotypes seem to characterize the body composition in the several endocrine disorders.

Adipose Tissue↗
PubMed2005

[Androstenedione].

Explore the source record for details and available documents.

Adrenal Hyperplasia, Congenital↗
PubMed1992

Urine cortisol:creatinine ratio as a screening test for hyperadrenocorticism in dogs.

A urine cortisol:creatinine (c:c) ratio, determined from a free-catch morning sample, was evaluated in each of 83 dogs as a screening test for hyper-adrenocorticism. The dogs evaluated were allotted to 3 groups, including 20 healthy dogs, 40 dogs with confirmed hyperadrenocorticism (HAC), and 23 dogs with polyuria and polydipsia not attributable to HAC (polyuria/polydipsia group; PU/PD). Overlap in the urine c:c ratios (mean +/- SEM), comparing results from the healthy dogs (5.7 x 10(-6) +/- 0.9) with those from the HAC dogs (337.7 x 10(-6) +/- 72.0) was not found. However, 11 (64%) of the 18 values from the PU/PD dogs (42.6 x 10(-6) +/- 9.4) were above the lowest ratio in the HAC group and 50% of the HAC group had a urine c:c ratio below the highest value in the PU/PD group. When the mean urine c:c ratio (+/- 2 SD) for the group of healthy dogs was used as a reference range, 100% of the HAC dogs and 18 (77%) of 23 dogs in the PU/PD group had abnormal urine c:c ratios. The sensitivity of the urine c:c ratio to discriminate dogs with HAC was 100%. The specificity of the urine c:c ratio was 22% and its diagnostic accuracy was 76%. On the basis of our findings, a urine c:c ratio within the reference range provides strong evidence to rule out HAC. However, abnormal urine c:c ratios are obtained from dogs with clinical diseases other than HAC. Therefore, measurement of a urine c:c ratio should not be used as the sole screening test to confirm a diagnosis of HAC.

Adrenocortical Hyperfunction↗
PubMed1992

Steroid hepatopathy in a horse with glucocorticoid-induced hyperadrenocorticism.

Steroid hepatopathy was diagnosed in a horse with glucorticoid-induced hyperadrenocorticism on the basis of anamnesis, serum biochemical data, and histologic findings of hepatic biopsy. Initially, clinical signs of polyuria, polydypsia, and muscular degeneration were seen. The horse developed laminitis during hospitalization.

Adrenocortical Hyperfunction↗
PubMed2005

A case of adrenal gland dependent hyperadrenocorticism with mitotane therapy in a Yorkshire terrier dog.

Hyperadrenocorticism, a disorder characterized by excessive production of cortisol by the adrenal cortex, is well-recognized in dogs. A 10-year-old, intact male, Yorkshire terrier dog was evaluated because of corneal ulceration and generalized alopecia. Diagnosis was made based on history taking, clinical signs, physical examination, and results of routine laboratory testing (complete blood count, serum biochemical analysis, and urinalysis). In addition, adrenocorticotropic hormone (ACTH) stimulation test and abdominal ultrasonography were also used to diagnose this case. The patient was diagnosed as adrenal gland neoplasia and medical therapy using the adrenocorticolytic agent, mitotane, was initiated. An ACTH stimulation test was performed after initial therapy. After successful induction was obtained, maintenance therapy with mitotane still continued.

Adrenal Gland Neoplasms↗