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Results for “Adrenocortical Hyperfunction”

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At least 1,549 records · Page 86Linked to original sources
PubMed1991

Serum free thyroxine concentration in healthy dogs, dogs with hypothyroidism, and euthyroid dogs with concurrent illness.

Serum free thyroxine (fT4), thyroxine (T4), and 3,5,3'-triiodothyronine (T3) concentrations were determined in 62 healthy dogs, 51 dogs with hypothyroidism, and 59 euthyroid dogs with concurrent dermatopathy or concurrent illness for which hypothyroidism was a diagnostic consideration. Status of thyroid function was based on history, physical findings, results of thyrotropin response testing, requirement for thyroid hormone replacement therapy, and in 31 dogs, on results of histologic examination of a thyroid gland biopsy specimen. Serum fT4 concentration was determined, using a single-stage radioimmunoassay. Mean (+/- SD) serum fT4 concentration was significantly (P less than 0.05) greater in healthy dogs vs dogs with hypothyroidism (0.51 +/- 0.27 ng/dl vs 0.10 +/- 0.07 ng/dl). Significant difference in mean serum fT4 concentration was not evident between dogs with hypothyroidism and euthyroid dogs with hyperadrenocorticism (0.16 +/- 0.13 ng/dl) or peripheral neuropathy (0.19 +/- 0.10 ng/dl). Mean serum fT4 concentration in all other groups of euthyroid dogs with concurrent illness was similar to values in healthy dogs and was significantly (P less than 0.05) greater, compared with values in dogs with hypothyroidism. Similar results were found for mean serum T4 concentration. Comparison of serum fT4 vs T4 concentration revealed: sensitivity, 0.97 vs 0.98; specificity, 0.78 vs 0.73; predictive value for a positive test result, 0.79 vs 0.80; predictive value for a negative test result, 0.97 vs 0.97; and accuracy, 0.78 vs 0.86, respectively. Ten (17%) and 12 (20%) of 59 serum fT4 and T4 concentrations, respectively, were inappropriately low in euthyroid dogs with concurrent illness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocortical Hyperfunction↗
PubMed1991

Plasma free cortisol concentrations in dogs with hyperadrenocorticism.

Unbound or free cortisol constitutes a small fraction of total plasma cortisol, but is believed to represent the biologically active portion of this circulating glucocorticoid. We tested the hypothesis that the percentage free cortisol was altered in plasma from dogs with hyperadrenocorticism, which could account for a greater target tissue response to this circulating hormone. The percentage free cortisol in plasma samples from human beings, healthy dogs, and dogs with hyperadrenocorticism was estimated, using centrifugal ultrafiltration-dialysis. Total cortisol concentrations were determined by use of radioimmunoassay. Total cortisol concentrations appeared greater in plasma from human beings than in plasma from either group of dogs. However, the percentage free cortisol was lower in plasma from human beings, resulting in a calculated concentration of free cortisol that was quite similar between plasma from human beings and healthy dogs. Total plasma cortisol concentrations were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (190 +/- 113 nmol/L; mean +/- SD) than in healthy dogs (102 +/- 85 nmol/L), but the percentage free cortisol was not different between these 2 groups (dogs with hyperadrenocorticism, 16 +/- 9%; healthy dogs, 13 +/- 6%). However, plasma free cortisol concentrations (product of total and the percentage of free cortisol) were greater (P less than 0.01) in samples from dogs with hyperadrenocorticism (36 +/- 41 nmol/L) than in those from healthy dogs (16 +/- 9 nmol/L). Significant (P less than 0.001) positive linear relationships were found between total cortisol concentrations and percentage free cortisol in plasma samples from healthy dogs and dogs with hyperadrenocorticism.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1991

[Cushing's syndrome due to bilateral adrenal macronodular hyperplasia. From ACTH-dependent hypercortisolism to ACTH-independent hypercortisolism].

A 35 year old female with Cushing's syndrome and bilateral adrenal macronodular hyperplasia, in whom a change from ACTH dependency to autonomy was observed, is presented. The diagnosis of Cushing's syndrome was based on the failure of suppression of urinary ketogenic steroids (17 KCS) and free cortisol (uF) with the administration of 2 mg of dexamethasone daily for 2 days. CT scan of the abdomen showed adrenal bilateral multinodular hyperplasia and the sellar CT scan was normal. Initially 8 mg for 2 days of dexamethasone suppressed 17 KCS and uF; however, a few months later this effect was lost as well as the effect of endogenous ACTH on cortisol. Bilateral adrenalectomy was carried out, prior to attainment of normal cortisol levels with Ketoconazole. The adrenal glands has multiple nodules and they weighed 10 and 21 grams. Her postoperative plasmatic cortisol levels were imperceptible. Physiopathologic mechanisms involved in bilateral macronodular adrenal hyperplasia are reviewed.

Adrenal Glands↗
PubMed2005

[Asymptomatic tumors of the adrenals (incidentalomas): criteria for the endoscopic removal].

An algorithm of using modern methods of the laboratory and X-ray examination and of operative treatment of patients by laparoscopic techniques was developed on the basis of an analysis of the results of diagnosis, endovideosurgical treatment of 132 patients with adrenal tumors without clear clinical signs, hypercortisolism and hyperadrenalinectomy (incidentalomas). Laparoscopic techniques were shown to be less traumatic and dangerous under conditions of regular using them in specialized clinics.

Adolescent↗
PubMed2006

[Diabetes mellitus and frequently associated endocrine diseases].

The simultaneous occurrence of type 1 or type 2 diabetes with various hormonal diseases (e.g. thyroid, adrenal, pituitary disease) is a frequent observation. A chronically poorly controlled metabolism can alter the hormone parameters of the diabetic. In contrast, an acute loss of metabolic control may be a sign of a newly manifesting hormonal disease, and needs always prompt an appropriate diagnostic work-up and treatment. In view of the frequency both of diabetes mellitus and thyroid disease, a regular check--at least yearly and always in case of unclear worsening of diabetic control--of thyroid gland function is mandatory. The aim is to provide appropriate treatment, and thus to stabilize the patient's metabolic status, as early as possible.

Adrenal Insufficiency↗
PubMed2006

Unravelling the mystery in a case of persistent ACTH-independent Cushing's syndrome.

INTRODUCTION: We present a rare variety of adrenocorticotrophic hormone (ACTH)-independent Cushing's syndrome known as primary pigmented nodular adrenocortical disease (PPNAD). CLINICAL PICTURE: The patient initially underwent unilateral adrenalectomy for what was thought to be a left adrenal adenoma. OUTCOME: Partial resolution of symptoms and demonstrable persistent hypercortisolism after surgery prompted further evaluation with findings leading to the diagnosis of Carney complex. A review of the adrenal histology was consistent with PPNAD. CONCLUSION: This entity of PPNAD, which has rarely been reported in Asians, forms part of the Carney complex. The diagnosis may not be simple and straightforward, as illustrated in this patient.

Adrenal Glands↗
PubMed1976

Human adenohypophysis in Nelson syndrome. Ultrastructural and clinical study.

The manifestations that comprise the disease known as Nelson syndrome are pituitary hyperplasia and cutaneous hyperpigmentation, which sometimes follow bilateral adrenalectomy, in patients with hypercortisolism. We present a comprehensive endocrinologic, structural study of a patient in whom the evidence obtained supports the hypotheses that: (a) the primary disorder in this form of hypercortisolism is probably hypothalamic; (b) the hyperplasia of the adenohypophysis, following adrenalectomy, is closely associated with lowered plasma cortisol levels; and (c) the cillular hyperplasia in the adenohypophysis involves primarily the corticotroph, a cell believed to be associated with the secretion of adrenocorticotrophic hormone and melanocyte-stimulating hormone.

17-Ketosteroids↗
PubMed1991

Ultrasonography of the adrenal gland.

A current review of ultrasonographic adrenal imaging is presented with emphasis on the clinical and problematic aspects of adrenal disease in the dog. Examples are presented to illustrate the usefulness of ultrasonography in distinguishing between canine pituitary- and adrenal-dependent hyperadrenocorticism. Adrenal imaging in the cat and ferret are discussed briefly. When coordination of sonographic findings with clinical and biochemical results is implemented properly, ultrasonography becomes a powerful and specific diagnostic tool for adrenal disease.

Adrenal Gland Diseases↗