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adrenocortical hyperfunction/kalium

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ArtiklarKliniska testerPatent
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OBJECTIVE To evaluate the effect of trilostane on serum concentrations of aldosterone, cortisol, and potassium in dogs with pituitary-dependent hyperadrenocorticism (PDH), compare the degree of reduction of aldosterone with that of cortisol, and compare aldosterone concentrations of healthy dogs

ADRENOCORTICAL HYPERFUNCTION AND POTASSIUM METABOLISM IN PATIENTS WITH "NON- ENDOCRINE" TUMORS AND CUSHING'S SYNDROME.

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Effect of trilostane and mitotane on aldosterone secretory reserve in dogs with pituitary-dependent hyperadrenocorticism.

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BACKGROUND Maximal aldosterone secretion in healthy dogs occurs 30 minutes postadrenocorticotropin (ACTH; 5 μg/kg IV) stimulation. The effect of trilostane and mitotane on aldosterone at that time is unknown. OBJECTIVE To assess the effect of trilostane and mitotane in dogs with pituitary-dependent

Prevalence and risk factors associated with systemic hypertension in dogs with spontaneous hyperadrenocorticism

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Background: Systemic hypertension (SH) is common in dogs with hyperadrenocorticism (HAC) however there are not many studies assessing its prevalence and risk factors. Objectives:

Results of non-selective adrenocorticolysis by o,p'-DDD in 129 dogs with pituitary-dependent hyperadrenocorticism.

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One hundred and twenty-nine dogs with pituitary-dependent hyperadrenocorticism were treated according to a protocol aimed at the complete destruction of the adrenal cortices by the administration of o,p'-DDD (mitotane) at a daily dose of 50 to 75 mg/kg bodyweight for 25 days. On the third day,

Hyperadrenocorticism in six cats.

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The case records of six cats with hyperadrenocorticism presented to the Department of Clinical Veterinary Medicine, University of Cambridge, over an 11-year period were reviewed. Signalment and clinical signs were similar to previous reports but, in contrast to other reports, only three cats had

[Shifts in the electrolyte and energy metabolism of rat myocardium in experimental hypercorticism].

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Experiments were conducted on 612 albino male rats; a complex study was made in the myocardium of K+, Na+, Ca2+, Mg2+, Cl-, water, creatinphosphate, inorganic phosphorus, adenylic system components. A study was made of the effect of exogenous hypercorticism created by the administration of

Plasma concentration of atrial natriuretic hormone during endogenous glucocorticoid hypercorticism.

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In vitro studies have shown that glucocorticoids may increase atrial natriuretic-hormone (ANH) synthesis and/or release. This action of glucocorticoids has also been suggested in vivo in patients with Cushing's syndrome. However, in this circumstance, plasma AH elevation might be due to humoral
The aim of this study was to evaluate the role of aldosterone as an initiating and/or perpetuating factor in hypertension associated with pituitary-dependent hyperadrenocorticism (PDH) in dogs. Thirteen dogs with PDH and 11 healthy control dogs were used. In all dogs, arterial blood pressure and
Although cardiovascular complications are the major determinant of the prognosis of Cushing's syndrome (CS), factors contributing to the cardiovascular lesions are still unclear. We investigated clinical factors determining cardiac function in patients with adrenal CS. Fifty patients with adrenal CS

Effect of trilostane on hormone and serum electrolyte concentrations in dogs with pituitary-dependent hyperadrenocorticism.

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BACKGROUND The effects of trilostane on key hormones and electrolytes over 24 hours in dogs with pituitary-dependent hyperadrenocorticism (PDH) are unknown. OBJECTIVE To determine the plasma concentration of cortisol, endogenous adrenocorticotropic hormone (ACTH), aldosterone, sodium, potassium, and

[Effects of activity of 11β-hydroxysteroid dehydrogenase type 2 on serum potassium levels in Cushing's syndrome patients].

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OBJECTIVE To explore the effects of different forms of glucocorticoid excess on cortisol/cortisone ratio and to reveal the mechanisms of hypokalemia in Cushing's syndrome patients. METHODS The levels of urinary free cortisol (UFF) and urinary free cortisone (UFE) were determined in 6 adult patients

Hypoadrenocorticism following therapy with o,p-DDD for hyperadrenocorticism in four dogs.

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Hypoadrenocorticism developed in 4 of 26 dogs treated with mitotane (o,p-DDD) for hyperadrenocorticism. Evidence of the hypoadrenocorticism was detected from 2-8 weeks after the beginning of weekly or bimonthly maintenance o,p-DDD therapy. The adversely affected dogs had hyponatremia plus

Hyperadrenocorticism in a ferret.

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A 7-year-old adult male ferret had progressive hair loss that was bilaterally symmetric. Also clinically evident were severe dehydration, polydipsia, muffled heart sounds, weak femoral pulses, hepatomegaly, lethargy, weakness, temporal muscular atrophy, dyspnea, and weakness. The blood profile of
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