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PubMed1988

Diabetes insipidus and hyperadrenocorticism associated with high plasma adrenocorticotropin concentration and a hypothalamic/pituitary mass in a dog.

Central diabetes insipidus was diagnosed in association with a dexamethasone-insuppressible adrenocorticotropin-secreting tumor in a dog. Over the 3 years before the dog's death, the combination of specific pituitary function tests, peptide hormone radioimmunoassays, and visualization of the tumor by use of x-ray computed tomography of the skull, allowed an etiologic diagnosis. Because initial signs of glucocorticoid excess were questionable and adrenolytic therapy was not allowed by the owners, treatment consisted only of administration of synthetic vasopressin, which was successful in the management of the diabetes insipidus.

Adrenocortical Hyperfunction↗
PubMed1986

The nature of neuroendocrine abnormalities in depression: a controversial issue in contemporary psychiatry.

Neuroendocrine abnormalities in depression have been regarded, by many authors, as relatively specific markers of nosological subtypes of the disorder, e.g. primary vs. secondary, endogenous vs. non-endogenous or unipolar vs. bipolar depression. They should reflect the same changes in central neurotransmitters (e.g. noradrenergic insufficiency and/or cholinergic hyperactivity) that were hypothesized as the cause of clinical symptoms. This view is challenged on the basis of our own neuroendocrine investigations in 317 psychiatric patients and 103 normal controls. According to these studies the abnormalities are nosologically rather unspecific. They are induced by a large variety of factors, e.g. emotional stress associated with the clinical symptomatology, weight loss due to malnutrition as a consequence of reduced appetite, medication and drug withdrawal. Stress-induced hypercortisolism appears to be the most common abnormality that may trigger other neuroendocrine dysfunctions, such as a blunted TSH response to TRH. Differences in neuroendocrine abnormalities of depressives are probably due to variations in the manifold factors influencing the hormonal axes involved, to temporal changes in hormonal patterns (e.g. one abnormality triggering another) and to individual differences in the basic activity and the responsiveness of the various axes.

Adrenocortical Hyperfunction↗
PubMed1985

Evaluation of a combined dexamethasone suppression/ACTH stimulation test in dogs with hyperadrenocorticism.

Twenty-one dogs with hyperadrenocorticism were studied. Six dogs had functioning adrenocortical tumors and 15 had pituitary-dependent hyperadrenocorticism. Each dog was evaluated, using endogenous plasma ACTH, ACTH stimulation, dexamethasone screening, dexamethasone suppression, and combined dexamethasone suppression/ACTH stimulation tests. The ACTH stimulation portion of the combined test was less reliable as a screening test in diagnosing hyperadrenocorticism than was the isolated ACTH stimulation test or the dexamethasone screening test. The dexamethasone suppression portion of the combined test was less reliable in distinguishing dogs with adrenocortical tumors from those with pituitary-dependent hyperadrenocorticism than was the endogenous ACTH or isolated dexamethasone suppression test. The combined test is not recommended for use. The ACTH stimulation test is the recommended screening test because of its diagnostic reliability and its subsequent importance as a base line in determining success of mitotane therapy.

Adrenal Cortex Function Tests↗
PubMed1985

Effect of o,p'DDD therapy on endogenous ACTH concentrations in dogs with hypophysis-dependent hyperadrenocorticism.

The effect of o,p'DDD therapy on the endogenous plasma ACTH concentration was evaluated in 15 dogs with hypophysis-dependent hyperadrenocorticism. Adequate control of hyperadrenocorticism with o,p'DDD was based on the reduction of water consumption to within the normal range, disappearance of clinical signs of lethargy, weakness, alopecia, thin skin, or pendulous abdomen, and an increase in blood cortisol below the normal range after exogenous ACTH administration. Endogenous ACTH concentrations were determined for each dog after the disease was controlled and while they were given o,p'DDD on a maintenance schedule. Endogenous ACTH concentrations increased in 14 of 15 dogs after o,p'DDD therapy, indicating a lack of suppressive effects of o,p'DDD on hypophysis ACTH secreting cells.

Adrenal Cortex Function Tests↗
PubMed1986

Facial dermatosis in four dogs with hyperadrenocorticism.

In hyperadrenocorticism in the dog, cutaneous lesions may include alopecia, thin, hypotonic skin, hyperpigmentation, comedones, calcinosis cutis, secondary bacterial and fungal infections, and demodicosis. Skin lesions affecting only the face have not been reported in reviews of hyperadrenocorticism, nor has the disease been included in the differential diagnoses of facial dermatoses. This report involves 4 dogs with hyperadrenocorticism in which cutaneous signs were limited to the face.

Adrenocortical Hyperfunction↗
PubMed1986

Evaluation of canine hyperadrenocorticism, using computed tomography.

Abdominal computed tomography was performed in 9 dogs with hyperadrenocorticism and in 2 healthy dogs. Both adrenal glands were identified in all dogs. Computed tomography allowed accurate identification of the sites of adrenal gland dysfunction, when interpreted in combination with a biochemical diagnosis of canine hyperadrenocorticism. This accuracy permitted the retroperitoneal approach to be used for all adrenalectomies. Use of contrast medium (although not essential) was helpful in the computed tomographic identification of blood vessels, kidneys, and other abdominal organs.

Adrenal Cortex Neoplasms↗
PubMed1986

Pituitary-dependent hyperadrenocorticism in a cat.

Pituitary-dependent hyperadrenocorticism was diagnosed in a 9-year-old, male castrated cat that had polyuria, polyphagia, pendulous abdomen, truncal hair loss, congestive heart failure, and insulin-resistant diabetes mellitus. Results of pituitary-adrenal function testing revealed inadequate serum cortisol suppression following dexamethasone administration, exaggerated serum cortisol responses after exogenous ACTH stimulation, and high plasma ACTH concentrations. The pathologic findings of bilateral adrenocortical hyperplasia and a pituitary adenoma that immunostained well for ACTH-related peptides confirmed pituitary-dependent hyperadrenocorticism.

Adenoma, Chromophobe↗
PubMed1986

Evaluation of a six-hour combined dexamethasone suppression/ACTH stimulation test in dogs with hyperadrenocorticism.

Seventeen dogs with hyperadrenocorticism were studied. Three dogs had functioning adrenocortical tumors and 14 had pituitary-dependent hyperadrenocorticism. Each dog was evaluated by determining the endogenous plasma ACTH concentration and by performing 4 tests: ACTH stimulation, dexamethasone screening, dexamethasone suppression, and a 6-hour combined dexamethasone suppression/ACTH stimulation test. The combined test was less reliable as a screening test in diagnosing hyperadrenocorticism than was the dexamethasone screening test or the ACTH stimulation test. Compared with the endogenous plasma ACTH concentration, results of the dexamethasone suppression portion of the combined test were less reliable in distinguishing dogs with adrenocortical tumors from those with pituitary-dependent hyperadrenocorticism. It was concluded that the combined test cannot be recommended for use.

Adrenal Cortex Function Tests↗
PubMedDate not supplied

[Similarity and differences of the pathogenesis of Itsenko-Cushing syndrome variants].

Proceeding from a study of the results of the investigation of 152 patients with Icenko-Cushing's syndrome the authors have arrived at the conclusion that hyperplasia, clear cell adenoma of monomorphous structure, dark cell and mixed adenomas of polymorphous structure, cancer of the adrenal cortex are different stages of a common pathological process. Such formation of morphological changes in the adrenal gland is one of the ways of development of Icenko-Cushing's syndrome. To confirm the proposed concept of the pathogenesis of this disease the authors provide some evidence of hyperplasia or the normal structure of nontumorous adrenocortical tissue in adenoma and cancer, of the absence of difference in a rise of the mean ACTH level in the blood in hyperplasia and different adrenocortical tumors. An increase in ACTH production in most of the patients should be regarded as one of the primary factors of the above morphological changes. The absence of suppression of 17-oxycorticosteroid excretion with urine in a test with 8 mg of dexamethasone in most of the patients with dark cell and mixed adenoma of polymorphous structure and adrenocortical cancer suggests a possibility of the development of certain autonomy of these neoplasms.

17-Hydroxycorticosteroids↗
PubMed1987

Corticotropin releasing hormone: relevance to normal physiology and to the pathophysiology and differential diagnosis of hypercortisolism and adrenal insufficiency.

CRH is a 41 amino acid peptide first isolated from ovine and subsequently from rat and human hypothalami. We have conducted a series of clinical studies with oCRH and hCRH in volunteers and patients with various disorders of hypothalamic-pituitary-adrenal function. In volunteers, it was demonstrated that hCRH administration produced ACTH and cortisol responses which closely mimic naturalistically occurring secretory episodes. This data, as well as the demonstration that pulsatile hCRH can reestablish normal ACTH and cortisol secretion in patients with hypothalamic CRH deficiency, strongly argue that CRH is of physiological relevance to the human pituitary-adrenal axis. However, since the ACTH response to an insulin tolerance test is greater than the maximal ACTH response to CRH, other factors such as vasopressin may be relevant to stress-induced ACTH secretion in man. Following the demonstration that CRH seems to be of physiological relevance to human subjects, a CRH stimulation test was developed based on pharmacokinetic and dose response studies with oCRH and hCRH. Based on these data, which revealed that oCRH functions as a long-acting analogue of hCRH, and the demonstration that hormonal responses to CRH are greatest in the evening, patient groups with abnormalities of the hypothalamic-pituitary-adrenal axis were tested with intravenous oCRH with a dose of 1 micrograms/kg given at 2000 hours. This CRH stimulation test has proved helpful in clarifying the pathophysiology of hypercortisolism in a variety of psychiatric disorders characterized by this endocrine abnormality. Thus, blunted ACTH responses in hypercortisolemic patients with depression, anorexia nervosa, and panic anxiety disorder indicate normality of the pituitary corticotroph in these patient subgroups. These data, along with the finding that a continuous infusion of CRH to normal volunteers, reproduces the pattern and magnitude of hypercortisolism in depression and anorexia nervosa, suggest that the hypercortisolism in these disorders represents a defect at or above the hypothalamus resulting in the hypersecretion of CRH. This hypothesis is particularly intriguing in light of the demonstration that CRH administration to experimental animals produces many of the physiological and behavioral responses classically associated with depression and anorexia nervosa, including hypercortisolism, hypothalamic hypogonadism, and decreases in libido and appetite. The CRH stimulation test has also helped to resolve one of the oldest endocrinological dilemmas, namely whether the hypercortisolism of depression and Cushing's disease share a common or dissimilar pathophysiological basis.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Insufficiency↗
PubMed1977

Influence of single peroral dose of aminoglutethimide on the rat adrenal cortex.

In female albino rats force fed with a single dose of 50 mg of aminoglutethimide (AG) lipoid adrenocortical hyperplasia was found within 24 h. In addition, a marked focal increase in cytoplasmic transparency was found which ultrastructurally appeared to result from optically empty vacuoles and membrane-bound spaces. Later, an increase occurred in the translucency of the cytoplasmic matrix, mitochondrial swelling, destruction of cell membranes and disappearance of adrenocortical cells presenting as cytolysis. Some of the damaged cortical cells contained protein vacuoles with fibrillar structures and occasionally also blood cells. All such changes were associated with a marked infiltration by neutrophilic granulocytes, the most severe of them resembling an acute purulent epinephritis. Ultrastructural examination showed blood monocytes with signs of initial phagocytic activity at sites of disintegration of adrenocortical cells. Focal decrease of dehydrogenase activity was demonstrated in areas of cellular destruction, while no alteration in acid phosphatase activity was detected. Moreover, an absolute increase in corticosterone production form endogeneous precursors in vitro was found which could be partially explained by an increase in adrenocortical size. Formation of 18-hydroxycorticosterone and aldosterone from 4-14C-progesterone was decreased. However, no appreciable changes were revealed in the zona glomerulosa. From these findings it may be assumed that high doses of AG not only block the conversion of cholesterol into pregnenolone, but also injure some other cellular enzymatic systems necessary for the integrity of the adrenocortical cell.

Adrenal Cortex↗
PubMed1988

Polycystic ovarian disease and congenital and late-onset adrenal hyperplasia.

This article surveys the congenital and late-onset forms of the common steroidogenic enzyme defects of the adrenal cortex--steroid 21-hydroxylase, steroid 11 beta-hydroxylase, and 3 beta-hydroxysteroid dehydrogenase deficiencies--in connection with the occurrence of polycystic ovarian disease.

3-Hydroxysteroid Dehydrogenases↗
PubMed1988

Glucocorticoid excess syndromes causing hypertension.

The adrenal glucocorticoid secretions undoubtedly perform necessary physiologic functions in maintaining normal blood pressure when secreted at their ordinary rate or in response to short term stress. Sustained glucocorticoid excess, in Cushing's syndrome or during prolonged therapy with synthetic steroids, leads to arterial hypertension and arteriosclerotic cardiovascular disease through a plentiful variety of pathogenetic mechanisms. Naturally occurring Cushing's syndrome should be readily detected, treated, and reversed unless due to metastatic malignancy. The benefits of glucocorticoid treatment as immunosuppressive and anti-inflammatory therapy are genuine, but the price includes cardiovascular disease. It is likely that the past role of glucocorticoid therapy will be supplanted by new strategies that minimize steroid dose, employ nonsteroid regimens, and perhaps lead to the development of specific steroids that possess only beneficial actions without potential for cardiovascular toxicity.

Adrenocortical Hyperfunction↗