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At least 217 records · Page 12Linked to original sources
PubMed1986

[Results of the diagnosis of adrenal masses using percutaneous CT-guided fine needle biopsy].

This paper reports the results of 42 CT-aided fine needle biopsies of adrenal masses in 40 patients (26 were smaller than 3 cm., six smaller than 1 cm.). There were 25 adenomas, seven metastases, one primary carcinoma, one case of tuberculosis, two phaeochromocytomas and four post-inflammatory lesions. Diagnostic material was obtained in 88%. There was one incorrect diagnosis and on five occasions the result was indefinite, leading to an accuracy of 73%. Exclusion or demonstration of malignancy was, however, correct in 85%. There were no complications except for one unimportant pneumothorax.

Addison Disease↗
PubMed1988

Cosecretion of peptides derived from gamma-human atrial natriuretic polypeptide in normal volunteers and patients with essential hypertension and adrenal disorders.

Using two radio-immunoassays for N-terminal and C-terminal fragments of human atrial natriuretic polypeptide (ANP) precursor, gamma-hANP [human atrial natriuretic factor-(1-126)], that is gamma-hANP(1-25) [human atrial natriuretic factor-(1-25)] and alpha-hANP [human atrial natriuretic factor-(99-126)], we studied the secretion of gamma-hANP-derived peptides into circulation from the heart in normal subjects and patients with essential hypertension and adrenal disorders. Volume expansion with 2 litres physiological saline increased plasma gamma-hANP(1-25)-like immunoreactivity concomitantly with plasma alpha-hANP-like immunoreactivity in normal subjects. Infusion of angiotensin II (20 ng/kg per min) or noradrenaline (200 ng/kg per min) also caused a parallel increase in plasma gamma-hANP(1-25)-like and alpha-hANP-like immunoreactivity. Plasma gamma-hANP(1-25)-like immunoreactivity levels were changed together with alpha-hANP-like immunoreactivity in patients with essential hypertension and adrenal disorders. These results indicate that gamma-hANP-derived peptides, alpha-hANP and the 10-k N-terminal fragment of gamma-hANP (N-peptide) are cosecreted from the heart and that the simultaneous measurement of N-peptide and alpha-hANP serves as an indicator of the cardiac endocrine function. The significance of N-peptide as a hormone must await further clarification.

Addison Disease↗
PubMed1985

ACTH and cortisol responses to ovine corticotrophin-releasing factor in patients with primary and secondary adrenal failure.

The ACTH and cortisol responses to an intravenous bolus injection of 100 micrograms ovine CRF were studied in 19 patients with adrenal failure. In all eight patients with primary adrenal failure, plasma ACTH levels increased from a mean basal level of 1494 +/- 431 (SEM) pg/ml to peak value of 2601 +/- 1220 pg/ml at 10 min. In comparison with healthy subjects absolute ACTH increments after ovine CRF were significantly augmented in the patients with Addison's disease (P* less than 0.001), and the absolute ACTH responses after ovine CRF were positively correlated with the basal plasma ACTH levels. The 11 patients with secondary adrenal insufficiency could be subdivided into two groups: (A) those having little or no ACTH and cortisol response to ovine CRF (five patients) and (B) those having prolonged and pronounced ACTH responses with a biphasic pattern and a delayed second peak (six patients), followed in all patients by a marked cortisol increase. These data demonstrate that the CRF-test can discriminate between hypothalamic and pituitary causes of secondary adrenal failure.

Addison Disease↗
PubMed2004

The adrenal.

During the past 15 years, considerable progress has been made in our understanding of the genetic basis of adrenal development and function. More than 30 single gene disorders have now been identified that can affect the hypothalamic-pituitary-adrenal axis in humans (fig. 1, 2; table 1). This review highlights recent advances in the molecular pathology of: (1) adrenal hypoplasia, (2) adrenal destruction, (3) disorders of adrenal steroidogenesis, (4) adrenal steroid resistance and (5) activation of the adrenal axis/tumorigenesis. Characterizing the molecular basis and natural history of these conditions is providing fascinating insight into adrenal development and function and can help to focus treatment and counselling of patients appropriately. However, ongoing translation of research findings into clinical practice is needed if patient care is to be influenced significantly.

Addison Disease↗
PubMed1975

Isolated glucocorticoid insufficiency.

Two cases of isolated glucocorticoid insufficiency or congenital adrenocortical unresponsiveness to ACTH-a variant of adrenocortical failure without mineralocorticoid insufficiency-are presented. Familial incidence was present only in case 1 since two of the siblings died after convulsions, possible related to hypoglycemia. The pathology specimens of one sibling were available for review showing complete lack of the fascicular zone and degenerative changes in the adrenals and evidence of increased ACTH secretion in the pituitary. In the patients who were given substitution therapy with hydrocortisone, studies of plasma renin and aldosterone revealed impairment of plasma aldosterone response to salt restriction, orthostatism and furosemide-induced diuresis combined with postural change. We conclude that in some cases of isolated glucocorticoid insufficiency, impairment of mineralocorticoid function may gradually develop, which is in contrast to the assumption of a congenital defect in the action of ACTH.

Adrenal Cortex Diseases↗