Diagnosis and therapy surveillance in Addison's disease: rapid adrenocorticotropin (ACTH) test and measurement of plasma ACTH, renin activity, and aldosterone

1992 ◽  
Vol 75 (1) ◽  
pp. 259-264 ◽  
Author(s):  
W. Oelkers
Keyword(s):  
Addison’S Disease ◽  
Renin Activity ◽  
Addison's Disease ◽  
Acth Test ◽  
Plasma Acth ◽  
Diagnosis And Therapy

scholarly journals A high-sensitivity test in the assessment of adrenocortical insufficiency: 10 microg vs 250 microg cosyntropin dose assessment of adrenocortical insufficiency

1998 ◽  
Vol 159 (2) ◽  
pp. 275-280 ◽  
Author(s):  
JG Gonzalez-Gonzalez ◽  
NE De la Garza-Hernandez ◽  
LG Mancillas-Adame ◽  
J Montes-Villarreal ◽  
JZ Villarreal-Perez
Keyword(s):  
Healthy Subjects ◽  
Low Dose ◽  
Standard Dose ◽  
Addison’S Disease ◽  
High Sensitivity ◽  
Serum Cortisol ◽  
Dose Assessment ◽  
Addison's Disease ◽  
Acth Test ◽  
Adrenocortical Insufficiency

The short cosyntropin (synthetic ACTH) test is recognized as the best screening manoeuvre in the assessment of adrenocortical insufficiency. Recent data, however, suggest that i.v. administration of 250 microg cosyntropin could be a pharmacological rather than a physiological stimulus, losing sensitivity for detecting adrenocortical failure. Our objective was to compare 10 vs 250 microg cosyntropin in order to find differences in serum cortisol peaks in healthy individuals, the adrenocortical response in a variety of hypothalamic-pituitary-adrenal axis disorders and the highest sensitivity and specificity serum cortisol cut-off point values. The subjects were 83 healthy people and 37 patients, the latter having Addison's disease (11), pituitary adenomas (7), Sheehan's syndrome (9) and recent use of glucocorticoid therapy (10). Forty-six healthy subjects and all patients underwent low- and standard-dose cosyntropin testing. In addition, 37 controls underwent the low-dose test. On comparing low- and standard-dose cosyntropin testing in healthy subjects there were no statistical differences in baseline and peaks of serum cortisol. In the group of patients, 2 out of 11 cases of Addison's disease showed normal cortisol criterion values during the standard test but abnormal during the low-dose test. In our group of patients and controls, the statistical analysis displayed a better sensitivity of the low-dose vs standard-dose ACTH test at 30 and 60 min. In conclusion, these results suggest that the use of 10 microg rather than 250 microg cosyntropin i.v. in the assessment of suspicious adrenocortical dysfunction gives better results.

No inhibition of corticotrophin (ACTH)-hypersecretion in adrenal insufficiency by somatostatin

1980 ◽  
Vol 95 (1) ◽  
pp. 71-74 ◽  
Author(s):  
A. Jara-Albarrán ◽  
J. Bayort ◽  
A. Caballero ◽  
R. Eusebio ◽  
P. García-Peris ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Primary Adrenal Insufficiency ◽  
No Inhibition ◽  
Infusion Period

Abstract. Somatostatin (250 μg as a bolus iv and 250 μg as a I h infusion) was administered to 6 patients with primary adrenal insufficiency (Addison's disease). The fall in plasma ACTH during the infusion period ranged between 0–30% with a mean reduction of 11.2 ± 11.6%. These findings suggest that with the method employed, somatostatin is not an inhibitor of ACTH secretion in a condition in which glucocorticoids are lacking.

Effect of angiotensin II on plasma ACTH in patients with Addison's disease

1985 ◽  
Vol 110 (4) ◽  
pp. 451-455
Author(s):  
Hermann Haller ◽  
Volker Bähr ◽  
Petra Exner ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Time Lag ◽  
Addison’S Disease ◽  
Major Effect ◽  
Addison's Disease ◽  
Base Line ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Short Term ◽  
Sodium Deficiency

Abstract. Short-term angiotensin II (All) infusions (3 ng/kg/min) were performed in 5 patients with Addison's disease in order to assess the effect of AII on ACTH secretion. Base line ACTH levels were elevated due to a 9-h time lag between hydrocortisone administration and onset of the study. In 2 separate infusion periods of 30-min duration, All had no unidirectional effect on plasma ACTH. Mean ACTH increased slightly but insignificantly. Mean blood pressure rose by about 10 mmHg. The degree of angiotensinaemia induced is probably similar to the state of moderate to severe sodium deficiency. Short-term changes of All in this order of magnitude have obviously no major effect on ACTH secretion.

Low dose (1 μg) ACTH test in the evaluation of adrenal dysfunction in pre-clinical Addison's disease

2000 ◽  
Vol 53 (1) ◽  
pp. 107-115 ◽  
Author(s):  
Stefano Laureti ◽  
Emanuela Arvat ◽  
Paola Candeloro ◽  
Lidia Di Vito ◽  
Ezio Ghigo ◽  
...  
Keyword(s):  
Low Dose ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Acth Test

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

1982 ◽  
Vol 99 (3) ◽  
pp. 357-363 ◽  
Author(s):  
Barbara Krautli ◽  
J. Müller ◽  
A. M. Landolt ◽  
F. von Schulthess
Keyword(s):  
Visual Fields ◽  
Sella Turcica ◽  
Addison’S Disease ◽  
Surgical Removal ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Cell Adenoma ◽  
Feedback Suppression ◽  
Secondary Hypothyroidism ◽  
Transsphenoidal Microsurgery

Abstract. In 2 women with known Addison's disease, progressive hyperpigmentation reappeared years after an initial remission under conventional substitution therapy with cortisone. Excessively elevated plasma ACTH concentrations and radiological evidence of sella turcica deformation led to the diagnosis of ACTH-producing adenomas and prompted their removal by transsphenoidal microsurgery. In one patient, a large Crooke's cell adenoma with extensive extrasellar expansion had caused severe and irreversible bilateral defects of the visual fields and unilateral optic atrophy. Surgical removal of the tumour and radiotherapy brought about a permanent disappearance of the hyperpigmentation, but eventually led to secondary hypothyroidism. In the second patient, the selective removal of a small intrasellar eosinophilic adenoma consisting of ACTH-producing cells did not alleviate the hyperpigmentation and did not lower the plasma ACTH concentration. However, hyperpigmentation regressed markedly within a year of treatment with a higher dose of cortisone. The rarity of similar cases in the literature seems to indicate that insufficient feedback suppression of ACTH-producing cells in treated Addison's disease does not by itself induce the development of a pituitary adenoma, but might promote the growth of an independently and coincidentally occurring microadenoma, which would have caused Cushing's disease in a person with intact adrenal glands.

Probable ACTH-secreting pituitary tumour in association with Addison's disease

1985 ◽  
Vol 110 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Toshihiko Yanase ◽  
Kensaku Sekiya ◽  
Masaaki Ando ◽  
Hajime Nawata ◽  
Ken-ichi Kato ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Sella Turcica ◽  
Addison’S Disease ◽  
Pituitary Tumour ◽  
Cortisone Acetate ◽  
University Hospital ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Old Japanese ◽  
Acth Secreting

Abstract. A 61 year old Japanese man with a diagnosis of Addison's disease was admitted to Kyushu University Hospital for further investigation of high ACTH levels and hyperpigmentation which 37.5 mg of cortisone acetate failed to alleviate. The basal level of plasma ACTH was 700—1000 pg/ml, and following 25—37.5 mg cortisone acetate or 1 mg dexamethasone the levels were 300—600 pg/ml. The general pigmentation showed little improvement with such medication. Radiographic studies revealed a double floor of the sella turcica and cisternal herniation. These observations suggested the existence of a pituitary ACTH-secreting tumour. Plasma ACTH showed a circadian rhythm ranging from 440 to 1570 pg/ml and it was not suppressed to a normal range by oral administration of dexamethasone, 8 mg/day or by continuous infusion of dexamethasone, 1.25 mg/h for 2 h. Plasma ACTH responses of 80% above basal level to lysine-vasopressin (LVP), and 12% above basal to synthetic ovine corticotrophin releasing factor (CRF) were observed. FK 33-824, a methionine-enkephaline analogue, suppressed plasma ACTH to 85% of basal level, while bromocriptine (CB-154) caused no significant change. These findings led to a diagnosis of pituitary ACTHsecreting adenoma (corticotropinoma) in association with Addison's disease. The persistent circadian rhythm of plasma ACTH suggested that this adenoma may not be completely free from regulation by the central nervous system. This case may be clinically significant for investigation of the pathogenesis of pituitary adenoma, particularly in Nelson's syndrome.

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