Suppression of ACTH Secretion by Synthetic MSH-Release Inhibiting Factor PRO-LEU-GLY-NH2in Addison's Disease

1977 ◽  
Vol 9 (02) ◽  
pp. 150-152 ◽  
Author(s):  
K. Voigt ◽  
H. Fehm ◽  
R. Lang ◽  
K. Beinert ◽  
E. Pfeiffer
Keyword(s):  
Addison’S Disease ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Inhibiting Factor

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.

Inhibitory effect of cyproheptadine on ACTH secretion in patients with Addison's disease

1983 ◽  
Vol 102 (1) ◽  
pp. 111-115
Author(s):  
P. Loli ◽  
F. Frascatani ◽  
D. Gelli ◽  
M. Maggioni ◽  
F. Muratori ◽  
...  
Keyword(s):  
Oral Dose ◽  
Single Oral Dose ◽  
Drug Administration ◽  
Plasma Levels ◽  
Addison’S Disease ◽  
Inhibitory Effect ◽  
Feedback Mechanism ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Acth Release

Abstract. In 14 patients with Addison's disease plasma levels of ACTH were studied after administration of a single oral dose (16 mg) of cyproheptadine. The drug administration was followed by an inhibition of ACTH release. These results support the view that cyproheptadine may exert an inhibitory effect on ACTH secretion in subjects whose corticosteroid feedback mechanism is normal. We hypothesize that the effect of cyproheptadine might be related to its anti-serotonin or anti-histaminergic action.

A pituitary tumour with possible ACTH and TSH hypersecretion in a patient with Addison's disease and primary hypothyroidism

1980 ◽  
Vol 95 (2) ◽  
pp. 181-184 ◽  
Author(s):  
Sylvi Aanderud ◽  
Hans H. Bassøe
Keyword(s):  
Differential Diagnosis ◽  
Replacement Therapy ◽  
Addison’S Disease ◽  
Pituitary Tumour ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Pituitary Enlargement

Abstract. A patient with Addison's disease, who was inadequately substituted with corticosteroids for twenty-five years, developed a pituitary tumour. The diagnosis of autoimmune thryroiditis with asymptomatic hypothyroidism was also made. ACTH and TSH plasma values were abnormally elevated. The ACTH secretion was suppressed by cortisone administered perorally. It seems possible that the pituitary enlargement is due to prolonged insufficient adrenocortical replacement therapy. The differential diagnosis and possible pathogenetic factors are discussed.

Effects of fludrocortisone withdrawal on plasma angiotensin II, ACTH, vasopressin, and potassium in patients with Addison's disease

1987 ◽  
Vol 115 (3) ◽  
pp. 325-330 ◽  
Author(s):  
W. Oelkers ◽  
V. Bähr
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Feedback Inhibition ◽  
Addison’S Disease ◽  
Plasma Potassium ◽  
Dietary Sodium ◽  
Addison's Disease ◽  
Acth Secretion ◽  
Plasma Angiotensin ◽  
Acth Release

Abstract. We attempted to answer to the question whether excessive rises in endogenous plasma angiotensin II (All) stimulate ACTH secretion by measuring PRA, All, AVP, ACTH, and cortisol in 8 patients with Addison's disease before and after withdrawal of fludrocortisone substitution. Blood was drawn at 14.30 h, exactly 6½ h after the morning dose of hydrocortisone had been taken. PRA and All were initially higher than normal in 4 patients. After withdrawal of fludrocortisone for 1 or 2 weeks, PRA and All rose markedly in 4 patients (up to 260 ng/l) without concomitant changes in plasma ACTH levels (r = −0.081, All vs ACTH). Changes in plasma cortisol could not have obscured a stimulatory effect of All on ACTH by variable feedback inhibition of ACTH release. The increase in plasma All levels in the 4 patients was larger than that observed in a previous study in normal subjects after rigorous dietary sodium restriction. In all patients, hyperkalaemia developed after fludrocortisone withdrawal, independent of changes in PRA and AII. Rises in PRA, All, and plasma potassium were partially reversed by increased sodium intake and further suppressed by resumption of fludrocortisone therapy. Plasma AVP remained in the normal range after fludrocortisone withdrawal, but was slightly elevated after increasing salt intake without fludrocortisone administration. Conclusions: 1) Rises of endogenous plasma All to levels tenfold higher than normal do not stimulate ACTH release. All is probably not a physiological modulator of ACTH secretion. 2) Mineralocorticoid substitution in Addison's disease should be monitored by plasma potassium measurement. Hyperkalaemia may coexist with normal PRA.

Addison's disease as a rare cause of chronically elevated transaminases

2004 ◽  
Vol 42 (05) ◽  
Author(s):  
GC Gurakuqi ◽  
V Stadlbauer ◽  
H Warnkross ◽  
M Trauner
Keyword(s):  
Addison’S Disease ◽  
Addison's Disease ◽  
Elevated Transaminases

"STEROID-CELL" ANTIBODY IN ENDOCRINE DISEASES

1974 ◽  
Vol 76 (4) ◽  
pp. 729-740 ◽  
Author(s):  
Peter Kamp ◽  
Per Platz ◽  
Jørn Nerup
Keyword(s):  
Leydig Cells ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Hormone Production ◽  
Cortical Cells ◽  
Endocrine Diseases ◽  
Cell Antibody ◽  
Indirect Immunofluorescence Technique ◽  
Males And Females ◽  
Adrenal Cortical Cells

ABSTRACT By means of an indirect immunofluorescence technique, sera from 116 patients with Addison's disease, an equal number of age and sex matched controls and 97 patients with other endocrine diseases were examined for the occurrence of antibody to steroid-producing cells in ovary, testis and adrenal cortex. Fluorescent staining was observed in the theca cells of growing follicles, the theca lutein cells, testicular Leydig cells and adrenal cortical cells, i. e. cells which contain enzyme systems used in steroid hormone production. The "steroid-cell" antibody was present in 24 % of the patients with idiopathic Addison's disease, equally frequent in males and females, and in 17 % of the patients with tuberculous Addison's disease, but was rarely found in controls, including patients with other endocrine diseases. Female hypergonadotrophic hypogonadism made an exception, since the "steroid-cell" antibody was found in about half the cases with this condition.

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