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 ◽  
...  

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.

2015 ◽  
Vol 55 ◽  
pp. 1-7 ◽  
Author(s):  
Katharina Schultebraucks ◽  
Katja Wingenfeld ◽  
Jana Heimes ◽  
Marcus Quinkler ◽  
Christian Otte

1985 ◽  
Vol 110 (4) ◽  
pp. 451-455
Author(s):  
Hermann Haller ◽  
Volker Bähr ◽  
Petra Exner ◽  
Wolfgang Oelkers

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.


2006 ◽  
Vol 91 (12) ◽  
pp. 4849-4853 ◽  
Author(s):  
Ragnhildur Bergthorsdottir ◽  
Maria Leonsson-Zachrisson ◽  
Anders Odén ◽  
Gudmundur Johannsson

Abstract Background: The survival rate of patients with primary adrenal insufficiency (Addison’s disease) undergoing currently accepted replacement therapy is not known, although well-informed patients are considered to have a normal survival rate. In this study, we evaluated the mortality of patients with Addison’s disease in Sweden. Methods: A population-based, retrospective, observational study was performed, using the National Swedish Hospital and Cause of Death Registers, covering the period from 1987–2001. After a diagnosis of Addison’s disease, each patient was followed until the end of follow-up or death. Mortality was compared with that of the Swedish background population. Findings: We identified 1675 patients (995 women and 680 men) diagnosed with primary adrenal insufficiency. The average follow-up from initial diagnosis was 6.5 yr. Five hundred seven patients died during the study period compared with an expected 199. The risk ratio for all-cause mortality was 2.19 (confidence interval 1.91–2.51) for men and 2.86 (confidence interval 2.54–3.20) for women. The excess mortality in both men and women was attributed to cardiovascular, malignant, and infectious diseases. Concomitant diabetes mellitus was observed in 12% of the patients, but only contributed to the increased mortality to a minor extent. Interpretation: Compared with the background population, we observed that the risk ratio for death was more than 2-fold higher in patients with Addison’s disease. Cardiovascular, malignant, and infectious diseases were responsible for the higher mortality rate.


2015 ◽  
Vol 103 (3-4) ◽  
pp. 315-320 ◽  
Author(s):  
Katharina Schultebraucks ◽  
Katja Wingenfeld ◽  
Christian Otte ◽  
Marcus Quinkler

1981 ◽  
Vol 97 (1) ◽  
pp. 98-102 ◽  
Author(s):  
B. Allolio ◽  
W. Winkelmann ◽  
F. X. Hipp

Abstract. In order to evaluate the possible role of endogenous histamine in ACTH secretion we investigated the effect of the H1 antagonist meclastine on plasma ACTH in patients with ACTH hypersecretion. Seven patients with primary adrenal insufficiency (group 1) and 5 patients with ACTH dependent Cushing's syndrome (group 2) were given an iv infusion of meclastine (4.8 mg/90 min). In patients of group 2 plasma ACTH was unaffected by meclastine infusion. However, in patients of group 1 with intact steroid feedback meclastine was followed by a significant drop in plasma ACTH as compared with ACTH levels after saline infusion (46.0 ± 4.6% vs 85.0 ± 7.0%, P < 0.01). These results suggest that histamine is involved in the control of ACTH secretion, possibly by stimulation of CRF release.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Ni Wayan Wina Dharmesti ◽  
Made Ratna Saraswati ◽  
Ketut Suastika ◽  
Wira Gotera ◽  
I Made Pande Dwipayana

Primary adrenal insufficiency, also known as Addison’s disease, is a rare but potentially fatal condition resulting from the failure of the adrenal cortex to produce glucocorticoid and/or mineralocorticoid hormones. Unfortunately, the clinical manifestation of primary adrenal insufficiency is not specific and often progresses insidiously, resulting in late diagnosis, or in severe cases, life-threatening circulatory collapse. Adrenal insufficiency should be considered in patients with unexplained vascular collapse. We report the case of a woman who presented to the emergency ward with unexplainable shock that was later diagnosed as adrenal crisis due to Addison’s disease. The presence of hyperpigmentation in patients with rapid progression of adrenal insufficiency suggests the diagnosis of Addison’s disease presenting with adrenal crisis.


2021 ◽  
Vol 15 (1) ◽  
Author(s):  
M. Abdalla ◽  
J. A. Dave ◽  
I. L. Ross

Abstract Background Primary adrenal insufficiency (Addison's disease) is a rare medical condition usually associated with hyperkalemia or normokalemia. We report a rare case of Addison's disease, coexisting with hypokalemia, requiring treatment. Case presentation In this case, a 42-year-old man was admitted to the intensive care unit with a history of loss of consciousness and severe hypoglycemia. His blood tests showed metabolic acidosis, low concentrations of cortisol 6 nmol/L (normal 68–327 nmol/L), and high plasma adrenocorticotropic hormone 253 pmol/L (normal 1.6–13.9 pmol/L), and he was diagnosed with primary adrenal insufficiency. Surprisingly, his serum potassium was low, 2.3 mmol/L (normal 3.5–5.1 mmol/L), requiring replacement over the course of his admission. Computed tomography scan of the adrenal glands showed features suggestive of unilateral adrenal tuberculosis. Investigations confirmed renal tubulopathy. The patient responded favorably to cortisol replacement, but never required fludrocortisone. Conclusions Coexistence of hypokalemia with Addison’s disease is unusual. We recommend investigation of the cause of hypokalemia in its own right, if it occurs with primary adrenal insufficiency.


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