CONTROL OF MINERALOCORTICOID SUBSTITUTION IN ADDISON'S DISEASE BY PLASMA RENIN AND ANGIOTENSIN II MEASUREMENT

1975 ◽  
Vol 80 (1_Suppla) ◽  
pp. S136
Author(s):  
W. Oelkers ◽  
M. L'age
Keyword(s):  
Angiotensin Ii ◽  
Addison’S Disease ◽  
Plasma Renin ◽  
Addison's Disease

scholarly journals Addison’s Disease Presenting with Cerebral Edema

1996 ◽  
Vol 23 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Caroline Geenen ◽  
Ingrid Tein ◽  
Robert M. Ehrlich
Keyword(s):  
Cerebral Edema ◽  
Addison’S Disease ◽  
Plasma Renin ◽  
Urine Osmolality ◽  
Early Morning ◽  
Unknown Etiology ◽  
Addison's Disease ◽  
Acth Stimulation ◽  
Serum Acth

ABSTRACT:Background: Increased intracranial pressure with encephalopathy has rarely been reported in Addison’s disease. Method: Case Study. Results: A 16-year-old female who presented with cerebral edema of unknown etiology was eventually diagnosed as having Addison’s disease. She had early morning headaches, fatiguability, diarrhea and deterioration in school performance. She was hyponatremic with a serum sodium of 128 mmol/L and hyperkalemic with a serum potassium of 5.9 mmol/L. She had a low serum osmolality (264 mosm), high urine osmolality (533 mosm) and high urine sodium (87 mosm). She had a postural drop in blood pressure and diffuse hyperpigmentation. An ACTH stimulation test revealed a low baseline Cortisol and no response to ACTH. Plasma renin activity was increased. Serum ACTH was elevated. She responded well to intravenous fluids and solu-cortef and was discharged on hydrocortisone and florinef. She remains well 18 months after the acute episode with no neurologic complaints or findings. Conclusion: Addison’s Disease should be considered in the differential diagnosis of symptomatic cerebral edema and idiopathic intracranial hypertension.

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.

The natural history of autoimmune Addison’s disease with a non-classical presentation: a case report and review of literature

2018 ◽  
Vol 56 (6) ◽  
pp. 896-900 ◽  
Author(s):  
Jacopo Manso ◽  
Raffaele Pezzani ◽  
Riccardo Scarpa ◽  
Nicoletta Gallo ◽  
Corrado Betterle
Keyword(s):  
Natural History ◽  
Adrenal Cortex ◽  
Clinical Manifestations ◽  
Addison’S Disease ◽  
Plasma Renin ◽  
Dehydroepiandrosterone Sulfate ◽  
Addison's Disease ◽  
Acth Stimulation ◽  
Basal Cortisol ◽  
History Of

Abstract Autoimmune Addison’s disease (AAD) is the most frequent cause of adrenocortical insufficiency. The natural history of AAD usually comprises five consecutive stages with the first stage characterized by the increase of plasma renin consistent with the impairment of pars glomerulosa, which is usually the first affected layer of the adrenal cortex. We describe a 19-year-old female with Hashimoto’s thyroiditis (HT) who underwent an autoantibody screening due to having the personal and family history of other autoimmune diseases in the absence of relevant clinical manifestations. She was positive for adrenal cortex autoantibodies (ACA) and steroid 21-hydroxylase autoantibodies (21-OH Ab) at high titers. She had increased basal levels of ACTH with normal basal cortisol not responding to ACTH stimulation, reduced levels of dehydroepiandrosterone-sulfate but normal levels of orthostatic renin and aldosterone. This scenario was consistent with a subclinical AAD presenting with first impairments in pars fasciculata and reticularis and conserved pars glomerulosa function. Only subsequently, progressive deficiency in pars glomerulosa function has become evident. Review of the literature showed that there was only one case, reported to date, with a similar atypical natural history of AAD. The strategies for screening for ACA/21-OH Ab in patients with HT are discussed.

Blood Pressure, Renal and Metabolic Effects of ACTH in Normotensive Man

1981 ◽  
Vol 61 (s7) ◽  
pp. 269s-272 ◽  
Author(s):  
Judith A. Whitworth ◽  
Dianne Saines ◽  
Robyn Thatcher ◽  
Aldona Butkus ◽  
B. A. Scoggins ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Diastolic Pressure ◽  
Addison’S Disease ◽  
Plasma Renin ◽  
Plasma Potassium ◽  
Urinary Sodium Excretion ◽  
Metabolic Effects ◽  
Plasma Sodium ◽  
Addison's Disease ◽  
Normotensive Subjects

1. The blood pressure, renal and metabolic effects of adrenocorticotropic hormone (ACTH) have been studied in six normotensive subjects and two patients with Addison's disease on maintenance steroid therapy. 2. In normotensive subjects, 5 days ACTH treatment (0.5 mg 12 hourly) was associated with a rise in systolic blood pressure and mean arterial pressure. There was a small rise in diastolic pressure but no consistent change in heart rate. Plasma sodium increased and plasma potassium fell. Serum creatinine and urea concentrations were unchanged. Fluid intake increased and urine output was unchanged but ACTH withdrawal was associated with a diuresis. There was an initial reduction in urinary sodium excretion and a natriuresis after ACTH withdrawal. Plasma volume and body weight rose. 3. ACTH produced increases in plasma cortisol, 11-deoxycortisol, corticosterone, deoxycorticosterone, aldosterone, 17α-hydroxyprogesterone and 17α,20α-dihydroxyprogesterone. Plasma renin concentration fell. 4. Patients with Addison's disease showed no change in blood pressure or in any other metabolic variable studied. 5. The effects of ACTH in man resembled those found in sheep.

The natural history of adrenal function in autoimmune patients with adrenal autoantibodies

1988 ◽  
Vol 117 (3) ◽  
pp. 467-475 ◽  
Author(s):  
C. Betterle ◽  
C. Scalici ◽  
F. Presotto ◽  
B. Pedini ◽  
L. Moro ◽  
...  
Keyword(s):  
Addison’S Disease ◽  
Plasma Renin ◽  
Autoimmune Disorder ◽  
Adrenal Function ◽  
Adrenocortical Function ◽  
Diabetic Patients ◽  
Addison's Disease ◽  
Gonadal Dysfunction ◽  
Insulin Dependent Diabetic ◽  
Low Cortisol

ABSTRACT Adrenal autoantibodies (AA) were found in 23 of 2571 (0·9%) patients with organ-specific autoimmune diseases, in one of 632 first-degree relatives of insulin-dependent diabetic patients, and in none of 375 normal controls. In AA-positive subjects the prevalence of human leucocyte antigens (HLA)-A1, -B8 and -DR3 was significantly higher with respect to the general population. Two groups were followed (15 subjects persistently positive for AA and 51 negative subjects) for a mean period of 3·2 years. Yearly tests were made for AA and adrenal function. Of the 15 subjects persistently positive for AA, six developed Addison's disease after a period varying from 6 months to 10 years. Of the 51 subjects initially negative, two became positive during follow-up, and one of these developed Addison's disease 16 months later. In contrast, all the remaining 49 persistently negative subjects maintained normal adrenal function tests. Overall, of the 17 positive subjects, seven (41%) developed Addison's disease, three (18%) showed various degrees of subclinical adrenocortical failure and the remaining seven maintained normal glandular function. In the positive patients the yearly incidence of detriment in adrenal function was 19%. Patients who developed Addison's disease showed significant association with HLA-B8 phenotype. The development from normal adrenocortical function to overt Addison's disease seemed to progress through four distinct stages of functional impairment: increased plasma renin activity with normal/low aldosterone (stage 1), low cortisol response after i.v. administration of ACTH (stage 2), increased ACTH (stage 3), and low basal cortisol (stage 4). Thus, idiopathic Addison's disease appears to be a chronic autoimmune disorder with a genetic predisposition and a long preclinical period marked by the presence of AA. Steroid-producing cell antibodies were also evaluated but they were not found to be markers of gonadal dysfunction. J. Endocr. (1988) 117, 467–475

DECREASED BLOOD PRESSURE IN RESPONSE TO AN ANGIOTENSIN II ANTAGONIST IN ADDISON'S DISEASE

1979 ◽  
Vol 10 (4) ◽  
pp. 377-381 ◽  
Author(s):  
TOSHIO OGIHARA ◽  
TAKESHI HATA ◽  
MITSUAKI NAKAMARU ◽  
HIROSHI MIKAMI ◽  
ANNA MARUYAMA ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Angiotensin Ii ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Angiotensin Ii Antagonist

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.

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