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

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.

1987 ◽  
Vol 38 (4) ◽  
pp. 435-437 ◽  
Author(s):  
Katsuyoshi Mineura ◽  
Tsuneo Goto ◽  
Motohiro Yoneya ◽  
Masayoshi Kowada ◽  
Yoshihara Tamakawa ◽  
...  

2000 ◽  
Vol 52 (6) ◽  
pp. 775-780 ◽  
Author(s):  
Gennet Gebre-Medhin ◽  
Eystein S. Husebye ◽  
Hans Mallmin ◽  
Lotti Helström ◽  
Christian Berne ◽  
...  

1987 ◽  
Vol 114 (3) ◽  
pp. 389-395 ◽  
Author(s):  
F. Laczi ◽  
T. Janáky ◽  
T. Iványi ◽  
J. Julesz ◽  
F. A. László

Abstract. The osmoregulation of arginine-8-vasopressin (AVP) was investigated in 14 patients with primary hypothyroidism and in 6 with Addison's disease. Plasma AVP was measured by radioimmunoassay. Patients with primary hypothyroidism were classified into subgroups with elevated (6.81 ± 1.12 pmol/l) or normal (3.92 ± 0.96 pmol/l) basal levels of plasma AVP. Following the infusion of 2.5% saline, a positive correlation was established between plasma AVP and plasma osmolality. A decreased osmotic threshold was found in hypothyroid patients with augmented basal AVP levels (pAVP = 0.37 (pOs-265), r = 0.71, P < 0.01) as compared with that in hypothyroid patients with a normal AVP level (pAVP = 0.42 (pOs-280), r = 0.93, P < 0.001). A relationship was demonstrated between the alteration in the AVP osmoregulation and the severity of the thyroid insufficiency. Patients with Addison's disease exhibited an increased basal level of plasma AVP (9.59 ± 1.25 pmol/l) and a decreased osmotic threshold (pAVP = 0.42 (pOs-261), r = 0.63, P < 0.01) contrasted to that of healthy volunteers (pAVP = 0.41 (pOs-280), r = 0.83, P < 0.001). The osmoregulation disturbance of the AVP secretion may play a major role in the impaired water metabolism in primary hypothyroidism and in Addison's disease.


1977 ◽  
Vol 9 (02) ◽  
pp. 150-152 ◽  
Author(s):  
K. Voigt ◽  
H. Fehm ◽  
R. Lang ◽  
K. Beinert ◽  
E. Pfeiffer

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.


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.


2013 ◽  
Vol 49 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Kathryn M. McGonigle ◽  
John F. Randolph ◽  
Sharon A. Center ◽  
Richard E. Goldstein

A dog with an unexpected presentation of primary hypoadrenocorticism was evaluated for clinical signs and electrolyte abnormalities characteristic of Addison’s disease. Although the initial adrenocorticotropic hormone (ACTH) stimulation test documented serum cortisol concentrations within the reference range, subsequent assessments confirmed hypoaldosteronism. Mineralocorticoid replacement promptly normalized electrolytes and transiently improved clinical illness. Six weeks after initial ACTH stimulation testing, the dog became glucocorticoid deficient. Concurrent primary hypothyroidism was also documented. Hypoaldosteronism preceding hypocortisolemia is a unique presentation of canine Addison’s disease.


2021 ◽  
Vol 14 (3) ◽  
pp. e238488
Author(s):  
Monu Rani ◽  
Rakesh Garg ◽  
Venkatesh Darshan Agraharabachalli Nanjunde ◽  
Rajesh Rajput

A 41-year-old man presented with vomiting and loose stools. He had a history of long-term intermittent fever, generalised skin hyperpigmentation, dragging sensation in the left hypochondrium and unintentional weight loss. He was receiving combination antiretroviral therapy since 2010 for HIV infection. He also received antitubercular therapy for tuberculous spondylitis. During the hospital stay, he was found to have postural hypotension, hypoglycaemia, hyponatraemia, hyperkalaemia, pancytopenia, hypothyroidism, hyperglobulinaemia and hypoalbuminaemia with reversal of serum albumin/globulin ratio. The morning plasma cortisol was lower than normal and could not be appropriately stimulated after the Synacthen test. The bone marrow histopathology was suggestive of visceral leishmaniasis. He was diagnosed as a case of visceral leishmaniasis and HIV coinfection with primary adrenal insufficiency (Addison’s disease) and primary hypothyroidism, as a rare and unusual presentation.


PEDIATRICS ◽  
1970 ◽  
Vol 46 (1) ◽  
pp. 131-134
Author(s):  
Frances W. Baker ◽  
Frederic M. Kenny ◽  
James R. Zuberbuhler

A 7-year-old patient with idiopathic hypoparathyroidism, Addison's disease, malabsorption, and unilateral diaphragmatic flutter synchronous with the heart beat (SDF) is reported. The flutter occurred shortly after the onset of malabsorption syndrome and disappeared after appropriate correction of serum magnesium, calcium, and Potassium levels. This unusual condition should be considered in the differential diagnosis of abdominal pulsations. The exact biochemical abnormalities that permit synchronous diaphragmatic flutter remain to be defined.


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