Addison's disease caused by adrenal gland tuberculosis

2016 ◽  
Author(s):  
Antonela Sabati Rajic ◽  
Maja Ivartnik Merkac ◽  
Petra Svetina
BMJ ◽  
1941 ◽  
Vol 1 (4190) ◽  
pp. 617-618 ◽  
Author(s):  
F. Katz ◽  
F. Mainzer

2020 ◽  
Vol 48 (02) ◽  
pp. 132-138
Author(s):  
Anna-Lena Proksch ◽  
Andreas Brühschwein ◽  
Katrin Hartmann ◽  
Astrid Wehner

AbstractA 13-year old miniature poodle presented with a 3-day episode of vomiting, anorexia, and lethargy. Lack of micturition had been noted for 2 days. Clinical examination indicated dehydration and a tense, painful abdomen. Laboratory parameters (severe azotaemia, hyperkalaemia, severe hyponatraemia, hypochloraemia, and hyperphosphataemia with glucosuria and proteinuria) were consistent with anuric acute kidney injury (AKI). Abdominal ultrasound revealed bilateral adrenal masses. ACTH stimulation test was diagnostic for Addison’s disease. Computed tomography confirmed bilateral adrenal masses and indicated multifocal liver nodules. Additionally, infiltration of the caudal vena cava with partial luminal occlusion was demonstrated. Surgical removal of the adrenal masses with venous plasty intervention and stenting of the vessels deemed unrewarding in this patient in respect to progressed tumour growth with assumed metastatic spread. The dog was treated for Addison’s disease and discharged with good overall condition. Eight weeks later, the dog was euthanized due to progressive caudal vena cava occlusion. Whilst hypoadrenocoticism typically affects young to middle aged dogs, in old dogs primary Addison’s disease might be caused by neoplastic bilateral adrenal gland destruction. This is the first case report of hypovolaemia leading to AKI secondary to bilateral adrenal masses causing Addison’s disease in a dog.


2003 ◽  
Vol 181 (5) ◽  
pp. 1433-1434 ◽  
Author(s):  
Angela M. O. Leal ◽  
Angela D. Bellucci ◽  
Valdair F. Muglia ◽  
Fabiano R. Lucchesi

Endocrinology ◽  
1934 ◽  
Vol 18 (3) ◽  
pp. 341-349 ◽  
Author(s):  
M. M. CANTOR ◽  
JOHN W. SCOTT

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