Suspected bilateral adrenal gland tumour causing primary Addison’s disease in a dog

2020 ◽  
Vol 48 (02) ◽  
pp. 132-138
Author(s):  
Anna-Lena Proksch ◽  
Andreas Brühschwein ◽  
Katrin Hartmann ◽  
Astrid Wehner
Keyword(s):  
Adrenal Gland ◽  
Vena Cava ◽  
Kidney Injury ◽  
Addison’S Disease ◽  
Abdominal Ultrasound ◽  
Surgical Removal ◽  
Addison's Disease ◽  
Acth Stimulation ◽  
First Case ◽  
Adrenal Masses

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.

Addison's disease caused by adrenal gland tuberculosis

2016 ◽  
Author(s):  
Antonela Sabati Rajic ◽  
Maja Ivartnik Merkac ◽  
Petra Svetina
Keyword(s):  
Adrenal Gland ◽  
Addison’S Disease ◽  
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.

scholarly journals First presentation of Addison's disease as hyperkalaemia in acute kidney injury

2016 ◽  
pp. bcr2015213375 ◽  
Author(s):  
Sara Maki ◽  
Caroline Kramarz ◽  
Paula Maria Heister ◽  
Kamran Pasha
Keyword(s):  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Addison’S Disease ◽  
Addison's Disease

Atypical Addison's disease in the dog: a retrospective survey of 14 cases

1996 ◽  
Vol 32 (2) ◽  
pp. 159-163 ◽  
Author(s):  
D Sadek ◽  
M Schaer
Keyword(s):  
Adrenocorticotropic Hormone ◽  
Clinical Signs ◽  
Addison’S Disease ◽  
Normal Serum ◽  
Definitive Diagnosis ◽  
Addison's Disease ◽  
Serum Electrolyte ◽  
Acth Stimulation ◽  
Retrospective Survey ◽  
Adrenocortical Response

Fourteen dogs diagnosed with Addison's disease and having atypical serum electrolyte levels are described. Seventy-eight percent were female, and most showed signs of inappetence, weakness, or vomiting. Ninety-three percent of the cases had either hyponatremia without hyperkalemia or normal serum electrolyte concentrations. Hemogram features were variable and were not useful in suggesting a diagnosis of hypoadrenocorticism. The results of this study show that normal or mild serum electrolyte changes in a dog with clinical signs compatible with Addison's disease should not exclude this diagnosis from consideration. Definitive diagnosis depends on the demonstration of inadequate adrenocortical response to adrenocorticotropic hormone (ACTH) stimulation.

Mineralocorticoid Before Glucocorticoid Deficiency in a Dog with Primary Hypoadrenocorticism and Hypothyroidism

2013 ◽  
Vol 49 (1) ◽  
pp. 54-57 ◽  
Author(s):  
Kathryn M. McGonigle ◽  
John F. Randolph ◽  
Sharon A. Center ◽  
Richard E. Goldstein
Keyword(s):  
Clinical Signs ◽  
Addison’S Disease ◽  
Serum Cortisol ◽  
Primary Hypothyroidism ◽  
Addison's Disease ◽  
Acth Stimulation Test ◽  
Acth Stimulation ◽  
Clinical Illness ◽  
Glucocorticoid Deficiency ◽  
Electrolyte Abnormalities

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.

scholarly journals Metachronous Periadrenal Fatty Tissue Metastasis from Contralateral Renal Cell Carcinoma

2013 ◽  
Vol 2013 ◽  
pp. 1-3
Author(s):  
Erdal Alkan ◽  
Oguz Ozkanli ◽  
Derya Balbay
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
De Novo ◽  
English Literature ◽  
Vena Cava ◽  
Surgical Removal ◽  
Fatty Tissue ◽  
Metachronous Tumor ◽  
First Case

Contralateral adrenal metastases from renal cell carcinomas are not commonly seen. To our knowledge, we are presenting the first case of extraadrenal metastasis in the English literature, from the contralateral RCC 6 months after radical nephrectomy. Patient was treated with robotic right adrenalectomy for continuous growing of a de novo right adrenal mass of 6 × 4 × 3 cm in diameter. Tissue between vena cava, renal capsule, and inferior diaphragmatic surface was removed en block. Pathological evaluation revealed renal cell carcinoma within the fatty tissue abutting the adrenal capsule from outside with negative surgical margins. Our experience dictates that removing adrenal tissue only after identifying the adrenal borders may sometimes result in insufficient tumor removal. Therefore, adrenal containing tissue within the anatomic boundaries should be removed en block, if surgical removal is planned for metachronous tumor metastasis in the treatment of renal cell carcinoma.

scholarly journals Successful Grafting of Adrenal Gland in a Case of Addison's Disease

BMJ ◽  
1941 ◽  
Vol 1 (4190) ◽  
pp. 617-618 ◽  
Author(s):  
F. Katz ◽  
F. Mainzer
Keyword(s):  
Adrenal Gland ◽  
Addison’S Disease ◽  
Addison's Disease

scholarly journals Addison’s Disease Presenting as Acute Renal Failure and Hyperkalemic Paralysis: A Rare Presentation

2021 ◽  
Vol 2021 ◽  
pp. 1-4
Author(s):  
Kundan Jana ◽  
Kalyana Janga ◽  
Sheldon Greenberg ◽  
Amit Gulati
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Adrenal Insufficiency ◽  
Delayed Diagnosis ◽  
Kidney Injury ◽  
Addison’S Disease ◽  
Adrenal Crisis ◽  
Addison's Disease ◽  
Medication History ◽  
Rare Presentation

Hyperkalemic paralysis in the setting of acute renal failure can lead to a missed or delayed diagnosis of adrenal insufficiency as the raised potassium can be attributed to the renal failure. Acute kidney injury as the presenting manifestation in an adrenal crisis due to Addison’s disease has been rarely reported in the literature. Here, we present the case of a young 37-year-old male who came with hyperkalemic paralysis and acute renal failure needing emergent hemodialysis. He had no past medical history and no medication history. His hyponatremia, hypotension, and hyperkalemia pointed to a picture of adrenal insufficiency confirmed by undetectable serum cortisol, elevated ACTH, renin, and low aldosterone levels and imaging. Replacement steroid therapy was given, and the patient made a steady recovery. He was advised on the importance of compliance to treatment at discharge to prevent another crisis event. Acute renal failure with hyperkalemia as a presenting manifestation of Addison’s disease can be very misleading. It is especially important to be vigilant of adrenal insufficiency in such patients as the hyperkalemia is resistant to standard therapy of insulin dextrose and can precipitate fatal arrhythmia if treatment is delayed.

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.

Bilateral adrenal masses in Addison's disease: primary tumors or tuberculosis?

2019 ◽  
Author(s):  
Mădălina Protop ◽  
Ambărus Popovici Ioana Alexandra ◽  
Ioan Bianca ◽  
Chelaru Alina ◽  
Rosu Andreea ◽  
...  
Keyword(s):  
Addison’S Disease ◽  
Addison's Disease ◽  
Primary Tumors ◽  
Adrenal Masses
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