Adrenal Pheochromocytoma With Contralateral Adrenocortical Adenoma in a Cat

2010 ◽  
Vol 46 (1) ◽  
pp. 36-42 ◽  
Author(s):  
Jon David R. Calsyn ◽  
Rebecca A. Green ◽  
Garrett J. Davis ◽  
Christopher M. Reilly
Keyword(s):  
Adrenal Gland ◽  
Low Dose ◽  
Clinical Signs ◽  
Adrenocortical Adenoma ◽  
Left Adrenal Gland ◽  
Adrenal Pheochromocytoma ◽  
History Of ◽  
Suppression Test ◽  
The Right ◽  
Dexamethasone Suppression

A 7-year-old, neutered male cat was presented with a 6-month history of progressive polyuria, polydipsia, polyphagia, aggression, and weight gain. Previous blood work, urinalysis, and radiographs did not delineate a cause for the clinical signs. An ultrasound revealed bilateral adrenal gland enlargement. A low-dose dexamethasone suppression test was consistent with hyperadrenocorticism. Based on these findings, bilateral adrenalectomy was attempted and successfully performed. Histopathology was consistent with a cortical adenoma in the right adrenal gland and a pheochromocytoma in the left adrenal gland. This association has never been reported in the cat.

scholarly journals Gynaecomastia in a male neutered cat with an adrenal tumour and associated hyperprogesteronism, hypercortisolism and hyperaldosteronism

2021 ◽  
Vol 7 (2) ◽  
pp. 205511692110456
Author(s):  
Jane Yu ◽  
Jason Lenord ◽  
Michelle Lau ◽  
Laurencie Brunel ◽  
Rachael Gray ◽  
...  
Keyword(s):  
Low Dose ◽  
Clinical Signs ◽  
Adrenal Tumour ◽  
Serum Progesterone ◽  
Adrenal Hormones ◽  
Case Summary ◽  
Suppression Test ◽  
Dexamethasone Suppression ◽  
Test Serum ◽  
Adrenocortical Tumour

Case summary A 7-year-old male neutered domestic longhair cat was presented with chronic progressive gynaecomastia, polydipsia, polyphagia, weight loss and poor fur regrowth. Sexualised behavioural changes were not reported and virilisation was not present on physical examination. Pertinent haematology, biochemistry and urinalysis findings at the time of referral included mild hypokalaemia. Left adrenomegaly and mild prostatomegaly were identified on a CT scan. Evaluation of adrenal hormones with a low-dose dexamethasone suppression test, serum progesterone, testosterone, oestradiol, plasma aldosterone, renin, plasma metanephrine and normetanephrine measurement supported a diagnosis of hyperprogesteronism, hyperaldosteronism and hypercortisolism. Adrenalectomy was performed and histopathology was consistent with an adrenocortical tumour. Clinical signs and hormone elevations resolved postoperatively. Relevance and novel information To our knowledge, this is the second report of gynaecomastia secondary to an adrenal tumour in a male neutered cat and the first associated with hyperprogesteronism.

scholarly journals SAT-196 The Use of 11C-metomidate PET-CT to Detect Unilateral Primary Hyperaldosteronism

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sumitro Harjanto ◽  
Aye Chan Maung ◽  
Troy Puar ◽  
Daphne Gardner
Keyword(s):  
Blood Pressure ◽  
Adrenal Gland ◽  
Primary Hyperaldosteronism ◽  
Left Adrenal Gland ◽  
Active Renin ◽  
Potassium Supplementation ◽  
Serum Aldosterone ◽  
Pet Ct ◽  
History Of ◽  
The Right

Abstract Background Identifying causative adrenal lesions presents a significant diagnostic burden for physicians and radiologists. We describe the use of radiolabelled metomidate to lateralise primary hyperaldosteronism. Case presentation A 52-year old Chinese man with a 5-year history of hypertension was referred for hypokalemia [K 2.7 mmol/L (3.6 - 5.0)]. He had been on Telmisartan 80 mg and Amlodipine 10 mg daily and blood pressure at home ranged 110-120 / 70-80 mmHg. There was no history of poor oral intake, persistent diarrhea or vomiting, and he was not on any other prescription or alternative medications. There was no significant family history of hypertension or sudden cardiac death. Clinic blood pressure was 140/84 mmHg. There were no features suggestive of Cushing’s syndrome. Repeat biochemical tests confirmed hypokalemia (K 3.1 mmol/L), and associated raised bicarbonate 37.3 mmol/L [19 - 29]. Magnesium and creatinine were normal. Aldosterone-renin Ratio was elevated at 8.1 (serum Aldosterone 611 pmol/L [97.3 - 834.0], active renin 2.7 pg/ml [1.8 – 59.4]). Post-saline infusion, non-suppressible serum aldosterone levels of 1137 pmol/L was demonstrated, consistent with autonomous aldosterone production. A computed tomography of the adrenal revealed a 2.3 cm x 1.9 cm nodule on the left adrenal gland consistent with lipid rich adenoma. Adrenal vein sampling (AVS) under continuous synacthen infusion was performed. Adrenal to peripheral cortisol ratio was ≥10 for either adrenal veins, confirming cannulation of the adrenal veins. Aldosterone-cortisol ratios showed lateralization to the left adrenal gland (lateralization ratio of 10.35). There was contralateral suppression of the right adrenal gland with ratio of 0.41. 11C-Metomidate PET-CT scan demonstrated a maximum standardised uptake value (SUVmax) of 26.8 over the left adrenal nodule, while the SUVmax of the right adrenal gland was 16.2. Ratio of the left to right adrenal gland SUVmax was 1.65 (above the threshold of 1.25); and was concordant with AVS. This confirmed that the patient had a left functional adrenal adenoma responsible for hyperaldosteronism. Our patient underwent a left adrenalectomy, and histology was consistent with adrenal cortical adenoma. Prior to surgery he required 72 mmol/l of potassium supplementation daily to maintain K levels of 3.3 – 4.0 mmol/L. Two weeks post-operatively, he was normokalemic (K 4.9 mmol/L) without potassium supplementation. Serum aldosterone normalized to 159.3 pmol/L (active renin 9.3 pg/ml). Blood pressure is well controlled on amlodipine 5mg daily. Conclusion Targeted molecular imaging such as 11C-Metomidate PET-CT could aid localisation of functional adrenal disease to guide definitive surgical management. In the future, this could obviate the need for invasive and technically complex procedures like AVS.

Ovarian Steroid Cell Tumor Resembling Luteoma Associated with Hyperadrenocorticism (Cushing's Disease) in a Dog

1997 ◽  
Vol 34 (1) ◽  
pp. 57-60 ◽  
Author(s):  
B. Yamini ◽  
P. L. VanDenBrink ◽  
K. R. Refsal
Keyword(s):  
Low Dose ◽  
Cystic Mass ◽  
Dexamethasone Suppression Test ◽  
Cell Tumor ◽  
Ovarian Steroid ◽  
Steroid Cell Tumor ◽  
Suppression Test ◽  
Polyhedral Cells ◽  
The Right ◽  
Dexamethasone Suppression

An ovarian steroid cell tumor was diagnosed in a 6.5-year-old female Rottweiler. The animal was polydipsic and polyuric, with an enlarged, pot-bellied abdomen. Radiographs and ultrasound examinations revealed an approximately 13-cm-diameter cystic mass below the right kidney. A low-dose dexamethasone suppression test was consistent with hyperadrenocorticism. Surgical exploration revealed an enlarged, lobulated left ovary approximately 10 cm in diameter, weighing 550 gs. Histologically, the ovarian tumor consisted of dense sheets and nests of round to polyhedral cells with abundant, finely vesiculated cytoplasm. The overall features were most consistent with ovarian steroid cell tumor resembling luteoma and associated with hyperadrenocorticism.

scholarly journals Acquired Skin Fragility Syndrome and Diabetes Mellitus Secondary to Hyperadrenocorticism in a Cat

2018 ◽  
Vol 46 ◽  
pp. 6
Author(s):  
Ana Paula Da Silva ◽  
Rafael Almeida Fighera
Keyword(s):  
Diabetes Mellitus ◽  
Adrenal Gland ◽  
Insulin Therapy ◽  
Skin Lesions ◽  
Dexamethasone Suppression Test ◽  
Skin Fragility ◽  
History Of ◽  
Suppression Test ◽  
Dexamethasone Suppression ◽  
Gland Enlargement

Background: Acquired skin fragility syndrome is a rare disorder which affects adult to senior cats with no history of skin trauma. Acquired skin fragility syndrome and diabetes mellitus, unlike the dog, are highly associated to feline hyperadrenocorticism (HAC) and, often, undiagnosed, what may accentuate the skin lesions and cause management complications. This report aimed to describe a case of acquired skin fragility syndrome and diabetes mellitus secondary to spontaneoushyperadrenocorticism in a cat, focusing on the chronic dermatological signs and their management, as well as on the treatment of the primary disease.Case: An approximately 7 year-old male mixed breed feline was admitted to the University Veterinary Hospital of an Institution with a history of polyphagia, polyuria and polydipsia, and skin ulcers on the trunk and in the cervical region about 2 months after onset and difficult to heal. Laboratory examinations indicated leukocytosis with lymphopenia, decreased urine specific gravity, glycosuria and hyperglycemia. The fasting plasma glucose level, the dexamethasone suppression test and the bilateral adrenal gland enlargement, visualized by ultrasonography, revealed diabetes mellitus and spontaneous hyperadrenocorticism, respectively. Histological skin findings indicated feline acquired skin fragility syndrome. Skin wound treatment through cleaning, protection and antibiotic therapy, and administration of insulin and trilostane were performed. After 6 months of trilostane therapy, adrenocorticotropic hormone (ACTH) stimulation test was performed, which demonstratednormal cortisol values 4 h after administration, which allowed maintenance of the dosage. After 12 months of the diagnosis of skin fragility syndrome and diabetes mellitus secondary to HAC, the patient did not present new skin lesions, fasting glycemia was within the reference values without insulin therapy and maintained only the prescription of trilostane.Discussion: The pituitary-dependent hyperadrenocorticism was the cause of the skin fragility syndrome, and it could be confirmed by the dexamethasone suppression test and the ultrasonography, which demonstrated bilateral adrenal gland enlargement. Healing of the wounds caused by the acquired skin fragility syndrome as well as the absence of new lesions may occur if the primary cause is found and treated adequately. Signs of polyuria, polydipsia and polyphagia verified inthe patient of this report are nonspecific and allow the suspicion of both diabetes mellitus and hyperadrenocorticism. The return of glycemia to basal levels and the interruption of insulin demonstrated that diabetes mellitus was transient and secondary to hyperadrenocorticism. Therefore, it is indicated in situations similar to the clinical condition described in thepatient of this report, to perform tests for diabetes mellitus and HAC. Trilostane can reduce the clinical signs of hyperadrenocorticism, but sometimes maintenance of insulin therapy is needed. The use of the drug improved the skin lesions in the cat of the current report and also allowed for the interruption of insulin administration. Those skin lesions which areof spontaneous occurrence and persistent, with no previous history of trauma and that do not respond to treatment, may alert clinicians to investigate underlying causes of non-dermatological origin and guide owners through the likely slow skin lesions healing until diagnosis and adequate therapeutic response of the primary disease.Keywords: Cushing disease, feline, skin, trilostane, wound healing.

scholarly journals Familial Acromegaly and Bilateral Asynchronous Pheochromocytomas in a Female Patient With a MAX Mutation: A Case Report

2021 ◽  
Vol 12 ◽  
Author(s):  
Elizaveta Mamedova ◽  
Evgeny Vasilyev ◽  
Vasily Petrov ◽  
Svetlana Buryakina ◽  
Anatoly Tiulpakov ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Medical History ◽  
Female Patient ◽  
Clinical Presentation ◽  
Left Adrenal Gland ◽  
Case Presentation ◽  
Whole Exome ◽  
History Of ◽  
The Right ◽  
Insight Into

BackgroundThere are very few cases of co-occurring pituitary adenoma (PA) and pheochromocytomas (PCC)/paragangliomas caused by MAX mutations. No cases of familial PA in patients with MAX mutations have been described to date.Case PresentationWe describe a 38-year-old female patient, presenting with clinical and biochemical features of acromegaly and PCC of the left adrenal gland. Whole-exome sequencing was performed [NextSeq550 (Illumina, San Diego, CA, USA)] identifying a nonsense mutation in the MAX gene (NM_002382) [c.223C>T (p.R75X)]. The patient had a medical history of PCC of the right adrenal gland diagnosed aged 21 years and prolactinoma diagnosed aged 25 years. Cabergoline treatment was effective in achieving remission of prolactinoma at age 33 years. The patient’s father who died at age 56 years of a heart attack had a medical history of PA and prominent acromegalic features, which supports the familial presentation of the disease.ConclusionThis clinical case gives an insight into the clinical presentation of familial PA and PCC probably associated with a MAX mutation.

scholarly journals Patterns of the low‐dose dexamethasone suppression test in canine hyperadrenocorticism revisited

2021 ◽  
Author(s):  
Florian K. Zeugswetter ◽  
Alejandra Carranza Valencia ◽  
Kerstin Glavassevich ◽  
Ilse Schwendenwein
Keyword(s):  
Low Dose ◽  
Dexamethasone Suppression Test ◽  
Suppression Test ◽  
Dexamethasone Suppression

Effective Therapy of Insulinoma by Using Long-Acting Somatostatin Analogue. A Case Report and Literature Review

2011 ◽  
Vol 120 (02) ◽  
pp. 68-72 ◽  
Author(s):  
A. Jawiarczyk ◽  
M. Bolanowski ◽  
J. Syrycka ◽  
G. Bednarek-Tupikowska ◽  
M. Kałużny ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Somatostatin Receptors ◽  
Subcutaneous Administration ◽  
Pancreatic Neuroendocrine Tumor ◽  
Somatostatin Analogue ◽  
Left Adrenal Gland ◽  
Glucose Levels ◽  
Long Acting ◽  
The Right

AbstractWe are reporting a case of 68-year-old woman with insulinoma, after a non-successful tumor surgery and a long-term diazoxide treatment. She had a lot of hypoglycemia cases, and a weight gain of 50 kg. An abdominal CT scan demonstrated a tumor 28 mm in the diameter, in the head of the pancreas. The patient did not agree for the repeated insulinoma surgery. Furthermore, we found a lesion in the left adrenal gland (14 mm in the diameter) and in the right lung (8 mm in the diameter). Pheochromocytoma was diagnosed on the basis of hypertension, elevated levels of normetanephrine in the 24-h urine collection, and an elevated level of norepinephrine in a plasma sample. After the left adrenal gland removal we observed lower blood pressure. Since we had revealed the presence of somatostatin receptors by the somatostatin receptors scintigraphy, we decided to control hypoglycemia by a monthly subcutaneous administration of the long-acting lanreotide. Because of higher glucose levels (300–400 mg/dl) we started an intense insulin therapy. Nowadays, the patient feels better, she has lost 20 kg of her body weight, and we have observed normal blood glucose levels during the long-term lanreotide treatment. We have noticed neither side effects nor hypoglycemic episodes and we have reduced the dose of insulin. The presented case can be an evidence of the effective treatment of the pancreatic neuroendocrine tumor of insulinoma type, with somatostatin analogue.

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