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Adrenal incidental adenomas
Published in Nadia Barghouthi, Jessica Perini, Endocrine Diseases in Pregnancy and the Postpartum Period, 2021
Cell typesAdrenal incidentalomas can arise from the adrenal cortex, adrenal medulla, or as metastatic disease from an extra-adrenal cancer.Tumors arising from the adrenal cortex include nonfunctional adrenocortical adenomas, cortisol-producing adenomas, aldosterone-producing adenomas, and adrenocortical carcinoma.A tumor arising from the adrenal medulla is a pheochromocytoma.5The most common etiology of an adrenal incidentaloma is a benign, non-hypersecreting adrenocortical adenoma.8
Neck and endocrine
Published in Michael Gaunt, Tjun Tang, Stewart Walsh, General Surgery Outpatient Decisions, 2018
MEN 1 is an autosomal dominant disease consisting of hyperparathyroidism, pituitary tumours and pancreatic tumours. It is caused by a defect on the long arm of chromosome 11. Hyperparathyroidism occurs in 90% of patients, characteristically hyperplasia.Pancreatic islet tumours occur in 30–75% and tend to be multiple. Gastrinomas occur in 30–60% and insulinomas in 35%. Others consist of glucagonomas and vasoactive intestinal peptide tumors (VIPomas).Pituitary adenomas occur in 15–40%. Prolactinomas are the most common, with acromegaly (growth hormone) and Cushing’s syndrome (ACTH hypersecretion) less common.Carcinoid tumours and thyroid neoplasia are more common, and adrenocortical adenomas are also found, although tending to be non-functional.
Endocrine and neuroendocrine tumours
Published in Pat Price, Karol Sikora, Treatment of Cancer, 2014
Ashley B. Grossman, Márta Korbonitis, P. Nicholas Plowman
Although benign adrenocortical adenomas are frequently found at autopsy, most are non-functioning and have no clinical importance. The majority of functioning cortical adenomas are found in female patients. Those occurring in pre-pubertal patients tend to present with virilization, whereas those in post-pubertal patients present with Cushing’s syndrome. An adrenal cortical adenoma producing aldosterone (Conn’s syndrome) is an uncommon cause of hypertension. Diagnostic tests include the endocrine demonstration of non-suppressible and excessive levels of circulating adrenal steroids and appropriate diagnostic imaging tests (e.g., MRI/CT scanning). Treatment is by surgical excision (adrenalectomy).
Using microwave thermal ablation to develop a subtotal, cortical-sparing approach to the management of primary aldosteronism
Published in International Journal of Hyperthermia, 2019
Padraig T. Donlon, Hojjatollah Fallahi, Warren L. Beard, Atif Shahzad, Lindsay Heflin, Whitney Cox, Brooke Bloomberg, James D. Lillich, Chanran K. Ganta, Gerard J. O’Sullivan, Giuseppe Ruvio, Paula M. O’Shea, Martin O’Halloran, Punit Prakash, Michael Conall Dennedy
A preclinical, swine model was chosen to reflect mean human adrenal volumes. It is noteworthy that we chose regional subtotal ablation of normal adrenal cortex rather than pathological nodules. There is no current animal model of benign adrenocortical adenomas of sufficient size to investigate the effects of MTA. Preparatory dielectric measurements validated our approach. APAs are homogenous, benign lesions, histologically similar to normal adrenal cortex and with dielectric properties that are no different to normal cortex [33]. We harvested the adrenals at 48 h post-ablation for two reasons. Firstly, this timepoint reliably allows coagulative necrosis to manifest. Secondly, this timepoint allowed a reasonable period following acute insult for clinical and biochemical evaluation of adrenocortical function in animals undergoing bilateral ablation.
Diagnostic evaluation in steroid-induced myopathy: case report suggesting clinical utility of quantitative muscle ultrasonography
Published in Endocrine Research, 2018
Marco Alessandro Minetto, Cristina Caresio, Valentina D’Angelo, Fabio Lanfranco, Lucia Ghizzoni, Silvestro Roatta, Emanuela Arvat, Santosh Kesari
A 39-year-old woman presented with muscle weakness and fatigability in association with hypertension and menstrual abnormalities. Laboratory work-up demonstrated increased 24-h excretion of urinary free cortisol (1733 µg/day) and lack of inhibition on the overnight dexamethasone suppression test (serum cortisol: 29.6 µg/dl). Computed tomography scan revealed a right adrenal mass of 40 mm in diameter, without invasion of surrounding tissues or intratumoral necrosis. The diagnosis of adrenal Cushing’s syndrome was confirmed by the pathological finding of an adrenocortical adenoma (the resected tumor was 40 mm in its greatest diameter, 75 g weight, and gray in color, and the tumor cells were immunohistochemically positive for chromogranin A, tyrosine hydroxylase, and vimentine) and by the occurrence of postoperative adrenal insufficiency (morning serum cortisol: 4 µg/dl) requiring hydrocortisone replacement therapy for 3 months (50 mg/day during the first 2 months and then 25 mg/day during the last month). Replacement therapy was discontinued after documentation of normal cosyntropin stimulation test (peak cortisol 30 min after adrenocorticotropic hormone: 25 µg/dl).
A Two-in-One Tumor in the Adrenal: A Functional Adrenocortical Adenoma with Myelolipomatous Differentiation
Published in Fetal and Pediatric Pathology, 2023
Sunny Bhardwaj, Rohit Sanjay Deshpande, Santosh Kumar, Suvradeep Mitra
Adrenocortical adenoma (ADA) and myelolipoma are two common benign neoplasms of the adrenal cortex. ADA can be nonfunctional or functional. A nonfunctional ADA is often detected incidentally, while a functional ADA can be associated with the hormonal manifestations. A myelolipoma is a benign tumor comprising of a combination of mature fat and marrow (hematopoietic lineage) elements in various proportions. Both ADA and myelolipoma are common although an ADA with myelolipomatous differentiation is an uncommon manifestation with only a few anecdotes [1]. This has not been reported in the pediatric age group, to the best of our knowledge. We describe a pediatric ADA with myelolipomatous differentiation.