scholarly journals A Unique Case of Corticomedullary Mixed Tumor Composed of Both Adrenal Cortical Cells and Pheochromocytes

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A106-A107
Author(s):  
Srinivas R Panja ◽  
Safrin Ali
Keyword(s):  
Adrenal Gland ◽  
Adrenal Adenoma ◽  
Pathology Report ◽  
Mixed Tumor ◽  
Unique Case ◽  
Cortical Cells ◽  
Post Surgery ◽  
Biochemical Testing ◽  
Abstract Submission ◽  
Mixed Tumors

Abstract Introduction or Background: Corticomedullary mixed tumors of the adrenal gland was first described in 1969 by Mathison and Waterhouse. It is defined as a single tumor mass of the adrenal gland that histopathologically has presence of adrenal cortical and medullary cells. Such mixed tumors involving the cortical and medullary components of the adrenal glands are very rare. Clinical Case (including diagnostic evaluation, treatment, and follow-up):A 67 year old woman with a history of hypertension and osteoporosis presents for incidental adrenal adenoma. Hypertension was controlled well with olmesartan 40mg, hctz 25mg, and amlodipine 2.5mg. Abdominal CT scan showed a 2.6 cm enhancing left adrenal nodule with delayed wash- out phase. Biochemical testing showed elevated plasma free metanephrine (132pq/ml, n < or = 57pq/ml) and abnormal 1mg dexamethasone suppression test (10.4mcg/dL, n <2mcg/dL). ACTH was suppressed. Patient underwent left adrenalectomy, after pretreatment with doxazosin. Surgical pathology report showed an unusual neoplasm consisting of a single nodule composed of intermixed aggregates of cortical cells and pheochromocytes displaying morphologic features of adrenal adenoma and pheochromocytoma. Also intermixed with the adenoma was a 3mm myelolipoma. Post surgery, the patient was treated with hydrocortisone for symptoms of adrenal insufficiency. Post surgery, she was able to stop amlodipine and hctz and is on 10 mg olmesartan on alternate days.. She remains on a weaning dose of hydrocortisone at the time of abstract submission. Clinical Lesson(s) or Conclusion(s) (emphasizing the learning point[s] and implications for clinical practice)This unique case report highlights the importance of appropriate workup for incidental adrenal adenoma and keeping in mind the rare possibility of mixed endocrine tumours. A single mixed tumor of the adrenal gland is rare but exhibits distinct morphologic features of both a cortisol producing tumor along with a pheochromocytoma. Furthermore, a concurrent intermixing of a myelolipoma within an adrenal corticomedullary mixed tumor is rarely reported.

scholarly journals Multiple Challenges: An Unusual Case of an Adrenal Mass With Plurihormonal Secretion of Catecholamines and Cortisol in a Patient With Several Neoplasms

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A144-A144
Author(s):  
Anna Elvira Seelin Arcellana ◽  
Franz Magnaye ◽  
Carmegie Caparida Saliba ◽  
Soriano Capaya ◽  
Jonathan Rivera ◽  
...  
Keyword(s):  
Case Report ◽  
Adrenal Gland ◽  
Adrenal Mass ◽  
Neuroendocrine Differentiation ◽  
Adrenocortical Adenoma ◽  
Mixed Tumor ◽  
Cardiovascular Risks ◽  
Cortical Cells ◽  
Plasma Aldosterone Concentration ◽  
Free Cortisol

Abstract Introduction: Simultaneous hypersecretion of both catecholamines and cortisol in one adrenal tumor is rarely seen because cortical cells, which produce cortisol, and medullary cells, which secrete catecholamines, are derived from different germ layers1. Formidable challenges ensue from a tumor with a complex behavior. We demonstrate here the clinical course and multi-modal management of the case of an adrenocortical adenoma which had neuroendocrine differentiation accounting for the excess of both catecholamine and cortisol hormones in a patient with multiple neoplasms. Clinical Case: An adrenal mass was incidentally discovered in a 61-year old female undergoing imaging as part of the metastatic work-up for an esophageal mass. The patient has insulin-requiring diabetes mellitus, hypertension and a history of breast cancer. A right adrenal gland mass, avidly enhancing, measuring 3.8 x 2.7 x 2.7 cm was found on abdominal imaging. The 24-hour urine metanephrine collections were done, and these were more than twice elevated in two instances at 2.516 mg/24 hours and 2.101 mg/24 hours (NV: 0–1 mg/24 hours). An unsuppressed cortisol level at 6.57 μg/dL (NV: ≤ 1.8 μg/dL) was obtained after the 1 mg dexamethasone suppression test. Hypercortisolism was confirmed with an elevated 24-hour urine free cortisol at 312.07 μg/24 hours (NV: 20–90 μg/24 hours). Adrenocorticotrophic hormone (ACTH) was low at 0.90 pg/ml, indicative of the presence of an adrenal form of Cushing’s. Primary aldosteronism was ruled out based on a ratio between plasma aldosterone concentration and plasma renin activity of less than 20. Pre-operative alpha blockade with terazosin was initiated. Right adrenalectomy was done. Histopathology revealed an adrenal mass of cortical origin, atypically staining positively for synaptophysin, which is indicative of neuroendocrine differentiation of the tumor. The patient had better blood pressure and glycemic control after the adrenalectomy. Clinical Lessons: An adrenocortical adenoma very seldom undergoes neuroendocrine differentiation. Pathophysiologic mechanisms include a genetic aberration in cortical cells leading to production of catecholamines2. This case underscores the importance of a comprehensive biochemical evaluation of a patient with an adrenal mass because control of hormonal hypersecretion is essential in reducing cardiovascular risks, morbidity and mortality. References: 1Duan L, Fang F, Fu W, et al. Corticomedullary mixed tumor resembling a small adrenal gland-involvement of cancer stem cells: case report. BMC Endocr Disord. 2017;17(1):9. Published 2017 Feb 13. doi:10.1186/s12902-017-0157-7.2Donatini G, Van Slycke S, Aubert S, Carnaille B. Corticomedullary mixed tumor of the adrenal gland-a clinical and pathological chameleon: case report and review of literature. Updates Surg. 2013 Jun;65(2):161–4. Epub 2012 Jan 7. PMID: 22228558.

Corticomedullary Mixed Tumor of the Adrenal Gland With Concurrent Adrenal Myelolipoma

2003 ◽  
Vol 127 (8) ◽  
pp. e329-e332 ◽  
Author(s):  
Albert Y. Chu ◽  
Virginia A. LiVolsi ◽  
Douglas L. Fraker ◽  
Paul J. Zhang
Keyword(s):  
Adrenal Gland ◽  
Adrenal Mass ◽  
Cushing Syndrome ◽  
Rare Tumor ◽  
Mixed Tumor ◽  
Left Adrenal Gland ◽  
Urinary Cortisol ◽  
Cortical Cells ◽  
Adrenal Myelolipoma ◽  
Adrenal Cortical Cells

Abstract We report the case of a corticomedullary mixed tumor of the adrenal gland in a 55-year-old woman with a left adrenal mass who presented with mild symptoms of Cushing syndrome and an elevated urinary cortisol level. The patient underwent a left adrenalectomy. A well-circumscribed 2.5-cm mass, composed of an admixture of adrenal cortical cells and pheochromocytes, and an incidental 0.7-cm myelolipoma were present in the resected left adrenal gland. The diagnosis of adrenal corticomedullary mixed tumor was confirmed by both immunohistochemistry and electron microscopy. To our knowledge, this is the eighth well-documented report of this rare tumor.

Ultrastructural Cytopiasmic Changes of Adrenal Cortex During Pregnancy

1969 ◽  
Vol 27 ◽  
pp. 298-299
Author(s):  
T. M. Murad ◽  
Karen Israel ◽  
Jack C. Geer
Keyword(s):  
Adrenal Gland ◽  
Steroid Hormones ◽  
Adrenal Cortex ◽  
Lipid Droplets ◽  
Plasma Cholesterol ◽  
Adrenal Steroids ◽  
Dynamic Changes ◽  
Cortical Cells ◽  
Acetyl Coenzyme A ◽  
Adrenal Cortical Cells

Adrenal steroids are normally synthesized from acetyl coenzyme A via cholesterol. Cholesterol is also shown to enter the adrenal gland and to be localized in the lipid droplets of the adrenal cortical cells. Both pregnenolone and progesterone act as intermediates in the conversion of cholesterol into steroid hormones. During pregnancy an increased level of plasma cholesterol is known to be associated with an increase of the adrenal corticoid and progesterone. The present study is designed to demonstrate whether the adrenal cortical cells show any dynamic changes during pregnancy.

Corticomedullary mixed tumor of the adrenal gland

2009 ◽  
Vol 70 (6) ◽  
pp. 473-476 ◽  
Author(s):  
S. Trimeche Ajmi ◽  
M. Chadli Chaieb ◽  
M. Mokni ◽  
R. Braham ◽  
K. Ach ◽  
...  
Keyword(s):  
Adrenal Gland ◽  
Mixed Tumor

scholarly journals Intravascular Papillary Endothelial Tumor of the Adrenal Gland: A Case Report and Review of Literature

2019 ◽  
Vol 4 (3) ◽  
Keyword(s):  
Case Report ◽  
Adrenal Gland ◽  
Blood Clot ◽  
Adrenal Adenoma ◽  
Vascular Tumor ◽  
Review Of Literature ◽  
Intravascular Papillary Endothelial Hyperplasia ◽  
Papillary Endothelial Hyperplasia ◽  
Malignant Lesions ◽  
Head Neck

Intravascular Papillary Endothelial Hyperplasia (IPEH) or Masson’s Tumor is a benign vascular tumor, most commonly seen on the skin and usually on the head, neck or extremities. It is more common in women with no age predilection. Visceral involvement is very rare, with about 30 intra-abdominal reports. We present a case report of a 58 year old woman who underwent a CT scan due to dysphagia complaints, with an incidental known finding of growth in the adrenal adenoma, which was 5 cm in diameter on hospitalization. The patient underwent laparoscopic adrenalectomy. Biopsy results demonstrated a brownish yellow lesion, 2.8 cm in diameter, composed of a blood clot and septate. Immunochemical staining for CD31 and CD34 was positive and the lesion was diagnosed as an IPEH of pure form. Our review of literature examines different forms of IPEH, previous reports and characteristics of Masson’s tumors in the adrenal gland and stratifies ways of differentiation it from other benign or malignant lesions of the adrenal.

scholarly journals SAT-199 Diagnostic Dilemma: An Adrenal Incidentaloma in a Young Adult

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Sonia Sharma ◽  
Steven N Levine ◽  
Xin Gu
Keyword(s):  
Adrenal Gland ◽  
Adrenal Mass ◽  
Adrenal Adenoma ◽  
Adrenal Incidentaloma ◽  
Significant Loss ◽  
Phase Imaging ◽  
African American Female ◽  
Hounsfield Units ◽  
Diagnostic Dilemma ◽  
Ki 67

Abstract Introduction: In an adult endocrine clinic, the majority of patients referred for evaluation of an adrenal incidentaloma are older than 30 years of age. It is important to be reminded that a patient may be diagnosed with an adrenal mass at any age but the etiology may vary depending on the age at presentation. Clinical case: An 18 year-old African American female with no significant past medical problems presented with a 2 month history of flank and abdominal pain associated with nausea and vomiting. An abdominal CT scan and a dedicated adrenal CT showed a right adrenal mass measuring 2.2 x 2.6 cm. The noncontrast Hounsfield units were 23, enhanced Hounsfield units 210, and delayed Hounsfield units 72. The calculated washout was 44%, not consistent with an adrenal adenoma. An MRI of the abdomen showed a 2.5 cm right adrenal nodule. The lesion did not demonstrate significant loss of signal between in and out of phase imaging, therefore the characteristics were not consistent with a lipid rich adenoma. Laboratory tests included an ACTH of 31 pg/mL (6-48 pg/mL), cortisol 8.7 ug/mL at 10:57 am (7-9 am 5.27-22.45 ug/mL), aldosterone 10.1 ng/dL (6-48 ng/dL), renin 2.2 ng/mL/hr (upright 0.5-4.0 ng/mL/hr), DHEA-sulfate 129 ug/dL (44-248 ug/dL), plasma free metanephrine 0.10 nmol/L (0.00-0.49 nmol/L), and plasma free normetaneprhine 0.41 nmol/L (0.00-0.89 nmol/L). The 24-hour urine norepinephrine, epinephrine, and metanephrine were all normal, however the 24-hour urine dopamine was elevated, 824 ug/24 hrs (52-480 ug/24 hrs). Subsequently, plasma dopamine, norepinephrine, and epinephrine were all within the reference range. The patient had a robotic-assisted right adrenalectomy removing a 5.7 x 3.5 x 1.7 cm gland, weighing 16.3 grams. The pathology demonstrated a ganglioneuroma within the right adrenal gland measuring 2.2 x 2.0 x 2.7 cm, negative for neuroblastoma or blastic components. Focal hemorrhage was noted, there was no tumor necrosis, and no mitotic figures were present. The tumor appeared to be encapsulated in the adrenal gland and the Ki-67 stain was negative in ganglioneuroma cells. Conclusion: Adrenal adenomas that appear as incidentalomas in young adulthood are extremely rare. Evaluating younger versus older adults found to harbor an adrenal “incidentaloma“ requires a unique approach for each age group, as the differential diagnosis varies widely. In our patient, the imaging was extremely concerning and diagnostic considerations included neuroblastoma, adrenocortical malignancy, pheochromocytoma, or ganglioneuroma. Adrenal ganglioneuromas are most frequently diagnosed in fourth and fifth decades of life. In younger adults ganglioneuromas are usually found in the retroperitoneum and posterior mediastinum. For our patient, surgical resection of the adrenal mass confirmed the pathologic diagnosis and provided definitive cure.

scholarly journals SUN-196 Persistent Hyperkalemia After Unilateral Adrenalectomy for Aldosteronoma

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Hima Reddy Ammana ◽  
Susan Yuditskaya
Keyword(s):  
Adrenal Gland ◽  
Sodium Bicarbonate ◽  
Antihypertensive Agents ◽  
Kidney Dysfunction ◽  
Hypertensive Nephropathy ◽  
Unilateral Adrenalectomy ◽  
Post Surgery ◽  
Aldosterone To Renin Ratio ◽  
Potassium Binders ◽  
Patients Experience

Abstract Introduction Following unilateral adrenalectomy, some patients experience persistent hyperkalemia. This has been attributed to hypoaldosteronism due to severe suppression of aldosterone synthesis in the contralateral adrenal gland. Additionally, excess aldosterone leads to glomerular hyperfiltration masking kidney dysfunction, which can then manifest after cure with CKD-related hyperkalemia. Case Presentation We report a case of 51-year-old male who was diagnosed with hypertension in his late 30s. He required a beta-blocker and calcium channel blocker (CCB) for 10 years, and eventually developed hypertensive nephropathy. With worsening lower extremity edema, he was switched from a CCB to an angiotensin receptor blocker. Soon afterwards, he presented with hypertensive emergency and was discovered to have significant hypokalemia (K 2.1 mmol/L), prompting work up for primary aldosteronism. Biochemical evaluation revealed an elevated aldosterone to renin ratio of 38 [(ng/dL)/(ng/mL/hr)] and adrenal protocol CT scan revealed a 1.9 cm left adrenal nodule with benign characteristics. Adrenal vein sampling showed marked lateralization of excess aldosterone to the left adrenal gland, with proper catheter placement demonstrated in each adrenal veins (5-fold cortisol gradient bilaterally). He was started on spironolactone and 6 weeks later, underwent an uncomplicated laparoscopic left adrenalectomy. Spironolactone was discontinued Serum K level was normal at 4.8 mmol/L immediately postoperatively. Ten hours later, his K went up to 6.6 mmol/L which was confirmed by repeat blood work, accompanied by worsened renal function (Cr 2.5 mg/dL up from a of baseline 2.0). His hyperkalemia persisted in the 5.0 – 6.0 range despite IV Calcium Gluconate, Insulin and D50. Oral potassium binders were avoided due to concerns about ileus. Upon recognition of the possibility of hypoaldosteronism, we recommended a NaHCO3 gtt, with subsequent normalization of serum K. We avoided initiating fludrocortisone in the short term, due to uncertainty about duration of hypoaldosteronism, & because he was still requiring two antihypertensive agents. Plasma aldosterone 2 wks after surgery was fully suppressed, confirming suspicion of hypoaldosteronism. He has been managed successfully with oral sodium bicarbonate tablets, remaining normokalemic at 3 weeks post-surgery. Conclusion: Here we present a case of persistent hyperkalemia following resection of a signficantly biochemically active and long-standing aldosteronoma, which was successfully managed with sodium bicarbonate. We attribute the post-operative hyperkalemia in this patient to a combination of hypoaldosteronism due to deep suppression of the mineralocorticoid production of the contralateral adrenal, as well as unmasking of more severe kidney dysfunction than was he previously thought to have once aldosterone excess was withdrawn.

Unique case of metachronous adrenal and hepatic myelolipomas

2021 ◽  
Vol 14 (3) ◽  
pp. e240894
Author(s):  
Paul David Morris ◽  
Chow P'Ng ◽  
Henry Pleass
Keyword(s):  
Adrenal Gland ◽  
Postoperative Period ◽  
Case Reports ◽  
Unique Case ◽  
Mesenchymal Tumour

We present a unique case of metachronous adrenal and hepatic myelolipomas in a 62-year-old man. Myelolipomas are most commonly found in the adrenal gland, with extra-adrenal sites such as the lung, retroperitoneum and liver reported. They are a form of benign mesenchymal tumour, with only 25 case reports of a hepatic location published to date. The are no guidelines to its management. Our patient underwent resection due to pain, and after a complicated postoperative period is pain free.

FORMATION OF STEROID HORMONES IN THE ADRENAL ADENOMA AND ADJACENT ADRENAL TISSUE OF A PATIENT WITH PRIMARY ALDOSTERONISM

1963 ◽  
Vol 41 (1) ◽  
pp. 1955-1959
Author(s):  
Elizabeth MacArthur ◽  
V. J. O'Donnell
Keyword(s):  
Adrenal Gland ◽  
Steroid Hormones ◽  
Primary Aldosteronism ◽  
Incubation Medium ◽  
Adrenal Adenoma ◽  
Adrenal Vein ◽  
Adrenal Tissue

The in vitro steroidogenic capacity of an adrenal adenoma and adjacent adrenal tissue of a patient with primary aldosteronism was studied. The adenoma slices elaborated into the incubation medium 7.07 μg/g tissue of cortisol (78.2%), corticosterone (7.6%), and aldosterone (14.2%), while the slices of adjacent adrenal gland released 19.88 μg/g tissue of cortisol (79.1%), corticosterone (14.9%), 11β-hydroxyandrostenedione (3.9%), androstenedione (2.1%), and a trace of aldosterone. The steroid content of the adenoma and the adrenal slices after incubation was 4.22 and 3.19 μg/g tissue respectively. From the former, cortisol (51.1%), corticosterone (36.6%), and progesterone (12.4%) were isolated and from the latter cortisol (13.2%), corticosterone (56.1%), progesterone (17.2%), and androstenedione (13.5%). A sample of adrenal vein blood obtained prior to adrenalectomy exhibited a cortisol/corticosterone ratio of 2.45.

Adrenocorticotrophic hormone (ACTH) stimulation of sheep fetal adrenal cortex can occur without increased expression of ACTH receptor (ACTH-R) mRNA

2002 ◽  
Vol 14 (1) ◽  
pp. 1 ◽  
Author(s):  
A. M. Carter ◽  
Y. M. Petersen ◽  
M. Towstoless ◽  
D. Andreasen ◽  
B. L. Jensen
Keyword(s):  
Adrenal Gland ◽  
Mrna Expression ◽  
Ribonuclease Protection Assay ◽  
Acth Stimulation ◽  
Cortical Cells ◽  
Fetal Plasma ◽  
Chain Cleavage ◽  
Ribonuclease Protection ◽  
Sheep Fetus

In the present study, it was hypothesized that the adrenocorticotrophin hormone receptor (ACTH-R) would be up-regulated in the adrenal gland of the sheep fetus following infusion of physiological amounts of ACTH, as shown for adrenal cortical cells in culture. In chronically catheterized sheep, an intravenous infusion of ACTH1–24 was given to 6 fetuses for 24 h at a rate of 0.5 g h–1, starting on Day 126 or 127 of gestation (term ~147 days). Four control fetuses received an infusion of vehicle (saline). Total RNA was extracted from the fetal adrenal glands by the guanidinium thiocyanate method. Expression of specific mRNAs was determined by ribonuclease protection assay using cRNA probes directed against: ACTH-R; the steroid enzymes side-chain cleavage (P450scc), 3β-hydroxysteroid dehydrogenase (3β-HSD), 17 α-hydroxylase (P450c17) and 21β-hydroxylase (P450c21); and β-actin. Ratios of mRNA expression to β-actin mRNA expression (arbitrary units) were calculated to correct for differences in RNA quality between samples. The concentration (mean SEM) of immunoreactive cortisol in fetal plasma was greater after ACTH infusion than after vehicle infusion (47 3 v. 13 2 ng mL–1 respectively; (P<0.001). Adrenal expression of P450scc and P450c21 mRNA increased after ACTH infusion (P<0.05), whereas expression of P450c17 and 3β-HSD mRNA was unchanged. There was no difference in ACTH-R mRNA expression between ACTH- and vehicle-infused fetuses (254 48 v. 305 76 arbitrary units respectively). It was concluded that ACTH is able to increase plasma cortisol concentrations in the sheep fetus by up-regulating cortisol synthesis in the adrenal gland, but that in vivo this does not require up-regulation of ACTH-R mRNA.

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