Appearance of a thymic mass after treatment of Cushing’s syndrome

2016 ◽  
Vol 25 (2) ◽  
pp. 150-153 ◽  
Author(s):  
Alessandro P Delitala ◽  
Laura Olita ◽  
Carla Piras ◽  
Rossella Cosseddu ◽  
Giorgio Bagella ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Weight Gain ◽  
Adrenal Gland ◽  
Thoracic Surgery ◽  
Sex Hormones ◽  
Laboratory Tests ◽  
Adrenocorticotropic Hormone ◽  
Thymic Hyperplasia ◽  
Adrenal Carcinoma ◽  
Irregular Menses

A 23-year-old woman was referred to our center with hirsutism, acne, weight gain, weakness, and irregular menses. Laboratory tests revealed increased levels of cortisol and sex hormones, and reduced adrenocorticotropic hormone levels. The patient underwent a right adrenalectomy. Pathology of the resected right adrenal gland showed an adrenal carcinoma. Computed tomography 8 months after the surgery revealed a thymic mass that was not detected preoperatively. The frequency of rebound thymic hyperplasia after normalization of hypercortisolism is not known, but possibly as high as 40%. Physicians must be aware of this phenomenon to avoid unnecessary thoracic surgery.

Hypothyroidism and Precocious Sexual Development: Another Case

PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 149-150
Author(s):  
Adolfo Perez Comas
Keyword(s):  
Weight Gain ◽  
Short Stature ◽  
Growth Retardation ◽  
Sexual Development ◽  
Similar Case ◽  
Pubic Hair ◽  
Breast Development ◽  
Attention Span ◽  
Admission Data ◽  
Irregular Menses

Recently, an article in Pediatrics by Costin et al.1 described two new cases of hypothyroidism and precocious sexual development. I would like to report another similar case with our available data. M.L.M., a 13-year-old girl was first seen by us at age 12-4/12 for short stature. Her history included growth retardation, diminution of attention span, somnolence, anorexia with weight gain, and constipation beginning between ages 4 to 6. At 9½ years of age irregular menses began, breast development was first noticed at 10 years, and pubic hair at 11½ years. Her initial admission data are in Table I.

Pediatricians in Court

PEDIATRICS ◽  
1992 ◽  
Vol 89 (6) ◽  
pp. 1267-1268
Author(s):  
JOHN T. BENJAMIN
Keyword(s):  
Magnetic Resonance Imaging ◽  
Computed Tomography ◽  
Magnetic Resonance ◽  
Medical Care ◽  
Laboratory Tests ◽  
Resonance Imaging

To the Editor.— I have been a practicing pediatrician for 18 years. There have been many changes in our specialty during that time. Some of the changes have been good and others more troublesome. Good changes have included greater recognition of the importance of our specialty; higher pay scale for residents, and, for that matter, practitioners; our greater ability to diagnose and treat patients: computed tomography, magnetic resonance imaging, and marvelous laboratory tests not even imagined 20 years ago; increased numbers and complexities of medications and methods of monitoring those medications—all of these changes have contributed to improved medical care for children.

scholarly journals Imaging of the adrenal gland lesions

2014 ◽  
Vol 47 (4) ◽  
pp. 228-239 ◽  
Author(s):  
Keith Herr ◽  
Valdair F. Muglia ◽  
Walter José Koff ◽  
Antonio Carlos Westphalen
Keyword(s):  
Computed Tomography ◽  
Magnetic Resonance ◽  
Adrenal Gland ◽  
Photon Emission ◽  
Resonance Imaging ◽  
Cross Sectional ◽  
Contrast Enhanced ◽  
Cross Sectional Imaging ◽  
Contrast Enhanced Ultrasonography ◽  
Photon Emission Tomography

With the steep increase in the use of cross-sectional imaging in recent years, the incidentally detected adrenal lesion, or "incidentaloma", has become an increasingly common diagnostic problem for the radiologist, and a need for an approach to classifying these lesions as benign, malignant or indeterminate with imaging has spurred an explosion of research. While most incidentalomas represent benign disease, typically an adenoma, the possibility of malignant involvement of the adrenal gland necessitates a reliance on imaging to inform management decisions. In this article, we review the literature on adrenal gland imaging, with particular emphasis on computed tomography, magnetic resonance imaging, and photon-emission tomography, and discuss how these findings relate to clinical practice. Emerging technologies, such as contrast-enhanced ultrasonography, dual-energy computed tomography, and magnetic resonance spectroscopic imaging will also be briefly addressed.

Direct effect of hypothalamic neuropeptides on the release of catecholamines by adrenal medulla in sheep – study ex vivo

2017 ◽  
Vol 20 (2) ◽  
pp. 339-346 ◽  
Author(s):  
D. Wrońska ◽  
B.F. Kania ◽  
M. Błachuta
Keyword(s):  
Adrenal Gland ◽  
Adrenal Medulla ◽  
Noradrenaline Release ◽  
Adrenocorticotropic Hormone ◽  
Ex Vivo ◽  
Adrenal System ◽  
Adrenaline Release ◽  
Hormone Control

Abstract Stress causes the activation of both the hypothalamic-pituitary-adrenocortical axis and sympatho-adrenal system, thus leading to the release from the adrenal medulla of catecholamines: adrenaline and, to a lesser degree, noradrenaline. It has been established that in addition to catecholamines, the adrenomedullary cells produce a variety of neuropeptides, including corticoliberine (CRH), vasopressin (AVP), oxytocin (OXY) and proopiomelanocortine (POMC) – a precursor of the adrenocorticotropic hormone (ACTH). The aim of this study was to investigate adrenal medulla activity in vitro depending, on a dose of CRH, AVP and OXY on adrenaline and noradrenaline release. Pieces of sheep adrenal medulla tissue (about 50 mg) were put on 24-well plates and were incubated in 1 mL of Eagle medium without hormone (control) or supplemented only once with CRH, AVP and OXY in three doses (10−7, 10−8 and 10−9 M) in a volume of 10 μL. The results showed that CRH stimulates adrenaline and noradrenaline release from the adrenal medulla tissue. The stimulating influence of AVP on adrenaline release was visible after the application of the two lower doses of this neuropeptide; however, AVP reduced noradrenaline release from the adrenal medulla tissue. A strong, inhibitory OXY effect on catecholamine release was observed, regardless of the dose of this hormone. Our results indicate the important role of OXY in the inhibition of adrenal gland activity and thus a better adaptation to stress on the adrenal gland level.

scholarly journals Metastatic renal cell carcinoma of unknown primary site. Clinical follow-up

2020 ◽  
Vol 22 (3) ◽  
pp. 149-153
Author(s):  
N. A. Ognerubov ◽  
T. S. Antipova ◽  
G. E. Gumareva
Keyword(s):  
Computed Tomography ◽  
Renal Cell Carcinoma ◽  
Adrenal Gland ◽  
Cell Carcinoma ◽  
Renal Cell ◽  
Clear Cell ◽  
Cell Cancer ◽  
Primary Site ◽  
The Right

Renal cell cancer metastases without evidence of a primary tumor are extremely rare. These variants are usually showed as a spontaneous description of single clinical cases. Aim.This contribution is a clinical follow-up of synchronous renal cell cancer metastases of unknown primary site. Results.A 52-year-old patient U. with a history of increased blood pressure, up to 170/100 mmHg for the last 5 years, who had undergone many instrumental examinations, including ultrasound examination, because of this disease. The computed tomography of the abdomen showed a 4975 mm heterogeneous tumor in the right adrenal gland in October 2017. The combined positron emission and X-ray computed tomography showed a 795441 mm mass in the right adrenal gland, associated with elevated fluorodeoxyglucose metabolic activity SUVmax 7.25. Focal accumulation of the radiopharmaceutical SUVmax 4.31 in a 171124 mm mass was detected in the space of bifurcation in the mediastinum. The lytic lesion (1015 mm) was found in right superior L3 articular process. The patient underwent retroperitoneoscopic adrenalectomy and thoracoscopic removal of mediastinal tumor in November 2017 because of the oligometastatic nature of the process. The histological study identified clear-cell carcinoma with areas of papillary structure in the right adrenal gland. The immunohistochemical study showed carcinoma cells intensively expressing CD10, and some other cells RCC. The immune phenotype of the tumor was identified as clear-cell renal cell carcinoma. The immunohistological and immunohistochemical analysis reviled the metastases of the same variant of renal cell carcinoma in one of 9 lymph nodes. The patient was treated with pazopanib. The primary renal tumor was not detected during the dynamic observation, including the application of annual combined positron emission and X-ray computed tomography. The patient is alive without disease progression with a follow-up of 32 months. Conclusion.Metastases of clear-cell renal cell carcinoma, including adrenal gland, without evidence of a primary site are extremely rare. The main method of treatment is a combination of surgery and targeted therapy, providing long-term local control of the course of the disease.

scholarly journals PRIMARY ADRENAL INSUFFICIENCY SECONDARY TO CHRONIC POSACONAZOLE USE

2020 ◽  
Vol 6 (2) ◽  
pp. e62-e64
Author(s):  
Daniela Pirela Araque ◽  
Gabriela Zuniga ◽  
Alejandro R. Ayala
Keyword(s):  
Computed Tomography ◽  
Adrenal Insufficiency ◽  
Side Effect ◽  
Adrenocorticotropic Hormone ◽  
Fungal Infections ◽  
Plasma Renin ◽  
Primary Adrenal Insufficiency ◽  
The Third ◽  
Abdominal Computed Tomography ◽  
Morning Cortisol

Objective: Posaconazole (PSO) is commonly used in the treatment of invasive fungal infections. PSO-induced primary adrenal insufficiency (PAI) is rare, and we present what we think to be the third case report of its incidence. We want to bring awareness to this rare but significant side effect that can impact management and monitoring of patients on this medication. Methods: After clinical assessment, the patient was evaluated with diagnostic studies including measurements of cortisol, adrenocorticotropic hormone, renin activity, and aldosterone levels. Imaging studies such as abdominal computed tomography were also performed. Results: A 65-year-old man with a history of hemophagocytic lymphohistiocytosis on a dexamethasone taper, complicated with mucormycosis on PSO presented to the emergency department with weakness, fatigue, decreased appetite, orthostatic hypotension, low morning cortisol (0.4 μg/dL), low adrenocorticotropic hormone (3.4 pg/mL), elevated plasma renin (16.7 ng/mL/hour), and low-normal aldosterone (1.7 ng/dL). Abdominal computed tomography imaging revealed bilaterally intact adrenal glands. A diagnosis of PSO-induced PAI was made. Fludrocortisone was initiated in addition to glucocorticoids with improvement of fatigue, appetite, blood pressure, and normalization of sodium and potassium. A month after discontinuing PSO, steroids and fludrocortisone were discontinued with measured morning cortisol of 13 μg/dL and an adrenocorticotropic hormone level of 53.9 pg/mL, both normal. Conclusion: Available data suggest that the adverse effect profile of PSO is more favorable than other triazoles. However, our case is the third report suggesting that PAI may be an underrecognized side effect. Awareness of this complication is particularly important in patients with severe or resistant fungal infections.

scholarly journals Adrenal incidentaloma. Part 1. Computed tomography of adrenal incidentaloma: the possibilities and difficulties of differential diagnosis

2020 ◽  
Vol 92 (12) ◽  
pp. 185-194
Author(s):  
S. A. Buryakina ◽  
N. V. Tarbaeva ◽  
N. N. Volevodz ◽  
G. G. Karmazanovsky ◽  
L. D. Kovalevich ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Differential Diagnosis ◽  
Adrenal Gland ◽  
Correct Diagnosis ◽  
Adrenal Incidentaloma ◽  
Diagnostic Study ◽  
Specific Organ ◽  
Adequate Management ◽  
Active Can

The adrenal incidentaloma is a lesion of a different etiology and found incidentally in patients who underwent a diagnostic study not about the disease of this organ. Lesions can be both hormonally inactive and hormonally active, can arise from different zones of the adrenal gland or have non-specific organ affiliation, can be benign or malignant. Computed tomography characterization of these lesions, especially the differential diagnosis of benign and malignant, is extremely important for the correct diagnosis in order to provide adequate management of the patient. The article presents the key computed tomography criteria that allow radiologist to characterize the lesion most accurately and consider appropriate diagnosis.

scholarly journals Virilization in a Girl with Adrenocortical Adenoma: A Case Report

2013 ◽  
Vol 6 (2) ◽  
pp. 70-72
Author(s):  
Tahniyah Haq ◽  
SM Ashrafuzzaman ◽  
Zafar A Latif
Keyword(s):  
Case Report ◽  
Soft Tissue ◽  
Adrenal Gland ◽  
Ct Scan ◽  
Dehydroepiandrosterone Sulfate ◽  
Adrenocortical Adenoma ◽  
Adrenal Carcinoma ◽  
Mass Size ◽  
The Right ◽  
Androgen Levels

We present a case of Cushing’s syndrome and virilization in a 15 year old girl which was suspected to be due to an adrenal carcinoma. She presented with features of virilization in addition to those of hypercortisilism. Her high androgen levels especially dehydroepiandrosterone sulfate (DHEAS) were also in favor of an adrenal carcinoma. An unenhanced computerized tomography (CT) scan showed a mass (size: 5.3 cm) in the right adrenal gland with a soft tissue intensity of more than 10 HU which was suggestive of adrenal carcinoma. But, histopathology of the resected mass revealed a benign adrenocortical adenoma. DOI: http://dx.doi.org/10.3329/imcj.v6i2.14736 Ibrahim Med. Coll. J. 2012; 6(2): 70-72

Cushing Syndrome

2019 ◽  
Author(s):  
Lynnette Nieman
Keyword(s):  
Chronic Exposure ◽  
Laboratory Tests ◽  
Adrenocorticotropic Hormone ◽  
Cushing Syndrome ◽  
Treatment Options ◽  
Clinical Manifestations ◽  
Screening Tests ◽  
Imaging Studies ◽  
Common Cause ◽  
Pituitary Adrenal Axis

Cushing syndrome is a condition with protean manifestations that are caused by chronic exposure to excess glucocorticoids. Treatment with supraphysiologic doses of glucocorticoids is the most common cause. Pathologic hypercortisolism may result from autonomous adrenal production or as a result of the action of excessive adrenocorticotropic hormone (ACTH) production by a tumor, which stimulates adrenal cortisol production. Primary adrenal forms include unilateral adenoma or carcinoma or, rarely, bilateral hyperplasia and/or nodules. This chapter covers the epidemiology, etiology, pathophysiology, and diagnosis of Cushing syndrome. Clinical manifestations, physical examination findings, and laboratory tests, including tests of the blood and other body fluids, imaging studies, and biopsy, are discussed. The differential diagnosis, treatment options, complications, and prognosis are described. Tables outline clinical features and causes of Cushing syndrome, abnormalities associated with primary adrenal causes of Cushing syndrome, diagnostic accuracy of screening tests, endogenous hypercortisolism without Cushing syndrome, and medical therapy for Cushing syndrome. Figures illustrate the causes of Cushing syndrome and a comparison of the hypothalamic-pituitary-adrenal axis in patients with ACTH-dependent Cushing syndrome and those with pseudo–Cushing syndrome. Algorithms show the evaluation of possible Cushing syndrome and evaluation of the causes of Cushing syndrome. Second-line treatments for Cushing syndrome when surgery fails or is not possible are also detailed. This chapter contains 5 figures, 7 tables, 50 references.

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