scholarly journals Dual Adenomas: Detection of Cushing’s Syndrome of Adrenal Origin During Evaluation of Pituitary Macroadenoma

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A127-A128
Author(s):  
Madeline Fasen ◽  
Kent R Wehmeier ◽  
Poonam Kalidas Kapadia

Abstract Cushing’s syndrome is a rare and often severe disease associated with increased mortality and major metabolic complications with cardiovascular disease as the main cause of death. Adrenal masses are most often found by radiographic studies or autopsy as incidentalomas. The prognosis of Cushing’s syndrome is mainly affected by the difficulties in timely diagnosis and treatment of the disease, which remain a challenge due to its nonspecific presentation and multitude of etiologies. Herein, we present an atypical case of adrenal Cushing’s syndrome unveiled by the workup of a nonfunctioning pituitary macroadenoma. A 62 year-old woman presented with new intermittent headaches and worsening vision changes for the past year. She was found to have a large sellar mass measuring 2.7 x 2.4 x 3.0 cm invading the right cavernous sinus with displacement of the optic chiasm on brain magnetic resonance imaging (MRI). In the interim to neurosurgical evaluation, lab work performed to assess pituitary function showed an elevated late night salivary cortisol at 0.200 UG/DL (0.010–0.090 UG/DL range). Low early morning ACTH and elevated late night salivary cortisol, dexamethasone suppression test and 24 hour urine cortisol were observed and confirmed with repeat studies. These findings warranted a computed tomography (CT) adrenal mass protocol which revealed a left adrenal lesion consistent with a lipid rich adenoma measuring 4.9 x 3.5 x 4.1 cm in size. Subsequent urine catecholamines and metanephrines were within normal limits. The patient was admitted for transphenoidal pituitary resection with perioperative stress dose corticosteroids, but was only able to achieve partial resection due to large tumor size. Post-operatively the patient did well on a quick corticosteroid taper down to hydrocortisone 15 mg in AM and 5 in afternoon with hope to wean in the near future. Post-operative workup showed ACTH 4.6 pg/mL (7.2 – 63.3 pg/mL) and 8 am cortisol 24.7 MCG/DL (6.2–19.4 MCG/DL) which suggests autonomous adrenal secretion of cortisol. Once the patient has recovered from her partial pituitary resection she will be referred to general surgery for adrenalectomy. This case provided a review of a classic pituitary macroadenoma workup with an interesting twist to Cushing’s etiology as the cause was not from the pituitary as originally thought.

2015 ◽  
Vol 38 (2) ◽  
pp. E4 ◽  
Author(s):  
Vivek Bansal ◽  
Nadine El Asmar ◽  
Warren R. Selman ◽  
Baha M. Arafah

Despite many recent advances, the management of patients with Cushing's disease continues to be challenging. Cushing's syndrome is a complex metabolic disorder that is a result of excess glucocorticoids. Excluding the exogenous causes, adrenocorticotropic hormone–secreting pituitary adenomas account for nearly 70% of all cases of Cushing's syndrome. The suspicion, diagnosis, and differential diagnosis require a logical systematic approach with attention paid to key details at each investigational step. A diagnosis of endogenous Cushing's syndrome is usually suspected in patients with clinical symptoms and confirmed by using multiple biochemical tests. Each of the biochemical tests used to establish the diagnosis has limitations that need to be considered for proper interpretation. Although some tests determine the total daily urinary excretion of cortisol, many others rely on measurements of serum cortisol at baseline and after stimulation (e.g., after corticotropin-releasing hormone) or suppression (e.g., dexamethasone) with agents that influence the hypothalamic-pituitary-adrenal axis. Other tests (e.g., measurements of late-night salivary cortisol concentration) rely on alterations in the diurnal rhythm of cortisol secretion. Because more than 90% of the cortisol in the circulation is protein bound, any alteration in the binding proteins (transcortin and albumin) will automatically influence the measured level and confound the interpretation of stimulation and suppression data, which are the basis for establishing the diagnosis of Cushing's syndrome. Although measuring late-night salivary cortisol seems to be an excellent initial test for hypercortisolism, it may be confounded by poor sampling methods and contamination. Measurements of 24-hour urinary free-cortisol excretion could be misleading in the presence of some pathological and physiological conditions. Dexamethasone suppression tests can be affected by illnesses that alter the absorption of the drug (e.g., malabsorption, celiac disease) and by the concurrent use of medications that interfere with its metabolism (e.g., inducers and inhibitors of the P450 enzyme system). In this review, the authors aim to review the pitfalls commonly encountered in the workup of patients suspected to have hypercortisolism. The optimal diagnosis and therapy for patients with Cushing's disease require the thorough and close coordination and involvement of all members of the management team.


2007 ◽  
Vol 51 (8) ◽  
pp. 1191-1198 ◽  
Author(s):  
Margaret de Castro ◽  
Ayrton C. Moreira

Cushing's syndrome (CS) results from sustained pathologic hypercortisolism. The clinical features are variable and the most specific features for CS include abnormal fat distribution, particularly in the supraclavicular and temporal fossae, proximal muscle weakness, wide purple striae, and decreased linear growth with continued weight gain in a child. Clinical presentation of CS can be florid and in this case the diagnosis is usually straightforward. However, the diagnosis can be difficult particularly in states of mild or cyclical or periodical hypercortisolism. Several tests based on the understanding of the physiologic characteristics of the hypothalamic-pituitary-adrenal axis have been used extensively to confirm the diagnosis of Cushing's syndrome, but none has proven fully capable of distinguishing all cases of CS from normal and/or pseudo-Cushing individuals. Three first-line diagnostic tests are currently used to screen for CS: measurement of free cortisol in 24-hour urine (UFC), cortisol suppressibility by low doses of dexamethasone (DST), and assessment of cortisol circadian rhythm using late-night serum and/or salivary cortisol. This paper discusses the effectiveness regarding best cut-off values, the sensitivity and the specificity of these tests to screen for CS. Late-night salivary cortisol appears to be the most useful screening test. UFC and DST should be performed to provide further confirmation of the diagnosis.


2019 ◽  
Vol 181 (4) ◽  
pp. C9-C11
Author(s):  
Hershel Raff ◽  
Eric P Cohen ◽  
James W Findling

The diagnosis of endogenous hypercortisolism (Cushing's syndrome) is extremely challenging. Chronic kidney disease (CKD) increases the activity of the hypothalamic-pituitary-adrenal axis making the diagnosis of Cushing's syndrome even more challenging. This is particularly so since urine free cortisol (UFC) testing is not useful in CKD. The case report by Stroud et al. in this issue of the European Journal of Endocrinology highlights this problem by finding normal UFC in a patient with pituitary ACTH-dependent Cushing's syndrome. Elevated late-night salivary cortisol (LNSC) testing was diagnostic and pituitary adenomectomy was curative. LNSC measurement is the diagnostic test of choice in patients with suspected Cushing's syndrome, particularly in the presence of CKD..


2017 ◽  
Author(s):  
Urszula Ambroziak ◽  
Agnieszka Kondracka ◽  
Jadwiga Rojek-Trębicka ◽  
Paweł Gajkowski ◽  
Agnieszka Stańczyk ◽  
...  

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