Cushing’s Disease/ Cushing’s Syndrome/ Nelson’s Syndrome

2003 ◽  
pp. 85-87
Author(s):  
Stanley E. Order ◽  
Sarah S. Donaldson
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing’S Disease ◽  
Cushing's Syndrome ◽  
Cushing's Disease ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome

BIOSYNTHESIS OF CORTICOIDS AND ANDROGENS IN AN ADENOMA FROM A CUSHING'S SYNDROME PATIENT

1963 ◽  
Vol 42 (2) ◽  
pp. 187-194
Author(s):  
Menek Goldstein ◽  
Marcel Gut ◽  
Ralph I. Dorfman ◽  
Louis J. Soffer ◽  
J. Lester Gabrilove
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing’S Disease ◽  
Cushing's Syndrome ◽  
Cushing's Disease ◽  
Syndrome Patient ◽  
Adrenal Tissue

ABSTRACT Incubation of cholesterol-4-14C and pregnenolone-7-3H with a homogenate of adenomatous adrenal tissue from a patient with Cushing's disease yielded 14C and 3H labelled, cortisol, cortisone, 11-deoxycortisol, deoxycorticosterone, dehydroepiandrosterone, and 11β-hydroxy-androst-4-3,17-dione.

Gastrin in pituitary tumours

1987 ◽  
Vol 115 (3) ◽  
pp. 419-422 ◽  
Author(s):  
Linda Bardram ◽  
Jörgen Lindholm ◽  
Jens F. Rehfeld
Keyword(s):  
Cushing’S Syndrome ◽  
Pituitary Adenomas ◽  
Cushing's Syndrome ◽  
Pituitary Tumours ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome

Abstract. Twelve of 87 pituitary adenomas from patients with acromegaly, Cushing's syndrome, Nelson's syndrome, hyperprolactinaemia and without symptoms of hormone hypersecretion contained gastrin in concentrations from 0.5 to 166 pmol/g. Only ACTH-producing tumours contained gastrin, which occurred in forms smaller than those present in the normal adenohypophysis. The results indicate that corticotropic tumours may synthesize gastrin in moderate amounts.

Pitfalls in the diagnosis and management of Cushing's syndrome

2015 ◽  
Vol 38 (2) ◽  
pp. E4 ◽  
Author(s):  
Vivek Bansal ◽  
Nadine El Asmar ◽  
Warren R. Selman ◽  
Baha M. Arafah
Keyword(s):  
Cushing’S Syndrome ◽  
Cushing’S Disease ◽  
Salivary Cortisol ◽  
Clinical Symptoms ◽  
Cushing's Syndrome ◽  
Cushing's Disease ◽  
Biochemical Tests ◽  
Late Night ◽  
Late Night Salivary Cortisol ◽  
Free Cortisol

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.

scholarly journals Nelson's Syndrome

2007 ◽  
Vol 51 (8) ◽  
pp. 1392-1396 ◽  
Author(s):  
Alia Munir ◽  
John Newell-Price
Keyword(s):  
Cushing’S Disease ◽  
Pituitary Tumour ◽  
Bilateral Adrenalectomy ◽  
Cushing's Disease ◽  
Treatment Modalities ◽  
Pituitary Mass ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome ◽  
Great Heterogeneity ◽  
The One

Nelson's syndrome is a potentially severe complication of bilateral adrenalectomy performed in the treatment of Cushing's disease, and its management remains difficult. Of all of the features of Nelson's syndrome, the one that causes most concern is the development of a locally aggressive pituitary tumour, which, unusually for pituitary disease, may occasionally cause death from the tumour itself. This feature is especially pertinent given the increasing use in Cushing's disease of laparoscopic bilateral adrenal surgery as a highly effective treatment modality to control cortisol-excess. Despite numerous studies and reports, there is no formal consensus of what defines Nelson's syndrome. Thus, some will define Nelson's syndrome according to the classical description with an evolving pituitary mass after bilateral adrenalectomy, whereas others will rely on increasing plasma ACTH levels, even in the absence of a clear pituitary mass lesion on MRI. These factors need to be borne in mind when considering the reports of Nelson's syndrome, as there is great heterogeneity, and it is likely that overall the modern 'Nelson's syndrome' represents a different disease entity from that of the last century. In the present paper, clinical and epidemiological features of Nelson's syndrome, as well as its treatment modalities, are reviewed.

Demonstration of pro-opiomelanocortin mRNA in pituitary adenomas and para-adenomatous gland in cushing's disease and Nelson's syndrome

1993 ◽  
Vol 169 (3) ◽  
pp. 335-339 ◽  
Author(s):  
Marita Fehn ◽  
Maura A. Farquharson ◽  
Doris Sautner ◽  
Wolfgang Saeger ◽  
Dieter K. Lüdecke ◽  
...  
Keyword(s):  
Cushing’S Disease ◽  
Pituitary Adenomas ◽  
Cushing's Disease ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome
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