scholarly journals The effect of sodium valproate in Cushing's disease, Nelson's syndrome and Addison's disease

1988 ◽  
Vol 66 (15) ◽  
pp. 686-689 ◽  
Author(s):  
M. Reincke ◽  
B. Allolio ◽  
D. Kaulen ◽  
C. Jaursch-Hancke ◽  
W. Winkelmann
Keyword(s):  
Sodium Valproate ◽  
Cushing’S Disease ◽  
Addison’S Disease ◽  
Cushing's Disease ◽  
Addison's Disease ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome

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

scholarly journals Nelson's syndrome

2010 ◽  
Vol 163 (4) ◽  
pp. 495-507 ◽  
Author(s):  
T M Barber ◽  
E Adams ◽  
O Ansorge ◽  
J V Byrne ◽  
N Karavitaki ◽  
...  
Keyword(s):  
Predictive Factors ◽  
Cushing’S Disease ◽  
Pituitary Tumour ◽  
Cushing's Disease ◽  
Current Evidence ◽  
Pituitary Mass ◽  
Nelson’S Syndrome ◽  
Nelson's Syndrome ◽  
Tertiary Centre ◽  
Threatening Condition

Nelson's syndrome is a potentially life-threatening condition that does not infrequently develop following total bilateral adrenalectomy (TBA) for the treatment of Cushing's disease. In this review article, we discuss some controversial aspects of Nelson's syndrome including diagnosis, predictive factors, aetiology, pathology and management based on data from the existing literature and the experience of our own tertiary centre.Definitive diagnostic criteria for Nelson's syndrome are lacking. We argue in favour of a new set of criteria. We propose that Nelson's syndrome should be diagnosed in any patient with prior TBA for the treatment of Cushing's disease and with at least one of the following criteria: i) an expanding pituitary mass lesion compared with pre-TBA images; ii) an elevated 0800 h plasma level of ACTH (>500 ng/l) in addition to progressive elevations of ACTH (a rise of >30%) on at least three consecutive occasions. Regarding predictive factors for the development of Nelson's syndrome post TBA, current evidence favours the presence of residual pituitary tumour on magnetic resonance imaging (MRI) post transsphenoidal surgery (TSS); an aggressive subtype of corticotrophinoma (based on MRI growth rapidity and histology of TSS samples); lack of prophylactic neoadjuvant pituitary radiotherapy at the time of TBA and a rapid rise of ACTH levels in year 1 post TBA. Finally, more studies are needed to assess the efficacy of therapeutic strategies in Nelson's syndrome, including the alkylating agent, temozolomide, which holds promise as a novel and effective therapeutic agent in the treatment of associated aggressive corticotroph tumours. It is timely to review these controversies and to suggest guidelines for future audit.

QUANTITATIVE ESTIMATION OF ADRENOCORTICAL HORMONES AND THEIR α-KETOLIC METABOLITES IN URINE

1963 ◽  
Vol 42 (1) ◽  
pp. 61-68 ◽  
Author(s):  
W. S. Cost ◽  
J. Pol ◽  
A. Korten
Keyword(s):  
Cushing’S Disease ◽  
Late Effects ◽  
Quantitative Estimation ◽  
Addison’S Disease ◽  
Cushing's Disease ◽  
Addison's Disease ◽  
Adrenogenital Syndrome ◽  
Adrenocortical Hormones ◽  
Before And After

ABSTRACT Urinary corticosteroid patterns were estimated before and after adrenocortical stimulation by exogenous corticotrophin (ACTH). The results indicate that changes in corticosteroid biosynthesis and metabolism depend on the duration of stimulation. Immediate effects are an increase in corticosterone production above that of cortisol (low F/B-ratio) and a shift in the metabolism of both cortisol and corticosterone in favour of all 11-hydroxycompounds. Late effects are characteristic of the patterns in Cushing's disease including a high F/B-ratio and low values for the 11-hydroxy-allocompounds (allotetrahydrocortisol and allotetrahydrocorticosterone). Changes in the ratios between cortisol, corticosterone and Reichstein's S as observed in Cushing's disease, adrenogenital syndrome and Addison's disease can be imitated by ACTH-induced acceleration of corticosteroid biosynthesis.

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