CUSHING'S DISEASE IN A PATIENT WITH GONADAL DYSGENESIS AND PITUITARY TUMOUR

1965 ◽  
Vol 48 (1) ◽  
pp. 72-80 ◽  
Author(s):  
H. H. Bassøe ◽  
H. Gadeholt ◽  
K. Ronold ◽  
K. F. Støa

ABSTRACT A thirty-nine years old woman with primary amenorrhoea and increased excretion of gonadotrophins, developed a chromophobe adenoma in the pituitary gland. Only a few years before she died, the diagnosis of Cushing's disease was made which progressed despite hypophysectomy. Evidence is given for the conclusion, that the patient suffered from ovarian dysgenesis, which secondarily led to hyperfunction and tumour formation of the pituitary gland and also to development of Cushing's disease. It is concluded that patients with hypogonadism should be observed for pituitary tumour formation, and that adequate substitution therapy may prevent formation of pituitary tumours.

1969 ◽  
Vol 62 (4) ◽  
pp. 647-652 ◽  
Author(s):  
J. Lindholm ◽  
P. Rasmussen ◽  
O. Korsgaard

ABSTRACT Two patients with concurrent Cushing's disease and chromophobe adenoma of the pituitary gland are presented. In one case the tumour was present before adrenalectomy, in the other it was not recognized until after adrenalectomy. The characteristic symptoms and findings are described – including the results of corticotrophin determinations in the blood. Some aspects of the treatment of Cushing's disease are discussed.


1969 ◽  
Vol 60 (1) ◽  
pp. 112-120 ◽  
Author(s):  
Sara Leiba ◽  
Baruch Landau ◽  
Artur Ber

ABSTRACT Three patients with pituitary tumours are described. The first is a patient with myxoedema who 28 years ago was treated for thyrotoxicosis with irradiation of the thyroid gland. It is the author's opinion that the long-standing hypothyroidism may have induced a hypersecretion of TSH and secondary hyperplasia of the pituitary gland which resulted in an enlargement of the sella. The second patient presented signs of a pituitary tumour with a compression of the chiasma and hypofunction of the thyroid and gonads. One year previously she had a febrile disease diagnosed as morbili. After she was treated with substitution therapy with thyroid hormones there was an improvement in her condition, with disappearance of the ocular signs of the glandular insufficiency. It is assumed that this patient developed a primary hypothyroidism due to thyroiditis which probably induced a mucopolysaccharide infiltration around the pituitary gland. This infiltration in turn resulted in the rapid enlargement of the sella and signs of compression of the optic chiasma. Thyroid therapy probably caused disappearance of the mucopolysaccharides infiltration with a consequent return of the ocular signs to normal. The sella remained enlarged. The third patient also presented an enlarged sella. The pituitary gland produced high levels of gonadotrophins, but the levels of GH, ACTH and TSH were normal. The patient had premature ovarian failure. In this case the tumour was discovered when the patient was still menstruating. This tumour seems to be of a dependent type since oestrogen therapy induced inhibition of the high levels of gonadotrophins. It is suggested that the prolonged subnormal levels of oestrogens stimulated the development of the pituitary tumour. The relation between the target gland insufficiency and the development of the pituitary tumours is discussed.


2021 ◽  
pp. 123-248
Author(s):  
Niki Karavitaki ◽  
Chris Thompson ◽  
Iona Galloway

This chapter covers the pituitary gland. It starts with the anatomy and physiology, then moves on to imaging, and pituitary function. It then covers common tests, including ITT, glucagon, ACTH stimulation, arginine, clomiphene, hCG, and TRH. It then begins to cover disorders of pituitary function, with treatment, hormone replacement, and investigation all included. Pituitary tumours are described, along with investigation, diagnosis, and treatment. Other disorders, including Cushing’s disease, cysts, inflammatory conditions are all included. Complications from other conditions are also described.


1983 ◽  
Vol 96 (2) ◽  
pp. 303-309 ◽  
Author(s):  
A. M. McNicol ◽  
H. Thomson ◽  
C. J. R. Stewart

The distribution of specifically stained corticotrophic cells has been studied in the pituitary glands of 11 dogs with pituitary-dependent hyperadrenocorticism. The results suggest that the disease is not a single entity, and that some cases are caused by primary abnormality of the pituitary gland whereas others appear to be the result of dysfunction of the hypothalamus or central nervous system. The patterns correspond closely to those demonstrated in the human pituitary gland in Cushing's disease, and confirm that the canine disease is a useful model for the study of the pathogenesis of the variants of the condition.


1985 ◽  
Vol 143 (3) ◽  
pp. 221-223 ◽  
Author(s):  
H. Stegner ◽  
D. K. Lüdecke ◽  
M. Kadrnka-Lovrenćić ◽  
N. Stahnke ◽  
R. P. Willig

1978 ◽  
Vol 88 (2) ◽  
pp. 239-249 ◽  
Author(s):  
Loren G. Lipson ◽  
Inese Z. Beitins ◽  
Paul D. Kornblith ◽  
Janet W. Mc Arthur ◽  
Henry G. Friesen ◽  
...  

ABSTRACT A tissue culture study was undertaken to determine if human non-functioning pituitary tumours secrete polypeptide anterior pituitary hormones in vitro and to study the spectrum of hormone release by functioning pituitary neoplasms. Fragments from 48 human pituitary tumours (from patients - 2 with Cushing's disease, 1 with Nelson's syndrome, 5 with amenorrhoea-galactorrhoea, 10 with acromegaly and 30 with non-functioning pituitary tumours) and three normal human anterior pituitary glands (controls) were placed in tissue culture immediately after surgery. The in vitro release of human growth hormone (HGH), prolactin (Prl), thyrotrophin (TSH), adrenocorticotrophin (ACTH), luteinizing hormone (LH) and follicle stimulating hormone (FSH) were measured by radioimmunoassays at the end of one week in culture. Clinical and pathological data were compared to hormone release patterns. In the culture media from control pituitaries the concentrations of the six hormones tested were 100 to 10 000 times greater than in peripheral blood. The medium surrounding the fragments from functioning pituitary tumours contained the following: a) Acromegaly - high levels of HGH and variable concentrations of the other hormones. b) Cushing's disease - ACTH and Prl predominantly. c) Amenorrhcea-galactorrhoea syndrome - prolactin in 4 out of 5 patients, all six polypeptides in one patient. In the media from the 30 patients diagnosed as having non-functioning pituitary tumours, 60 % of the samples contained at least one hormone at a concentration similar to that of the controls and 100 % of the samples contained detectable quantities of at least one hormone.


2007 ◽  
Vol 51 (8) ◽  
pp. 1392-1396 ◽  
Author(s):  
Alia Munir ◽  
John Newell-Price

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.


2010 ◽  
Vol 163 (4) ◽  
pp. 495-507 ◽  
Author(s):  
T M Barber ◽  
E Adams ◽  
O Ansorge ◽  
J V Byrne ◽  
N Karavitaki ◽  
...  

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.


2015 ◽  
Vol 26 (1) ◽  
pp. 271-277 ◽  
Author(s):  
Alexandra A. J. de Rotte ◽  
Amy Groenewegen ◽  
Dik R. Rutgers ◽  
Theo Witkamp ◽  
Pierre M. J. Zelissen ◽  
...  

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