Probable ACTH-secreting pituitary tumour in association with Addison's disease

1985 ◽  
Vol 110 (1) ◽  
pp. 36-41 ◽  
Author(s):  
Toshihiko Yanase ◽  
Kensaku Sekiya ◽  
Masaaki Ando ◽  
Hajime Nawata ◽  
Ken-ichi Kato ◽  
...  
Keyword(s):  
Circadian Rhythm ◽  
Sella Turcica ◽  
Addison’S Disease ◽  
Pituitary Tumour ◽  
Cortisone Acetate ◽  
University Hospital ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Old Japanese ◽  
Acth Secreting

Abstract. A 61 year old Japanese man with a diagnosis of Addison's disease was admitted to Kyushu University Hospital for further investigation of high ACTH levels and hyperpigmentation which 37.5 mg of cortisone acetate failed to alleviate. The basal level of plasma ACTH was 700—1000 pg/ml, and following 25—37.5 mg cortisone acetate or 1 mg dexamethasone the levels were 300—600 pg/ml. The general pigmentation showed little improvement with such medication. Radiographic studies revealed a double floor of the sella turcica and cisternal herniation. These observations suggested the existence of a pituitary ACTH-secreting tumour. Plasma ACTH showed a circadian rhythm ranging from 440 to 1570 pg/ml and it was not suppressed to a normal range by oral administration of dexamethasone, 8 mg/day or by continuous infusion of dexamethasone, 1.25 mg/h for 2 h. Plasma ACTH responses of 80% above basal level to lysine-vasopressin (LVP), and 12% above basal to synthetic ovine corticotrophin releasing factor (CRF) were observed. FK 33-824, a methionine-enkephaline analogue, suppressed plasma ACTH to 85% of basal level, while bromocriptine (CB-154) caused no significant change. These findings led to a diagnosis of pituitary ACTHsecreting adenoma (corticotropinoma) in association with Addison's disease. The persistent circadian rhythm of plasma ACTH suggested that this adenoma may not be completely free from regulation by the central nervous system. This case may be clinically significant for investigation of the pathogenesis of pituitary adenoma, particularly in Nelson's syndrome.

ACTH-producing pituitary adenomas in Addison's disease: two cases treated by transsphenoidal microsurgery

1982 ◽  
Vol 99 (3) ◽  
pp. 357-363 ◽  
Author(s):  
Barbara Krautli ◽  
J. Müller ◽  
A. M. Landolt ◽  
F. von Schulthess
Keyword(s):  
Visual Fields ◽  
Sella Turcica ◽  
Addison’S Disease ◽  
Surgical Removal ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Cell Adenoma ◽  
Feedback Suppression ◽  
Secondary Hypothyroidism ◽  
Transsphenoidal Microsurgery

Abstract. In 2 women with known Addison's disease, progressive hyperpigmentation reappeared years after an initial remission under conventional substitution therapy with cortisone. Excessively elevated plasma ACTH concentrations and radiological evidence of sella turcica deformation led to the diagnosis of ACTH-producing adenomas and prompted their removal by transsphenoidal microsurgery. In one patient, a large Crooke's cell adenoma with extensive extrasellar expansion had caused severe and irreversible bilateral defects of the visual fields and unilateral optic atrophy. Surgical removal of the tumour and radiotherapy brought about a permanent disappearance of the hyperpigmentation, but eventually led to secondary hypothyroidism. In the second patient, the selective removal of a small intrasellar eosinophilic adenoma consisting of ACTH-producing cells did not alleviate the hyperpigmentation and did not lower the plasma ACTH concentration. However, hyperpigmentation regressed markedly within a year of treatment with a higher dose of cortisone. The rarity of similar cases in the literature seems to indicate that insufficient feedback suppression of ACTH-producing cells in treated Addison's disease does not by itself induce the development of a pituitary adenoma, but might promote the growth of an independently and coincidentally occurring microadenoma, which would have caused Cushing's disease in a person with intact adrenal glands.

No inhibition of corticotrophin (ACTH)-hypersecretion in adrenal insufficiency by somatostatin

1980 ◽  
Vol 95 (1) ◽  
pp. 71-74 ◽  
Author(s):  
A. Jara-Albarrán ◽  
J. Bayort ◽  
A. Caballero ◽  
R. Eusebio ◽  
P. García-Peris ◽  
...  
Keyword(s):  
Adrenal Insufficiency ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Primary Adrenal Insufficiency ◽  
No Inhibition ◽  
Infusion Period

Abstract. Somatostatin (250 μg as a bolus iv and 250 μg as a I h infusion) was administered to 6 patients with primary adrenal insufficiency (Addison's disease). The fall in plasma ACTH during the infusion period ranged between 0–30% with a mean reduction of 11.2 ± 11.6%. These findings suggest that with the method employed, somatostatin is not an inhibitor of ACTH secretion in a condition in which glucocorticoids are lacking.

Effect of angiotensin II on plasma ACTH in patients with Addison's disease

1985 ◽  
Vol 110 (4) ◽  
pp. 451-455
Author(s):  
Hermann Haller ◽  
Volker Bähr ◽  
Petra Exner ◽  
Wolfgang Oelkers
Keyword(s):  
Angiotensin Ii ◽  
Time Lag ◽  
Addison’S Disease ◽  
Major Effect ◽  
Addison's Disease ◽  
Base Line ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Short Term ◽  
Sodium Deficiency

Abstract. Short-term angiotensin II (All) infusions (3 ng/kg/min) were performed in 5 patients with Addison's disease in order to assess the effect of AII on ACTH secretion. Base line ACTH levels were elevated due to a 9-h time lag between hydrocortisone administration and onset of the study. In 2 separate infusion periods of 30-min duration, All had no unidirectional effect on plasma ACTH. Mean ACTH increased slightly but insignificantly. Mean blood pressure rose by about 10 mmHg. The degree of angiotensinaemia induced is probably similar to the state of moderate to severe sodium deficiency. Short-term changes of All in this order of magnitude have obviously no major effect on ACTH secretion.

Technetium-99m pentavalent dimercaptosuccinic acid imaging in patients with pituitary adenomas

1995 ◽  
Vol 133 (1) ◽  
pp. 38-47 ◽  
Author(s):  
Secondo Lastoria ◽  
Annamaria Colao ◽  
Emilia Vergara ◽  
Diego Ferone ◽  
Paola Varrella ◽  
...  
Keyword(s):  
Pituitary Adenomas ◽  
Addison’S Disease ◽  
Primary Hypothyroidism ◽  
Dimercaptosuccinic Acid ◽  
Addison's Disease ◽  
Klinefelter’S Syndrome ◽  
Klinefelter's Syndrome ◽  
Technetium 99M ◽  
Before And After ◽  
Acth Secreting

Lastoria S, Colao A, Vergara E, Ferone D, Varrella P, Merola B, Lombardi G, Salvatore M. Technetium-99m pentavalent dimercaptosuccinic acid imaging in patients with pituitary adenomas. Eur J Endocrinol 1995;133:38–47. ISSN 0804–4643 We studied the tumor-seeking agent technetium-99m-labeled pentavalent dimercaptosuccinic acid ([99mTc](V)DMSA) to visualize 21 growth hormone (GH)-, nine prolactin (PRL)-, two mixed GH/PRL-, six adrenocorticotropin (ACTH)-secreting and 15 clinically non-functioning pituitary adenomas, three craniopharyngiomas and one dysgerminoma of the sella. All non-adenomas and 31 out of 53 adenomas were studied before treatment: 22 after surgery and/or radiotherapy. Eight cases of acromegaly were studied before and after chronic treatment with octreotide, whereas three cases of acromegaly, one of prolactinoma and two of non-functioning adenoma were imaged before and after adenomectomy. As a control group, 27 patients without any clinical evidence of pituitary adenoma were studied: 10 of them were operated on previously and treated with iodine-131 for metastatic thyroid carcinoma, 10 had brain tumors and the remaining seven patients had functional pituitary hypersecretion (four Klinefelter's syndrome, two primary hypothyroidism and one Addison's disease). The scintigraphy was repeated after testosterone in Klinefelter's syndrome, l-thyroxine in primary hypothyroidism and cortisone administration in Addison's disease. Seventeen GH-secreting (81%), seven PRL-secreting (78%), three ACTH-secreting (50%), 15 non-functioning (100%) and one (50%) mixed adenoma significantly concentrated [99mTc](V)DMSA, showing elevated tumor-to-background (T/B) ratios. The T/B ratios were similar in untreated and surgically treated adenomas (11.2 ± 5.6 vs 11.8 ± 6.2). Radiotherapy significantly lowered the [99mTc](V)DMSA uptake to 5.1 ± 2.8 (p < 0.1 vs untreated patients). Non-adenomatous lesions of the sella turcica did not concentrate [99mTc](V)DMSA in the pituitary as well as brain tumors and 8 out of 10 metastatic thyroid cancers. The treatment with octreotide normalized GH and insulin-like growth factor I levels and reduced [99mTc](V)DMSA from 15.7 ± 4.8 to 13.5 ± 3.9 (p < 0.05). Conversely, adequate substitutive therapy completely inhibited the uptake of the radiotracer in Klinefelter's syndrome, in primary hypothyroidism and in Addison's disease. The [99mTc](V)DMSA scintigraphy showed an overall sensitivity of 81% (43/53) in detecting pituitary adenomas, which was increased to 95% for lesions greater than 10 mm in size. High-quality images with minimal total body radiation were obtained, enabling a good in vivo characterization of viable adenomatous tissue as well as an accurate monitoring of the effects of different therapeutic regimens. Secondo Lastoria, Department of Nuclear Medicine, National Cancer Institute, Fondazione G Pascale, via M Semmola, 80131 Napoli, Italy

Pituitary ACTH-secreting adenoma in Addison's disease: A case report

2013 ◽  
Vol 115 (12) ◽  
pp. 2543-2546 ◽  
Author(s):  
Siyuan Fan ◽  
Ying Jiang ◽  
Yong Yao ◽  
Renzhi Wang ◽  
Bing Xing
Keyword(s):  
Case Report ◽  
Addison’S Disease ◽  
Addison's Disease ◽  
Acth Secreting
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