SPONTANEOUS RESOLUTION OF PRIMARY HYPERCORTISOLISM OF CUSHING DISEASE AFTER PITUITARY HEMORRHAGE.
Journal
AACE clinical case reports
ISSN: 2376-0605
Titre abrégé: AACE Clin Case Rep
Pays: United States
ID NLM: 101670593
Informations de publication
Date de publication:
Historique:
received:
19
06
2019
accepted:
14
09
2019
entrez:
28
9
2020
pubmed:
29
9
2020
medline:
29
9
2020
Statut:
epublish
Résumé
To describe a case of spontaneous resolution of primary hypercortisolism from Cushing disease (CD) due to pituitary apoplexy (PA). Clinical, laboratory, and pathologic information are described. A 59-year-old female presented with a headache, a 2.3 cm sellar mass with a questionable hemorrhagic component, and clinical signs of hypercortisolism. On further evaluation, she had an increased 24-hour urine free cortisol, abnormal serum cortisol during a low dose dexamethasone suppression test, and an elevated plasma adrenocorticotropic hormone (ACTH), consistent with pituitary CD. As she was being prepared for surgical resection, she was noted to have spontaneous biochemical remission associated with resolution of her symptoms of hypercortisolism, and a repeat magnetic resonance imaging scan showed shrinkage of the sellar mass. She has been managed conservatively since and remains in clinical/biochemical remission until present time, 18 months following her initial presentation. We report a case of spontaneous resolution of CD from symptomatic hemorrhage within an ACTH-secreting pituitary adenoma, or PA. This has been rarely reported in the medical literature. The fact that she did not pass through a phase of adrenal withdrawal, makes us suspect a residual functional adenoma within or around the sella which may eventually grow, causing her disease to recur, as has been reported. Hence, continued monitoring will be required.
Identifiants
pubmed: 32984518
doi: 10.4158/ACCR-2019-0292
pmc: PMC7279773
doi:
Types de publication
Case Reports
Langues
eng
Pagination
e23-e29Informations de copyright
Copyright © 2020 AACE.
Déclaration de conflit d'intérêts
DISCLOSURE The authors have no multiplicity of interest to disclose.
Références
Endocr Pract. 2003 Mar-Apr;9(2):147-51
pubmed: 12917078
J Clin Endocrinol Metab. 2008 Jul;93(7):2454-62
pubmed: 18413427
Pituitary. 2015 Jun;18(3):283-9
pubmed: 24803324
Endocr J. 2000 Dec;47(6):793-7
pubmed: 11228056
J Neurosurg. 2006 Jun;104(6):931-7
pubmed: 16776337
Neth J Med. 2015 Jun;73(5):242-6
pubmed: 26087804
J Clin Endocrinol Metab. 2005 Aug;90(8):4963-9
pubmed: 15886242
Pituitary. 2012 Sep;15(3):428-35
pubmed: 21927887
Endocr Rev. 2015 Dec;36(6):622-45
pubmed: 26414232
Am J Emerg Med. 2008 Nov;26(9):1068.e1-3
pubmed: 19091287
Pituitary. 2005;8(2):81-7
pubmed: 16195779
J Clin Endocrinol Metab. 2004 Dec;89(12):6348-57
pubmed: 15579802
Neurosurgery. 1990 Jun;26(6):980-6
pubmed: 2362675
Turk Neurosurg. 2018;28(2):323-325
pubmed: 27593808
Insights Imaging. 2014 Dec;5(6):753-62
pubmed: 25315035
Arq Bras Endocrinol Metabol. 2013 Aug;57(6):486-9
pubmed: 24030190
J Neurosurg. 1979 Dec;51(6):866-9
pubmed: 228016
Pituitary. 2018 Apr;21(2):138-144
pubmed: 29383476
Endocrine. 2010 Oct;38(2):143-6
pubmed: 21046475
Neurol India. 2002 Dec;50(4):490-3
pubmed: 12577104
Arch Intern Med. 1993 Jan 25;153(2):251-5
pubmed: 8422213
Neurosurg Focus. 2015 Feb;38(2):E7
pubmed: 25639325
Endocrine. 2017 Apr;56(1):10-18
pubmed: 27189147