Does pituitary stalk compression cause hyperprolactinemia?

Singer, William

doi:10.1007/bf02915621

Cited by 7 publications

(2 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Although, a hyperprolactinemia could not be detected in our patient, immunohistochemistry of the fi rst recurrence revealed a weak prolactin-positivity. As several POMC derivates, especially ßendorphin, stimulate the release of prolactin and the clinical silence of silent corticotroph adenomas may be the result of abnormal cleavage of the POMC molecule, these features may account for the prolactin abnormalities ( Chabre et al, 1991 ;Lloyd et al, 1990 ;Singer, 1990 ). In a series of 12 patients with silent corticotroph adenomas investigated in a US referral center for pituitary diseases, only 4 were predominantly chromophobic ( Lopez et al, 2004 ).…”

Section: Discussionmentioning

confidence: 99%

Atypical Type II Silent Corticotrophic Adenoma Developing into Cushing's Disease upon Second Recurrence

Psaras

Honegger²,

Buslei³

et al. 2007

Exp Clin Endocrinol Diabetes

View full text Add to dashboard Cite

Herein, we report the case of a 73-year old male patient who presented with two recurrences of a pituitary adenoma within a period of 15 years. The first tumor resection 15 years ago revealed a non-functioning pituitary macroadenoma. 11 years later, the first recurrence of the tumor was reoperated. Throughout the early course of the disease, he suffered from secondary adrenal insufficiency and required replacement therapy with hydrocortisone. Currently, he presented with the second recurrence and clinical examination revealed signs of Cushing's disease. This was clearly confirmed by endocrinological evaluation. A retrospective analysis of all histological and immunohistochemical slides rendered an adenoma exhibiting chromophobia, ACTH-positivity and features of atypia such as elevated p53 and Ki67 expression as well as nuclear polymorphism. According to the revised WHO classification it was classified as atypical type II silent corticotroph adenoma at the time of the first and second surgery. The specimen removed during the recent surgery displayed the same histological features and was classified as corticotroph adenoma. The combination of an atypical type II adenoma and the switch in the hormone status to an endocrinologically active adenoma makes this case exceedingly rare.

show abstract

Section: Discussionmentioning

confidence: 99%

Atypical Type II Silent Corticotrophic Adenoma Developing into Cushing's Disease upon Second Recurrence

Psaras

Honegger²,

Buslei³

et al. 2007

Exp Clin Endocrinol Diabetes

View full text Add to dashboard Cite

show abstract

“…Approximately 30% of surgically removed pituitary adenomas are unaccompanied by clinical and biochemical evidence of hormone excess [4, 11, t4], with the exception of mild hyperprolactinemia, which may occur m some patients, particularly in those harboring large tumors. The elevation of serum prolactm levels is explained by the so-called stalk section effect [18]; it is claimed that the growing tumor compresses or impairs the h)~pothalamus or the hypophyseal stalk, thereby suppressing the synthesis, release, or adenohypophyseal transport ofdopamine, the main hypothalamic factor inhibiting prolactiu discharge [18]. Nonfunctioning pituitary tumors are discovered either incidentally at autopsy or by various imaging techniques during thc patient's lifc or because of local symptoms, such as visual disturbances, various cranial nerve palsies, headache, nausea, increased intracranial pressure, or various degrees ofhypopituitaris,n [ 9, 1 t ].…”

mentioning

confidence: 99%