TY - JOUR
T1 - Endocrine function after spontaneous infarction of the human pituitary
T2 - Report, review, and reappraisal
AU - Veldhuis, Johannes D.
AU - Hammond, James M.
PY - 1980/1
Y1 - 1980/1
N2 - NO COMPREHENSIVE review has been available to define preservation or loss of pituitary function after acute hemorrhagic infarction of the hypophysis in man. Published experience is limited to individual reports emphasizing unusual features of pituitary apoplexy, such as “autohypophysectomy” in acromegaly (1–4), atypical presentations such as pituitary “pseudotumor” (5), or the occurrence of “hypothalamic hypopituitarism” (6–8). In the following work, we have collated data from the gynecological, neurological, neurosurgical, radiological, and internal medicine literature, to permit systematic examination of residual endocrine function after pituitary apoplexy. These data are supported by detailed hormonal evaluations of four additional patients with pathologically proven pituitary apoplexy. Collectively, our observations document a high prevalence of multiple adenohypophyseal deficits, and illustrate the diversity of etiological settings in which pituitary apoplexy has been described. Our studies with the administration of hypothalamic releasing factors have prompted critical reappraisal of the precise mechanisms causing hypopituitarism after pituitary infarction.
AB - NO COMPREHENSIVE review has been available to define preservation or loss of pituitary function after acute hemorrhagic infarction of the hypophysis in man. Published experience is limited to individual reports emphasizing unusual features of pituitary apoplexy, such as “autohypophysectomy” in acromegaly (1–4), atypical presentations such as pituitary “pseudotumor” (5), or the occurrence of “hypothalamic hypopituitarism” (6–8). In the following work, we have collated data from the gynecological, neurological, neurosurgical, radiological, and internal medicine literature, to permit systematic examination of residual endocrine function after pituitary apoplexy. These data are supported by detailed hormonal evaluations of four additional patients with pathologically proven pituitary apoplexy. Collectively, our observations document a high prevalence of multiple adenohypophyseal deficits, and illustrate the diversity of etiological settings in which pituitary apoplexy has been described. Our studies with the administration of hypothalamic releasing factors have prompted critical reappraisal of the precise mechanisms causing hypopituitarism after pituitary infarction.
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U2 - 10.1210/edrv-1-1-100
DO - 10.1210/edrv-1-1-100
M3 - Article
C2 - 6785084
AN - SCOPUS:0019249499
SN - 0163-769X
VL - 1
SP - 100
EP - 107
JO - Endocrine Reviews
JF - Endocrine Reviews
IS - 1
ER -