Improvement of pituitary function after surgical decompression for pituitary tumor apoplexy.
Hypopituitarism is a major manifestation of pituitary adenoma apoplexy. We postulated that the acute deterioration in pituitary function may be caused by compression of portal vessels and the pituitary stalk, secondary to a sudden increase in intrasellar contents. If this were the case, one would predict improvement in pituitary function to occur after surgical decompression. We studied pituitary function in eight patients presenting with the clinical syndrome of pituitary adenoma apoplexy before and on multiple occasions after urgent surgical decompression. Partial or complete hypopituitarism was seen in all subjects at the time of presentation. Serum cortisol levels were inappropriately low (5.9 +/- 1.4 micrograms/dL; 162.8 +/- 38 nmol/L) for the degree of stress in seven patients and appropriately elevated in only one subject (55.3 micrograms/dL; 1525.7 nmol/L). High normal increments in cortisol levels were noted in three subjects given test doses of cosyntropin. Patients were given glucocorticoids before, during, and for 2 days after surgery. Serum cortisol concentrations measured on or after the third day when glucocorticoids had already been stopped were normal in seven subjects and consistently low in one. These seven subjects were discharged on no replacement and were subsequently documented by dynamic testing to have normal pituitary-adrenal function. Gonadal function improved in two of four men and in one of two women who had hypogonadism on presentation. Improvement in thyroid function was documented in two of three subjects with preoperative hypothyroidism. Gradual improvement and almost complete resolution of the neuroophthalmological abnormalities occurred days to weeks after decompression. These observations demonstrate that urgent surgical decompression after pituitary tumor apoplexy was associated with improvement not only in neurological defects but also in pituitary function. The rapid improvement in pituitary function indicates not only that the hypopituitarism was reversible, but also that it might be caused by compression of the portal circulation and pituitary stalk by the sudden increase in intrasellar contents.
Arafah
B M
BM
Division of Endocrinology, Case Western Reserve University School of Medicine, Cleveland, Ohio.
Harrington
J F
JF
Madhoun
Z T
ZT
Selman
W R
WR
D000324:Adrenocorticotropic Hormone / Q000032:analysis; D000328:Adult; D002561:Cerebrovascular Disorders / Q000209:etiology* / Q000601:surgery; D005260:Female; D005640:Follicle Stimulating Hormone / Q000032:analysis; D013006:Growth Hormone / Q000032:analysis; D006801:Humans; D007018:Hypopituitarism / Q000209:etiology / Q000503:physiopathology*; D007124:Immunoenzyme Techniques; D007986:Luteinizing Hormone / Q000032:analysis; D008297:Male; D008875:Middle Aged; D010911:Pituitary Neoplasms / Q000150:complications / Q000503:physiopathology / Q000601:surgery*; D011388:Prolactin / Q000032:analysis; D013739:Testosterone / Q000097:blood; D013972:Thyrotropin / Q000032:analysis
D013739:Testosterone; D000324:Adrenocorticotropic Hormone; D011388:Prolactin; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D013972:Thyrotropin; D013006:Growth Hormone