脳下垂体腺腫の石灰沈着

PITUITARY ADENOMA CALCIFICATION

　抄録　脳下垂体腺腫の318症例を対象に，石灰沈着の出現率および発現機序を，光顕，電顕，免疫組織化学的に検討した。光顕的に石灰沈着を認めたのは44例（13.8％）であった。その内訳けは，PRL腫瘍23例，GH腫瘍7例，PRL＋GH腫瘍2例，ACTH腫瘍2例，FSH腫瘍1例，non-functioning adenoma9例であった。頭蓋単純レ線フィルム上，トルコ鞍または鞍上部に石灰沈着を認めたのは7例（2.2％）で，CT上Caと考えられる高吸収域を鞍内または鞍上部に認めたのは4例（1.3％）であった。PRL腫瘍にみられる石灰沈着は，腺腫摘出後に血中PRL値の正常化と共に血中Caの正常化ないし減少傾向がみられることより，PRLそれ自身がCa代謝の異常を招来することに起因すると考えられる。GH腫瘍も同様である。nonfunctioning adenomaにみられる石灰沈着はdystrophic calclficationに由来するものと考えられるが，functioning adenomaにみられる石灰沈着は，metastatic calcificationを中心に，dystrophicおよびarterial calcificationさらにcalcinosisが互いに係り合って発現されるものと考えた。

Three hundred and eighteen cases of functioning and non-functioning pituitary adenoma were exa-mined by histological, immunocytochemical and electronmicroscopic technique. Fourty-four of them (13.8%) showed evidence of calcospherites in the tumor tissues. A high incidence of calco-spherite is found in functioning adenoma, but not in non-functioning adenoma. Calcification was seen most frequently in cases of prolactinoma (23), GH secreting (7), or GH+PRL tumor (2) and less in adrenocorticotropic hormone secreting adenoma (2) and follicle stimulating hormone secreting adenoma (1). Prolactin and growth hormone might be involved in the control of calcium meta-bolism. This is because, following adenomectomy in patients with prolactinoma or GH-secreting adenoma with hypercalcemia, there is normaliza-tion of serum PRL and GH with reduction in serum calcium. Calcospherite is produced in all of metastatic calcification, arterial calcification, dystrophic calcification and calcinosis. In cases of non-functioning adenoma however, the mechanism is believed to by dystrophic calcification.