REMISSION OF ACROMEGALY CAUSED BY PITUITARY CARCINOMA AFTER SURGICAL EXCISION OF GROWTH HORMONE-SECRETING METASTASIS DETECTED BY 111-INDIUMPENTETREOTIDE SCAN
Y. Greenman et al., REMISSION OF ACROMEGALY CAUSED BY PITUITARY CARCINOMA AFTER SURGICAL EXCISION OF GROWTH HORMONE-SECRETING METASTASIS DETECTED BY 111-INDIUMPENTETREOTIDE SCAN, The Journal of clinical endocrinology and metabolism, 81(4), 1996, pp. 1628-1633
GH-secreting carcinomas of the pituitary are extremely rare. We descri
be a 37-yr-old woman with refractory acromegaly 15 yr after transpheno
idal surgery and radiotherapy, with no evidence of a recurrent pituita
ry mass. Scanning with Ill-indium pentetreotide revealed an area of in
tense activity in the left neck. A 3.5 x 2.5-cm mass was excised from
the neck after demonstrating an arterio-venous GH gradient of 7:1. GH
levels (50 ng/mL) dropped to 0.8 ng/mL 3 h after surgery and remained
normal. GH gene expression was demonstrated in the metastasis by North
ern and Western blot analyses and by positive immunocytochemistry and
immunoelectron microscopy. In vitro cultured cells responded to GHRH a
nd TRH by increasing GH levels (P < 0.01). Medium GH was identical to
authentic pituitary GH, as demonstrated by high pressure liquid chroma
tography. RT-PCR of hypothalamic hormone receptor messenger RNA in the
mass revealed somatostatin receptor subtypes 2, 3, and 5 and GHRH, TR
H, and dopamine receptor expression. No GH gene amplification, rearran
gement, or gsp mutation was found. RE gene deletion and H-ras mutation
s, previously reported in PRL- and ACTH-secreting carcinomas, were not
detected. In conclusion, clinical and molecular features of a GH-secr
eting pituitary carcinoma are presented. This metastatic lesion synthe
sized GH and expressed functional hypothalamic hormone receptors.