PubMed · 7205948
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
A D Parent. 1981. Acromegaly.. https://pubmed.ncbi.nlm.nih.gov/7205948/
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
An echocardiographic follow-up of 25 patients (pts) was performed, after the first examinations in 1978-1979. 15 pts have died in the last 15 years (Group 1), while 10 still living (Group 2). In Group 1 either the impaired global left ventricular at the time of the first echocardiography predicted a high mortality i.e. there were only two pts with normal echocardiographic findings. The other 6 acromegalic pts with a "normal heart" have survived. The left ventricular hypertrophy of pts in Group 2 was observed to increase during the 15-year follow-up, because of the development of systemic hypertension. In conclusion, the echocardiographic findings are of a good predictive value in estimations of the survival rate in acromegalic pts.
Local expansion of pituitary tumors causes nonspecific symptoms, including hormone insufficiency, that may exist for years before diagnosis. Although they are more specific, symptoms of pituitary hormone oversecretion may also remain unrecognized and give rise to difficult diagnostic problems. Gonadotropic tumors do not elicit specific endocrine symptoms, whether they secrete complete gonadotropins or their biologically inactive free subunits. Hyperprolactinemia is not due to tumor secretion in the majority of cases, including some with a tumor in the pituitary (compressive hyperprolactinemia). When acromegaly is suspected, the unequivocal proof of excess growth hormone secretion is not easy to obtain, due to intermittent growth hormone secretion, both in normals and in acromegalics. The large variety of tests available for the etiological diagnosis of hypercorticism indicates the diagnostic difficulties that can be encountered. Corticotrope pituitary adenomas may be minute, and ectopic corticotropin secretion may remain occult. But on the other hand, the quality of the diagnostic tools available improves constantly. This includes new hormone measurements, such as insulin-like growth factor 1 and its binding proteins, dynamic tests, selective pituitary blood drawing by inferior petrosal sinus catheterism, pituitary nuclear magnetic resonance imaging and somatostatin-analogue scintiscan. In addition to the improving techniques of transphenoidal neurosurgery and pituitary radiotherapy, medical management of pituitary tumors remains a distinct possibility. Tumor hormone secretion can be controlled in some cases by drugs such as dopaminergic agents, somatostatin analogues and gonadoliberin analogues, which may also exert an antitumoral mass effect. Within the next few years we will be confronted with an increasing number of incidentally discovered pituitary tumors, due to the frequent use of high-resolution intracranial imaging.
L-692,429 is a non-peptidyl GH secretagogue. We examined the effects of L-692,429 on cultured human pituitary tumors removed from patients with acromegaly. Dose-dependent stimulation of GH secretion was observed, with 1 mumol/L leading to 2 or 3-fold increases. Prolactin (PRL) secretion by a mixed somatotrophic-lactotrophic tumor was also stimulated. The effects of L-692,429 were abolished by phloretin and W7 but not Rp-cAMPS. Rate of phosphatidylinositol turnover was markedly increased up to 3-fold by L-692,429. These results show that L-692,429 increases hormone secretion by human pituitary cells via a protein kinase C and Ca2+ dependent mechanism.