ABSTRACT
Intracarotid CDDP infusion in combination with angiotensin II was performed in two patients with metastatic brain tumor, lung carcinoma (LC) and ovarian carcinoma (OC). The patient with OC received 40 mg/m2 CDDP while the other patient with LC was administered intra-arterially with 50 mg/m2 CDDP, 30 mg/m2 ADM and 2.5 mg/m2 MMC. 50% or greater reduction in the size of metastatic lesions was observed in both patients in whom no neurological toxicities developed. Intra-arterial infusion of CDDP either alone or in combination with ADM or MMC seems to present an aggressive approach in dealing with other metastatic neoplasms without increasing toxicity, especially if intra-arterial angiotensin II is infused concomitantly.
Subject(s)
Angiotensin II/administration & dosage , Antineoplastic Combined Chemotherapy Protocols/therapeutic use , Brain Neoplasms/drug therapy , Cisplatin/administration & dosage , Adenocarcinoma, Papillary/drug therapy , Adenocarcinoma, Papillary/secondary , Aged , Brain Neoplasms/secondary , Carotid Arteries , Doxorubicin/administration & dosage , Female , Humans , Infusions, Intra-Arterial , Lung Neoplasms/pathology , Male , Middle Aged , Mitomycin , Mitomycins/administration & dosage , Ovarian Neoplasms/pathologyABSTRACT
In an attempt to test the hypothesis that pituitary adenomas of acromegaly may possess altered cellular membrane receptors, the response of growth hormone (GH) secretion to ovine corticotrophin-releasing factor (CRF) in cultured adenoma cells of acromegaly was studied. In three out of seven experiments using different pituitary adenoma cells in culture, nanomolar concentrations of CRF caused a significant increase in GH release. The CRF-induced GH release was reproducible and a dose-response relationship was observed between the CRF concentrations and the amounts of GH released into the incubation media. Hydrocortisone, at a concentration of 1 microM, on the other hand, resulted in a significant decrease in GH secretion in four out of five experiments. When adenoma cells were co-incubated with CRF and 1 microM hydrocortisone, CRF-induced GH release was partially overcome. In one experiment, the inhibitory effect of hydrocortisone was reversed by co-incubation with CRF, although CRF alone was ineffective in the stimulation of GH. These results suggest that CRF may stimulate GH release in some, though not all, patients with acromegaly, and that glucocorticoids may block this effect of CRF acting directly on the pituitary adenoma cells of acromegaly.
