SOMATOSTATIN ANALOG OCTREOTIDE AND INHIBITION OF TUMOR-GROWTH IN METASTATIC ENDOCRINE GASTROENTEROPANCREATIC TUMORS

Citation
R. Arnold et al., SOMATOSTATIN ANALOG OCTREOTIDE AND INHIBITION OF TUMOR-GROWTH IN METASTATIC ENDOCRINE GASTROENTEROPANCREATIC TUMORS, Gut, 38(3), 1996, pp. 430-438
Citations number
46
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
GutACNP
ISSN journal
00175749
Volume
38
Issue
3
Year of publication
1996
Pages
430 - 438
Database
ISI
SICI code
0017-5749(1996)38:3<430:SAOAIO>2.0.ZU;2-6
Abstract
Antiproliferative treatment of patients with metastatic endocrine gast roenteropancreatic tumours (GEP) is based mainly on chemotherapeutic p rotocols whereby drug toxicity is a major handicap. Octreotide is the first choice in the control of hormone mediated symptoms. From retrosp ective and a few prospective studies it has been suggested that octreo tide exhibits antiproliferative properties. The prospective German San dostatin multicentre phase II trial investigated the effects of 200 mu g octreotide thrice daily for one year on tumour growth and endocrine abnormalities in 103 patients. Octreotide treatment was continued in those patients responding to the drug until tumour progression occurre d. In 28 of those with tumour progression during 200 mu g thrice daily octreotide dose was increased to 500 pg thrice daily. The study sampl e consisted of 52 patients with computed tomography confirmed tumour p rogression and 13 patients with stable disease before octreotide treat ment, whereas no preobservation period was available in 38 patients. N ineteen patients (36.5%) with computed tomography confirmed tumour pro gression experienced stabilisation of tumour growth lasting for at lea st three months. Median duration of stable disease was 18 months. At m onth 12, stable disease continued in 12 patients, declined after 24 mo nths to nine patients, and after 36 months to five patients. Tumour re gression has not been seen in this or other subgroups. In the subgroup with stable disease before octreotide, stable disease continued in 53 .8% of patients over 12 months. Increase of octreotide dose to 500 mu g thrice daily did not influence progression seen during the lower dos e with the exception of one patient in whom tumour progression changed to stable disease, No association of tumour size response and patient s' characteristics could be detected. The results suggest that octreot ide inhibits tumour growth in patients with metastasised endocrine GEP tumours. The antiproliferative effect is, at least in some patients, longlasting. Currently, octreotide can only be recommended as an antip roliferative drug if patients with clearly progressive disease show st abilisation after treatment for three to six months.