572 ASSOCIATION BETWEEN SOMATOSTATIN ANALOGUE TREATMENT AND DIABETES MELLITUS IN GI NEUROENDOCRINE TUMOR PATIENTS: A STUDY OF 4,664 SEER-MEDICARE DATABASE PATIENTS

2020 ◽  
Vol 158 (6) ◽  
pp. S-119-S-120
Author(s):  
Katherine Ni ◽  
Kiwoon Joshua Baeg ◽  
Juan P. Wisnivesky ◽  
Michelle Kim
Keyword(s):  
Diabetes Mellitus ◽  
Neuroendocrine Tumor ◽  
Somatostatin Analogue ◽  
Tumor Patients ◽  
Medicare Database

scholarly journals Can an amino acid mixture alleviate gastrointestinal symptoms in neuroendocrine tumor patients?

BMC Cancer ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Aman Chauhan ◽  
Satya Das ◽  
Rachel Miller ◽  
Laura Luque ◽  
Samuel N. Cheuvront ◽  
...  
Keyword(s):  
Amino Acid ◽  
Neuroendocrine Tumor ◽  
Gastrointestinal Symptoms ◽  
Retrospective Chart Review ◽  
Final Analysis ◽  
Acid Mixture ◽  
Tumor Patients ◽  
Short Gut Syndrome ◽  
Oral Rehydration ◽  
The Mean

Abstract Background Neuroendocrine tumors, although relatively rare in incidence, are now the second most prevalent gastrointestinal neoplasm owing to indolent disease biology. A small but significant sub-group of neuroendocrine tumor patients suffer from diarrhea. This is usually secondary to carcinoid syndrome but can also be a result of short gut syndrome, bile acid excess or iatrogenic etiologies. Recently, an amino acid based oral rehydration solution (enterade® Advanced Oncology Formula) was found to have anti-diarrheal properties in preclinical models. Methods A retrospective chart review of all NET patients treated with enterade® AO was performed after IRB approval. Results Ninety-eight NET patients who had received enterade® AO at our clinic from May 2017 through June 2019 were included. Patients (N = 49 of 98) with follow up data on bowel movements (BMs) were included for final analysis. Eighty-four percent of patients (41/49) had fewer BMs after taking enterade® AO and 66% (27/41) reported more than 50% reduction in BM frequency. The mean number of daily BMs was 6.6 (range, 3–20) at baseline before initiation of therapy, while the mean number of BMs at 1 week time point post enterade® AO was 2.9 (range, 0–11). Conclusions Our retrospective observations are encouraging and support prospective validation with appropriate controls in NET patients. This is first published report of the potential anti-diarrheal activity of enterade® AO in NET patients.

Endogenous hyperglycemia restores insulin release impaired by somatostatin analogue

1981 ◽  
Vol 240 (4) ◽  
pp. E407-E413
Author(s):  
G. J. Taborsky ◽  
D. Porte
Keyword(s):  
Diabetes Mellitus ◽  
Insulin Release ◽  
Beta Cell Function ◽  
Cell Function ◽  
Dependent Diabetes Mellitus ◽  
Somatostatin Analogue ◽  
Base Line ◽  
Glucagon Release ◽  
Insulin Deficiency ◽  
Insulin Responses

These studies assessed the ability of des-Asn5-[D-Trp8-D-Ser13]-somatostatin (d-ATS-SS) to selectively inhibit insulin release and produce a hyperglycemia sufficient to compensate for the original impairment. d-ATS-SS at 0.017 micrograms/min inhibited basal insulin output (delta = -38 +/- 6%, P less than 0.005) and increased basal pancreatic glucagon output (delta - +21 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.17 micrograms/min markedly inhibited insulin output (delta = -84 +/- 4%, P less than 0.0005) and slightly inhibited glucagon output (delta = -14 +/- 6%, P less than 0.05, n = 5). d-ATS-SS at 0.055 micrograms/min decreased basal and stimulated insulin release but not basal nor stimulated glucagon release. By 3.5 of analogue infusion, plasma glucose had risen by 116 +/- 13 mg/dl, and base-line insulin levels and the insulin responses to both isoproterenol and arginine, but not glucose, increased toward control values. We conclude that d-ATS-SS produces selective insulinopenia resulting in hyperglycemia which in turn compensates for the original impairment. Thus, the hyperglycemia observed in other states of selective insulin deficiency (e.g., noninsulin-dependent diabetes mellitus) may compensate for defects in beta-cell function.

scholarly journals Inflammation-Based Index and 68Ga-DOTATOC PET–Derived Uptake and Volumetric Parameters Predict Outcome in Neuroendocrine Tumor Patients Treated with 90Y-DOTATOC

2019 ◽  
Vol 61 (7) ◽  
pp. 1014-1020 ◽  
Author(s):  
Elin Pauwels ◽  
Sofie Van Binnebeek ◽  
Vincent Vandecaveye ◽  
Kristof Baete ◽  
Hubert Vanbilloen ◽  
...  
Keyword(s):  
Neuroendocrine Tumor ◽  
Tumor Patients

scholarly journals Management of Small Bowel Neuroendocrine Tumors

Cancers ◽  
2019 ◽  
Vol 11 (9) ◽  
pp. 1395 ◽  
Author(s):  
Larouche ◽  
Akirov ◽  
Alshehri ◽  
Ezzat
Keyword(s):  
Small Bowel ◽  
Neuroendocrine Tumor ◽  
Neuroendocrine Tumors ◽  
Management Strategies ◽  
Mammalian Target Of Rapamycin ◽  
Peptide Receptor Radionuclide Therapy ◽  
Somatostatin Analogue ◽  
Important Landmark ◽  
Cancer Network ◽  
Compare And Contrast

Several important landmark trials have reshaped the landscape of non-surgical management of small bowel neuroendocrine tumors over the last few years, with the confirmation of the antitumor effect of somatostatin analogue therapy in PROMID and CLARINET trials as well as the advent of therapies with significant potential such as mammalian target of rapamycin inhibitor (mTor) everolimus (RADIANT trials) and peptide receptor radionuclide therapy (PRRT) with 177-Lutetium (NETTER-1 trial). This narrative summarizes the recommended management strategies of small bowel neuroendocrine tumors. We review the main evidence behind each recommendation as well as compare and contrast four major guidelines, namely the 2016 Canadian Consensus guidelines, the 2017 North American Neuroendocrine Tumor Society guidelines, the 2018 National Comprehensive Cancer Network guidelines, and the 2016 European Neuroendocrine Tumor Society guidelines. Different clinical situations will be addressed, from loco-regional therapy to metastatic unresectable disease. Carcinoid syndrome, which is mostly managed by somatostatin analogue therapy and the serotonin antagonist telotristat etiprate for refractory diarrhea, as well as neuroendocrine carcinoma will be reviewed. However, several questions remain unanswered, such as the optimal management of neuroendocrine carcinomas or the effect of combining and sequencing of the aforementioned modalities where more randomized controlled trials are needed.

Activity of Sunitinib in Patients With Advanced Neuroendocrine Tumors

2008 ◽  
Vol 26 (20) ◽  
pp. 3403-3410 ◽  
Author(s):  
Matthew H. Kulke ◽  
Heinz-Josef Lenz ◽  
Neal J. Meropol ◽  
James Posey ◽  
David P. Ryan ◽  
...  
Keyword(s):  
Growth Factor ◽  
Tyrosine Kinase ◽  
Neuroendocrine Tumor ◽  
Neuroendocrine Tumors ◽  
Objective Response ◽  
Pancreatic Neuroendocrine Tumor ◽  
Endocrine Tumor ◽  
Pancreatic Endocrine Tumor ◽  
Tumor Patients ◽  
Patient Reported

Purpose Standard cytotoxic chemotherapy has limited efficacy in metastatic neuroendocrine tumor patients. Neuroendocrine tumors express vascular endothelial growth factor (VEGF) and its receptor (VEGFR). Sunitinib malate, an oral tyrosine kinase inhibitor, has activity against VEGFRs as well as platelet-derived growth factor receptors, stem-cell factor receptor, glial cell line–derived neurotrophic factor, and FMS-like tyrosine kinase-3. We evaluated the efficacy of sunitinib in a two-cohort, phase II study of advanced carcinoid and pancreatic neuroendocrine tumor patients. Patients and Methods Patients were treated with repeated 6-week cycles of oral sunitinib (50 mg/d for 4 weeks, followed by 2 weeks off treatment). Patients were observed for response, survival, and adverse events. Patient-reported outcomes were assessed. Results Among 109 enrolled patients, 107 received sunitinib (carcinoid, n = 41; pancreatic endocrine tumor, n = 66). Overall objective response rate (ORR) in pancreatic endocrine tumor patients was 16.7% (11 of 66 patients), and 68% (45 of 66 patients) had stable disease (SD). Among carcinoid patients, ORR was 2.4% (one of 41 patients), and 83% (34 of 41 patients) had SD. Median time to tumor progression was 7.7 months in pancreatic neuroendocrine tumor patients and 10.2 months in carcinoid patients. One-year survival rate was 81.1% in pancreatic neuroendocrine tumor patients and 83.4% in carcinoid patients. No significant differences from baseline in patient-reported quality of life or fatigue were observed during treatment. Conclusion Sunitinib has antitumor activity in pancreatic neuroendocrine tumors; its activity against carcinoid tumors could not be definitively determined in this nonrandomized study. Randomized trials of sunitinib in patients with neuroendocrine tumors are warranted.

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