Influence of Sorafenib and Bevacizumab on pancreatic volume – A monocentric CT based analysis

Veit Phillip, Tina Zahel, Klaus Bärtl, Sebastian Rasch, Oliver Ebert, Roland M. Schmid, Ernst Rummeny, Hana Algül

Publikation: Beitrag in FachzeitschriftArtikelBegutachtung

9 Zitate (Scopus)

Abstract

Background/Objectives Angiogenesis plays a central role in tumor growth and metastasis and tyrosine kinases are crucial in the modulation of growth factor signaling. Several side effects of tyrosine kinase inhibitors have been reported, including diarrhea due to pancreatic insufficiency. The suspected mechanism is the anti-angiogenetic effect of the inhibited vascular endothelial growth factor (VEGF) causing a disturbance of the microvasculation. The aim of the present study was to determine the volume of the pancreas before and after a therapy both with the multi-tyrosine kinase inhibitor Sorafenib and Bevacizumab, which is a humanized monoclonal immunoglobulin G1 antibody against VEGF. Methods Retrospective monocentric study including 42 patients who received either Sorafenib, Bevacizumab combined with Flourouracil and/or Irinotecan, or singly Flourouracil and Irinotecan for different non-pancreatic malignancies. The volume of the pancreas was measured before and after therapy by CT-scan based volumetry. Results The pancreatic volume was statistically significantly lower after treatment with Sorafenib (75.4 mL vs. 71.0 mL; p = 0.006) or Bevacizumab and Fluorouracil ± Irinotecan (71.8 mL vs. 62.6 mL; p = 0.020). The pancreatic volume did not change statistically significantly after treatment with Fluorouracil ± Irinotecan only (51.1 mL vs. 49.9 mL; p = 0.142). Conclusions Pancreatic volume decreases statistically significantly under treatment with both the multi-tyrosine kinase inhibitor Sorafenib and the angiogenesis inhibitor Bevacizumab. This volume reduction is most likely due to a reduced microvasculation by inhibition of VEGF.

OriginalspracheEnglisch
Seiten (von - bis)621-624
Seitenumfang4
FachzeitschriftPancreatology
Jahrgang16
Ausgabenummer4
DOIs
PublikationsstatusVeröffentlicht - 1 Juli 2016
Extern publiziertJa

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