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

Veit Phillip1, Tina Zahel2, Klaus Bärtl3

  • 1II. Medizinische Klinik und Poliklinik, Klinikum rechts der Isar der Technischen Universität München, Ismaninger Straße 22, 81675 München, Germany.

Abstract

Insights

Pancreatic volume significantly decreased after treatment with Sorafenib and Bevacizumab, likely due to reduced microvasculation from inhibiting vascular endothelial growth factor (VEGF). This finding may explain side effects like diarrhea.

Area of Science:

  • Oncology
  • Vascular Biology
  • Pharmacology

Background:

  • Angiogenesis is vital for tumor growth and metastasis.
  • Tyrosine kinases regulate growth factor signaling, and their inhibitors can cause side effects like diarrhea.
  • Pancreatic insufficiency may result from anti-angiogenic effects on pancreatic microvasculation.

Purpose of the Study:

  • To assess changes in pancreatic volume following treatment with Sorafenib and Bevacizumab.
  • To investigate the relationship between anti-angiogenic therapies and pancreatic volume reduction.

Main Methods:

  • Retrospective monocentric study of 42 patients with non-pancreatic malignancies.
  • Patients received Sorafenib, Bevacizumab with chemotherapy, or chemotherapy alone.
  • Pancreatic volume was measured using CT-scan volumetry before and after treatment.

Main Results:

  • Pancreatic volume significantly decreased after Sorafenib treatment (75.4 mL to 71.0 mL, p=0.006).
  • Pancreatic volume significantly decreased after Bevacizumab and Fluorouracil ± Irinotecan treatment (71.8 mL to 62.6 mL, p=0.020).
  • No significant change in pancreatic volume was observed with Fluorouracil ± Irinotecan alone (51.1 mL to 49.9 mL, p=0.142).

Conclusions:

  • Both Sorafenib and Bevacizumab treatments led to a statistically significant reduction in pancreatic volume.
  • This volume reduction is likely attributed to decreased pancreatic microvasculation caused by VEGF inhibition.
  • The findings suggest a potential mechanism for treatment-related pancreatic side effects.

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