Pathogenesis of malignant ascites: Starling's law of capillary hemodynamics revisited

Ann Oncol. 2001 Oct;12(10):1353-7. doi: 10.1023/a:1012504904713.

Abstract

Peritonitis carcinomatosa, indicating the presence of malignant cells in the peritoneal cavity, is a well-known complication of malignant disease. As a result, so-called malignant ascites develops. Malignant ascites is a debilitating condition for which no effective anti-tumor therapy is available. Frequent draining may be necessary to relieve pain and discomfort. Most studies regarding malignant ascites focus on diagnosis and treatment. In this paper. we will address the subject from a pathophysiologic perspective, using the characteristics of malignant ascites, Starling's equation of capillary forces, and recent knowledge regarding biologically active peptides produced by tumor cells. Following this approach. apart from decreased lymphatic ascites absorption, increased net capillary fluid-production can be identified as a contributing feature of ascites formation. The increased net filtration is due to an increase of overall capillary membrane-surface, increased capillary permeability and a subsequent increase of intraperitoneal protein concentration leading to increased intraperitoneal oncotic pressure. This sequence might be the result of biologically active peptides produced by tumor cells such as vascular endothelial growth factor and basic fibroblast growth factor. Interference with these mediators may serve as a target in future therapeutic strategies.

Publication types

  • Review

MeSH terms

  • Ascites / physiopathology*
  • Capillary Permeability
  • Endothelial Growth Factors / pharmacology
  • Fibroblast Growth Factor 2 / pharmacology
  • Filtration
  • Hemodynamics
  • Humans
  • Lymphokines / pharmacology
  • Models, Biological*
  • Neoplasm Metastasis
  • Neoplasms / physiopathology
  • Neovascularization, Pathologic*
  • Regional Blood Flow
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors

Substances

  • Endothelial Growth Factors
  • Lymphokines
  • Vascular Endothelial Growth Factor A
  • Vascular Endothelial Growth Factors
  • Fibroblast Growth Factor 2