Abstract

e13543 Background: Tryptase is a serin protease stored in mast cell granules that plays a role in tumour angiogenesis. Data from experimental tumour models suggest that mast cells accumulate near tumour cells before the onset of angiogenesis and that they are required for the macroscopic expansion and metastatic spread of primary tumour cells. Hepatocellular cancer (HCC) is a well-established hypervascular tumour. This preliminary study aims to assess tryptase serum levels in 30 HCC patients before and after hepatic trans-arterial chemoambolization (TACE). Methods: In this study patients with intermediate stage (B) HCC (according to BCLC staging system) and adequate liver functional reserve (A or B status according Child-Pugh classification) were enrolled. Samples of blood were taken from HCC patients between 7 and 9 a.m.1 day before and 1 day after TACE. Venous blood was dispensed into a tube for serum (Becton Dickinson Hemogard Vacutainer Systems, Plymouth, UK). Serum blood samples were centrifuged at 1,500g for 10 minutes and then aliquoted and frozen at -80 °C. Tryptase levels were measured using the UniCAP Tryptase Fluoroenzymeimmunoassay (Pharmacia,Uppsala, Sweden). TACE was performed using doxorubicin loaded on microspheres (Dc-Bead; Biocompatibles, Farnham [GB]). Results: Mean ± s.d. tryptase level pre-TACE was 7.74 ± 3.62 μg/L, and mean ± s.d. tryptase level post TACE was 4.67 ± 2.79 μg/L. A statistically significant difference between pre-TACE and post-TACE tryptase level concentrations was found: p=0.000 by t-test. No correlation among tryptase levels and other important clinical-pathological features of patients were found. Conclusions: This is the first preliminary report that analyzes the possible significance of serum tryptase levels in HCC patients. Tryptase is one of the most powerful angiogenic mediators released by mast cells and it may be angiogenic via several mechanisms. On the other hand HCC is an hypervascular tumour. Our results demonstrated higher serum tryptase levels in HCC patients suggesting the release of tryptase from HCC tissue. As expected, after TACE, serum tryptase levels had decreased. We suggest that tryptase may play a role as a biomarker of response to TACE treatment in HCC patients.

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