Case Report

Over-expression of glutamine synthase in focal nodular hyperplasia (part 1): Early stages in the formation support the hypothesis of a focal hyper-arterialisation with venous (portal and hepatic) and biliary damage

Paulette Bioulac-Sage^1,2 , Hervé Laumonier³ , Gaëlle Cubel² , Jean Saric⁴ and Charles Balabaud^2,4

¹  Service d'Anatomie Pathologique Hôpital Pellegrin, CHU Bordeaux, France

²  GREF Inserm U889, Université Bordeaux 2, France

³  Service de Radiologie, Hôpital Saint André, CHU Bordeaux, France

⁴  Pôle HGE, Hôpital Saint André, CHU Bordeaux, France

author email corresponding author email

Comparative Hepatology 2008, 7:2doi:10.1186/1476-5926-7-2

Published:	29 February 2008

Abstract

Background

Most focal nodular hyperplasia (FNH) cases are diagnosed by chance. We studied a case of pre-FNH. We used glutamine synthase as an immunohistochemical marker for perivenous zones.

Results

Neither fibrotic scars nor hepatocytic nodules surrounded by fibrosis with a ductular reaction were observed in the sections studied. Most sections generally displayed preserved architecture. The glutamine synthase-positive hepatocyte areas were wider than those observed in non-tumoural surrounding liver, and they tended to extend outwards. Portal tracts bordering the nodule were more fibrotic, with an absence of portal veins and ducts and with arterial proliferation often in proximity with large draining veins; isolated arteries were present and hepatic veins were rare in the nodule. These features appeared prior to the identification of other major criteria characteristics of FNH, thus supporting the "hypothesis of Wanless".

Conclusion

The findings confirm that in FNH there is a portal tract injury leading to local portal vein injury. This leads to a cascade of events, including arterial venous shunts, ductular reaction, and scar formation.