BACKGROUND/ PURPOSE: Mesenchymal hamartoma (MH) of the liver is thought to develop from the ductal plates of the prenatal liver. This immunohistochemical study was performed to gain insight into the pathophysiology of its development. METHODS: Specimens from four MHs with adjacent liver, in one case from a biopsy and from the resected lesion after 6 years follow-up, were investigated with immunostaining on cryostatsectionswith antibodies against cytokeratins, vimentin, desmin and alpha-actin, as well as von Willebrand factor (factor VIII), fibroblast growth factor (FGF) receptors, FGF-1 (acidic FGF), FGF-2 (basic FGF), and the proliferation-associated Ki67 antigen. RESULTS: Fibrous tissue of MH stained positive not only for vimentin, but also for desmin and alpha-actin, whereas cytokeratins and factor VIII showed specific staining in biliary cysts and endothelial cells, respectively. All mesenchymal cells expressed proteins of the FGF receptor family. Although FGF-1 was only scarcely detectable, there was an accumulation of FGF-2 in borderline areas of liver to MH. Multiple Ki67-positive mesenchymal cells could be identified in these regions in all three MHs. However, we could not detect any proliferative activity in the MHs after follow-up. CONCLUSIONS: The proliferative process in MH is still active during early childhood. FGF-2 may have a role in promoting this process. The positivity for desmin and alpha-actin of the lesions suggests that fat-storing (Ito) cells of the immature liver may be involved in the development of MH.
BACKGROUND/ PURPOSE: Mesenchymal hamartoma (MH) of the liver is thought to develop from the ductal plates of the prenatal liver. This immunohistochemical study was performed to gain insight into the pathophysiology of its development. METHODS: Specimens from four MHs with adjacent liver, in one case from a biopsy and from the resected lesion after 6 years follow-up, were investigated with immunostaining on cryostatsectionswith antibodies against cytokeratins, vimentin, desmin and alpha-actin, as well as von Willebrand factor (factor VIII), fibroblast growth factor (FGF) receptors, FGF-1 (acidic FGF), FGF-2 (basic FGF), and the proliferation-associated Ki67 antigen. RESULTS: Fibrous tissue of MH stained positive not only for vimentin, but also for desmin and alpha-actin, whereas cytokeratins and factor VIII showed specific staining in biliary cysts and endothelial cells, respectively. All mesenchymal cells expressed proteins of the FGF receptor family. Although FGF-1 was only scarcely detectable, there was an accumulation of FGF-2 in borderline areas of liver to MH. Multiple Ki67-positive mesenchymal cells could be identified in these regions in all three MHs. However, we could not detect any proliferative activity in the MHs after follow-up. CONCLUSIONS: The proliferative process in MH is still active during early childhood. FGF-2 may have a role in promoting this process. The positivity for desmin and alpha-actin of the lesions suggests that fat-storing (Ito) cells of the immature liver may be involved in the development of MH.
Authors: Anand Pandey; Ajay N Gangopadhyay; Shiv P Sharma; Vijayendra Kumar; Dinesh K Gupta; Saroj C Gopal; Shashikant C Patne Journal: Saudi J Gastroenterol Date: 2011 Jan-Feb Impact factor: 2.485
Authors: Jan Scheele; Johannes Lemke; Thomas F E Barth; Markus Juchems; Mathias Wittau; Marko Kornmann; Doris Henne-Bruns Journal: GMS Interdiscip Plast Reconstr Surg DGPW Date: 2014-12-17