Hypervitaminosis A-induced liver fibrosis: stellate cell activation and daily dose consumption
Article first published online: 22 DEC 2005
Volume 26, Issue 2, pages 182–186, March 2006
How to Cite
Nollevaux, M.-C., Guiot, Y., Horsmans, Y., Leclercq, I., Rahier, J., Geubel, A.P. and Sempoux, C. (2006), Hypervitaminosis A-induced liver fibrosis: stellate cell activation and daily dose consumption. Liver International, 26: 182–186. doi: 10.1111/j.1478-3231.2005.01207.x
- Issue published online: 31 JAN 2006
- Article first published online: 22 DEC 2005
- Received 1 February 2005, accepted 13 September 2005
- hepatic stellate cells;
- hypervitaminosis A;
- liver fibrosis;
- vitamin A
Abstract: Hypervitaminosis A-related liver toxicity may be severe and may even lead to cirrhosis. In the normal liver, vitamin A is stored in hepatic stellate cells (HSC), which are prone to becoming activated and acquiring a myofibroblast-like phenotype, producing large amounts of extracellular matrix.
Aims: In order to assess the relationship between vitamin A intake, HSC activation and fibrosis, we studied nine liver biopsies from patients belonging to a well-characterized series of 41 patients with vitamin A hepatotoxicity.
Methods: Fibrosis was underlined by Sirius-red staining, whereas activated HSC were immunohistochemically identified using an antibody against α smooth muscle actin. The volume density (Vv) of sinusoidal and total fibrosis and of sinusoidal and total activated HSC was quantified by the point-counting method.
Results: Morphology ranged from HSC hypertrophy and hyperplasia as the sole features to severe architectural distortion. There was a significant positive correlation between Vv of perisinusoidal fibrosis and the daily consumption of vitamin A (P=0.004).
Conclusion: The close correlation between the severity of perisinusoidal fibrosis and the daily dose of the retinol intake suggests the existence of a dose–effect relationship.