Showing papers by "Frédéric Charlotte published in 2008"
TL;DR: In patients with NASH, rosiglitazone improves steatosis and transaminase levels despite weight gain, an effect related to an improvement in insulin sensitivity, however, there is no improvement in other parameters of liver injury.
554 citations
TL;DR: To the editor: Erdheim-Chester disease (ECD) is a non-Langerhans form of CD68+ CD1a− histiocytosis and Interferon α (IFNα) is effective in ECD.
78 citations
TL;DR: A new definition of inactive carriers was proposed with an algorithm combining “zero” scores for FT-AT (F0 and A0) and viral load classes, which accurately defined the prognosis and the inactive carrier status.
Abstract: Background
The combination of transaminases (ALT), biopsy, HBeAg and viral load have classically defined the inactive status of carriers of chronic hepatitis B. The use of FibroTest (FT) and ActiTest (AT), biomarkers of fibrosis and necroinflammatory activity, has been previously validated as alternatives to biopsy. We compared the 4-year prognostic value of combining FT-AT and viral load for a better definition of the inactive carrier status.
74 citations
TL;DR: In this paper, the authors reported four patients from a same family with ferroportin disease associated with the N144H mutation and showed that in this family the mutation which is fully penetrant, may act through an increased iron export from macrophages as suggested by the unexpected absence of iron overload in the spleen and bone marrow detected by magnetic resonance imaging.
Abstract: Summary Ferroportin is a putative transmembrane channel involved in the exit of iron out of the enterocytes, the macrophages and the hepatocytes. Mutations in the human gene coding ferroportin have been linked to an unusual form of iron overload, now referred to as “hemochromatosis type IV” or “ferroportin disease” characterized by a prevalent iron overload of macrophages and liver Kupffer cells. We report four patients from a same family with ferroportin disease associated with the N144H mutation. We show that in this family the mutation which is fully penetrant, may act through an increased iron export from macrophages as suggested by the unexpected absence of iron overload in the spleen and bone marrow detected by magnetic resonance imaging, that it co-segregates with a phenotype close to the classical form of HFE-associated hemochromatosis and was associated, in the oldest patient, with the development of hepatocellular carcinoma in a non cirrhotic liver. Our findings illustrate the existence of a genotype-phenotype relationship in “ferroportin disease”, suggest that MRI may be useful in determining this phenotype and show that hepatocellular carcinoma may occur in these patients even without cirrhosis. This observation justifies careful follow-up of this subgroup of patients.
14 citations
3 citations