Dysmetabolic iron overload syndrome.

Over the last few years the genetic basis of Gilbert’s syndrome has been clarified. This issue of the journal contains four papers on this condition. One paper describes a novel molecular mechanism responsible for decreased bilirubin-UDP-glucuronosyltransferase activity, while two articles evaluate the interaction between Gilbert’s syndrome and hematologic disorders associated with increase bilirubin production. Finally, a review article analyzes our present knowledge of the molecular pathogenesis of this condition. Why publish papers on Gilbert’s syndrome in a hematology journal? There are several reasons. First, Haematologica aims to be a journal of hematologic medicine in a broad sense: borderline subjects that may be of interest to our readers are therefore welcome. Second, Gilbert’s syndrome is borderline subject. This condition is characterized by mild unconjugated hyperbilirubinemia in the absence of overt hemolysis or evidence of liver disease. However, several studies have shown that red cell lifespan is shorter than normal in half the cases of Gilbert’s syndrome, suggesting a mild, compensated hemolytic state. Third, being a common condition, Gilbert’s syndrome frequently coexists and may interact with hematologic disorders that involve unconjugated hyperbilirubinemia, per se.