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Bilirubin levels in the acute hemolytic crisis of G6PD deficiency are related to Gilbert's syndrome
Author(s) -
Iolascon Achille,
Faienza Maria Felicia,
Giordani Lucia,
Perrαtta Silverio,
Ruggiu Giuseppina,
Meloni Gian Franco,
Giudice Emanuele Miraglia
Publication year - 1999
Publication title -
european journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0902-4441
DOI - 10.1111/j.1600-0609.1999.tb01907.x
Subject(s) - bilirubin , unconjugated hyperbilirubinemia , hemolytic anemia , medicine , polymorphism (computer science) , hemoglobin , gastroenterology , biology , endocrinology , genetics , gene , genotype
In this study we analyzed the effect of the (TA)7 polymorphism of the UGT1A gene associated with Gilbert's syndrome in G6PD‐deficient subjects during an acute hemolytic crisis (tabic crisis). DNA from 44 subjects originating from the same geographic area in Sardinia was analyzed for the UGT1A promoter polymorphism. The increase of unconjugated bilirubin level during fabic crisis and its relationship with UGT1A polymorphism was evaluated. The UGT1A (TA)7 TATA box variant was found in 9/44 (21%) of the G6PD deficient subjects examined. The median value for unit of increase of bilirubin (mg/dl)/unit of decrease of hemoglobin (g/dl) was higher in variant homozygous than in heterozygous and normal subjects. These findings imply a contribution of the UGT1A polymorphism associated to Gilbert's syndrome to development of the hyperbilirubinemia in G6PD deficient subjects during acute hemolytic anemia.