Abstract
Chronic infection with the hepatitis C virus (HCV) affects 170 million people worldwide and is an important cause of liver-related morbidity and mortality. The standard of care therapy combines pegylated interferon (pegIFN) alpha and ribavirin (RBV), and is associated with a range of treatment-limiting adverse effects. One of the most important of these is RBV-induced haemolytic anaemia, which affects most patients and is severe enough to require dose modification in up to 15% of patients. Here we show that genetic variants leading to inosine triphosphatase deficiency, a condition not thought to be clinically important, protect against haemolytic anaemia in hepatitis-C-infected patients receiving RBV.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Alleles
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Anemia, Hemolytic / chemically induced*
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Anemia, Hemolytic / complications
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Anemia, Hemolytic / genetics*
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Antiviral Agents
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Chromosomes, Human, Pair 20
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Europe / ethnology
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Genetic Variation / genetics*
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Genome-Wide Association Study
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Hemoglobins / deficiency
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Hemoglobins / metabolism
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Hepatitis C, Chronic / complications
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Hepatitis C, Chronic / drug therapy*
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Humans
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Inosine Triphosphatase
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Polymorphism, Single Nucleotide / genetics
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Pyrophosphatases / deficiency
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Pyrophosphatases / genetics*
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Pyrophosphatases / metabolism
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Racial Groups / genetics
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Ribavirin / therapeutic use
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United States
Substances
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Antiviral Agents
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Hemoglobins
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Ribavirin
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Pyrophosphatases
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ITPA protein, human