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Jaeckel, E., Cornberg, M., Wedemeyer, H., Santantonio, T., Mayer, J., Zankel, H., Dietrich, M., Trautwein, C. and Manns, M.P. (2001) Treatment of acute hepatitis C with interferon alfa-2b. The New England Journal of Medicine, 345, 1452-1457.
http://dx.doi.org/10.1056/NEJMoa011232

has been cited by the following article:

• TITLE: Hyperhomoysteinemia as a risk factor for coronary heart diseases in chronic hepatitis C patients

  AUTHORS: Ali Raza Kazmi, Andleeb Hanif, Muhammad Ismail, Javaria Qazi

  KEYWORDS: Hepatitis C Virus; Hyperhomocysteinemia (HHC); Coronary Heart Diseases (CHD); Chronic Hepatitis C (CHC)

  JOURNAL NAME: World Journal of Cardiovascular Diseases, Vol.3 No.8, November 18, 2013

  ABSTRACT: Hepatitis C virus is one of the major health problems worldwide. It affects mainly the liver but several extrahepatic manifestations are also accounted. Chronic hepatitis C patients are at an increased risk of developing hepatic steatosis, which share many clinical features with the metabolic syndrome. Hepatic steatosis has also been associated with elevated levels of markers of inflammation such as homocysteine, identified as hyperhomocysteinemia (HHC). HHC due to Methylenetetrahydrofolate Reductase (MTHFR) gene, in particular the C677T polymorphism, was recently associated with coronary heart diseases (CHD) in chronic hepatitis C (CHC) patients. Homocysteine is an intermediate in methionine metabolism, which takes place mainly in the liver metabolism. Deficiencies of micronutrients (folate, vitamin B 6 and possibly vitamin B 12) along with mild hyperhomocysteinemia, perhaps, act synergistically with other classical risk factors to further increase the risk of CHD. Clinical data indicate that HHC is associated with an increased incidence of CHD as well as with the severity of the disease in CHC patients. In conclusion, HHC might be a potential aetiological factor of CHD in CHC patients. The aim of this review is to investigate the progression of coronary heart diseases in chronic hepatitis C patients and correlate with levels of homocysteine in concurrence to genetic defects and nutrient deficiencies. However, future studies need to clarify the mechanistic role of HHC in CHD and CHC as a useful paradigm with most interesting therapeutic implications.