Potential conflict of interest: Nothing to report.
Article first published online: 7 JAN 2013
Copyright © 2012 American Association for the Study of Liver Diseases
Volume 57, Issue 1, page 422, January 2013
How to Cite
Petta, S. and Craxì, A. (2013), Reply. Hepatology, 57: 422. doi: 10.1002/hep.25916
- Issue published online: 7 JAN 2013
- Article first published online: 7 JAN 2013
- Accepted manuscript online: 22 JUN 2012 08:45AM EST
- Manuscript Accepted: 13 JUN 2012
- Manuscript Revised: 10 JUN 2012
- Manuscript Received: 4 JUN 2012
We thank Dr. de las Heras and colleagues for their interest in our recent paper.1 We recently found that patients with genotype 1 chronic hepatitis C (CHC) had a higher prevalence of carotid atherosclerosis compared with a control population, and identified older age and the presence of severe hepatic fibrosis as two factors independently associated with the presence of carotid plaques. According to these data, we speculated that the proinflammatory and profibrogenic environment prompting fibrogenesis in the liver of hepatitis C virus (HCV)-infected patients could also be systemically activated, enhancing the development of atherosclerotic lesions and explaining the higher prevalence of carotid plaques in this subgroup of CHC patients. Interestingly, Dr. de las Heras and colleagues suggest that other mechanism(s) could operate to explain the high prevalence of atherosclerotic disease in CHC. Specifically, in experimental studies on rats, they observed that induced long-term prehepatic portal hypertension (PH) led to development of a chronic inflammatory impairment of the abdominal aorta, rather than to the development of steatosis and dyslipidemia, which are potentially also responsible for the atherogenic pathogenic mechanism in the production of an aortic disease related to PH.2, 3 Although these results are interesting, they were obtained in experimental animals, and we were unable to validate them in our patients. In fact, in our study1 we enrolled patients with CHC (only 13 patients had cirrhosis) without significant PH and without data on portal pressure. Prospective studies aimed at evaluating the impact of PH on atherosclerotic lesions in HCV and non–HCV-infected patients with chronic liver diseases may be useful to assess the interesting finding suggested by Dr. de las Heras and colleagues.
- 1Carotid atherosclerosis and chronic hepatitis C: a prospective study of risk associations. HEPATOLOGY 2012; 55: 1317-1323., , , , , , et al.
- 2A wound-like inflammatory aortic response in chronic portal hypertensive rats. Mol Immunol 2012; 51: 177-187., , , , , , et al.
- 3Hepatic lipid metabolism changes in short- and long-term prehepatic portal hypertensive rats. World J Gastroenterol 2006; 12: 6828-6834., , , , , , et al.
Salvatore Petta M.D., Ph.D.*, Antonio Craxì M.D.*, * Section of Gastroenterology, Di.Bi.M.I.S., University of Palermo, Palermo, Italy.