Gut doi:10.1136/gutjnl-2013-306102
Leading article
Salvatore Petta, Fabio Salvatore Macaluso, Antonio Craxì
+ Author Affiliations
Correspondence to
Dr S Petta, Gastroenterologia and Epatologia, Piazza delle Cliniche 2, Palermo 90127, Italy;
petsa@inwind.it
Received 17 September 2013
Revised 14 November 2013
Accepted 17 November 2013
Published Online First 2 December 2013
Introduction
HCV infection, metabolic disorders and cardiovascular alterations, considered alone or in combination, are common conditions in a large proportion of the general population. Consequently, determining whether the association of HCV infection with cardiometabolic disorders is simply coincidental or, conversely, caused by pathogenetic mechanisms (in)directly linking chronic HCV infection to these disorders, would be of extreme relevance.
Several clinical studies have shown that metabolic disorders—namely, type 2 diabetes,1insulin resistance (IR)2 and hepatic steatosis3—are highly prevalent in patients with chronic hepatitis C (CHC) compared with non-infected patients. Experimental and clinical studies have shown that HCV is able to directly influence glucose and lipid metabolism and thus can perturb the metabolic homeostasis of the host, leading to extrahepatic consequences.4 ,5 However, unlike the classic forms of metabolic disturbances, CHC is associated with a favourable lipoprotein profile—that is, reduced levels of apolipoprotein B containing lipoproteins, such as low density lipoprotein and very low density lipoprotein cholesterol.6
The discordance between the increased prevalence of IR, steatosis and diabetes, and the favourable lipoprotein profile in CHC compared with non-infected individuals, may account for the similar prevalence of metabolic syndrome (ie, the presence of at least three of the following: visceral obesity, hyperglycaemia, arterial hypertension, low levels of high density lipoprotein cholesterol and high triglycerides levels)7 reported in data from the database of the third National Health and Nutrition Examination Survey (NHANES-III).8
These data raise the question of whether HCV infection per se and/or via induction of metabolic/inflammatory dysfunctions is associated with an increased cardiovascular risk.
With this in mind, cross sectional and prospective studies have evaluated the presence and occurrence of both cardiovascular alterations and cardiovascular mortality in HCV infected patients compared with non-infected patients, with contrasting results.6 ,9–34
This review was prompted by …
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