We acknowledge the appreciation and comments by Drs. Amedeo Lonardo and Paola Loria. In our review, the metabolic syndrome (MS) represents hepatitis C virus (HCV)-related insulin resistance (IR) and its clinical consequences, with IR being a common denominator.1 The intensity of IR and its consequences vary based on underlying cause(s) and the body's ability to compensate for IR.2 Although all HCV patients may not manifest the typical phenotype of MS, they have significant potential of developing these features due to similar underlying pathophysiology.1 MS has also been recently described in 26% of patients with HCV.3 It is also known that there is considerable interplay of both viral and host factors in accelerating the natural course of disease in HCV.4 It is therefore difficult to isolate pathogenic mechanisms induced by the virus from any coexisting additional insult(s). It seems premature to limit the spectrum of HCV-induced MS by labeling it as “dysmetabolic syndrome”.
The causes of mortality in patients with HCV are variable. It ranges from liver-related mortality to those attributable to drug, alcohol, trauma, suicide, and cardiovascular mortality.5 Moreover, onset of portal hypertension and decompensated cirrhosis can alter several clinical features of MS syndrome. On the other hand, there is presently a lot of controversy about the utility of MS to predict cardiovascular risk in an individual.6, 7 The role of IR in HCV is a relatively new subject, and more studies are needed in order to clearly delineate the effect it has on the natural history of the disease process. The difficulty lies in the complex natural history of chronic liver disease and unraveling the effects of specific factors that may alter its course over the lifespan of an individual.