HIV/Hepatitis C Virus-Coinfected Patients: Is There a Better Marker for Atherogenicity?

E ditor: We read with great interest the recent article by Kakinami et al. ¹ on the magnitude of change in the total cholesterol (TC)/high-density lipoprotein cholesterol (HDL) ratio after initiation of highly active antiretroviral therapy (HAART) in HIV patients and HIV/hepatitis C (HCV) coinfected patients. The authors have comprehensively discussed important results in this increasing cohort of HIV/HCV coinfected patients. We would like to add some comments.

In this interesting study, though the TC and HDL levels increased in both the HIV monoinfected and HIV/HCV coinfected population after HAART initiation, the TC/HDL ratio did not change significantly. In addition, the magnitude of change in the TC/HDL ratio was statistically similar between the two groups. The TC/HDL ratio is well-established as a risk factor for cardiovascular disease. ² Given the similar magnitude of change in both the groups, the authors concluded that the risk of atherosclerotic disease following HAART initiation might be equally high in coinfected patients as well, contrary to the results from previous studies. ³

Multiple clinical and animal studies have shown that HCV patients are at increased risk of both diabetes mellitus (DM) and insulin resistance (IR). ^4,5 Triglycerides (TG) and the TG/HDL ratio are closely related to IR and have been used as surrogate markers of IR in previous studies. ⁶ It would be worthwhile to evaluate on similar lines the changes in TG level and TG/HDL ratio in this cohort. The strong association between HCV and IR raises the possibility that the TG/HDL ratio might be a better marker than the TC/HDL ratio to assess atherogenicity in HCV patients.

Due to the increased risk of DM in HCV, it is possible that patients with HIV/HCV coinfection have a poor atherogenic profile compared to HIV monoinfected patients. In this study, as expected, there is a significantly higher prevalence of hyperglycemia in HIC/HCV coinfected patients. However, DM was not included as a significant risk factor in the multivariate linear analysis. Similarly, smoking, a known risk factor for metabolic syndrome, was not included in the adjusted analysis. It would be interesting to know if the results change after adjusting for these additional confounders.

This article underscores the need for further research on atherogenic risk in HIV/HCV coinfected patients, as the risk might be greater than currently appreciated. Further analyses in the same cohort by including the TG and TG/HDL ratio could add more strength to the results.