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Logo of bumcprocBaylor University Medical Center ProceedingsAbout the JournalBaylor Health Care SystemSubmit a Manuscript
Proc (Bayl Univ Med Cent). 2010 April; 23(2): 111–113.
PMCID: PMC2848083

Is statin therapy safe in patients with HIV/hepatitis C coinfection?

Jeffrey S. Stroup, PharmD, BCPScorresponding author and Bryan Harris, DO


Statins are effective therapy for hypercholesterolemia and are commonly indicated in patients with HIV and hepatitis C virus infections. Unfortunately, in patients coinfected with these viruses, the safety of statins has not been conclusively evaluated. We retrospectively evaluated five coinfected patients in our outpatient clinic who received statin therapy. Although the sample size was small, we found that statins were safe in this population and recommend that further evaluation with a prospective controlled trial be undertaken to definitively answer this safety issue.

In the United States, as of 2003, approximately 1.2 million people were living with HIV or AIDS (1). HIV, the virus that causes AIDS, is a retrovirus that can be spread through exposure to blood, semen, or vaginal fluid. Hepatitis C virus (HCV) is a single-strand RNA that infects liver cells. Currently, HCV infection is the leading cause of death due to liver disease in the US (2). HCV is transmitted primarily through blood exposure. In the US, approximately 3.2 million people are chronically infected with HCV (3). HIV and HCV coinfection is becoming more prevalent. In fact, worldwide, approximately 20% to 25% of all HIV-infected patients also have HCV infection (4). In the US, data published in 2002 estimate this coinfection rate at 16.1% (5). This is a concern because coinfected patients progress to cirrhosis faster that those with HCV infection alone (4, 6). It is also a concern because coinfection may complicate the delivery of effective HIV treatments in the setting of active liver disease (7).

Cholesterol-lowering drugs such as the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) have become a valuable tool to manage patients with cardiovascular disease because of their ability to decrease low-density lipoprotein (LDL) cholesterol, stabilize plaque, decrease inflammatory markers, and decrease mortality in patients with and without established vascular disease (8). In patients with HIV infection, dyslipidemia is prevalent due to the effects of highly active antiretroviral therapies (HAART) that may be utilized (9). In HIV patients, treatment of LDL is complicated by the interactions of statins with HAART, and some studies have shown that atorvastatin and pravastatin may be used with ritonavir and saquinavir, but that simvastatin should be avoided (10). Recent data have also been published that support the safety and efficacy of rosuvastatin and fluvastatin in patients with HIV infection on HAART therapy (11, 12). Statins have also been shown to have activity against HCV (2, 1315). In fact, some statins appear to have greater anti-HCV activity than others (14).

Statin use in the setting of active liver disease is a common concern of health care professionals. Some studies have demonstrated no significant short-term change in hepatic enzymes when statins are administered to HCV-infected patients (13, 1618). In other clinical scenarios, such as fatty liver disease, exposure to statin therapy has also not been demonstrated to affect the hepatic enzymes (19). One small study to date has evaluated statin use in the HIV/HCV-coinfected population and has shown no significant change in hepatic enzymes (20). The primary purpose of this study was to evaluate the safety of statin therapy in coinfected HIV/HCV patients.


This was a retrospective study in an outpatient HIV specialty clinic. To be included in the analysis, patients had to be seen in the clinic between January 1, 2007, and December 31, 2007, be HIV positive, be HCV positive, and be >18 years of age. Patients with acute hepatitis, active alcohol use, and hepatitis B coinfection were excluded.

After approval from the Oklahoma State University institutional review board, a data collection form was utilized to collect baseline data, including patient demographic data (sex, race, age, weight, and height), social history (tobacco and alcohol), concomitant disease states, and current medication use. HIV duration, HIV risk factors, HCV duration, and HCV genotype were also documented when available. Laboratory data—including albumin, alkaline phosphatase, aminotransferases, bilirubin, complete blood count, CD4 T-cell count, HCV RNA, HIV RNA, lipid profile, prothrombin time, serum creatinine, and Child-Pugh score—were collected at baseline and at follow-up time intervals. The specific statin used and the dosage were also recorded.


Of the 745 HIV-positive patients who were active clinic patients, 60 were coinfected with HCV. Ten of these patients were excluded because of active hepatitis B coinfection, 5 were excluded because of active alcoholism, and 40 were excluded because of lack of exposure to statin therapy. Of the 60 coinfected patients, only 5 received statin therapy.

The average age of the patients with HIV/HCV coinfection on statin therapy was 47.8 years. The average duration of infection was 5.2 years for HIV and 2.8 years for HCV. Of the five patients, four were men and one was a woman. In addition, four patients were Caucasian and one was African American. Two of the patients had received interferon and ribavirin therapy, and all of the patients were on HAART. Four of the patients had undetectable HIV viral loads, and the average CD4 cell count of the five patients was 389.4 cells/[multimap]L. The baseline and follow-up safety of statin therapy is presented in the Table. The average follow-up time in this population was 8 months (range, 4–15 months).

Safety of statins in five patients coinfected with HIV and hepatitis C


The safety of statin therapy has been documented in patients with HCV infection (13, 16, 17). Our experience with statin therapy in patients with HIV/HCV coinfection is limited but suggests that this therapy is safe in this population. This observation is consistent with a previously published retrospective analysis that assessed the safety of statins in HIV/HCV-coinfected patients (20). In that study, 38 coinfected patients were safely treated with atorvastatin, pravastatin, and rosuvastatin over a 6-month time period (20). In our population, only 5 of 60 patients with coinfection were on statin therapy. The primary reason identified for the lack of statin use in our population was fear of utilizing statins in patients with active liver disease, even though an indication existed.

In HIV-infected patients, drug interactions with HAART may also limit the use of certain statins (i.e., simvastatin). Simvastatin, lovastatin, and atorvastatin are primarily metabolized by the 3A4 system (21). Because atorvastatin is less lipophilic than simvastatin and lovastatin, the peak level of atorvastatin is less when administered with 3A4 inhibitors (21). Fluvastatin is primarily metabolized by 2C9, whereas pravastatin and rosuvastatin are eliminated unchanged by the liver and kidney (21). Approximately 10% of rosuvastatin is metabolized by 2C9 (21). It is common for prescribers to utilize pravastatin to avoid the interactions that can be encountered with several of the statin therapies (10). Unfortunately, pravastatin does not provide potent lowering of lipid values compared with other statins. Until recently, minimal data were available on the safety and efficacy of rosuvastatin in patients with HIV infection on HAART (11).

In coinfected patients, the choice of statin therapy may also make a difference, as certain statins have shown a more potent anti-HCV effect than others (2). In a study by Ikeda and colleagues, cell models identified that fluvastatin had the strongest anti-HCV activity compared with atorvastatin and simvastatin, which had moderate activity (14). Lovastatin and pravastatin showed minimal or no anti-HCV activity (14).

These effects on both HIV and HCV need to be considered when selecting a statin in the treatment of hypercholesterolemia or cardiovascular disease. The statins used in our population were varied, with pravastatin used in two patients and rosuvastatin, atorvastatin, and simvastatin each used in one patient. Because of the small sample size, no definitive conclusions can be drawn regarding the most appropriate statin to use in the HIV/HCV-coinfected patient.

Even though our experience, consistent with other retrospective studies, identified that statins were safe in HIV/HCV-coinfected patients, further controlled prospective studies should be conducted to truly identify those patients who may not be appropriate candidates for therapy and to identify the preferred statin in this management scenario.


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