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PCSK9 IS ELEVATED IN PATIENTS WITH HIV AND HEPATITIS C
A2156 JACC March 17, 2015 Volume 65, Issue 10S
Young Investigator Awards Competition PCSK9 Is Elevated in Patients with HIV and Hepatitis C Oral Contributions Room 4 Monday, March 16, 2015, 8:30 a.m.-8:45 a.m. Session Title: Young Investigator Awards Competition: Clinical Investigations, Congenital Heart Disease, and Cardiovascular Surgery Abstract Category: Clinical Investigations, Congenital Heart Disease, Cardiac Surgery Presentation Number: 909-05 Authors: Payal Kohli, Peter Ganz, Yifei Ma, Rebecca Scherzer, Kristinalisa Maka, Steven Deeks, Carl Grunfeld, Scott Wasserman, Rob Scott, Priscilla Hsue, University of California San Francisco, San Francisco, CA, USA, San Francisco General Hospital, San Francisco, CA, USA
Background: Proprotein convertase subtilisin kexin 9 (PCSK9) inhibitors are an effective strategy for lowering LDL-C. In an oral presentation from our group, we reported that PCSK9 is elevated in HIV infection, a state of heightened inflammation. Here, we aim to characterize the levels of PCSK9 in individuals with HIV and Hepatitis C (HCV) co-infection, another hyper-inflammatory state that may also impact the ability of hepatocytes to synthesize PCSK9.
Methods: We measured PCSK9 in 567 participants (111 HIV+/HCV+, 385 HIV+, 72 controls) from an outpatient cohort in San Francisco using a high affinity ELISA assay. Poisson regression models were used to determine associations between HIV/HCV and PCSK9 levels.
Results: The median age was 50 years (IQR 43-55) and 89% were male; 34% were smokers, 25% hypertensive, median LDL was 103 mg/dL (IQR 80-127), and 21% were on statins. HIV patients and controls had similar rates of traditional risk factors. Half of the HIV patients were treated and suppressed. PCSK9 levels were 21% higher in HIV/HCV co-infected patients vs. controls (95% CI 1.09-1.34) and 11% higher in co-infected patients vs. those with HIV alone (95% CI 1.03-1.20). In a fully adjusted model, HIV/HCV co-infection retained a highly significant association with 21% higher PCSK9 levels (95% CI 1.09-1.34, p=0.001) (Table).
Conclusion: PCSK9 is significantly increased in HIV and HCV co-infection. Future studies should explore whether PCSK9 inhibition may be used safely to treat dyslipidemia in such patients.
Young Investigator Awards Competition PCSK9 Is Elevated in Patients with HIV and Hepatitis C Oral Contributions Room 4 Monday, March 16, 2015, 8:30 a.m.-8:45 a.m. Session Title: Young Investigator Awards Competition: Clinical Investigations, Congenital Heart Disease, and Cardiovascular Surgery Abstract Category: Clinical Investigations, Congenital Heart Disease, Cardiac Surgery Presentation Number: 909-05 Authors: Payal Kohli, Peter Ganz, Yifei Ma, Rebecca Scherzer, Kristinalisa Maka, Steven Deeks, Carl Grunfeld, Scott Wasserman, Rob Scott, Priscilla Hsue, University of California San Francisco, San Francisco, CA, USA, San Francisco General Hospital, San Francisco, CA, USA
Background: Proprotein convertase subtilisin kexin 9 (PCSK9) inhibitors are an effective strategy for lowering LDL-C. In an oral presentation from our group, we reported that PCSK9 is elevated in HIV infection, a state of heightened inflammation. Here, we aim to characterize the levels of PCSK9 in individuals with HIV and Hepatitis C (HCV) co-infection, another hyper-inflammatory state that may also impact the ability of hepatocytes to synthesize PCSK9.
Methods: We measured PCSK9 in 567 participants (111 HIV+/HCV+, 385 HIV+, 72 controls) from an outpatient cohort in San Francisco using a high affinity ELISA assay. Poisson regression models were used to determine associations between HIV/HCV and PCSK9 levels.
Results: The median age was 50 years (IQR 43-55) and 89% were male; 34% were smokers, 25% hypertensive, median LDL was 103 mg/dL (IQR 80-127), and 21% were on statins. HIV patients and controls had similar rates of traditional risk factors. Half of the HIV patients were treated and suppressed. PCSK9 levels were 21% higher in HIV/HCV co-infected patients vs. controls (95% CI 1.09-1.34) and 11% higher in co-infected patients vs. those with HIV alone (95% CI 1.03-1.20). In a fully adjusted model, HIV/HCV co-infection retained a highly significant association with 21% higher PCSK9 levels (95% CI 1.09-1.34, p=0.001) (Table).
Conclusion: PCSK9 is significantly increased in HIV and HCV co-infection. Future studies should explore whether PCSK9 inhibition may be used safely to treat dyslipidemia in such patients.