Atorvastatin possibly interacts with the mechanism of the Zostavax vaccine by attenuating the immune responses that should occur after administration of the vaccine. Without a proper immune response, there is a decreased antibody production against the varicella zoster virus (VZV). Atorvastatin contains immunomodulating properties that as it inhibits HMG-CoA reductase, it causes a decrease in isoprenoid pyrophosphates. Isoprenoid pyrophosphates are necessary to activate Ras-related GTPases. Without this activation, there is a decline in the activation and proliferation of T-cells in the body.3 Atorvastatin causes an increased CD4+CD25+ regulatory T cells proliferation, and this contributes to age-linked immunosenescence and latent disease reactivation.3 The function of regulatory T cells is to regulate specific immune tolerance by suppressing the actions of CD4+ and CD8+ T cells. Additionally, statins cause an increase in Th2 helper T cells and this leads to a decrease in Th1 cell-mediated immunity, which helps prevent VZV replication.3 Th1 helper T cells function to activate CD8+ T cells that kill virus-infected cells. Other immunomodulatory effects of statins that weaken the serological response after vaccine administration are that they impair the MHC II pathway by interfering with antigen processing and presentation to T cells. In B cells, statins inhibit antigen internalization and that leads to a decreased antibody production. All of these lead to decreased vaccine efficacy. This patient already has depressed immunity due to suffering from autoimmune disorders like Sjögren’s syndrome and rheumatoid arthritis. His old age and comorbidities with the addition of long-term statin use, led to reduced boosting of VZV antibodies after Zostavax vaccination. Several studies support the interaction of atorvastatin as the possible cause of decreased efficacy of Zostavax vaccine in this patient.
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A study completed during the influenza seasons of 2009-2011 investigated the relationship between long-term statin therapy and its influence on influenza vaccine efficacy (VE). The results of this post hoc analysis of a cross-sectional observational study, along with a clinical trial, indicated that statins caused a decreased antibody titer after vaccine administration. Over 6000 adults over the age of 65 that had been on statin therapy for at least 28 days before influenza vaccine administration were included in this randomized, controlled, observer-blind clinical trial. Blood samples taken on the day of vaccination and 22 days after vaccination compared the hemagglutination-inhibiting (HAI) titers. Results from this study were that irrespective of the type of influenza vaccine, the geometric mean titer (GMT) ratio was consistently higher in the control group. In the controls, the GMT ratio was 38% higher for A(H1N1), 68% higher for A(H3N2), and 38% higher for influenza B. The HAI titers were also less in statin therapy patients that were male and patients that were using synthetically derived statins. The decreased HAI titers suggest that there was a decreased serological response to the vaccine in statin-user. Furthermore, another population-based cohort study analyzed the effect of statin exposure on influenza vaccine efficacy in over 3000 patients over 10 influenza seasons from 2004-2005 to 2014-2015. Patients of statin users and non-statin users gave respiratory samples to test for influenza virus to measure vaccine efficacy. Results from this study showed that for influenza A (H2N2), a significant interaction (p=0.03) was present for VE alteration by statin therapy. For patients that were non-statin users, the adjusted VE was 45% (95% CI, 27%-59%). For
A study completed during the influenza seasons of 2009-2011 investigated the relationship between long-term statin therapy and its influence on influenza vaccine efficacy (VE). The results of this post hoc analysis of a cross-sectional observational study, along with a clinical trial, indicated that statins caused a decreased antibody titer after vaccine administration. Over 6000 adults over the age of 65 that had been on statin therapy for at least 28 days before influenza vaccine administration were included in this randomized, controlled, observer-blind clinical trial. Blood samples taken on the day of vaccination and 22 days after vaccination compared the hemagglutination-inhibiting (HAI) titers. Results from this study were that irrespective of the type of influenza vaccine, the geometric mean titer (GMT) ratio was consistently higher in the control group. In the controls, the GMT ratio was 38% higher for A(H1N1), 68% higher for A(H3N2), and 38% higher for influenza B. The HAI titers were also less in statin therapy patients that were male and patients that were using synthetically derived statins. The decreased HAI titers suggest that there was a decreased serological response to the vaccine in statin-user. Furthermore, another population-based cohort study analyzed the effect of statin exposure on influenza vaccine efficacy in over 3000 patients over 10 influenza seasons from 2004-2005 to 2014-2015. Patients of statin users and non-statin users gave respiratory samples to test for influenza virus to measure vaccine efficacy. Results from this study showed that for influenza A (H2N2), a significant interaction (p=0.03) was present for VE alteration by statin therapy. For patients that were non-statin users, the adjusted VE was 45% (95% CI, 27%-59%). For