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Background: Myocardial infarction (MI) has been reported as a postinfection sequela of herpes zoster, but with limited data on incidence after zoster and protective effect of the zoster vaccine. This study investigates the risk of developing an MI 30 days postzoster, determines patient-specific risk factors, and investigates the impact of herpes zoster vaccination. Methods: This retrospective cohort study included patients who received care at a Veterans Affairs facility between 2015 and 2020. Time to MI was determined from either 30 days post-zoster infection (zoster cohort) or a primary care appointment (control cohort). Results: This study assessed a total of 2 165 584 patients. MI within 30 days occurred in 0.34% (n = 244) of the zoster cohort and 0.28% (n = 5782) of the control cohort (P = .0016). Patients with a documented herpes zoster infection during the study period were 1.35 times more likely to develop an MI within the first 30 days postinfection compared to the control cohort. Patients who received the recombinant zoster vaccine were less likely to have an MI postinfection (odds ratio, 0.82 [95% confidence interval, .74-.92]; P = .0003). Conclusions: Herpes zoster infection was associated with an increased risk of MI within the first 30 days postinfection. History of prior MI, male sex, age ≥50 years, history of heart failure, peripheral vascular disease, human immunodeficiency virus, prior cerebrovascular accident, and renal disease increased odds of MI 30 days postinfection with herpes zoster. Herpes zoster vaccination decreased the odds of developing an MI in patients aged ≥50 years.
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BACKGROUND: The human immune response to mercury is not well characterized despite the body of evidence that suggests that Hg can modulate immune responses, including the induction of autoimmune disease in some mouse models. Dysregulation of cytokine signaling appears to play an important role in the etiology of Hg-induced autoimmunity in animal models. OBJECTIVES: In this study, we systematically investigated the human immune response to Hg in vitro in terms of cytokine release. METHODS: Human peripheral blood mononuclear cells (PBMCs) were isolated from 20 volunteers who donated blood six separate times. PBMCs were cultured with lipopolysaccharide and concentrations of mercuric chloride (HgCl(2)) up to 200 nM. Seven cytokines representing important pathways in physiologic and pathologic immune responses were measured in supernatants. We used multilevel models to account for the intrinsic clustering in the cytokine data due to experimental design. RESULTS: We found a consistent increase in the release of the proinflammatory cytokines interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha, and concurrent decrease in release of the antiinflammatory cytokines interleukin 1-receptor antagonist (IL-1Ra) and IL-10 in human PBMCs treated with subcytotoxic concentrations of HgCl(2). IL-4, IL-17, and interferon-gamma increased in a concentration-response manner. These results were replicated in a second, independently recruited population of 20 different volunteers. CONCLUSIONS: Low concentrations of HgCl(2) affect immune function in human cells by dysregulation of cytokine signaling pathways, with the potential to influence diverse health outcomes such as susceptibility to infectious disease or risk of autoimmunity.