Perceived psychological stress and risk of herpes zoster: a nationwide population‐based cohort study

Summary Background Psychological stress may reduce cellular immunity, but its role in triggering latent infections, including herpes zoster (HZ), is controversial. Objectives To examine the association between perceived psychological stress and risk of HZ. Methods In a linked registry‐based cohort s...

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Published inBritish journal of dermatology (1951) Vol. 185; no. 1; pp. 130 - 138
Main Authors Schmidt, S.A.J., Sørensen, H.T., Langan, S.M., Vestergaard, M.
Format Journal Article
LanguageEnglish
Published England Oxford University Press 01.07.2021
John Wiley and Sons Inc
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Summary:Summary Background Psychological stress may reduce cellular immunity, but its role in triggering latent infections, including herpes zoster (HZ), is controversial. Objectives To examine the association between perceived psychological stress and risk of HZ. Methods In a linked registry‐based cohort study, we followed 77 310 persons aged 40 years or older who participated in the 2010 Danish National Health Survey from 1 May 2010 until HZ diagnosis, death, emigration or 1 July 2014, whichever occurred first. We computed hazard ratios (HRs) of HZ associated with Cohen’s Perceived Stress Scale (PSS) score (range 0–40) using Cox regression with age as the timescale, adjusted for sex, immunosuppressive and selected chronic conditions, immunosuppressive drugs, and sociodemographic, lifestyle and anthropometric factors. The PSS measures chronic stress perceived by an individual in response to various demands of daily life. We modelled the PSS score using quintiles and a restricted cubic spline function. Results The unadjusted rate of HZ varied from 5·53 to 7·20 per 1000 person‐years from the lowest to the highest PSS score quintile. Compared with the lowest PSS score quintile, the adjusted HR for HZ was 1·00 [95% confidence interval (CI) 0·86–1·16], 1·08 (95% CI 0·92–1·26), 1·05 (95% CI 0·90–1·23) and 1·14 (95% CI 0·97–1·34) for the second to the fifth quintile, respectively. In cubic spline analyses, PSS scores < 20 were not associated with increased HR of HZ, but thereafter the HR increased linearly from 1·10 (95% CI 0·85–1·41) to 2·22 (95% CI 1·32–3·75). Conclusions Our study indicated that high levels of psychological stress are associated with increased risk of HZ. What is already known about this topic? Psychological stress may reduce cellular immunity, but its role in triggering latent infections, such as herpes zoster (HZ), is controversial. Previous epidemiological studies have mainly focused on the effects of negative life events (e.g. bereavement) on HZ risk, and dose–response analyses are lacking. It is possible that the allostatic load (the cumulative ‘wear and tear’ on the body associated with stress) depends on the type of stress and coping mechanisms. What does this study add? In this large population‐based cohort study, we found that persons reporting the highest levels of perceived psychological stress in daily life had an increased risk of HZ. Perceived psychological stress may be a modifiable risk factor for HZ. Our study adds HZ to the growing list of potential negative health consequences of psychological stress and underscores the importance of supporting mental wellbeing and resilience in the general population. Linked Comment: A.W.M. Evers and S. van Beugen. Br J Dermatol 2021; 185:12–13.
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Funding sources This work was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation (grant number 100060), the Lundbeck Foundation (grant number R248‐2017‐521) and the Program for Clinical Research Infrastructure established by the Lundbeck Foundation and the Novo Nordisk Foundation. The funder had no role in the study design, data collection, data analysis, manuscript preparation and/or publication decisions.
Conflicts of interest S.A.J.S. reports receipt of grants from the Edel and Wilhelm Daubenmerkls Charitable Foundation during the study period. H.T.S. reports receipt of grants from the Lundbeck Foundation (R248‐2017‐521) during the study period, and the Department of Clinical Epidemiology, Aarhus University Hospital, receives funding for other studies from companies in the form of research grants to (and administered by) Aarhus University. None of these studies are related to the present study. S.M.L. reports receipt of grants from the Wellcome Trust and the National Institute for Health Research during the study period.
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ISSN:0007-0963
1365-2133
DOI:10.1111/bjd.19832