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  • 标题:Cumulative Risk of Guillain–Barré Syndrome Among Vaccinated and Unvaccinated Populations During the 2009 H1N1 Influenza Pandemic
  • 本地全文:下载
  • 作者:Claudia Vellozzi ; Shahed Iqbal ; Brock Stewart
  • 期刊名称:American journal of public health
  • 印刷版ISSN:0090-0036
  • 出版年度:2014
  • 卷号:104
  • 期号:4
  • 页码:696-701
  • DOI:10.2105/AJPH.2013.301651
  • 语种:English
  • 出版社:American Public Health Association
  • 摘要:Objectives. We sought to assess risk of Guillain–Barré syndrome (GBS) among influenza A (H1N1) 2009 monovalent (pH1N1) vaccinated and unvaccinated populations at the end of the 2009 pandemic. Methods. We applied GBS surveillance data from a US population catchment area of 45 million from October 15, 2009, through May 31, 2010. GBS cases meeting Brighton Collaboration criteria were included. We calculated the incidence density ratio (IDR) among pH1N1 vaccinated and unvaccinated populations. We also estimated cumulative GBS risk using life table analysis. Additionally, we used vaccine coverage data and census population estimates to calculate denominators. Results. There were 392 GBS cases; 64 (16%) occurred after pH1N1vaccination. The vaccinated population had lower average risk (IDR = 0.83, 95% confidence interval = 0.63, 1.08) and lower cumulative risk (6.6 vs 9.2 cases per million persons, P = .012) of GBS. Conclusions. Our findings suggest that at the end of the influenza season cumulative GBS risk was less among the pH1N1vaccinated than the unvaccinated population, suggesting the benefit of vaccination as it relates to GBS. The observed potential protective effect on GBS attributed to vaccination warrants further study. Guillain–Barré syndrome (GBS) is an acute, monophasic, autoimmune neurologic disorder of the peripheral nerves characterized primarily by muscle weakness and loss of reflexes. Estimates of GBS incidence range from 0.8 to 1.9 cases per 100 000 person-years, are higher in males, and increase with age. 1,2 Although the exact causes of GBS are unknown, they are thought to be triggered by antigenic stimulation resulting in demyelination and damage to the peripheral nerves. 3,4 GBS has been shown to be associated with antecedent gastrointestinal or upper respiratory tract illnesses, including influenza. 5–9 Rarely, GBS may follow vaccination. 10–12 During the 1976 swine-origin influenza A pandemic, the risk of GBS was found to be increased by nearly 8 fold in the 6 weeks following receipt of the swine-origin influenza vaccine. 11 After 1976, several studies have assessed the risk of GBS following seasonal inactivated influenza vaccines demonstrating either no increased risk or a small increased risk of approximately 1 to 2 additional GBS cases per 1 million vaccine doses administered. 13,14 However, the 1976 GBS incident influenced the approach to the 2009 H1N1 vaccine safety monitoring efforts, and GBS became a primary focus of surveillance activities. The pandemic (H1N1) 2009 influenza virus began widespread circulation during the first half of the influenza season with illness peaking during October and November 2009. 15 At the same time, influenza A (H1N1) 2009 monovalent vaccines (pH1N1 vaccines) became available in early October 2009 16 and were administered rapidly and broadly throughout the United States. During this time the United States and several countries worldwide implemented enhanced pH1N1 vaccine safety monitoring. 17–19 Many programs have subsequently published their surveillance and evaluation findings for the risk of GBS during the 6 weeks following the pH1N1 vaccine 20–25 ; some but not all of the surveillance systems found a significant but small increased risk of GBS following pH1N1 vaccination. Most, however, were unable to adequately evaluate the potential confounding because of exposure to the pandemic (H1N1) 2009 influenza virus. Influenza and other respiratory illnesses have been associated with GBS, 6–8,26,27 and it has been suggested that the absolute increase in risk of GBS is much higher after influenza-like illnesses (ILIs) than a potential increase in risk after vaccination. 7,27 We hypothesized that the overall risk of GBS at the end of the 2009 influenza season (October 2009 through May 2010) may have been lower among the pH1N1 vaccinated population than the unvaccinated population. Surveillance for GBS using active-case finding through US Centers for Disease Control and Prevention’s (CDC’s) Emerging Infections Program (EIP) was implemented as part of enhanced pH1N1 vaccine safety monitoring activities 25,28 ; we used these data to test our hypothesis. We evaluated the average and cumulative risk of incident GBS among those vaccinated with pH1N1 vaccine and those unvaccinated (did not receive pH1N1 vaccine) during the surveillance period of October 1, 2009, through May 31, 2010.
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