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© 1996 Oxford University Press
research-article |
Whooping Cough and Parkinson's Disease
VE§
*Department of Applied Epidemiology, National Centre for Epidemiology, Carlos III Institute of Health Madrid, Spain
**Division of Neurology, Department of Clinical Neuroscience and Family Medicine, Huddinge University Hospital, Karolinska Institute Huddinge, Sweden
Department of Neurology, National University Hospital Reykjavik, Iceland
Biostatistics Unit, RamÓn y Cajal Hospital, and the REUNI Centre, Carlos III Institute of Health Madrid, Spain
§Department of Microbiology, National University Reykjavik, Iceland
||Department of Social Medicine, National University Reykjavik, Iceland
¶Pharmaceutical Division, Ministry of Health Reykjavik, Iceland
Reprint requests: Jesús de Pedro Cuesta. Instituto de Salud Carlos III, Centro Nacional de Epidemilogía, Departmento de Epidemiología Aplicada, c/ Sinesio Delgado, 6, 28029 Madrid, Spain.
de Pedro-Cuesta J (Instituto de Salud Carlos III, Centro Nacional de Epidemiología, Departamento de Epidemiología Aplicada, c/ Sinesio Delgado, 6, 28029 Madrid, Spain), Gudmundsson G, Abraira V, Gudmundsson G, L
ve A, Tulinius H, Veiga J, Almazán J and Petersen I J for the EUROPARKINSON Preparatory Activity Research Group. Whooping Cough and Parkinson' Disease. International Journal of Epidemiology 1996; 25: 1301–1311.
BACKGROUND: We reported high levodopa use and prevalences of Parkinson's Disease (PD) in periodically, time-clustered, Icelandic cohorts born after major whooping cough epidemics (MWCE).
METHODS: In order to quantify a possible relationship between age at first post-birth MWCE and risk of PD we: 1) calculated cumulative incidences of PD during the period 1954–1963 in one-year Icelandic cohorts born between 1869 and 1927, using raw material from a reported survey; 2) identified MWCE from 1869 onwards in Iceland; 3) estimated cohort ages at onset of incidence period and at first MWCE; and 4) combined the above-mentioned information using log-linear models. In addition, we studied the prevalence of levodopa users in Icelandic birth cohorts during a recent period.
RESULTS: The curves of the above-mentioned incidences and prevalences in one-year birth-cohorts showed: 1) a similar, age-related, inverted V profile; and 2) a systematic notchy pattern, with peak values for one or both measurements for cohorts born during or after each of nine MWCE identified during the period 1869–1927. When 13 cohorts bom in years with MWCE were excluded from the analysis, the risk of PD rose with age at first defined MWCE, with the linear increase being 8.4% per year (95% Cl: –0.1–18.3%).
CONCLUSIONS: These results are consistent with reported effects of age at exposure in animal models of toxic parkinsonism, age-related changes in the dopamine receptor-GPT-binding protein-adenylatecyclase system observed in rats treated with pertussis toxin, and some PD epidemiological features. They suggest that pertussis neurotoxicity could be causally related to PD worldwide.
Keywords dopamine, drug use, epidemiology, aetiology, Parkinson's disease, pertussis
Revised 1 May 1996