Viral hepatitis and Parkinson disease: A national record-linkage study

This is a study led by Julia Pakpoor in the HES database, a very large UK cohort study using routinely collected medical data. Two previous studies from Taiwan showed a link between hepatitis and future Parkinson's, but here we show it on a larger scale and in a Western population. It is not clear whether this a feature peculiar to the virus, the treatment or a common risk factor that predisposes to both...

Neurology. 2017 Mar 29. pii: 10.1212/WNL.0000000000003848. doi: 10.1212/WNL.0000000000003848. [Epub ahead of print]
Pakpoor J, Noyce A, Goldacre R, Selkihova M, Mullin S, Schrag A, Lees A, Goldacre M.

http://www.neurology.org/content/early/2017/03/29/WNL.0000000000003848.short

OBJECTIVE: To study associations between viral hepatitis and Parkinson disease (PD).

METHODS: A retrospective cohort study was done by analyzing linked English National Hospital Episode Statistics and mortality data (1999-2011). Cohorts of individuals with hepatitis B, hepatitis C, autoimmune hepatitis, chronic active hepatitis, and HIV were constructed, and compared to a reference cohort for subsequent rates of PD.

RESULTS: The standardized rate ratio (RR) of PD following hepatitis B was 1.76 (95% confidence interval [CI] 1.28-2.37) (p < 0.001), based on 44 observed compared with 25 expected cases. The RR of PD following hepatitis C was 1.51 (95% CI, 1.18-1.9) (p < 0.001), based on 48.5 expected and 73 observed cases. There was no significant association between autoimmune hepatitis, chronic active hepatitis or HIV, and subsequent PD. When including only those episodes of care for PD that occurred first at least 1 year following each exposure condition, the RR for hepatitis B and hepatitis C were 1.82 (1.29-2.5) and 1.43 (1.09-1.84), respectively.

CONCLUSIONS: We report strong evidence in favor of an elevation of rates of subsequent PD in patients with hepatitis B and hepatitis C. These findings may be explained by factors peculiar to viral hepatitis, but whether it reflects consequences of infection, shared disease mechanisms, or the result of antiviral treatment remains to be elucidated. Further work is needed to confirm this association and to investigate pathophysiologic pathways, potentially advancing etiologic understanding of PD more broadly.