The viruses hepatitis B and C may both be associated with an increased risk of Parkinson's disease, according to an Oxford University and University College London study.
The hepatitis virus affects the liver. According to the Centres for Disease Control and Prevention (CDC), it is estimated that anywhere from 850,000 to 2.2m people in the US have chronic hepatitis B virus infection and anywhere from 2.7m to 3.9m people have chronic hepatitis C. While both can lead to serious illness, many people have few symptoms and do not realise they have the virus, especially at first.
Hepatitis B is spread through contact with blood and body fluids of an infected person, such as unprotected sex, sharing needles, getting a tattoo or piercing with unsterilised tools or sharing razors or toothbrushes with an infected person. Hepatitis C is spread through blood-to-blood contact such as sharing needles, razors and toothbrushes and is passed on at birth by infected mothers.
"The development of Parkinson's disease is complex, with both genetic and environmental factors," said study author Dr Julia Pakpoor, of the University of Oxford.
"It's possible that the hepatitis virus itself or perhaps the treatment for the infection could play a role in triggering Parkinson's disease or it's possible that people who are susceptible to hepatitis infections are also more susceptible to Parkinson's disease. We hope that identifying this relationship may help us to better understand how Parkinson's disease develops."
For the study, researchers examined hospital records from a large UK database. They looked for records of people with a first case of hepatitis B, hepatitis C, auto-immune hepatitis, chronic active hepatitis and HIV from 1999 to 2011. Then those people were compared to the hospital records of people with relatively minor conditions such as cataract surgery, bunions and knee replacement surgery.
For all of the participants, researchers looked at the records to see who later developed Parkinson's disease.
There were nearly 22,000 people with hepatitis B, 48,000 with hepatitis C, 6,000 with auto-immune hepatitis, 4,000 with chronic active hepatitis and nearly 20,000 with HIV. They were compared to more than 6m people with minor conditions.
The study found that people with hepatitis B were 76% more likely to develop Parkinson's disease than those in the comparison group, and people with hepatitis C were 51% more likely to develop Parkinson's disease. A total of 44 people with hepatitis B developed Parkinson's disease, compared to 25 cases that would be expected in the general population. For people with hepatitis C, 73 people developed Parkinson's disease, where about 49 cases would have been expected in the general population.
People with autoimmune hepatitis, chronic active hepatitis and HIV did not have an increased rate of Parkinson's disease.
A previous study from Taiwan showed a relationship between hepatitis C and Parkinson's disease, but it did not show any relationship for hepatitis B.
Pakpoor said that limitations of the current study include that they could not adjust for lifestyle factors such as smoking and alcohol use, which could affect Parkinson's disease risk, and that the study was based solely on people who were evaluated at a hospital.
Abstract
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.
Authors
Julia Pakpoor, Alastair Noyce, Raph Goldacre, Marianna Selkihova, Stephen Mullin, Anette Schrag, Andrew Lees, Michael Goldacre
[link url="https://www.sciencedaily.com/releases/2017/03/170331120225.htm"]American Academy of Neurology material[/link]
[link url="http://www.neurology.org/content/early/2017/03/29/WNL.0000000000003848"]Neurology abstract[/link]