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Elevated rates of Parkinson’s disease found in patients with viral hepatitis
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Researchers found significant evidence of elevated rates of subsequent Parkinson’s disease in patients with hepatitis B and hepatitis C, though the underlying correlation is yet to be determined, according to a recently published study.
“The development of Parkinson’s disease is complex, with both genetic and environmental factors,” Julia Pakpoor, BA, BM, BCh, from the Unit of Health-Care Epidemiology, University of Oxford, said in a press release. “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.”
The researchers analyzed data from the English National Hospital Episode Statistics between 1999 and 2011 for the retrospective study. Study cohorts included patients with HBV (n = 21,633), HCV (n = 48,428), autoimmune hepatitis (n = 6,225), chronic active hepatitis (n = 4,234) and HIV (n = 19,870). They also included a reference cohort (n = 6,132,124) of patients admitted for a variety of relatively minor medical and surgical conditions.
The standardized rate ratio of Parkinson’s disease following HBV was 1.76 (95% CI, 1.28-2.37), including 44 patients with observed Parkinson’s disease and 25 expected cases. For HCV, the standardized rate ratio was 1.51 (95% CI, 1.18-1.9), including 73 patients with observed Parkinson’s disease and 48.5 expected cases.
“Explaining a relationship between viral hepatitis and [Parkinson’s disease] is largely speculative. Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy,” the researchers wrote. “Further, all essential ...HCV receptors have been shown to be expressed on the brain microvascular endothelium, which constitutes the primary component of the blood–brain barrier, thus suggesting one mechanism by which the virus may affect the [central nervous system].” They did not cite any similar research in the realm of HBV. – by Talitha Bennett
Disclosure: The researchers report no relevant financial disclosures.