Hepatitis B, C appear to raise Parkinson’s risk

Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.

The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.

To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.

The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).

The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.

In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.

More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.

The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.

Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.

The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.

To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.

The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).

The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.

In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.

More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.

The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.

Hepatitis B and C appear to raise the risk of later Parkinson’s disease (PD), according to a report published in Neurology.

The etiology of Parkinson’s disease is complex, and several factors, including environmental toxins and head trauma, have been proposed that may increase risk for the disorder. Two recent epidemiologic studies in Taiwan found an association between hepatitis C and Parkinson’s risk, said Julia Pakpoor, BM BCh, of the Unit of Health-Care Epidemiology, Nuffield Department of Population Health, University of Oxford (England), and her associates.

To further explore that association, the investigators performed a retrospective cohort study using data from National Health Service hospitals across England for 1999-2011. They assessed the risk for developing PD among 21,633 people with hepatitis B, 48,428 with hepatitis C, 6,225 with autoimmune hepatitis, 4,234 with chronic active hepatitis, 19,870 with HIV, and 6,132,124 control subjects with other disorders.

The risk of developing PD was elevated for only 1 or more years following hospitalization for hepatitis B (relative risk, 1.76) or hepatitis C (RR, 1.51). “These findings may be explained by a specific aspect of viral hepatitis (rather than a general hepatic inflammatory process or general use of antivirals), but whether this reflects shared disease mechanisms, shared genetic or environmental susceptibility, sequelae of viral hepatitis per se, or a consequence of treatment remains to be determined,” Dr. Pakpoor and her associates said (Neurology. 2017;88:1-4).

The reason for this association is not yet known. “Neurotropic features of hepatitis C have been described previously and include the potential for cognitive impairment, independent of hepatic encephalopathy. Further, all essential hepatitis C virus receptors have been shown to be expressed on the brain microvascular endothelium. … suggesting one mechanism by which the virus may affect the CNS,” they noted.

In addition, parkinsonism has been described as an adverse effect of treatment with interferon and ribavirin, which are commonly used in hepatitis C infection. Parkinsonism also is known to develop in association with liver cirrhosis, and cirrhosis status was not available for the members of this study cohort.

More studies are needed to confirm this association and verify that it is causal. Such research will also provide insight into pathophysiologic pathways of PD, “which may be important to understanding the development of PD more broadly,” Dr. Pakpoor and her associates said.

The English National Institute for Health Research supported the study. Dr. Pakpoor and her associates reported having no relevant financial disclosures.