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Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.
“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.
The study was published online in Neurology.
Conflicting findings
Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.
It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.
To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.
Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.
Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).
There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.
However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.
Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.
The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.
They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.
The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.
“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.
The study was published online in Neurology.
Conflicting findings
Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.
It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.
To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.
Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.
Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).
There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.
However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.
Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.
The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.
They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.
The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Herpes zoster does not appear to increase dementia risk – on the contrary, the viral infection may offer some protection, a large population-based study suggests.
“We were surprised by these results [and] the reasons for the decreased risk are unclear,” study author Sigrun Alba Johannesdottir Schmidt, MD, PhD, with Aarhus (Denmark) University Hospital, said in a news release.
The study was published online in Neurology.
Conflicting findings
Herpes zoster (HZ) is an acute, cutaneous viral infection caused by the reactivation of varicella-zoster virus (VZV). Previous population-based studies have reported both decreased and increased risks of dementia after having HZ.
It’s thought that HZ may contribute to the development of dementia through neuroinflammation, cerebral vasculopathy, or direct neural damage, but epidemiologic evidence is limited.
To investigate further, Dr. Schmidt and colleagues used Danish medical registries to identify 247,305 people who had visited a hospital for HZ or were prescribed antiviral medication for HZ over a 20-year period and matched them to 1,235,890 people who did not have HZ. For both cohorts, the median age was 64 years, and 61% were women.
Dementia was diagnosed in 9.7% of zoster patients and 10.3% of matched control persons during up to 21 years of follow-up.
Contrary to the researchers’ expectation, HZ was associated with a small (7%) decreased relative risk of all-cause dementia during follow-up (hazard ratio, 0.93; 95% confidence interval, 0.90-0.95).
There was no increased long-term risk of dementia in subgroup analyses, except possibly among those with HZ that involved the central nervous system (HR, 1.94; 95% CI, 0.78-4.80), which has been shown before.
However, the population attributable fraction of dementia caused by this rare complication is low (< 1%), suggesting that universal vaccination against VZV in the elderly has limited potential to reduce dementia risk, the investigators noted.
Nonetheless, Dr. Schmidt said shingles vaccination should be encouraged in older people because it can prevent complications from the disease.
The research team admitted that the slightly decreased long-term risk of dementia, including Alzheimer’s disease, was “unexpected.” The reasons for this decreased risk are unclear, they say, and could be explained by missed diagnoses of shingles in people with undiagnosed dementia.
They were not able to examine whether antiviral treatment modifies the association between HZ and dementia and said that this topic merits further research.
The study was supported by the Edel and Wilhelm Daubenmerkls Charitable Foundation. The authors disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.