Shingles have been seen to increase the risks of issues such as stroke, according to the American College of Cardiology. Now, researchers have dug into why those dealing with shingles are more likely to develop stroke.
This was the focus of research conducted by the Anschutz Medical Campus of the University of Colorado. SciTechDaily notes how the assumed answer can be found within exosomes, lipid vesicles, that move genetic data and proteins across cells.
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Shingles Increases Risks of Developing Stroke
The study looks into the mechanisms underlying the link between the two focused conditions. It was published in the Infectious Diseases Journal.
Lead author and assistant research professor Andrew Bubak shared how most individuals are knowledgeable about the pain that comes with shingle rashes. However, they may not be aware of how the risk of stroke rises one year post-infection. Even if such a rash is completely cleared and the individual feels well, this person is still moving forward with elevated risks of getting a stroke.
Shingles, or herpes zoster (HZ), is typically caused by the virus varicella-zoster, which is also known to lead to chicken pox. Such a virus stays within the ganglionic brain cells and may activate again, leading to extreme pain.
However, on top of all this, the researchers noted how shingles elevate the risk of developing stroke. This is particularly true among those younger than 40-an age range where vaccination for shingles is not encouraged.
Those with rashes on their face have higher risks because of the proximity between the rash and the brain.
Why Does the Shingles Condition Heighten Stroke Risks?
The researchers looked into exosomes to better understand how this phenomenon works.
Bubak shared exosomes board pathogenic cargo that may lead to thrombosis and inflammation far from the actual infection site. This could result in a stroke.
As part of their procedures, the researchers gathered samples of plasma from 13 patients who had shingles and ten who did not. These samples were taken while the infection was ongoing. There was also a three-month follow-up. Exosome was taken from the plasma.
Upon analyzing the exosomes, the researchers noted prothrombotic exosomes, which may lead to blood clots among those infected. They also noted proinflammatory exosomes that pose a risk for developing stroke at the three-month follow-up.
According to Science Daily, Bubak notes how these findings connote that among the subset of those with singles, the virus may not be latent again, or the moving exosomes that lead to a lengthened state of prothrombosis may continue post-rash and post-therapy. He mentioned how using antiviral agents for lengthier periods alongside anti-inflammatory and antiplatelet agents could help.
Bubak also mentions how if these results can be verified with a bigger sample and a longitudinal scale, it may alter current clinical practices. He mentions how knowing the connection between these two conditions is extremely important. Moreover, it can also be mitigated easily by issuing antiplatelet agents.
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