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AppId is over the quota AppId is over the quota Main Category: Eczema / Psoriasis
Also Included In: Cardiovascular / Cardiology
Article Date: 14 May 2012 – 0:00 PST Current ratings for:
Psoriasis Linked To Increased Risk Of Cardiovascular Disease By Mechanistic Discovery
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The link between psoriasis and cardiovascular events has been observed for years, however the mechanics were unknown. For the first time, Case Western Reserve University School of Medicine researchers have discovered preclinical evidence demonstrating that the inflammatory skin disease leads to cardiovascular disease. Further, the research demonstrated that aggressive reversal of psoriasis reduces the cardiovascular risk as well. Psoriasis is a chronic disease of the immune system that appears as raised, inflamed, scaly red patches of skin and is often associated with intense itch. In the United States, it affects between two and a half to six million patients. http://www.eczemablog.net/

Published in the Journal of Investigative Dermatology, the study used a new, innovative mouse model to demonstrate a causal connection between the skin disease and cardiovascular disease. Dr. Ward and her research team demonstrated that mice engineered to overexpress a protein called Tie-2 in the skin, develop a skin condition similar to human psoriasis. Using this model, they showed that persistent, chronic inflammation confined to the skin can result in inflammation in large arteries, such as the aorta.

“This discovery is paradigm shifting. There has been a link between the two diseases but to date we had not been able to show cause. Epidemiologic evidence from thousands of patients was convincing that psoriasis patients had a much greater chance of developing cardiovascular disease and dying from it,” says Nicole Ward, PhD, senior author of the study, assistant professor of dermatology and neurosciences at Case Western Reserve School of Medicine, and scientist with the Murdough Family Center for Psoriasis at University Hospitals Case Medical Center.

There is a known increased risk of heart, cerebrovascular, and peripheral artery diseases, as well as risk of death, in individuals suffering from a variety of chronic inflammatory diseases, such as rheumatoid arthritis (RA), colitis, gum disease, lupus, and psoriasis. Many researchers showed, statistically, that having psoriasis leads to an increased risk for cardiovascular disease and heart complications, however it was unclear why this occurs and it was challenging to separate out the significance of other lifestyle factors and their contributions to this risk, she adds.

Based on published clinical reports demonstrating psoriasis patients had increased risk of developing and dying of heart attack and stroke, Dr. Ward and her team set-out to investigate whether their mouse model of psoriasis would also show cardiac complications, mimicking these seen in human disease. They teamed up with experts in the role of inflammation in vessel injury – Yunmei Wang, PhD, assistant professor of medicine at the School of Medicine and Daniel I. Simon, MD the Herman K. Hellerstein Professor of Cardiovascular Research at the School of Medicine, and chief, Cardiovascular Medicine at University Hospitals Case Medical Center.

“We believed that chronic inflammation over a large area of the body may be the reason for an increased risk of cardiovascular complications in skin disease patients; however, until now we had no way to model and definitively prove this,” says Dr. Wang.

Dr. Ward and her team measured blood clot formation in the psoriasis mouse model and normal mice, revealing that time was greatly shortened in the diseased mice. This shortened time to vessel blockage is akin to a greater risk for blood vessel blockage in humans that leads to stroke or heart attack. Further examination revealed that mice with the skin disease also exhibited inflammation of the vessel wall similar to that observed with atherosclerotic lesions or plaques.

Importantly, and highly meaningful for patients with psoriasis, Dr. Ward’s work was able to demonstrate that upon reversal of the skin disease, the cardiovascular inflammation and blood clot formation were also decreased.

“Our observations of improved vessel wall inflammation and decreased clot formation following skin-specific repression of disease provide further evidence that skin inflammation promotes vascular inflammation and thrombosis and strongly suggests that aggressive treatment of skin disease may block pathways that produce cardiovascular disease in psoriasis patients,” says Dr. Ward.

Article adapted by Medical News Today from original press release. Click ‘references’ tab above for source.
Visit our eczema / psoriasis section for the latest news on this subject. Dr. Ward presented these findings at the 2012 Society for Investigative Dermatology Annual Meeting in Raleigh, NC.
This research was funded by the National Institutes of Health, National Psoriasis Foundation, and the Murdough Family Center for Psoriasis.
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Eczema Blog

All over the media last week was the news that two scientists at the National Institutes of Health in Bethesda, MD had discovered “the molecule responsible for itch.”

This molecule, “Nppb,” relays signals from certain neurons that detect itch in the skin to other neurons that carry the signals up the spinal cord to the brain. The scientists, Santosh Mishra and Mark Hoon, engineered mice in which the gene for Nppb had been turned off. The mice could not, apparently, feel itch.

The media hype is evident. Nppb is not THE molecule responsible for itch. Several molecules are known to be involved in detecting itch in the first place, and we know many others must be involved in the signaling pathway.

What is remarkable, though, is that the scientists were able to define a model for how itch gets from the skin to the spinal cord.

Mishra and Hoon’s model of how neurons carry the itch signal. (Fig 4G from their Science paper.)

We now know that there are at least two pinch points: the synapse across which Nppb carries the signal, and a second downstream synapse across which another molecule, GRP, sends the information to the next stage of neurons.

Blocking the receptors for Nppb or GRP would seem to be a prime candidate for an anti-itch therapy.

But, of course, there are complications. Nppb was originally known because it is important in the heart, where it controls blood pressure. GRP controls digestion. The genetically engineered Nppb-free mice died early. (The scientists said so in their media interviews.)

So you can’t just take a pill that blocks Nppb receptors everywhere. That would be a disaster.

But this kind of restriction on where a drug can act is well-known in pharmacology. That’s why, e.g., I can use the anti-pain Voltaren gel (diclofenac) safely by rubbing it into my joints, but diclofenac is known to be pretty toxic if you swallow it.

You can’t design an Nppb receptor-blocking topical cream, because the important synapses are in the spinal cord. A cream would only be effective on the surface.

But it might be possible to take a pill that blocks Nppb only in the spinal cord. I’m not sure how, but that’s what major pharma companies are paying their scientists the big bucks to find out. Maybe the receptors in the spinal cord are subtly different than those elsewhere in the body.

This is very exciting stuff. The massive question is whether the work applies to humans. I would expect it did. Mice and human immune systems are quite different, but our nervous systems are not. We most likely have an analog of Nppb that carries our itch signals.

Just to put this in context—the new work tells us substantially more about itch signaling than previous work in the field. I’d been aware of studies that had identified a class of itch neurons, or certain molecules important in detecting itch in the skin, but this research builds on those foundations in a big way.
End Eczema