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The possible druggie way to address this;
Can Psoriasis Tx Diminish Atherosclerosis?
Observational study links improvements in skin, vascular inflammation
Treatments that eased psoriasis were tied to reductions in vascular inflammation as well, a small study found.After a year of treatment for the skin condition -- a mix of of topical therapy (60%), biological therapy (66%, mostly anti-tumor necrosis factor [anti-TNF] therapy), and phototherapy (15%) -- there was a median 33% improvement in psoriasis (P<0.001) that was linked to a 6% reduction in vascular inflammation as measured by PET/CT, even after adjusting for traditional risk factors (P=0.03), according to Nehai N. Mehta, MD, MSCE, of the National Heart, Lung, and Blood Institute in Bethesda, Md., and colleagues.
They noted in their JAMA Cardiology
study that patients achieving at least a 75% reduction in skin
inflammation severity had an 11% improvement in vascular inflammation (P<0.003).
"These findings suggest that controlling remote target organ inflammation (e.g., in the skin) may improve vascular diseases; however, randomized clinical trials are needed to confirm these findings," wrote Mehta's group.
For one, the randomized Vascular Inflammation in Psoriasis-Extension Trial is in the works as investigators study the effect of anti-TNF therapy with adalimumab on skin and vascular inflammation.
"These data are intriguing and support a rigorous testing of the hypothesis that intervening on psoriatic disease may mitigate vascular disorders, but there are several unanswered questions that frame our understanding of the role of inflammation in vascular disease," according to Calum A. MacRae, MD, PhD, of Brigham and Women's Hospital in Boston.
Writing in an accompanying editorial, MacRae said it was unclear "whether the correlation observed by [the authors] reflects a shared pathobiology or a serendipitous shared responsiveness to a specific anti-inflammatory intervention. It is difficult to infer from these data that treating skin inflammation directly results in diminished vascular inflammation."
"Even mild cases of psoriasis exhibit evidence of fluorodeoxyglucose uptake, particularly in the proximal aorta, but the distribution of these findings in the arterial tree and the absence of reliable correlates in typical atherosclerotic coronary disease complicates straightforward inferences regarding the underlying biology."
Mehta and colleagues admitted that their observational study left room for residual confounding despite adjustment. Furthermore, participants got a mix of therapies that precluded drawing any conclusions about the role of anti-TNF therapy.
Their prospective study had followed 220 patients, with 115 consecutive participants making it to 1-year follow-up. Mean age of the participants was 49.7 years; the group was 59% men. The study population also started with low baseline cardiovascular risk (Framingham risk score) and mild-to-moderate psoriasis (median Psoriasis Area and Severity Index score 5.2).
Psoriasis severity, measured as a Psoriasis Area and Severity Index score, was associated with vascular inflammation at baseline (P=0.03). Vascular inflammation, a well-known contributor to atherosclerosis, was quantified as target-to-background ratio on 18fluorodeoxyglucose positron emission tomography/CT.
Moving forward, it's important to further elucidate the role of inflammation in atherosclerosis, MacRae suggested.
"Inflammation affects multiple stages of human atherosclerosis. Cellular and humoral immunity have been implicated in the initiation and evolution of atherosclerotic plaques, in plaque vulnerability, and in acute coronary syndromes," he said. "Distinctive inflammation biology has also been implicated in other vascular syndromes, including aortic root disease, carotid arteriopathy, and peripheral arterial disease, revealing a substantial etiologic heterogeneity that has been confirmed by genetics and other studies."
"Despite these insights and increases in our understanding of the role of inflammation in atherosclerosis models, immunology has hardly influenced clinical cardiology."
"These findings suggest that controlling remote target organ inflammation (e.g., in the skin) may improve vascular diseases; however, randomized clinical trials are needed to confirm these findings," wrote Mehta's group.
For one, the randomized Vascular Inflammation in Psoriasis-Extension Trial is in the works as investigators study the effect of anti-TNF therapy with adalimumab on skin and vascular inflammation.
"These data are intriguing and support a rigorous testing of the hypothesis that intervening on psoriatic disease may mitigate vascular disorders, but there are several unanswered questions that frame our understanding of the role of inflammation in vascular disease," according to Calum A. MacRae, MD, PhD, of Brigham and Women's Hospital in Boston.
Writing in an accompanying editorial, MacRae said it was unclear "whether the correlation observed by [the authors] reflects a shared pathobiology or a serendipitous shared responsiveness to a specific anti-inflammatory intervention. It is difficult to infer from these data that treating skin inflammation directly results in diminished vascular inflammation."
"Even mild cases of psoriasis exhibit evidence of fluorodeoxyglucose uptake, particularly in the proximal aorta, but the distribution of these findings in the arterial tree and the absence of reliable correlates in typical atherosclerotic coronary disease complicates straightforward inferences regarding the underlying biology."
Mehta and colleagues admitted that their observational study left room for residual confounding despite adjustment. Furthermore, participants got a mix of therapies that precluded drawing any conclusions about the role of anti-TNF therapy.
Their prospective study had followed 220 patients, with 115 consecutive participants making it to 1-year follow-up. Mean age of the participants was 49.7 years; the group was 59% men. The study population also started with low baseline cardiovascular risk (Framingham risk score) and mild-to-moderate psoriasis (median Psoriasis Area and Severity Index score 5.2).
Psoriasis severity, measured as a Psoriasis Area and Severity Index score, was associated with vascular inflammation at baseline (P=0.03). Vascular inflammation, a well-known contributor to atherosclerosis, was quantified as target-to-background ratio on 18fluorodeoxyglucose positron emission tomography/CT.
Moving forward, it's important to further elucidate the role of inflammation in atherosclerosis, MacRae suggested.
"Inflammation affects multiple stages of human atherosclerosis. Cellular and humoral immunity have been implicated in the initiation and evolution of atherosclerotic plaques, in plaque vulnerability, and in acute coronary syndromes," he said. "Distinctive inflammation biology has also been implicated in other vascular syndromes, including aortic root disease, carotid arteriopathy, and peripheral arterial disease, revealing a substantial etiologic heterogeneity that has been confirmed by genetics and other studies."
"Despite these insights and increases in our understanding of the role of inflammation in atherosclerosis models, immunology has hardly influenced clinical cardiology."
Mehta and MacRae disclosed no relevant conflicts of interest.
Study co-authors reported numerous relationships with industry.
Study co-authors reported numerous relationships with industry.
Primary Source
JAMA Cardiology
Source Reference: Dey AK, et al "Association between skin and aortic vascular inflammation in patients with psoriasis: a case-cohort study using positron emission tomography/computed tomography" JAMA Cardiol 2017; DOI: 10.1001/jamacardio.2017.1213.Secondary Source
JAMA Cardiology
Source Reference: MacRae CA "Skin and vascular disease -- inside-out/outside-in" JAMA Cardiol 2017; DOI: 10.1001/jamacardio.2017.1420.
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