The severity of psoriasis appears to correlate with the degree of aortic vascular inflammation in patients who have psoriasis, according to a prospective observational study comparing patients with psoriasis with age- and sex-matched controls.
To better characterize the known relationship between psoriatic skin disease and atherosclerosis, they assessed vascular inflammation using 18F-fluorodeoxyglucose–positron emission tomography/computed tomography (FDG-PET/CT) of the aorta in 60 adults with moderate to severe psoriasis and 22 healthy control subjects (mean age, 44 years) during a 2-year period. FDG uptake in the blood vessel wall denotes activated endothelial cells and cellular infiltration in noncalcified atherosclerotic plaques and is a direct, reliable marker of vascular inflammation, said Dr. Haley B. Naik of the cardiovascular and pulmonary branch, National Heart, Lung, and Blood Institute in Bethesda Md., and her associates. The study was published online on Oct. 8 (Arterioscler Thromb Vasc Biol. 2015 Oct 8. doi: 10.1161/ATVBAHA.115.306460).
As the severity of psoriasis increased, as measured by scores on the Psoriasis Area Severity Index (PASI), the degree of vascular inflammation also increased. This association was stronger than would be expected, given the psoriasis patients’ already increased cardiovascular risk based on traditional risk factors (their higher incidence of obesity, dyslipidemia, hypertension, diabetes, and smoking) and their elevated Framingham risk scores and higher levels of C-reactive protein. This suggests that “psoriasis plaques are biologically active in promoting inflammation at remote sites,” the investigators concluded.
In addition, they found that the absolute neutrophil count in the circulation was significantly elevated in psoriasis patients, compared with control subjects (mean, 3.7 vs. 2.9). Immunophenotyping by flow cytometry identified a significant increase in neutrophil frequencies in whole blood (mean, 65.2 vs. 56.3). Protein markers of neutrophil activation also were significantly elevated. Levels of these markers correlated with both psoriasis severity and vascular inflammation, suggesting that the two disorders may share the same immune-mediated mechanism.
“Our observation that the psoriatic atherosclerotic milieu is upregulated in concert with markers of neutrophil activation underscores the concept that atherosclerosis may involve complex neutrophil biology, which future studies should focus on elucidating, especially after intervention,” Dr. Naik and her associates added.