title: Cardiovascular involvement in psoriatic arthritis.
abstract: Psoriasis is a chronic, genetically determined and immunomediated inflammatory skin disease that affects 2-3% of the Caucasian population. A considerable proportion of these patients develop a form of inflammatory arthritis known as psoriatic arthritis (PsA), although the prevalence of this has not been well defined. Patients with PsA have a higher mortality rate than the general population and the risk of mortality is related to disease severity at the time of presentation. Endothelial dysfunction and early atherosclerosis have been found in patients with PsA without any cardiovascular disease (CVD) risk factors, and experts believe that CVD is one of the leading causes of death, as it is in patients with rheumatoid arthritis (RA). Various disease-related mechanisms may be involved in the development of premature vascular damage in both cases, including an increased synthesis of proinflammatory mediators (such as cytokines, chemokines and adhesion molecules), autoantibodies against endothelial cell components, perturbations in T-cell subsets, genetic polymorphisms, hyperhomocysteinemia, oxidative stress, abnormal vascular repair, and iatrogenic factors. In a recent study of 22 patients with PsA without any signs of CVD, we found that the plasma concentration of asymmetric dimethylarginine (ADMA) levels were significantly high and coronary flow reserve (CFR) was significantly reduced. Moreover, there was a significant correlation between CFR and plasma ADMA levels in the PsA group. The significant correlation between the reduced CRF and increased ADMA levels suggests that, like patients with early RA, PsA patients suffer from endothelial dysfunction and impaired coronary microcirculation. Active PsA is a risk factor for CVD, and so PsA patients should be screened for subclinical forms of the disease and its risk factors, and an early treatment approach should be adopted.
authors.affiliation: Rheumatology Unit, L. Sacco University Hospital, Milan, Italy.
authors.forename: F
authors.initials: F
authors.lastname: Atzeni
authors.forename: M
authors.initials: M
authors.lastname: Turiel
authors.forename: L
authors.initials: L
authors.lastname: Boccassini
authors.forename: S
authors.initials: S
authors.lastname: Sitia
authors.forename: L
authors.initials: L
authors.lastname: Tomasoni
authors.forename: M
authors.initials: M
authors.lastname: Battellino
authors.forename: A
authors.initials: A
authors.lastname: Marchesoni
authors.forename: V
authors.initials: V
authors.lastname: De Gennaro Colonna
authors.forename: P
authors.initials: P
authors.lastname: Sarzi-Puttini
mesh_terms: D018501:Antirheumatic Agents / Q000494:pharmacology / Q000627:therapeutic use; D001120:Arginine / Q000031:analogs & derivatives / Q000097:blood; D015535:Arthritis, Psoriatic / Q000097:blood / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D003326:Coronary Circulation; D003327:Coronary Disease / Q000097:blood / Q000209:etiology / Q000517:prevention & control; D016207:Cytokines / Q000378:metabolism; D006331:Heart Diseases / Q000097:blood / Q000209:etiology* / Q000517:prevention & control; D006801:Humans; D007249:Inflammation; D008833:Microcirculation; D012307:Risk Factors; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors
chemical_list: D018501:Antirheumatic Agents; D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; C018524:N,N-dimethylarginine; D001120:Arginine