Background: Psoriasis is a chronic relapsing skin disease affecting 1-3% of the world’s population. One of the most severe disabling manifestations of this disease is psoriatic arthritis (PsA), which varied between 10% and 40% of the total number of cases. In addition to skin and joint involvement, there is a growing evidence suggesting that patients with PsA also have increased risk of cardiovascular (CV) disease, mostly due to endothelial dysfunction (ED). One of the novel CV risk factor among rheumatological patients, which is actively discussed in the current literature and has a direct impact on the state of the endothelium, is hyperhomocysteinemia (HHcy).

It has been established that homocysteine (HC) disrupts the normal production of nitric oxide by endothelial cells and reduces its bioavailability, promotes the accumulation of low-density lipoprotein in cell membranes and the intercellular space, as well as to a decrease in the synthesis of sulfur-containing glycosaminoglycans, which leads to a decrease in the elasticity of the vascular wall. As a result, vessels lose elasticity, which reduces their ability to vasodilate, which is one of the key stages of ED.

Objectives: To determine the role of homocysteine in the development of endothelial dysfunction and cardiovascular diseases in patients with psoriatic arthritis

Methods: In total, ninety-seven patients with PsA, who fulfilled the disease criteria (CASPAR) were examined using standard diagnostic methods (including C-reactive protein, lipid profile), evaluation endothelium-dependent vasodilation in response to reactive hyperemia (EDVD) and level of HC. The QRISK-3 scale were used to assess the 10-year risk of CV diseases. The control group, which were consisted from twenty-five healthy adults were also examined.

Results: Intermediate (6.56 ± 0.39 %) risk of adverse CV events within the next 10 years was estimated for PsA patients and it was 7 to 8 – fold higher than the Q - score of a healthy age, sex, and ethnicity – matched subjects. The results of the study of endothelial function in patients with PsA demonstrated that reduced EDVD (less than 10%), which is a direct sign of dysfunction of endothelium, was more common among examined patients compared to the control group (75.3% vs. 11.8%, respectively). Level of HC was quantified in patients with PsA (15.79 ± 0,74 mkmol/l) and in the control cohort (9,05 ± 0,41 mkmol/l). Comparing two groups, results were significantly different ( p = 0.0001). Finally, we analyzed the relationship between HC count, comorbidities, cardiovascular risk factors and EDVD in patients with PsA. Increased HC level (more than 10.0 mkmol/l) was associated with duration of disease (rs=0,61), increased CRP (rs=0,59), high blood pressure (rs=0,57), hypercholesterolemia (r=0,49), increased BMI (rs=0,45), decreased EDVD (rs=–0,89) and Q-risk index (rs=0,77).

Conclusion: Level of HC was significantly higher in patients with PsA, positively correlated with the CV risk index (Q-Risk) and the main factors of CV diseases, specific marker of ED - EDVD. Were also found associations with long standing disease activity, during which chronic inflammation plays a direct role in promoting vascular inflammation, vessel damage and clinical CV events. The causes of HHcy requires further studies while the effect of proinflammatory agents on the endothelial state and the development of dyslipidemia in the setting of a prolonged autoimmune process has already been described, the role of HC in the above conditions has not been studied well.

REFERENCES: [1] Armstrong AW, Read C. Pathophysiology, clinical presentation, and treatment of psoriasis: a review. JAMA. 2020;323(19):1945-1960.

[2] Peluso R, Caso F, Tasso M, et al. Cardiovascular Risk Markers and Major Adverse Cardiovascular Events in Psoriatic Arthritis Patients. Rev Recent Clin Trials . 2018;13(3):199-209.

[3] Yang Q, He GW. Imbalance of Homocysteine and H2S: Significance, Mechanisms, and Therapeutic Promise in Vascular Injury. Oxid Med Cell Longev. 2019 Nov 22; 2019:7629673.

Acknowledgements: NIL.

Disclosure of Interests: None declared.