Background: Cardiovascular risk is well-recognized in spondyloarthritis (SpA) and is primarily attributed to systemic inflammation and metabolic disturbances. Hyperhomocysteinemia, an established cardiovascular risk factor, may further contribute to this increased risk.

Objectives: The aim of this study was to assess the prevalence of hyperhomocysteinemia in patients with SpA and to examine its relationship with cardiovascular risk, as evaluated by the QRISK3 score.

Methods: This was a cross-sectional study conducted in the rheumatology department of the military hospital of Tunis over a two-month period (November–December 2024). Patients diagnosed with SpA according to the ASAS 2009 criteria were included. Sociodemographic, clinical, and biological data were collected. Homocysteine levels were measured in all patients, with hyperhomocysteinemia defined as a concentration > 15 µmol/L. Cardiovascular risk was evaluated using the QRISK3 score, calculated via an online application. This score estimates the 10-year risk of developing cardiovascular disease for patients aged 25 to 84 years. Cardiovascular risk was categorized into three levels: low risk (QRISK3 < 10%), moderate risk (QRISK3 10–20%), and high risk (QRISK3 > 20%).

Results: Sixty-one patients were included in the study. The sex ratio (M/F) was 5.77 (52 men and 9 women). The mean age was 40.84 ± 11.45 years. The mean age at disease onset was 34.71 ± 11.53 years. The mean disease duration was 5.80 ± 6.22 years. The SpA phenotypes were as follows: axial SpA in 32 cases (52.5%), axial and peripheral SpA in 21 cases (34.4%), arthritis associated with inflammatory bowel disease in 5 cases (8.2%), and psoriatic arthritis in 1 case (1.6%). Smoking was reported in 23 patients (37.7%), and alcohol consumption in 7 patients (11.5%). Five patients had a history of hypertension, and 2 were diabetic. The mean weight was 77.28 ± 13.58 kg (47–105 kg). The mean BMI was 25.88 kg/m² ± 4.61, and the mean waist circumference was 93.96 ± 11.59 cm (66–117 cm). The mean waist-to-hip ratio was 0.92± 0.07 (0.76–1.13). The mean systolic blood pressure was 124.57 ± 15.36 mmHg (95–169 mmHg). The mean levels of cholesterol, triglycerides, LDL-C, and HDL-C were 4.26 ± 0.87 mmol/L, 1.22 ±0.94 mmol/L, 2.61 ± 0.73 mmol/L, and 1.12 ± 0.28 mmol/L, respectively. The mean homocysteine level was 13.37 ± 4.16 µmol/L (7.55–24.89 µmol/L). The mean CRP and ESR levels were 12.87 ± 19.62 mg/L (0–91) and 26.94 ± 26.27 mm/h (5–105), respectively. The mean disease activity indices were: ASDAS-CRP 2.91 ± 1.27 (0–8.10), ASDAS-ESR 1.91 ± 1.27 (0–5.70), and BASDAI 2.30 ± 1.13 (0.70–6.20). Sixteen patients had hyperhomocysteinemia. The QRISK3 score was calculated for 60 patients, with a mean of 3.59% ± 5.69 (0.20–35.90%). Fifty-five patients (90.2%) had a low cardiovascular risk, 4 patients had a moderate risk, and 1 patient was at high cardiovascular risk. A positive correlation was observed between homocysteine levels and age (r = 0.431; p = 0.001), and age at disease onset (r = 0.311; p = 0.016). No significant correlation was found between homocysteine levels and other disease parameters: weight (p = 0.244), BMI (p = 0.802), waist circumference (p = 0.348), ASDAS-CRP (p = 0.909), ASDAS-ESR (p = 0.787), BASDAI (p = 0.765), CRP (p = 0.975), and ESR (p = 0.383). A positive correlation was found between the QRISK3 score and homocysteine levels (r = 0.382; p = 0.003), age (r = 0.946; p <0.001), age at disease onset (r = 0.737; p <0.001), disease duration (r= 0.405; p = 0.001), waist circumference (r = 0.324; p = 0.014), waist-to-hip ratio (r = 0.408; p = 0.002), cholesterol levels (r = 0.262; p = 0.049), and LDL-C levels (r = 0.571; p <0.001). However, no significant correlation was found between the QRISK3 score and disease activity indices, and inflammatory parameters.

Conclusion: This study highlights a significant association between homocysteine levels and cardiovascular risk, as assessed by the QRISK3 score, in patients with SpA. Screening for hyperhomocysteinemia may improve risk stratification and guide preventive strategies in this population.

REFERENCES: NIL.

Acknowledgements: NIL.

Disclosure of Interests: None declared.

© The Authors 2025. This abstract is an open access article published in Annals of Rheumatic Diseases under the CC BY-NC-ND license ( http://creativecommons.org/licenses/by-nc-nd/4.0/ ). Neither EULAR nor the publisher make any representation as to the accuracy of the content. The authors are solely responsible for the content in their abstract including accuracy of the facts, statements, results, conclusion, citing resources etc.