Patients with cutaneous lupus erythematosus may face a 72% higher risk of developing atherosclerotic cardiovascular disease compared with disease-free controls, according to a recent study.
In the retrospective cohort study, published in JAMA Dermatology, investigators evaluated the incidence and prevalence of atherosclerotic cardiovascular disease (ASCVD) in patients with cutaneous lupus erythematosus (CLE), systemic lupus erythematosus (SLE), psoriasis, and matched disease-free controls. The study utilized data from the IBM MarketScan database (2018 to 2020) and included 8,138 patients with CLE matched with 24,675 with SLE, 192,577 with psoriasis, and 81,380 controls, with all participants free of overlapping conditions. The investigators aimed to determine the independent association of CLE with ASCVD compared with SLE, psoriasis, and controls, adjusting for traditional cardiovascular risk factors.
The median age of the participants with CLE was 49 years, and 81% were female. Prevalence analysis showed ASCVD in 2.24% of those with CLE compared with 2.06% in SLE and 1.44% in psoriasis. Multivariable logistic regression revealed that patients with CLE had a significantly higher risk of ASCVD compared with controls (odds ratio [OR] = 1.72, 95% confidence interval [CI] = 1.45–2.02, P < .001), whereas the highest risk was observed in SLE (OR = 2.41, 95% CI = 2.14–2.70, P < .001). Psoriasis was not associated with an increased prevalence (OR = 1.03, 95% CI = 0.95–1.11, P = .48).
Over a median follow-up of 36 months, ASCVD incidence rates were highest in SLE (24.8 per 1,000 person-years), followed by CLE (15.2 per 1,000 person-years), psoriasis (14.0 per 1,000 person-years), and controls (10.3 per 1,000 person-years). Multivariable Cox regression showed increased risk for CLE (hazard ratio [HR] = 1.32, 95% CI = 1.13–1.55, P < .001) and SLE (HR = 2.23, 95% CI = 2.05–2.43, P < .001), but not psoriasis (HR = 1.06, 95% CI = 0.99–1.13, P = .09).
The association between CLE and ASCVD risk appeared to involve multiple factors, including direct contributions from inflammatory pathways such as the interferon signature observed in CLE, and indirect effects through comorbid conditions like metabolic syndrome, diabetes, and obesity. Smoking, a shared risk factor for both CLE and ASCVD, further complicated this relationship, but its impact could not be fully assessed as a result of limitations in smoking status data within the claims database. Additionally, the study's exclusion of patients aged older than 65 years limited the generalizability of findings to populations at higher absolute risk for ASCVD.
The researchers concluded that CLE was independently associated with increased ASCVD risk, warranting targeted screening and management. The findings emphasized the need to consider CLE as a risk enhancer in cardiovascular prevention strategies, with further studies required to elucidate the role of comorbidities and systemic therapies in this association.
Full disclosures can be found in the published study.