Subclinical Atherosclerosis in Alopecia Areata: Usefulness of Arterial Ultrasound for Disease Diagnosis and Analysis of Its Relationship with Cardiometabolic Parameters.

UNLABELLED: Background/

Objectives

Chronic systemic inflammation is a risk factor that increases the development of atherosclerosis and predisposes to cardiovascular diseases (CVDs). The systemic inflammatory profile of alopecia areata (AA) regarding IFNγ and Th1 cytokine dysregulation has previously been described, suggesting an increased incidence of CVDs in this population. No previous studies investigated the possible relationship between atherosclerosis and AA by cardiovascular imaging techniques. To determine the prevalence, distribution and burden of subclinical atherosclerosis in AA.

METHODS

We conducted a case-control study in 62 participants, including 31 patients with severe AA (SALT > 75) and 31 healthy controls, matched for age, sex and body mass index (BMI). The participants underwent a detailed history assessment and were subjected to the measurement of weight, height, abdominal circumference and blood pressure. A fasting blood sample was also collected. Subclinical atherosclerosis was evaluated by ultrasonography of the bilateral femoral and carotid arteries.

RESULTS

The AA patients had an increased prevalence of subclinical atherosclerosis (54.7%) compared to the healthy controls (22.6%, p = 0.010). The prevalence of atheroma plaques was significantly higher in the carotid arteries (41.90% vs. 12.9%, p = 0.009), while no significant differences were found in femoral plaque prevalence. The AA patients with atherosclerotic plaques were older (p < 0.001) and had a longer time since AA diagnosis (p = 0.11) and increased serum levels of glycated hemoglobin (p = 0.029) and triglycerides (p = 0.009). In a regression analysis, duration of disease and neutrophil/lymphocyte ratio were the main predictors of atherosclerosis.

CONCLUSIONS

AA patients have an increased prevalence of carotid subclinical atherosclerosis. The duration of AA, systemic inflammation and insulin resistance appear to play a role in the development of subclinical atherosclerosis in this population.