Key result
Lichen planus is linked to increased epicardial fat thickness, driven by longer disease duration.
Why the study?
Is epicardial fat tissue thickness increased in patients with lichen planus compared to controls?
Case-Control (n=104)
Is epicardial fat tissue thickness increased in patients with lichen planus compared to controls?
Patients with lichen planus have increased epicardial fat tissue thickness, which correlates with disease duration and inflammatory markers, suggesting an increased risk of subclinical atherosclerosis.
Should not change lichen planus management; hypothesis-generating for epicardial fat as cardiovascular risk marker.
Lichen planus (LP) is a mucocutaneous inflammatory disease. Inflammation plays a major role in the progression of atherosclerosis. Epicardial fat tissue (EFT) has been shown to produce and secrete various proatherogenic and proinflammatory hormones and cytokines. The aim of this study was to assess EFT in patients with lichen planus. Fifty-four patients with LP and 50 controls were enrolled in the study. LP was diagnosed according to the World Health Organization criteria. EFT was measured on the free wall of the right ventricle in parasternal long-axis view, as previously described and validated. There were positive correlations between EFT thickness and platelet/lymphocyte ratio, neutrophil/lymphocyte ratio, duration of LP, and high-sensitivity C-reactive protein (hsCRP) (p<0.001, p<0.001, p=0.002 and p<0.001, respectively). In multivariate analysis, after adjustments for relevant confounders, LDL cholesterol, hsCRP, platelet/lymphocyte ratio and duration of LP were independent predictors of EFT thickness in patients with LP (β=0.231, p=0.014; β=0.205, p=0.037; β=0.361, p=0.001 and β=0.133, p=0.047, respectively). EFT is increased in patients with LP compared to control subjects. Duration of LP is correlated with EFT, and duration of LP is also an independent predictor of increased EFT, which is a predictor of subclinical atherosclerosis. O líquen plano (LP) é uma doença inflamatória mucocutânea. A inflamação tem um papel importante na progressão da aterosclerose. Demonstrou-se que o tecido adiposo epicárdico (TAE) produz e segrega várias hormonas e citocinas pró-aterogénicas e pró-inflamatórias. O objetivo deste estudo foi a avaliação do TAE em pacientes com LP. Cinquenta e quatro pacientes com LP e 50 controlos foram inscritos no estudo. O LP foi diagnosticado de acordo com os critérios da Organização Mundial de Saúde. O TAE foi medido na parede livre do ventrículo direito, do ponto de vista do eixo longo para-esternal, conforme descrito e validado anteriormente. Verificaram-se correlações positivas entre a espessura da gordura epicárdica e a relação linfócitos-plaquetas, a relação neutrófilos-linfócitos, a longevidade do LP, e o hsCRP (p < 0,001, p < 0,001, p = 0,002 e p < 0,001, respetivamente). Após análises multivariadas e ajustamentos para confundidores relevantes (colesterol LDL, hsCRP, relação plaquetas-linfócitos e longevidade do LP), foram confirmados como preditores independentes da espessura da gordura epicárdica em pacientes com LP (β = 0,231, p = 0,014; β = 0,205, p = 0,037; β = 0,361, p = 0,001 e β = 0,133, p = 0,047, respetivamente). O TAE está aumentado em pacientes com LP em comparação com o grupo de controlo. A longevidade do LP está correlacionada com o TAE, e a sua longevidade é uma variável independente de previsão do TAE aumentado, que por sua vez é uma variável de previsão da aterosclerose subclínica.
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Ertem et al. (2016) conducted a case-control in Lichen planus (n=104). Lichen planus vs. Control subjects was evaluated on Epicardial fat tissue (EFT) thickness. Epicardial fat tissue thickness is increased in patients with lichen planus compared to controls, with disease duration acting as an independent predictor of this increase (β=0.133, p=0.047).
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