Abstract
Retinoic acid (RA), produced by the metabolism of vitamin A, makes effects on depression and stroke. This study was aimed to evaluate the relationship between RA levels in serum and post-stroke depression (PSD). A single-center (Chengdu, China) prospective cohort study was conducted on patients with acute ischemic stroke. The RA serum level was measured at admission. The PSD was assessed in the 3-month follow-up. The RA-PSD relationship was evaluated with conditional logistic regression. In total, 239 ischemic stroke cases and 100 healthy controls were included. The median RA serum level in patients with ischemic stroke was 2.45 ng/ml (interquartile range [IQR], 0.72-4.33), lower(P<0.001) than 3.89 ng/ml of those in control cases ([IQR]: 2.62-5.39). The crude and adjusted odds ratios [OR] (and 95% confidence intervals [CI]) of PSD associated with an IQR increase for RA were 0.54 (0.44, 0.67) and 0.66 (0.52, 0.79), respectively. Higher ORs of PSD associated with reduced RA levels (<cut-off=2.8ng/ml) were observed (OR=3.01 [95% CI, 2.34-4.98]; P<0.001). This study revealed that, in patients with ischemic stroke, reduced RA serum level was related to higher risk of PSD at 3 months, which may be applied as a predictive indicator.
Highlights
Stroke has been a leading cause of disability and death worldwide [1]
A multivariate model was constructed with reduced levels of Retinoic acid (RA) (
Previous studies have confirmed that Post-stroke depression (PSD) was caused by multiple factors, conformed to the biopsychosocial model of mental illness [18]
Summary
Stroke has been a leading cause of disability and death worldwide [1]. In China, stroke is associated with the highest disability-adjusted life-years loss of any disease, and with over 2 million new cases annually [2]. Since China contains a fast ageing population, it has been a challenge to prevent and control stroke as well as its complications [3]. A meta-analysis showed that PSD significantly increased risk of death in stroke patients [5]. Psychopathological mechanism of PSD has been complex and unclear, which may be associated with the neurobiological dysfunctions induced by ischemic stroke, such as the neuroinflammatory caused by ischemia, stress activation of the hypothalamic-pituitary-adrenal (HPA) axis, as well as the dysfunction of adaptive response [6]
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