Inflammation plays an important role in the pathophysiology of vascular disease. In this review, we consider the associations between the neutrophil-lymphocyte ratio (NLR; an indicator of inflammation) and vascular disease and its associated risk factors. The NLR has received attention due to its role as an independent prognostic factor for coronary artery disease. The NLR can also be affected by atherosclerotic risk factors, such as hypercholesterolemia, metabolic syndrome, diabetes, and hypertension. Importantly, it can predict mortality in cardiovascular diseases. There are also reports of a positive correlation between the NLR and commonly used inflammatory markers. Inflammation is important not only in pathophysiology but also clinical outcomes of many diseases. The NLR is a widely available, easily derived, and reproducible marker of inflammation. Unlike many other inflammatory markers, the NLR is inexpensive and readily available and it provides additional risk stratification beyond conventional risk scores.

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A full blood count is a routine, inexpensive and easy test that provides information about formed blood contents. The platelet-lymphocyte ratio (PLR) is a novel inflammatory marker, which may be used in many diseases for predicting inflammation and mortality. The PLR can be easily calculated and is widely available but it may be affected by several inflammatory conditions. Recent studies show that a high PLR reflects inflammation, atherosclerosis and platelet activation. More research is needed to determine how the PLR may be used in clinical practice.

Endothelial dysfunction is regarded as the initial lesion in the development of atherosclerosis. Endocan, previously called endothelial cell-specific molecule 1 (ESM-1), is a new candidate immunoinflammatory marker that may be associated with cardiometabolic risk factors. Therefore, we assessed serum levels of endocan in newly diagnosed patients with untreated essential hypertension (HT). A total of 18 patients with HT and 23 normotensive control participants were included in the study. Serum endocan levels, carotid intima-media thickness (cIMT), and high-sensitivity C-reactive protein (hsCRP) were measured. Serum endocan levels were significantly higher in the HT group (P < .001). In patients with HT, serum endocan levels correlated positively with cIMT and hsCRP (r = .551, P < .001 and r = .644, P < .001, respectively). Our findings suggest that circulating endocan levels represent a new marker in patients with essential HT. Endocan may be a surrogate endothelial dysfunction marker and may have a functional role in endothelium-dependent pathological disorders.

Circulating endocan may represent a new marker that correlates with cardiovascular risk as well as the severity of disease in patients with psoriasis vulgaris. Endocan may be a surrogate endothelial dysfunction marker and may have a functional role in endothelium-dependent pathological disorders. Whether endocan levels could become a treatment target merits further investigation.