Quantification of Circulating Ednothelial Cells as Surrogate Marker for Vascular Damage

The inner lining of our vascular system consists of approximately 1.2 trillion endothelial cells. Rather than being a mere wall between the blood and organs, the endothelium is a highly dynamic structure involved in many aspects of vascular biology. Endothelial cells play an important role in regulation of vasomotor tonus, hemostasis and coagulation, fluid and electrolyte transport, inflammation, and angiogenesis. Understanding the biology of the endothelium in specific diseases that can be associated with vascular damage could be of great interest for physicians. Quantification of specific endothelial features, such as the degree of proliferation (angiogenesis) or the extent of endothelial injury, could be of predictive or prognostic value, or could enable physicians to monitor the response to treatment. A novel endothelial biomarker currently under investigation, is the number of circulating endothelial cells (CEC). CEC are endothelial cells detached from the vessel wall, and as such are considered a promising marker for endothelial damage Increased numbers of CEC have been observed in diseases with documented vascular involvement such as vasculitis, sickle cell anemia, and cancer. Also, their number correlates to putative plasma markers of endothelial injury

Circulating endothelial cells: A potential parameter of organ damage in sickle cell anemia?

Objective laboratory tools are needed to monitor developing organ damage in sickle cell disease (SCD). Circulating endothelial cells (CECs) are indicative of vascular injury. We determined whether elevated CEC can be detected in asymptomatic SCD with the CellSearch system and whether the CEC count is related to clinical and blood-based biomarkers of disease severity. Fifteen consecutive clinically asymptomatic HbSS patients and 15 matched HbAA controls were analyzed for CEC counts, laboratory parameters of disease severity (Hb, leukocyte counts, HbF%), plasma levels of markers for endothelial activation (sVCAM-1, VWF:Ag) and of endogenous inhibitors of nitric oxide synthase (asymmetrical dimethylarginine [ADMA]). CEC counts were significantly higher in patients (12 cells/mL, IQR 8-29) as compared to controls (4 cells/mL, 3-10) (P=0.007). CEC counts were significantly higher in patients with pulmonary hypertension (PHT) (P=0.015), and increased with increasing number of affected organs (0-4 involved organs, P=0.002). No significant correlations between CEC and any other laboratory parameter were detected. In conclusion, CECs could prove to be an important new tool for assessing developing vasculopathy and organ damage in SC