Endocan Levels Research Articles

Evaluation of endothelial dysfunction in patients with familial Mediterranean fever: the relationship between the levels of asymmetric dimethylarginine and endocan with carotid intima–media thickness and endothelium-dependent vasodilation

It has been suggested that there is an ongoing subclinical inflammation in familial Mediterranean fever (FMF) patients also in attack-free periods as well. Due to this ongoing inflammation, endothelial dysfunction (ED) may develop. Previously, ED has been suggested to increase the risk of the atherosclerosis and cardiovascular disease (CVD). Endocan is recognized as a specific molecule of the endothelium and has been shown to increase in some cases associated with inflammation. However, there is not sufficient data whether those with FMF could develop ED in the early period of life. In this study, we aimed to investigate ED and its relation with endocan in young FMF patients. A total of 57 male patients diagnosed with FMF according to the Tel Hashomer criteria and a total of 33 healthy males with similar characteristics to the patient group were included in this research. Complete blood count, erythrocyte sedimentation rate (ESR), fibrinogen, serum glucose, serum LDL cholesterol (LDL-C) and triglyceride (TG), asymmetric dimethylarginine (ADMA), and endocan levels were tested from fasting blood samples. Moreover, carotid intima-media thickness (CIMT) and flow-mediated dilatation (FMD) were measured. The endocan levels of the FMF patients during an attack-free period were significantly higher than those of the control group (p<0.001). On the other hand, FMD measurements were significantly lower among FMF patients (p<0.001). ADMA levels were higher in the patient group; however, this difference was similar (p>0.05). CIMT values were similar among FMF patients and healthy controls (p>0.05). These results have suggested that ED may develop in the patients with FMF who have no additional CVD risk, even during young adulthood, and endocan may be a favorable biomarker at demonstration of ED than ADMA among FMF patients.

Diagnostic Significance of Measuring Vascular Endothelial Growth Factor for the Differentiation between Malignant and Tuberculous Pleural Effusion.

Malignancy and tuberculosis are common causes of lymphocytic exudative pleural effusion. However, it is occasionally difficult to differentiate malignant pleural effusion from tuberculous pleural effusion. Vascular endothelial growth factor (VEGF) is a critical cytokine in the pathogenesis of malignant pleural effusion. Endocan is a dermatan sulfate proteoglycan that is secreted by endothelial cells. Importantly, endocan mediates the vascular growth-promoting action of VEGF. The aim of this study was to evaluate the diagnostic significance of VEGF and endocan in pleural effusion. We thus measured the levels of VEGF and endocan in the pleural effusion and serum samples of patients with lung cancer (n = 59) and those with tuberculosis (n = 32) by enzyme-linked immunosorbent assay. Lung cancer included 40 cases of adenocarcinoma, 13 of squamous cell carcinoma, and 6 of small cell carcinoma. Pleural effusion VEGF levels were significantly higher in the malignant group than in the tuberculosis group (2,091.47 ± 1,624.80 pg/mL vs. 1,291.05 ± 1,100.53 pg/mL, P < 0.05), whereas pleural effusion endocan levels were similar between the two groups (1.22 ± 0.74 ng/mL vs. 0.87 ± 0.53 ng/mL). The areas under the curve of VEGF and endocan were 0.73 and 0.52, respectively. Notably, the VEGF levels were similar in malignant pleural effusion, irrespective of the histological type of lung cancer. Moreover, no significant difference was found in the serum VEGF and endocan levels between patients with lung cancer and those with tuberculosis. In conclusion, high VEGF levels in pleural effusion are suggestive of malignant pleural effusion.

Serum endocan levels before and after surgery on low-grade gliomas.

Background:Endocan has been shown to be a marker for several cancers and may show degree of malignancy. The aim of this study is to assess serum levels of endocan before and after surgery on low-grade gliomas (LGGs).Methods:Endocan was assayed by commercially available enzyme-linked immunosorbent assay (ELISA) kits in a total of 19 patients and 12 controls. Serial serum samples were obtained before and after surgery (1st day, 1st week, and 1st month of surgery). Control samples were collected from cord blood during cesarean section. The results were compared with control brain tissues.Results:Controls showed significantly lower serum endocan levels compared to before and after surgery (P < 0.05). There is a trend of increase in mean serum levels from before surgery and during the very early period after surgery (during first week); however, in the first month, mean serum levels became lower.Conclusion:Endocan, a vital molecule for angiogenesis, is highly expressed before and after surgery in LGGs, but long-term data is needed. Furthermore, future studies should include high-grade gliomas to discuss whether endocan is associated with recurrence and response to treatment.

Could “calprotectin” and “endocan” serve as “Troponin of Nephrologists”?

AKI, a serious, common and occasionally under-recognized condition, which is a significant contributor to the growing incidence of CKD and end-stage renal disease (ESRD). To date, the diagnosis of AKI is made by serial measurement of Cr and BUN which are late and imprecise markers of kidney injury. “Calprotectin” and “endocan” are two biomarkers that could reflect renal tubular injury and glomerular/endothelial-vascular damage, respectively. Measurement of urinary calprotectin could help the physicians to diagnose tubular degradation and differentiate prerenal AKI from intrinsic AKI. Serum level of endocan could signify endothelial damage. Herein it is hypothesized that calprotectin and endocan may help the clinicians to diagnose intrinsic AKI, earlier than rise of serum creatinine, differentiate AKI from acute presentation of CKD and also discriminate tubular injury from glomerular/vascular-endothelial injury, assess the prognosis and extent of renal damage and plan for appropriate therapy which may render these biomarkers as potentially applicable equivalents of Troponin in the field of nephrology.

Endocan is a predictor of increased cardiovascular risk in women with polycystic ovary syndrome

ABSTRACTPurpose: Endocan is a proteoglycan secreted mainly from endothelial cells. It has been implicated that there is a link between endocan and endothelial dysfunction. Polycystic ovary syndrome (PCOS) is a reproductive and metabolic disease associated with increased risk of cardiovascular events. The aims of this study were to ascertain whether circulating endocan levels are altered in women with PCOS, and whether there is an association between endocan and carotid intima media thickness (cIMT). Materials and methods: This cross-sectional study included 80 women with PCOS and 80 age- and BMI-matched controls without PCOS. Circulating endocan levels were measured using ELISA. Metabolic, hormonal parameters and cIMT were determined. 2-h oral glucose tolerance test (2-h OGTT) was performed on all women. Results: Circulating endocan levels were significantly elevated in women with PCOS compared with controls (5.99 ± 2.37 vs. 3.66 ± 1.79 ng/ml, P < 0.001). Endocan levels positively correlated with BMI, homeostasis model assessment of insulin resistance (HOMA-IR), free androgen index (FAI), high-sensitivity C-reactive protein (hs-CRP), and cIMT in both PCOS and control groups. Endocan levels did not correlate with fasting blood glucose, 2-h OGTT, A1C and lipid parameters. Multiple linear regression analysis revealed that endocan is an independent predictor for cIMT (β = 0.128, 95% CI = 0.118–0.138, P = 0.011). Conclusions: Circulating endocan levels are significantly higher in women with PCOS and endocan is independently associated with cIMT. Elevated endocan levels can be a predictor of increased cardiovascular risk in PCOS subjects.

Endocan and albuminuria in type 2 diabetes mellitus

Background: Endocan is a newly identified proteoglycan released from endothelium, stimulating angiogenesis and when increased, indicates endothelial activation (inflammation). Our aim was to examine the association between serum endocan levels and urine albumin–creatinine ratio (UACR).Method: One hundred and thirty-seven patients with type 2 diabetes mellitus and normal serum creatinine who had no co-morbidities other than hypertension, diabetic nephropathy, retinopathy, or neuropathy were divided into normoalbuminuria (G1), microalbuminuria (G2), and macroalbuminuria (G3) groups and compared cross-sectionally regarding serum endocan levels.Result: There were 55, 47, and 35 patients in G1, G2, and G3, respectively. The groups were comparable in terms of gender, age, duration of diabetes, diabetic neuropathy/retinopathy, fasting glucose, HbA1c, serum creatinine level, and eGFR. Patients in G3 had significantly higher blood pressure but lower serum albumin and endocan levels. UACR showed a negative bivariate correlation with serum endocan levels (r = −.282, p = .001). There was bivariate positive correlation between endocan and systolic blood pressure (r=.185, p = .030). In linear regression analysis, UACR was negatively correlated with endocan while positively correlated with systolic blood pressure, duration of diabetes, and platelet distribution width.Conclusion: Patients with macroalbuminuria had lower endocan levels, and increasing UACR was associated with decreasing serum endocan levels. Despite the occurrence of angiogenesis and glomerular hypertrophy in the early phase of diabetic nephropathy, ensuing significant renal injury over time may reduce the expression of endocan. Serum endocan levels may represent a novel marker for nephropathy progression.

Serum endocan levels in endometrial and ovarian cancers.

Ovarian and endometrial carcinomas are the two most common malignancies of the female reproductive system. Endocan is a proteoglycan that is specific to vascular endothelial cells. Increased serum levels have been reported in some tumors. The aim of this study was to investigate serum endocan levels in cases of endometrial and ovarian cancer. Levels of serum endocan were assessed in 27 patients with endometrial cancer and 20 with ovarian cancer, and in 38 control subjects with benign ovarian or endometrial disorders. Thirty-five healthy subjects were also included. Serum endocan levels were measured using a specific enzyme-linked immunosorbent assay. Serum CA-125 levels were also measured in the patient and control groups. All patients had detectable serum endocan levels among endometrial and ovarian cancer groups except six cases. However, in the benign and healthy control groups, all endocan levels were undetectable except for two cases in the benign group and three in the healthy control group. Serum endocan levels were significantly higher in the entire patient group than in the controls (P<.0001 for both). Serum endocan levels in cases of endometrial cancer and ovarian cancer were higher than in both the control groups (P<.0001 for both). Evaluation of all groups revealed a positive correlation between serum CA-125 and endocan levels (r=.43, P<.0001). Although benign ovarian or endometrial disorders do not lead to expression of endocan, malignant cases can result in measurable endocan levels. This may be useful in differentiating benign and malign diseases of the endometrium or ovary.

Vitamin D Treatment Effect on Serum Endocan and High-Sensitivity C-Reactive Protein Levels in Renal Transplant Patients.

Endocan is a marker showing endothelial dysfunction and inflammation. Significantly increased endocan levels have been observed in serum of patients with sepsis and cancer. Our aim was to investigate the relationship between vitamin D treatment and serum endocan and high-sensitivity C-reactive protein (hs-CRP) levels as inflammatory markers in transplant patients. Prospective. Nephrology clinic. Thirty-eight renal transplant patients with serum 25-hydroxy-vitamin D (25-OH-vitamin D) levels below 20 ng/mL and transplanted at least 12 months. One-time oral dose of 300 000 IU vitamin D3. Before and after vitamin D treatment, serum endocan, hs-CRP, calcium, phosphorus, and parathyroid hormone (PTH) levels were measured. Median serum endocan and PTH values before vitamin D were significantly higher than those of after treatment values ( P = .001 and P < .001, respectively). On the other hand, serum total calcium and phosphorus levels before vitamin D treatment were lower than the values obtained after vitamin D treatment ( P = .0013 and P < .001, respectively). Serum hs-CRP was lower after vitamin D therapy than before, but the difference was not statistically significant ( P = .06). A moderate negative correlation was determined between endocan and 25-OH-vitamin D levels after treatment with vitamin D ( r = -.36, P = .02). This study has revealed that vitamin D treatment reduced markers of endothelial dysfunction in patients with renal transplantation and vitamin D deficiency.

Endocan: a novel biomarker associated with well-developed coronary collateral circulation in patients with stable angina and chronic total occlusion.

Angiogenesis and arteriogenesis have a crucial role in the formation of coronary collateral vessels. It has been shown that endocan and vascular cell adhesion molecule-1 (VCAM-1) are potential angiogenetic factors. We investigated the relationship between serum endocan levels and grade of coronary collaterals, and also the correlation of endocan levels with serum VCAM-1 levels. Patients with stable angina and at least one total coronary occlusion at invasive coronary angiography were included in our study. Collateral degree was graded according to Rentrop and Cohen's classification. Patients who had grade 0 or 1 collateral vessels were included in the poorly-developed collateral group, and those with grade 2 or 3 coronary collateral vessels were included in the well-developed collateral group. Serum endocan and VCAM-1 levels were significantly higher in the well-developed collateral group (436.6 ± 213.3ng/mL vs. 216.1 ± 78.5ng/mL, p < .001; 11.02 ± 6.58ng/mL vs. 6.78 ± 1.14ng/mL, p < .001, respectively). In a logistic regression analysis, only serum endocan level remained as an independent predictor for good collateral development. In the ROC curve analysis, 282ng/mL endocan level had an a 82 % sensitivity and 86 % specificity for prediction of the well-developed collateral group. Higher endocan level was related to better coronary collateral development. In the event that these results are confirmed in further studies, endocan may be considered as an anti-ischemic treatment strategy in order to improve collateral development.

OS 01-02 ENDOCAN LEVEL IN ESSENTIAL HYPERTENSION

Objective: Endocan, human endothelial cell-specific molecule, which is expressed by the vascular endothelium may play role in endothelium-dependent inflammatory process leading to the development of hypertension. The aim of the study was to estimate endocan concentration in 121 patients with primary hypertension and proper renal function as also in healthy individuals from the control group and to estimate endocan levels in subgroups with proper blood pressure control and without. Design and Method: The endocan concentration was estimated in 121 hypertensive patients (median age 56 min-19, max-85). The medical history, office blood pressure measurements, 24 hour ambulatory blood pressure measurement (ABPM), laboratory tests and the echocardiography were taken, the medical therapy was analysed. The correlation between endocan levels and catecholamine concentration in blood, blood pressure control, type of pharmacological therapy and medical history were analysed. Results: The median endocan concentration in the whole study group was 1.91 ng/ml. The median endocan level was significantly higher in hypertensive patients than in control group (Me = 2,02 ng/ml vs 1.09 ng/ml, p = 0.0001). The median office blood pressure in hypertensive patients was 145,5/86 mmHg and was significantly higher than the median home blood pressure measurements, which was 135/80 mmHg, p < 0,05. Endocan was higher in patients without proper blood pressure control in ambulatory measurements (Me = 2.28ng/ml vs Me = 1.91ng/ml). There were no statistically significant differences between endocan level and office blood pressure measurements. Negative correlation was observed between endocan level and BMI (r = −0.19, p = 0.046). Conclusions: Endocan, as indicator of the endothelium dysfunction could be a predictor of cardiovascular events. Higher endocan concentration in patients with primary hypertension than in control group as also higher endocan levels in subgroup with inadequate blood pressure control in ambulatory measurements need further studies to find out the exact role of endocan in pathogenesis and treatment of primary hypertension.

Evaluation of Cardiovascular Risk Factors, Haematological and Biochemical Parameters, and Serum Endocan Levels in Patients with Lichen Planus

Background and Objective: The current study aimed to evaluate cardiovascular risk factors, haematological and biochemical parameters, and serum endocan concentrations in lichen planus (LP) patients. Methods: This study was conducted with 86 cases, including 43 LP patients and 43 healthy controls. Cardiovascular risk factors, haematological and biochemical parameters, and endocan levels were evaluated. Results: The serum endocan concentrations of LP patients were not significantly different from those of the healthy controls (p > 0.05). There were no significant differences in the serum endocan levels according to classification by cardiovascular risk factors and smoking history (p > 0.05). In the LP group, white blood cell count, platelet distribution width and monocyte count/high-density lipoprotein cholesterol ratios were significantly higher when compared to the healthy controls (p < 0.05). The LP group had a lower mean platelet volume than the healthy controls (p < 0.05). Conclusions: Serum endocan levels did not change significantly in patients with LP, and there were significant differences in haematological and biochemical parameters.

Effects of Dexmedetomidine on Intestinal Microcirculation and Intestinal Epithelial Barrier in Endotoxemic Rats.

Dexmedetomidine reduces cytokine production in septic patients and reduces inflammation and mortality in experimental models of endotoxemia and sepsis. This study investigated whether dexmedetomidine attenuates endothelial dysfunction, intestinal microcirculatory dysfunction, and intestinal epithelial barrier disruption in endotoxemic rats. Ninety-two male Wistar rats were randomly assigned to the following four groups: (1) Sham; (2) lipopolysaccharide, received IV lipopolysaccharide 15 and 10 mg/kg at 0 and 120 min; (3) dexmedetomidine, received IV dexmedetomidine for 240 min; and (4) lipopolysaccharide + dexmedetomidine, received both lipopolysaccharide and dexmedetomidine. Sidestream dark-field videomicroscope, tissue oxygen monitor, and full-field laser perfusion image were used to investigate the microcirculation of the terminal ileum. Serum endocan level was measured. The Ussing chamber permeability assay, lumen-to-blood gadodiamide passage by magnetic resonance imaging, and bacterial translocation were conducted to determine epithelial barrier function. Mucosal apoptotic levels and tight junctional integrity were also examined. The density of perfused small vessels in mucosa, serosal muscular layer, and Peyer patch in the lipopolysaccharide + dexmedetomidine group was higher than that of the lipopolysaccharide group. Serum endocan level was lower in the lipopolysaccharide + dexmedetomidine group than in the lipopolysaccharide group. Mucosal ratio of cleaved to full-length occludin and spleen bacterial counts were significantly lower in the lipopolysaccharide + dexmedetomidine group than in the lipopolysaccharide group. The study finding suggests that dexmedetomidine protects against intestinal epithelial barrier disruption in endotoxemic rats by attenuating intestinal microcirculatory dysfunction and reducing mucosal cell death and tight junctional damage. (Anesthesiology 2016; 125:355-67).

Prognostic value of endocan in prostate cancer: clinicopathologic association between serum endocan levels and biochemical recurrence after radical prostatectomy.

To assess the diagnostic capability of serum endocan level in association with clinicopathologic features and its impact on biochemical progression-free survival in patients with prostate cancer (PCa). A total of 86 patients with localized prostate cancer were treated with open radical prostatectomy (RP). The control group included 80 patients who were referred to the urology outpatient clinic with normal rectal examination and prostate-specific antigen (PSA) levels. The patients' characteristics, baseline PSA value, and serum endocan levels were recorded. The patients were followed up with the measurement of PSA concentration every 3 months during the first year, thereafter every 6 months until 5 years, then yearly after surgery. The primary endpoint of follow-up was the time of biochemical recurrence. The median serum endocan levels were 3.14 ng/mL in the RP group and 2.98 ng/mL in the control group (p = 0.122). A total of 86 patients who underwent RP for PCa were divided into 2 groups based on a cutoff serum endocan level of 1.8 ng/mL. The distribution of Gleason score and biochemical failure rate were significantly higher in patients with serum endocan ≥1.8 ng/mL (p = 0.031 and p = 0.047). The biochemical recurrence-free time for endocan ≥1.8 ng/mL and <1.8 ng/mL were 38 and 56 months, respectively (p = 0.041). Spearman correlation analysis showed a linear relationship between endocan expression and Gleason score (p = 0.025, p = 0.511). Multivariate analysis revealed that elevated serum endocan level (≥1.8 ng/mL) was a significant predictor of biochemical progression-free survival (hazard ratio 2.44; 95% confidence interval 1.78-3.23; p = 0.001). The current study indicates that endocan has a close relationship with tumor recurrence in PCa.

Endocan Levels and Subclinical Atherosclerosis in Patients With Systemic Lupus Erythematosus.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease of unknown etiology. A major cause of morbidity and mortality in SLE is accelerated atherosclerosis. Endothelial-specific molecule 1 (endocan) is a potential predictor of vascular events and is expressed in response to inflammatory cytokines in endothelial cells. We investigated the relationship between endocan and carotid intima-media thickness (cIMT) as a marker of early atherosclerosis. We included 44 women with SLE and 44 healthy women as controls. Disease severity of SLE was evaluated using the SLE Disease Activity Index. Endocan, C-reactive protein, erythrocyte sedimentation rate (ESR), and lipid panel were measured. The cIMT was 0.70 (range: 0.45-1.20) mm in patients with SLE and 0.40 (0.25-0.60) mm in controls (P < .001). Endocan value was 1.6 ± 0.9 ng/mL in controls and 2.2 ± 1.0 ng/mL in patients with SLE (P = .014). Endocan levels were positively correlated with cIMT (r = .469, P < .001), body mass index (r = .373, P = .013), and ESR (r = .393, P = .008). Endocan level may be associated with subclinical atherosclerosis in SLE. Consequently, endocan levels may be a promising clinical tool for patients with SLE as a guide for preventive strategy.

Serum and urinary endocan levels for bladder cancer diagnosis.

Serum and urinary endocan levels for bladder cancer diagnosis.

Plasma endocan level and prognosis of immunoglobulin A nephropathy

BackgroundEndocan, previously called endothelial cell–specific molecule-1, is a soluble proteoglycan that is secreted from vascular endothelial cells. Elevated plasma endocan levels were shown to be associated with poor cardiovascular outcomes in patients with chronic kidney disease (CKD). We investigated the clinical relevance of plasma and urine endocan levels in patients with immunoglobulin A nephropathy (IgAN). MethodsSixty-four patients with IgAN and 20 healthy controls were enrolled in this study. Plasma and urine endocan levels were measured. Clinical parameters, pathologic grades, and renal outcomes were compared among subgroups with different plasma and urine endocan levels. ResultsBoth plasma and urine endocan levels were significantly higher in patients with IgAN than in controls. Elevated serum phosphorus and C-reactive protein were independent determinants for plasma endocan, and elevated C-reactive protein was also an independent determinant for urine endocan levels in multivariate analysis. Plasma endocan level was not significantly different across CKD stages, but patients with higher plasma endocan levels showed adverse renal outcome. Urine endocan levels were also elevated in patients with poor renal function. Cox proportional hazard models showed that high plasma endocan was an independent risk factor for CKD progression after adjusting for the well-known predictors of outcome in patients with IgAN. ConclusionThis study suggested that plasma endocan might be useful as a prognostic factor in patients with IgAN.

Human cytomegalovirus infection contributes to glioma disease progression via upregulating endocan expression

The etiology of malignant glioma remains unclear. To examine the association between glioma and human cytomegalovirus (HCMV) infection and the possible mechanism through which HCMV contributes to malignant glioma, we investigated the expression of HCMV components and an angiogenesis marker, endocan, in 79 glioma specimens and 8 control brain samples. HCMV pp65 protein and DNA were detected in 65.8% (52 of 79) and 54.4% (43 of 79) of glioma specimens, respectively. The positive rate and expression levels of pp65 were significantly correlated with the glioma grades. The endocan expression was detected in 78.5% (62 of 79) of glioma specimens, and elevated endocan immunoreactivity was also significantly associated with high-grade glioma. The pp65 was predominantly detected and colocalized with endocan in the cytoplasm of tumor cells. Importantly, there was a significant positive correlation in detection rates between those 2 proteins. In control samples, neither HCMV pp65 nor endocan expression was detected. Moreover, the serum endocan levels in glioma patients were markedly higher than that in healthy subjects. In invitro study, HCMV infection induced the expression of interleukin 6 and tumor necrosis factor-α in human glioblastoma U87MG (U87) cells and human umbilical vein endothelial cells (HUVECs). Furthermore, elevated endocan levels were also observed in HCMV-infected U87cells and HUVECs and antiviral treatment with ganciclovir reduced the endocan expression. These results suggest HCMV infection leads to glioma progression through an upregulation of endocan and the secretion of inflammatory cytokines. Thus, anti-HCMV treatment may represent a potentially novel therapeutic strategy for glioma.

Admission Endocan Level may be a Useful Predictor for In-Hospital Mortality and Coronary Severity Index in Patients With ST-Segment Elevation Myocardial Infarction.

We assessed the prognostic role of serum endocan level in patients with ST-segment elevation myocardial infarction (STEMI) and compared the results with a normal coronary angiography group. A total of 133 patients were included in the study (88 patients with STEMI and 45 patients with normal coronary arteries). The SYNTAX score was determined based on the baseline coronary angiogram. Multivariate logistic regression analysis indicated that endocan independently correlated with the presence of STEMI. Moreover, high-sensitivity C-reactive protein (hsCRP), peak troponin I, and left ventricular ejection fraction (LVEF) were found to be independently associated with STEMI. Endocan level correlated significantly with hsCRP and SYNTAX score. We analyzed the discriminatory capability of endocan level for the presence of STEMI using a receiver-operating characteristics curve. A cutoff endocan level of 1.7 (ng/mL) predicted the presence of STEMI with a sensitivity of 76.1% and specificity of 73.6%. In conclusion, a high endocan level on hospital admission is an independent predictor of a worse cardiovascular outcome and a high SYNTAX score in patients with STEMI.

Human Endothelial Cell-Specific Molecule-1 (Endocan) and Coronary Artery Disease and Microvascular Angina.

Endothelial cell-specific molecule-1 (endocan) is an immunoinflammatory marker linked to endothelial activation and dysfunction. We investigated the relationship between obstructive coronary artery disease (CAD), microvascular angina (MVA), and plasma levels of endocan. We included 53 healthy individuals as controls, 40 MVA patients, and 120 patients with obstructive CAD. The severity of CAD was assessed by the Gensini and SYNergy between percutaneous coronary intervention with TAXUS and Cardiac Surgery (SYNTAX) scores. Endocan levels were 382.7 (313.8-470.2) pg/mL in patients with obstructive CAD; 324.3 (277.1-460.7) pg/mL in MVA group, and 268.0 (226.4-336.5) pg/mL (P < .001) in controls. Endocan levels in obstructive CAD and MVA groups were similar but both were significantly higher than for the control group (P < .001 and P = .002, respectively). In subgroup analysis, similar to the hypertensive subgroup results, endocan was still an independent predictor of presence of obstructive CAD in normotensives (odds ratio = 1.005, 95% confidence interval = 1.001-1.010, P = .024). There was also an independent positive correlation between endocan levels and SYNTAX score both in the hypertensives (β = 0.414, t = 3.21, P = .002) and in the normotensives (β = .301, t = 2.23, P = .031). In conclusion, endocan could be a common predictor of the endothelium-dependent inflammatory processes, rather than related with specific risk factors.

Plasma Endocan Levels in Patients With Isolated Coronary Artery Ectasia.

Endocan is a soluble proteoglycan, secreted by human vascular endothelial cells. Endocan is a marker for vascular pathologies and an important mediator of angiogenesis, strongly associated with inflammation, vascular endothelial dysfunction, and atherosclerosis. The relationship between coronary artery ectasia (CAE) and endocan has not been evaluated. We aimed to investigate this association. Fifty-four patients with isolated CAE without coronary stenosis and 30 controls with normal coronary angiogram were included in this study. Endocan plasma concentrations were measured using an enzyme-linked immunosorbent assay. Patients with isolated CAE had significantly higher levels of endocan compared to the controls (18.9 ± 7.3 vs 15.6 ± 3.6 ng/mL; P = .007). There was a significant correlation between endocan levels and severity of isolated CAE according to the Markis classification ( r = -.593, P < .001). Plasma endocan levels may reflect the presence and severity of isolated CAE, suggesting that endocan may be involved in pathogenesis of isolated CAE.