ESPE Abstracts (2019) 92 P1-236

Serum Endocan Levels as a Marker of Endothelial Dysfunction in Turner Syndrome and Correlation with Cardiac Findings

Ali Genco Gencay1, Feyza Darendeliler2, Kemal Nişli3, Serra Karaca4, Aslı Derya Kardelen2, Şükran Poyrazoğlu2, Firdevs Baş2

1Istanbul University, Istanbul Faculty of Medicine, Department of Pediatrics, Istanbul, Turkey. 2Istanbul University, Istanbul Faculty of Medicine, Pediatric Endocrinology Unit, Istanbul, Turkey. 3Istanbul University, Istanbul Faculty of Medicine, Pediatric Cardiology Unit, Istanbul, Turkey. 4Samsun Hospital for Women and Children, Samsun, Turkey

Background: The most common reason for the increased mortality and morbidity in TS, which results from partial or complete deficiency of an X chromosome in a female, is acquired cardiovascular disease, which is the result of endothelial dysfunction that causes atherosclerosis. Endocan, an inflamatory marker, has been found elevated in several diseases with endothelial dysfunction (ED). There is no study of endocan levels in TS.

Objective: To investigate the significance of serum endocan level in evaluating ED in TS.

Methods: 41 girls with TS and 25 healthy females were enrolled. Patients were examined, weight, height, waist circumference (WC) were measured, body mass index (BMI) values were calculated, systolic (SBP) and diastolic blood pressure (DBP) were measured and expressed as SDS. Samples for serum endocan levels (pg/mL) were obtained and the patients underwent ultrasound (USG) evaluation for measurement of carotid intima media thickness (cIMT) (expressed as SDS) and flow mediated dilation (FMD) (%). Karyogram, fasting blood glucose and insulin levels, total cholesterol (TC), high density lipoprotein (HDL), low density lipoprotein (LDL), triglyceride (TG), C-reactive protein (CRP), thyroid hormone and antibody levels and echocardiogram findings were obtained from patient files. Homeostatic model assessment – insulin resistance index (HOMA-IR) was calculated.

Results: Mean age of the patients was 14.7 ± 3.6 years. Mean age of the controls was 11.1 ± 2.9 years (P = 0.001). SDS values were used instead of absolute values wherever possible to minimize the effects of age difference on our results. Height SDS of the study group was lower than the control group (P=0.001). WC SDS (P=0.033) and BMI SDS (P=0.003) of the study group were higher than that of the control group. The study group had a higher SBP SDS (P=0.001) and DBP SDS (P=0.001). The study group had higher levels of TC (P=0.001), LDL (P=0.025), fasting insulin (P=0.027) and HOMA-IR (P=0.016). Both groups had similar endocan levels, cIMT and FMD. Karyotype, pubertal status, cardiac anomalies, IR and thyroiditis did not alter endocan, cIMT or FMD. Overweight and obese patients were found to have lower FMD than non-overweight patients (P=0.038) and the controls (P=0.018). WC (r=-0.348, P=0.005) and BMI SDS (r=-0.368, P=0.002) were found negatively correlated with FMD.

Conclusion: Our data do not support the use of endocan levels to evaluate for ED in TS. Lower FMD in obese TS patients and negative correlation of FMD with BMI and visceral obesity show that controlling obesity is important for future vascular pathology.

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