ESPE Abstracts (2014) 82 P-D-1-1-208

ESPE2014 Poster Presentations Reproduction (12 abstracts)

GH Therapy in Turner Syndrome Patients: the Effects on Nutritional Status, Adipokines, and Aortic Dilatation

Hanna Magnuszewska a , Maria Gnacinska-Szymanska b , Piotr Wisniewski b , Piotr Potaz c , Dorota Birkholz-Walerzak a , Maria Korpal-Szczyrska a & Krzysztof Sworczak b


aDepartment of Paediatrics, Diabetology and Endocrinology, Medical University of Gdansk, Gdansk, Poland; bDepartment of Endocrinology and Internal Medicine, Medical University of Gdansk, Gdansk, Poland; cDepartment of Pediatric Cardiology and Congenital Heart Defects, Medical University of Gdansk, Gdansk, Poland


Background: Turner syndrome (TS) patients are at increased obesity risk. Additionally body composition in TS is distinctly altered. The percentage of body fat mass (BFM) is higher. Also adipokine dysregulation is observed. TS is associated with aortic dilatation, which is seen not only in patients with congenital aortic defects but also in patients without underlying pathology. Considering different co-morbidities common in TS, it’s extremely important to evaluate wide spectrum of GH effects in these patients. Till now there are very few studies analyzing long-term effects of GH therapy on obesity and cardiovascular complications in TS.

Objective and hypotheses: Assessment of long-term GH therapy effects on nutritional status and aortic dilatation in TS.

Method: Fifty three TS patients with confirmed diagnosis. Group 1: n=37, after GH therapy. Age 20.87 (±3.69), age at start of GH therapy 11.73, treatment duration 4.83, interval between GH discontinuation and study 4.46 years. Group 2: n=16, never treated with GH, age 23.16 (±5.8) years. Exclusion criteria: diabetes mellitus, unbalanced thyroid pathology, aortic defects: aortic coarctation and bicuspid aortic valve. Study protocol contained: measurements: height, weight, BMI, WHR; bioelectrical impedance analysis; laboratory tests: adiponectin, obestatin, omentin, wisfatin; echocardiography, including different aortic diameters, which were indexed to BSA.

Results: BMI, WHR didn’t differ between groups. BFM was significantly lower in group 1 vs 2 (27.4 vs 31.8%, P=0.03). There was no difference in adipokines between groups. Also aortic diameters didn’t differ. Negative correlation between aortic size index (ASI) and obestatin was noted (r=−0.6117, P=0.0015). ASI correlated with karyotype (r=−0.4886, p=0.0083) and didn’t correlate with GH treatment duration.

Conclusion: GH therapy in TS has beneficial impact on body composition. GH therapy has no direct effect on aortic dimension. However, the association between obestatin, negatively correlating with nutritional status, and aortic size, suggest that GH may decrease aortic dilatation risk in TS.

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