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Endocrine Abstracts (2013) 32 P873 | DOI: 10.1530/endoabs.32.P873

1Endocrinology Department. Hospital de la Santa Creu i Sant Pau. Universitat Autònoma de Barcelona (UAB), Barcelona, Barcelona, Spain; 2Sant Pau Biomedical Research Institute, Barcelona, Barcelona, Spain; 3Department of Genetics and Microbiology. Universitat Autònoma de Barcelona (UAB), Bellaterra, Barcelona, Spain; 4Center for Biomedical Research on Rare Diseases (CIBERER Unit 745), Valencia, Valencia, Spain; 5Endocrinology Department. Hospital Universitari Mútua de Terrassa, Terrassa, Barcelona, Spain; 6Biomedical Research Networking Center on Bioenginnering, Biomaterials and Nanomedicina. CIBER-BBN, Barcelona, Barcelona, Spain; 7Center for Biomedical Research on Rare Diseases (CIBERER Unit 747). Instituto de Salud Carlos III (ICSIII), Barcelona, Barcelona, Spain.


Introduction: Cushing’s syndrome (CS) is associated with increased mortality and morbidities. Hypercortisolism is also present in chronic mood disorders (CMD) and stress, where telomere length (TL) has been found to be shorter than in matched controls. Since hypercortisolism is present in CS and CMD, we hypothesized that telomere shortening could also be present in CS. The aim of this study was to investigate TL in CS patients compared to matched controls.

Methods/design: Transversal study. Thirty-four CS (seven males, 26 pituitary and eight adrenal; six with active disease and 28 cured from hypercortisolism) and 34 matched control (for age, gender, smoking). Mean age was 48+13.7 in CS vs 48.09+13.5 years in controls (ns). Manual DNA extraction from leukocytes using the phenol/chloroform method was performed. Leukocyte TL was measured by TRF-Southern technique (kit-telo TTAGGG Telomere length Assay, Roche).

Results: CS patients had a greater waist:hip ratio than controls (0.91±0.07 vs 0.84±0.08, P<0.01), more prevalence of hypertension (47 vs 11%, P<0.001) and osteoporosis (29 vs 11%, P<0.05). No other baseline differences were found. TL did not differ in CS (7788±752 base pairs –bp vs 7446±1100 bp) compared to controls. CS with dyslipidemia (n=12, 35%; two with active hypercortisolism) had shorter telomers than those without (7248±715 bp vs 8060±865 bp, P<0.05). No correlation was found with concomitant cortisol values, length of exposure to hypercortisolism or endocrine cure.

Conclusion: In this small group of matched CS/controls, we did not find any differences in TL; however, in CS with dyslipidemia, TL was shortened compared to CS patients with normal lipid values. Further studies will be necessary to confirm this finding and define any possible relationship between hypercortisolism and TL.

AA is supported by a grant from ISCIII, PI 11-0001.

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