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Disease Markers
Volume 33, Issue 2, Pages 69-76

Elevated Asymmetric Dimethylarginine in Young Adult Survivors of Childhood Acute Lymphoblastic Leukemia: A Preliminary Report

Joanna Sulicka,1,4 Andrzej Surdacki,2,4 Magdalena Strach,1,4 Aleksander Kwater,1,4 Barbara Gryglewska,1,4 Magdalena Ćwiklińska,3,5 Walentyna Balwierz,3,5 and Tomasz K. Grodzicki1,4

1Department of Internal Medicine and Gerontology, Faculty of Medicine, Jagiellonian University, Cracow, Poland
22nd Department of Cardiology, Faculty of Medicine, Jagiellonian University, Cracow, Poland
3Department of Pediatric Oncology and Hematology, Polish-American Institute of Pediatrics, Faculty of Medicine, Jagiellonian University, Cracow, Poland
4University Hospital, Cracow, Poland
5University Children's Hospital, Cracow, Poland

Received 11 July 2012; Accepted 11 July 2012

Copyright © 2012 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Background: Adult survivors of childhood malignancy are predisposed to late cardiovascular (CV) complications. Our aim was to estimate plasma levels of the endogenous nitric oxide formation inhibitor asymmetric dimethylarginine (ADMA), in long-term survivors of childhood acute lymphoblastic leukemia (ALL) treated with only chemotherapy.

Methods: ADMA and its isomer symmetric dimethylarginine (SDMA) were measured in 25 former ALL patients (aged 18–28 years) who had survived without recurrent disease ≥ 5 years from completing chemotherapy without cranial irradiation, and in 20 healthy controls (aged 20–31 years).

Results: Characteristics of the both groups were similar, except for lower high-density lipoproteins-cholesterol (HDL-C) in ALL survivors. Compared to controls, the former ALL patients exhibited significant, albeit small, rises in levels of ADMA (0.63 ± 0.09 [SD] vs. 0.57 ± 0.07 μmol/L; p = 0.016), but not SDMA, with a consequently increased ADMA to SDMA ratio (1.08 ± 0.22 vs. 0.91 ± 0.16; p = 0.004). The effect of former ALL on ADMA was attenuated (intergroup p = 0.10 [ANCOVA]) upon adjustment for HDL-C (ADMA vs. HDL-C regression coefficient: −0.065 ± 0.030 [SEM]; p = 0.03).

Conclusions: ADMA is elevated in adult childhood ALL survivors, which can reflect late detrimental chemotherapy effects, partially related to minor lipid profile changes. Whether these subtle ADMA elevations might herald future CV morbidity, remains to be elucidated.