Aqueous humour and serum concentration of asymmetric dimethyl arginine in pseudoexfoliation syndrome
- 1Department of Medical Biochemistry, Faculty of Medicine, Abant Izzet Baysal University, Bolu, Turkey
- 2Department of Ophthalmology, Faculty of Medicine, Abant Izzet Baysal University, Bolu, Turkey
- 3Department of Internal Medicine, Faculty of Medicine, Abant Izzet Baysal University, Bolu, Turkey
- Correspondence to Dr Mehmet Tosun, Department of Medical Biochemistry, Faculty of Medicine, Abant Izzet Baysal University, Bolu 14280, Turkey;
Contributors All authors have contribution to study design, acquisition of data and final approval of the study.
- Accepted 31 May 2012
- Published Online First 22 June 2012
Objective Asymmetric dimethyl arginine (ADMA) is the major endogenous inhibitor of nitric oxide synthase. ADMA is related to endothelial dysfunction and is an independent cardiovascular risk factor. This study aimed to evaluate the concentration of ADMA in aqueous humour and serum samples of patients with pseudoexfoliation (PEX) syndrome.
Materials and Methods 21 cataract patients with PEX syndrome (PEX group) and 18 cataract patients without PEX syndrome (control group) were enrolled in the study. ADMA was measured in the aqueous humour and serum of the PEX and control groups. ELISA was used to determine the ADMA concentration.
Results Mean aqueous humour ADMA concentration in the PEX group was 0.39±0.07 μmol/l and in the control group was 0.34±0.06 μmol/l. Mean serum ADMA concentration in the PEX group was 0.56±0.21 μmol/l and in the control group was 0.44±0.12 μmol/l. ADMA concentration of aqueous humour in the PEX group was significantly higher than the control group (p=0.026). Similarly, ADMA concentration of serum in the PEX group was significantly higher than the control group (p=0.039).
Conclusions The findings of the present study could suggest that ADMA might play a role in the aetiopathogenesis of PEX syndrome. Higher aqueous and serum levels of ADMA might be potential evidence of endothelial dysfunction in PEX syndrome.
Funding This work was supported by Abant Izzet Baysal University scientific research projects funds grant no: BAP–2011.08.01.427.
Competing interests None.
Patient consent Obtained.
Ethics approval The study was approved by the Abant Izzet Baysal University Clinical Research Ethics Committee and followed the Declaration of Helsinki for research involving human subjects.
Provenance and peer review Not commissioned; externally peer reviewed.