Association of Asymmetric Dimethylarginine With Acute Pancreatitis–Induced Hyperglycemia. Issue 5 (May 2016)

• Record Type: Journal Article
• Authors: Trgo, Gorana; Zaja, Ivan; Bogut, Ante; Kovacic Vicic, Vesna; Meter, Ivana; Vucic Lovrencic, Marijana; Radman, Maja
• Is Part Of: Pancreas. Volume 45:Issue 5(2016)
• Publication Date: 2016-05
• Subjects: acute pancreatitis -- asymmetric dimethylarginine -- reactive oxygen species -- reactive nitrogen species -- diabetes mellitus; Pancreas -- Diseases -- Periodicals; Pancreas -- Periodicals; Neuroendocrine tumors -- Periodicals; 616.37005
• DOI: 10.1097/MPA.0000000000000516
• Languages: English
• ISSNs: 0885-3177

Abstract

Abstract : Objective: The objective of this study was to investigate the relationship between asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, oxidative-nitrosative damage, and glucoregulation in acute pancreatitis (AP). Methods: The study evaluated serum levels of ADMA, nitrotyrosine, and urinary 8-hydroxydeoxyguanosine in 40 male patients hospitalized for AP at baseline and at 2 and 10 days of treatment, respectively. The patients were classified into a mild and a moderately severe AP group (MAP and MSAP, respectively) according to Atlanta classification criteria. Glycemic status was evaluated by a 75-g oral glucose tolerance test 1 month after AP onset. Forty age-matched healthy subjects served as control subjects. Results: Significant decrease of ADMA and increased levels of nitrotyrosine and urinary 8-hydroxydeoxyguanosine were found in MSAP, but not in MAP at baseline, with ADMA correction toward control levels at the 10th day of treatment. Fructosamine was found to significantly influence ADMA levels ( r = −0.362, P = 0.002). After AP recovery, either impaired glucose tolerance or diabetes was identified with the oral glucose tolerance test in 10.5% and 92.8% of patients with MAP and MSAP, respectively. Conclusions: Insufficient inhibition of nitric oxide synthesis, through reduced bioavailability of ADMA, might be a novel significant contributory factor to the severity of AP and subsequent development of hyperglycemia.