Malondialdehyde in early phase of acute pancreatitis.

AIMS to assess oxidative stress in acute pancreatitis, its evolution over time and its relationship with the severity of the disease. METHODS during a two-year period, patients with acute pancreatitis with less than 24 hours of pain were evaluated. Serum was obtained the first, second and fourth day from admittance, if complications were detected, and after recovery. Malondialdehyde was determined by high performance liquid chromatography. Twenty healthy volunteers constituted the control group. Malondialdehyde between groups was compared with Mann-Whitney and Kruskal-Wallis tests; malondialdehyde evolution was studied with Wilcoxon test. RESULTS one hundred and sixty-nine patients were included (91 women, median age 67 years, range 20-95); 33 suffered a severe episode. Malondialdehyde decreased from first to fourth day (0.600 vs. 0.451 vs. 0.343 M, respectively, p < 0.05). When complications were detected, malondialdehyde level was similar to that of first and second day (0.473 M, p > 0.05). In severe attacks malondialdehyde was higher than in control group at day 2 (severe: 0.514; mild: 0.440; control: 0.347 M, p < 0.05 severe vs. control). CONCLUSIONS an early oxidative stress is observed in acute pancreatitis. In severe attacks, oxidative stress remains high longer than in mild episodes. The onset of complications is associated with high malondialdehyde concentration.

[1]  T. Shimosegawa,et al.  Role of Free Radicals in Pancreatitis , 2011 .

[2]  J. Pérez-Hernández,et al.  Corelation among clinical, biochemical and tomographic criteria in order to evaluate the severity in acute pancreatitis. , 2010, Revista espanola de enfermedades digestivas : organo oficial de la Sociedad Espanola de Patologia Digestiva.

[3]  A. Saraya,et al.  Variations in the levels of oxidative stress and antioxidants during early acute pancreatitis. , 2009, Tropical gastroenterology : official journal of the Digestive Diseases Foundation.

[4]  A. Siriwardena,et al.  Randomised, double blind, placebo controlled trial of intravenous antioxidant (n-acetylcysteine, selenium, vitamin C) therapy in severe acute pancreatitis , 2007, Gut.

[5]  R. Parks,et al.  Association between early systemic inflammatory response, severity of multiorgan dysfunction and death in acute pancreatitis , 2006, The British journal of surgery.

[6]  M. Mcphail,et al.  Malondialdehyde and superoxide dismutase as potential markers of severity in acute pancreatitis. , 2006, JOP : Journal of the pancreas.

[7]  S. Milnerowicz,et al.  Blood Plasma Antioxidant Defense in Patients With Pancreatitis , 2006, Pancreas.

[8]  Changbin Shi,et al.  Potential Role of Reactive Oxygen Species in Pancreatitis-Associated Multiple Organ Dysfunction , 2005, Pancreatology.

[9]  C. Johnson,et al.  Painful ascites , 2004, Gut.

[10]  E. Sierka,et al.  The Dynamics of the Oxidant-Antioxidant Balance in the Early Phase of Human Acute Biliary Pancreatitis , 2004, Pancreatology.

[11]  M. McMahon,et al.  Association of antioxidant enzyme gene polymorphisms and glutathione status with severe acute pancreatitis. , 2004, Gastroenterology.

[12]  B. Mroczko,et al.  The Importance of Interleukin 18, Glutathione Peroxidase, and Selenium Concentration Changes in Acute Pancreatitis , 2004, Digestive Diseases and Sciences.

[13]  W. Du,et al.  Therapeutic efficacy of high-dose vitamin C on acute pancreatitis and its potential mechanisms. , 2003, World journal of gastroenterology.

[14]  J. Windsor,et al.  Elevated Protein Carbonyls as Plasma Markers of Oxidative Stress in Acute Pancreatitis , 2003, Pancreatology.

[15]  J. Kang,et al.  Role of oxygen free radicals in patients with acute pancreatitis. , 2003, World journal of gastroenterology.

[16]  P. Puolakkainen,et al.  Multiple organ dysfunction associated with severe acute pancreatitis , 2002 .

[17]  S. Evans,et al.  Dynamic nature of early organ dysfunction determines outcome in acute pancreatitis , 2002, The British journal of surgery.

[18]  P. Puolakkainen,et al.  Multiple organ dysfunction associated with severe acute pancreatitis* , 2001, Critical care medicine.

[19]  J. Braganza.  Towards a Novel Treatment Strategy for Acute Pancreatitis , 2001, Digestion.

[20]  J. Braganza.  Towards a Novel Treatment Strategy for Acute Pancreatitis , 2001, Digestion.

[21]  J. Windsor,et al.  Severity of acute pancreatitis: a multivariate analysis of oxidative stress markers and modified Glasgow criteria , 2002, The British journal of surgery.

[22]  D. Talwar,et al.  Relationship of carotenoid and vitamins A and E with the acute inflammatory response in acute pancreatitis , 2000, The British journal of surgery.

[23]  J. Windsor,et al.  Early ascorbic acid depletion is related to the severity of acute pancreatitis , 1999, The British journal of surgery.

[24]  J. Norman.  New Approaches to Acute Pancreatitis: Role of Inflammatory Mediators , 1999, Digestion.

[25]  F. J. Romero,et al.  Serum malondialdehyde: possible use for the clinical management of chronic hepatitis C patients. , 1998, Free radical biology & medicine.

[26]  M. Jedynak,et al.  Oxidative Stress as an Early Prognostic Factor in Acute Pancreatitis (AP): Its Correlation with Serum Phospholipase A2 (PLA2) and Plasma Polymorphonuclear Elastase (PMN‐E) in Different‐Severity Forms of Human AP , 1998, Pancreas.

[27]  G. Glazer,et al.  United Kingdom guidelines for the management of acute pancreatitis , 1998, Gut.

[28]  F. Chang,et al.  Oxidative stress: an important phenomenon with pathogenetic significance in the progression of acute pancreatitis , 1998, Gut.

[29]  J. Norman.  The role of cytokines in the pathogenesis of acute pancreatitis. , 1998, American journal of surgery.

[30]  L. Hunt,et al.  Evidence for early oxidative stress in acute pancreatitis , 1995, International journal of pancreatology : official journal of the International Association of Pancreatology.

[31]  R. McCloy,et al.  Vitamin C status in patients with acute pancreatitis , 1993, The British journal of surgery.

[32]  E L Bradley,et al.  A clinically based classification system for acute pancreatitis. Summary of the International Symposium on Acute Pancreatitis, Atlanta, Ga, September 11 through 13, 1992. , 1993, Archives of surgery.

[33]  Bradley El rd,et al.  A clinically based classification system for acute pancreatitis. , 1993 .

[34]  E. Bradley.  A clinically based classification system for acute pancreatitis. , 1993, Annales de chirurgie.

[35]  A. Favier,et al.  High-performance liquid chromatographic separation of malondialdehyde-thiobarbituric acid adduct in biological materials (plasma and human cells) using a commercially available reagent. , 1992, Journal of chromatography.

[36]  I. Young,et al.  Measurement of Malondialdehyde in Plasma by High Performance Liquid Chromatography with Fluorimetric Detection , 1991, Annals of clinical biochemistry.

[37]  D. Janero,et al.  Malondialdehyde and thiobarbituric acid-reactivity as diagnostic indices of lipid peroxidation and peroxidative tissue injury. , 1990, Free radical biology & medicine.

[38]  C. Babbs,et al.  A rapid, widely applicable screen for drugs that suppress free radical formation in ischemia/reperfusion. , 1988, Journal of pharmacological methods.

[39]  J. Cameron,et al.  The Role of Oxygen‐derived Free Radicals in the Pathogenesis of Acute Pancreatitis , 1984, Annals of surgery.

[40]  J. Cameron,et al.  Source of oxygen derived free radicals in the pathogenesis acute of pancreatitis , 1984 .