Intermediate products of purine metabolism in an experimental model of pancreatic necrosis Purine bases as predictors of pancreatic necrosis

Main Article Content

Grigoriy Abramov
Yelena Pozdnyakova
Neila Tankibaeva
Kairat Shakeev
Maida Tusupbekova
Dmitriy Shestakov


purines, purine metabolism intermediates, predictors of necrosis, pancreas, pancreatitis, pancreatic necrosis


Background and aim: Determine the level of purines in the blood plasma of experimental animals at three stages of induced pancreatic necrosis. Find out the potential of purines as predictors of the severity of pancreatitis.

Methods: The experiment was carried out on white outbred rabbits. The pancreatic necrosis was modeled by introducing self-bile into the pancreatic parenchyma. The pancreas of rabbits, after isolation, was subjected to microscopic description. Blood was also taken from rabbits to determine the plasma levels of adenine, guanine, hypoxanthine, xanthine, and uric acid.

Results: 12 hours after the administration of self-bile, the level of xanthine significantly increases and the concentration of uric acid in the blood plasma increases by 3 times. 24 hours after the introduction of self-bile, there is a slight decrease in the level of adenine, xanthine and uric acid, and the indicators of purine metabolism remain elevated. 48 hours after the introduction of self-bile, the levels of guanine, hypoxanthine and xanthine are reduced.

Conclusions: The concentration indices of absolute and relative intermediate products of purine metabolism were increased at the initial stage of pancreatic necrosis. The activity of enzymes and metabolites of purine metabolism involved in the formation of reactive oxygen species and free radicals increased. The hypothesis that intermediate products of purine metabolism can be predictors of pancreatic necrosis was confirmed.


Download data is not yet available.


Metrics Loading ...
Abstract 191 | PDF Downloads 139


1. Sekimoto M, Takada T, Kawarada Y, et al. Guidelines for the management of acute pancreatitis: epidemiology, etiology, natural history, and outcome predictors in acute pancreatitis. J Hepatobiliary Pancreat Surg 2006; 13(1):10–24. doi:
2. Trikudanathan G, Wolbrink DRJ, van Santvoort HC, Mallery S, Freeman M, Besselink MG. Current concepts in severe acute and necrotizing pancreatitis: an evidence-based approach. Gastroenterology 2019; 156(7):1994-2007.e3. doi:
3. Wu D, Tang M, Zhao Y, et al. Impact of seasons and festivals on the onset of acute pancreatitis in Shanghai, China. Pancreas 2017; 46(4):496–503. doi:
4. Bertilsson S, Håkansson A, Kalaitzakis E. Acute pancreatitis: impact of alcohol consumption and seasonal factors. Alcohol and Alcoholism 2017; 52(3):383–9. doi:
5. Guarino M, Bologna A, Ursini F, et al. Chronobiology of acute pancreatitis in a single Italian centre. Eur Rev Med Pharmacol Sci 2020; 24(4):1988–94. doi:
6. Banks PA, Bollen TL, Dervenis C, et al. Classification of acute pancreatitis – 2012: revision of the Atlanta classification and definitions by international consensus. Gut 2013; 62(1):102–11. doi:
7. Basnayake C, Ratnam D. Abnormal laboratory results: Blood tests for acute pancreatitis. Aust Prescr 2015; 38(4):128–30. doi:
8. Leppäniemi A, Tolonen M, Tarasconi A, et al. 2019 WSES guidelines for the management of severe acute pancreatitis. World J Emerg Surg 2019; 14(1):27. doi:
9. Furey C, Buxbaum J, Chambliss AB. A review of biomarker utilization in the diagnosis and management of acute pancreatitis reveals amylase ordering is favored in patients requiring laparoscopic cholecystectomy. Clin Biochem 2020; 77:54–6. doi:
10. Cardoso FS, Ricardo LB, Oliveira AM, et al. C-reactive protein prognostic accuracy in acute pancreatitis: timing of measurement and cutoff points. Eur J Gastroenterol Hepatol 2013; 25(7):784–9. doi:
11. Muddana V, Whitcomb DC, Khalid A, Slivka A, Papachristou GI. Elevated serum creatinine as a marker of pancreatic necrosis in acute pancreatitis. Am J Gastroenterol 2009; 104(1):164–70. doi:
12. Wu BU, Bakker OJ, Papachristou GI, et al. Blood urea nitrogen in the early assessment of acute pancreatitis: an international validation study. Arch Intern Med 2011; 171(7):669–76. doi:
13. Mentula P, Kylänpää ML, Kemppainen E, et al. Early prediction of organ failure by combined markers in patients with acute pancreatitis. Br J Surg 2005; 92(1):68–75. doi:
14. Lipinski M, Rydzewski A, Rydzewska G. Early changes in serum creatinine level and estimated glomerular filtration rate predict pancreatic necrosis and mortality in acute pancreatitis. Pancreatology 2013; 13(3):207–11. doi:
15. Rainio M, Lindström O, Penttilä A, et al. Serum serine peptidase inhibitor kazal-type 1, trypsinogens 1 to 3, and complex of trypsin 2 and α1-antitrypsin in the diagnosis of severe acute pancreatitis. Pancreas 2019; 48(3):374–80. doi:
16. Shu W, Wan J, Chen J, et al. Initially elevated arterial lactate as an independent predictor of poor outcomes in severe acute pancreatitis. BMC Gastroenterol 2020; 20(1):116.1 doi:
17. Zhang Y, Guo F, Li S, et al. Decreased high density lipoprotein cholesterol is an independent predictor for persistent organ failure, pancreatic necrosis and mortality in acute pancreatitis. Sci Rep 2017; 7(1):8064. doi:
18. Roggenbuck D, Goihl A, Hanack K, et al. Serological diagnosis and prognosis of severe acute pancreatitis by analysis of serum glycoprotein 2. Clin Chem Lab Med 2017; 55(6):854–64. doi:
19. Tenner S, Baillie J, DeWitt J, Vege SS, American College of Gastroenterology. American College of Gastroenterology guideline: management of acute pancreatitis. Am J Gastroenterol 2013; 108(9):1400–15; 1416. doi:
20. Dale N, Frenguelli BG. Measurement of purine release with microelectrode biosensors. Purinergic Signal 2012; 8(Suppl 1):27–40. doi:
21. Saugstad OD. Hypoxanthine as an indicator of hypoxia: its role in health and disease through free radical production. Pediatr Res 1988; 23(2):143–50. doi:
22. Castro-Gago M, Rodríguez-Núñez A, Novo-Rodríguez MI, Eirís-Puñal J. Biochemical parameters predictive of neuronal damage in childhood. Rev Neurol 2001; 32(12):1141–50. doi:
23. Del Castillo Velasco-Martínez I, Hernández-Camacho CJ, Méndez-Rodríguez LC, Zenteno-Savín T. Purine metabolism in response to hypoxic conditions associated with breath-hold diving and exercise in erythrocytes and plasma from bottlenose dolphins (Tursiops truncatus). Comp Biochem Physiol A Mol Integr Physiol 2016; 191:196–201. doi:
24. Meng X, Wang SC, Shan JJ., Xu JY., Shen CS., Xie T. Regulation of jinxin oral liquid on metabolites in spleen of mice with RSV pneumonia based on GC-MS. CTHD 2016; 47: 4408-4415.
25. Vareed SK, Bhat VB, Thompson C, et al. Metabolites of purine nucleoside phosphorylase (NP) in serum have the potential to delineate pancreatic adenocarcinoma. PLoS One 2011; 6(3):e17177. doi:
26. Zuccarini M, Giuliani P, Frinchi M, et al. Uncovering the signaling pathway behind extracellular guanine-induced activation of NO system: new perspectives in memory-related disorders. Front Pharmacol 2018; 9:110. doi:
27. Abramov G, Shakeyev K, Tusupbekova M, Tagaev E, Shestakov D, Zhumanbaev S. Experimental model of pancreonecrosis induced by auto-bile injection. Open Access Maced J Med Sci 2020; 8(A):472–5. doi:
28. Oreshnikov EV, Gunin AG, Madyanov IV. Purines of blood and cerebrospinal fluid during pregnancy. Problems of reproduction 2008; 6:74-80. Russian.
29. Cruz-Santamaría DM, Taxonera C, Giner M. Update on pathogenesis and clinical management of acute pancreatitis. World J Gastrointest Pathophysiol 2012; 3(3):60–70. doi:
30. Rau B, Poch B, Gansauge F, et al. Pathophysiologic role of oxygen free radicals in acute pancreatitis: initiating event or mediator of tissue damage? Ann Surg 2000; 231(3):352–60. doi:
31. Sanfey H, Bulkley GB, Cameron JL. The role of oxygen-derived free radicals in the pathogenesis of acute pancreatitis. Ann Surg 1984; 200(4):405–13. doi:
32. Eltzschig HK, Thompson LF, Karhausen J, et al. Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism. Blood 2004; 104(13):3986–92. doi:
33. Nagao H, Nishizawa H, Tanaka Y, et al. Hypoxanthine secretion from human adipose tissue and its increase in hypoxia. Obesity. Silver Spring 2018; 26(7):1168–78. doi:
34. Furuhashi M, Koyama M, Higashiura Y, et al. Differential regulation of hypoxanthine and xanthine by obesity in a general population. J Diabetes Investig 2020; 11(4):878–87. doi:
35. Yarilin AA. Apoptosis and its role in the whole organism. Glaucoma 2003; 2:46–54. Russian.
36. El Ridi R, Tallima H. Physiological functions and pathogenic potential of uric acid: A review. J Adv Res. 2017; 8:487–493. doi:
37. Huang H, Huang B, Li Y, et al. Uric acid and risk of heart failure: a systematic review and meta-analysis. Eur J Heart Fail 2014; 16(1):15–24. doi:

Similar Articles

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 > >> 

You may also start an advanced similarity search for this article.