ENDOCRINE PANCREATIC FUNCTION IN ACUTE PANCREATITIS
DOI:
https://doi.org/10.14739/2310-1210.2014.1.23809Keywords:
acute pancreatitis, hormones of pancreasAbstract
Introduction Among the organs of internal secretion pancreas has a special place thanks to active exocrine function and a wide range of physiological actions of produced hormones. Violations of endocrine pancreas arises in 6.5-38 % of patients with acute pancreatitis. However, there is still no clear understanding of the pathogenetic mechanisms of hormonal dysfunction of the pancreas in acute pancreatitis, there is no uniform algorithms for its correction.
Aim of the research was to study the endocrine function of pancreas in acute pancreatitis. To define the role of endocrine pancreatic function in the etiology and pathogenesis of the acute pancreatitis. To assess the prospects of the use of pancreatic hormones in the treatment and predicting the outcomes of acute pancreatitis.
Materials and methods of the research Survey of publications in specialized periodical medical journals, PubMed sources developed by the National Center for Biotechnology Information. Search in PubMed was carried out in the following databases: MEDLINE, Pre MEDLINE.
Results of the research. In a significant proportion of patients who recovered from acute pancreatitis, exocrine and endocrine functional impairments were found. This finding was not detected only in patients after severe acute pancreatitis. Routine evaluation of pancreatic function after acute pancreatitis should be considered. The comparative analysis of the synthetic analogues (somatostatin, calcitonin, leu-enkefalin-dalargin) influence on the glucose metabolism of rats in acute pancreatitis of was made. Physiological reaction of beta-cells is preserved in infusion of somatostatin. However, infusion of calcitonin results in the distortion of counterregulatory action of insulin and glucagon. It was detected that pancreatic renin-angiotensin system is markedly activated in the experimental rat models of chronic hypoxia and acute pancreatitis. The activation of the pancreatic renin-angiotensin system by chronic hypoxia and experimental pancreatitis could play role in the physiology and pathophysiology of the pancreas. The significant changes of pancreatic renin-angiotensin system may have clinical relevance in acute pancreatitis and hypoxia-induced injury in the pancreas. Detection of the pancreatic polypeptide level, oral glucose tolerance test assesses the state of the pancreas after acute pancreatitis in the long term.
Conclusions:
- The biggest impact in the hormonal secretion of pancreatic islet has pancreatic renin-angiotensin system. Permissive factor for pancreatic endocrine dysfunction is chronic hypoxia due to violation of organ perfusion.
- Endocrine function of the pancreas are more affected after resection treatment of acute pancreatitis.
- Serological tests of pancreatic polypeptide promising for early diagnosis and prediction of the outcome of acute pancreatitis.
References
Цвиркун В.В. Влияние регуляторных пептидов на эндокринную функцию поджелудочной железы при экспериментальном остром панкреатите / В.В. Цвиркун, В.П. Григоревский, К.В. Боцманов, В.С. Бочарова // Бюллетень экспериментальной биологии и медицины. – 1989. – № 108 (12). – С. 748–751.
Шевердин Ю.П. Эндокринная функция поджелудочной железы у больных острым панкреатитом / Ю.П. Шевердин // Хирургия. – 1992. – № 1. – С. 62–64.
Abe N. Pancreatic endocrine function and glucose transporter (GLUT)-2 expression in rat acute pancreatitis / N. Abe, T. Watanabe, S. Ozawa, T. Masaki [et al.] // Pancreas. – 2002. – № 25 (2). – Р. 149–153.
Andersson B. Pancreatic function, quality of life and costs at long-term follow-up after acute pancreatitis / B. Andersson, M.L. Pendse, R. Andersson // World J Gastroenterol. – 2010. – № 16 (39). – Р. 4944–4951.
Buscher H.C. Beta-cell function of the pancreas after necrotizing pancreatitis / H.C. Buscher, M.L. Jacobs, G.L. Ong, H. van Goor [et al.] // Dig Surg. – 1999. – № 16(6). – Р. 496–500.
Cai K. TNF-α acutely upregulates amylin expression in murine pancreatic beta cells / K. Cai, D. Qi, O. Wang, J. Chen [et al.] // Diabetologia. – 2011. – № 54 (3). – Р. 617–626.
Chen X. Glucagonlike peptide 2 protects intestinal barrier in severe acute pancreatitis through regulating intestinal epithelial cell proliferation and apoptosis / X. Chen, H.X. Zhao, X.S. Fu, C.P. Li, X.L. Zhong // Pancreas. – 2012. – № 41 (7). – Р. 1080–1085.
Czakó L. Interactions between the endocrine and exocrine pancreas and their clinical relevance / L. Czakó, P. Hegyi, Z.Jr. Rakonczay, T. Wittmann, M. Otsuki // Pancreatology. – 2009. – № 9 (4). – Р. 351–359.
Dembinski A. Ghrelin attenuates the development of acute pancreatitis in rat / A. Dembinski, Z. Warzecha, P. Ceranowicz, R. Tomaszewska [et al.] // J Physiol Pharmacol. – 2003. – № 54 (4). – Р. 561–573.
Deng W.H. Effects of ORP150 on appearance and function of pancreatic beta cells following acute necrotizing pancreatitis / W.H. Deng, C. Chen, W.X. Wang, J. Yu, J.Y. Li, L. Liu // Pathol Res Pract. – 2011. – № 207 (6). – Р. 370–376.
Díaz-Rubio J.L. Diabetes mellitus in acute pancreatitis / J.L. Díaz-Rubio, A. Torre-Delgadillo, G. Robles-Díaz // Rev Gastroenterol Mex. – 2002. – № 67 (4). – Р. 278–284.
Hennig R. Pancreatic polypeptide in pancreatitis / R. Hennig, P.B. Kekis, H. Friess, T.E. Adrian, M.W. Büchler // Peptides. – 2002. – № 23 (2). – Р. 331–338.
Krska Z. Developments in pancreatic surgery at the 1st Surgical Department 1st Faculty of Medicine, Charles University and General University Hospital in Prague / Z. Krska, J. Sváb // Rozhl Chir. – 2012. – № 91 (5). – P. 262–266.
Leung P.S. Local renin-angiotensin system in the pancreas: the significance of changes by chronic hypoxia and acute pancreatitis / P.S. Leung // JOP. – 2001. – № 2 (1). – Р. 3–8.
Leung P.S. Tissue renin-angiotensin system: its expression, localization, regulation and potential role in the pancreas / P.S. Leung, P.O. Carlsson // J Mol Endocrinol. – 2001. – № 26 (3). – Р. 155–164.
Li Y.Y. Alteration of the pancreatic endocrine component in the early stage of acute necrotic pancreatitis in rats / Y.Y. Li, G.Y. Zhu, Y.X. Gao, Z.Y. Yang, Z.Y. Wang // Chin J Dig Dis. – 2006. – № 7 (3). – Р. 164–169.
Luyckx A. The role of glucagon in hyperglycemia. A review (author's transl) / A. Luyckx // Diabete Metab. – 1975. – № 1 (3). – Р. 201–208.
Mario C. Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands / C. Mario, L. Luciana, R. Valeria, H. Vanesa [et al.] // Res Ther. – 2009. – № 11 (2). – Р. 53–56.
Mayerle J. Course of illness in acute pancreatitis / J. Mayerle, M.M. Lerch // Kongressbd Dtsch Ges Chir Kongr. – 2001. – № 118. – Р. 296–300.
Nikou G.C. Changes of plasma levels of gastrointestinal peptides over the course of acute pancreatitis. Any significance for the pathophysiology and treatment of acute pancreatitis? / G.C. Nikou, E.J. Giamarellos-Bourboulis, C. Toumpanakis, T.P. Arnaoutis [et al.] // Hepatogastroenterology. – 2002. – № 49 (45). – Р. 706–708.
Pappas T.N. Pancreatic polypeptide in acute pancreatitis and small-bowel infarction in dogs / T.N. Pappas, J.G. Yovos, E.C. Ellison, T.M. O'Dorisio [et al.] // Digestive Diseases and Sciences. – 1981. – № 26 (11). – Р. 1013–1018.
Pitt H.A. Hepato-pancreato-biliary fat: the good, the bad and the ugly / H.A. Pitt // HPB (Oxford). – 2007. – № 9 (2). – Р. 92–97.
Qader S.S. Acute pancreatitis, expression of inducible nitric oxide synthase and defective insulin secretion / S.S. Qader, M. Ekelund, R. Andersson, S. Obermuller, A. Salehi // Cell Tissue Res. – 2003. – № 313 (3). – Р. 271–279.
Sabater L. Pancreatic function after severe acute biliary pancreatitis: the role of necrosectomy / L. Sabater, E. Pareja, L. Aparisi, J. Calvete [et al // Pancreas. – 2004. – № 28 (1). – Р. 65–68.
Shen J.Q. Expression of insulin-like growth factor binding protein-4 (IGFBP-4) in acute pancreatitis induced by L-arginine in mice / J.Q. Shen, J. Shen, X.P. Wang // Acta Histochem. – 2012. – № 114 (4). – Р. 379–385.
Singh S. Glucagonlike peptide 1-based therapies and risk of hospitalization for acute pancreatitis in type 2 diabetes mellitus: a population-based matched case-control study / S. Singh, H.Y. Chang, T.M. Richards, J.P. Weiner [et al.] // JAMA Intern Med. – 2013. – № 173 (7). – Р. 534–539.
Symersky T. The outcome of a long-term follow-up of pancreatic function after recovery from acute pancreatitis / T. Symersky, B. van Hoorn, A.A. Masclee // JOP. – 2006. – № 7 (5). – Р. 447–453.
Tanjoh K. Changes in glucagon kinetics and processing in patients with acute pancreatitis / K. Tanjoh, R. Tomita, Y. Ishikawa, T. Izumi [et al.] // Hepatogastroenterology. – 2007. – № 54 (76). – Р. 1250–1255.
Terada T. Minute mixed ductal-endocrine carcinoma of the pancreas with predominant intraductal growth / T. Terada, M. Kawaguchi, K. Furukawa, Y. Sekido, Y. Osamura // Pathol Int. – 2002. – № 52 (11). – Р. 740–746.
Toma H. Characterization of the neurotrophic response to acute pancreatitis / H. Toma, J.H. Winston, M.A. Micci, H. Li [et al.] // Pancreas. – 2002. – № 25 (1). – Р. 31–38.
Uemura K. Main pancreatic duct obstruction due to a small nonfunctioning endocrine tumor of the pancreas / K. Uemura, Y. Murakami, Y. Hayashidani, T. Sudo [et al.] // Hiroshima J Med Sci. – 2009. – № 58 (1). – Р. 45–48.
Weidenbach H. Vasoactive mediators and the progression from oedematous to necrotising experimental acute pancreatitis / H. Weidenbach, M.M. Lerch, T.M. Gress, D. Pfaff [et al // Gut. – 1995. – № 37 (3). – Р. 434–440.
Wu D. Endocrine pancreatic function changes after acute pancreatitis / D. Wu, Y. Xu, Y. Zeng, X. Wang // Pancreas. – 2011. – № 40 (7). – Р. 1006–1011.
Zhongkai L. Vasoactive intestinal peptide promotes gut barrier function against severe acute pancreatitis / L. Zhongkai, Y. Jianxin, C. Weichang // Mol Biol Rep. – 2012. – № 39 (4). – Р. 3557–3563.
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