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Endocrine Pancreatic Function During and Following Acute Pancreatitis

  • J. E. Domínguez-Muñoz
  • P. di Sebastiano
  • P. Malfertheiner
Conference paper

Abstract

The metabolic response during acute pancreatitis may depend on the one hand on acute stress, which is similar to that seen in other diseases such as sepsis or clinical situations such as surgical interventions, and on the other hand on damage to the Langerhans’s islets related to pancreatic inflammation. Hyperglycemia develops rather often in the early phase of acute pancreatitis, mainly in patients with severe disease [1–3]. This hyperglycemia could thus be the result of a hyperglucagonemia secondary to stress or the result of decreased synthesis and release of insulin secondary to the damage of pancreatic β-cells [4–7].

Keywords

Acute Pancreatitis Insulin Release Severe Acute Pancreatitis Pancreatic Necrosis Exocrine Pancreatic Function 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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References

  1. 1.
    Ranson JHC (1982) Etiology and prognostic factors in human acute pancreatitis: a review. Am J Gastroenterol 77: 633–63PubMedGoogle Scholar
  2. 2.
    Imrie CW, Benjamin IS, McKay AJ, Mackenzie I, O’neill J, Blumgart LH (1978) A single centre double blind trial of Trasylol therapy in primary acute pancreatitis. Br J Surg 65: 337–341PubMedCrossRefGoogle Scholar
  3. 3.
    Fan ST, Choi TK, Lai ECS, Wong J (1989) Prediction of severity of acute pancreatitis: An alternative approach. Gut 30: 1591–1595PubMedCrossRefGoogle Scholar
  4. 4.
    Drew SI, Joffe B, Vinik A, Seftel H, Singer F (1978) The first 24 hours of acute pancreatitis. Am J Med 64: 795–803PubMedCrossRefGoogle Scholar
  5. 5.
    Solomon SS, Duckworth WC, Jallepalli P, Bobal MA, Iyer R (1980) The glucose intolerance of acute pancreatitis: Hormonal response to arginine. Diabetes 29: 22–26PubMedCrossRefGoogle Scholar
  6. 6.
    Dunowitz M, Hendler R, Spiro HM, et al (1975) Glucagon secretion in acute and chronic pancreatitis. Ann Intern Med 83:778–781Google Scholar
  7. 7.
    Day JL, Knight M, Condon JR (1972) The role of pancreatic glucagon in the pathogenesis of acute pancreatitis. Clin Sci 43: 597–603PubMedGoogle Scholar
  8. 8.
    Domínguez-Muñoz JE, Uhl W, Lohr C, DiSebastiano P, Büchler M, Malfertheiner P (1992) Endocrine pancreatic response to arginine stimulation during the early phase of human acute pancreatitis. Gastroenterology 102: A263Google Scholar
  9. 9.
    Angelini G, Pederzoli P, Caliari S, et al (1984) Long-term outcome of acute necrohemorrhagic pancreatitis. Digestion 30: 131–137PubMedCrossRefGoogle Scholar
  10. 10.
    Büchler M, Hauke A, Malfertheiner P (1987) Follow-up after acute pancreatitis: Morphology and function. In: Beger HG, Büchler M, eds. Acute pancreatitis. Springer-Verlag: Berlin-Heidelberg 367–374Google Scholar
  11. 11.
    Doepel M, Erikson J, Halme L, Kumpulainen T, Hockerstedt K (1993) Good long-term results in patients surviving severe acute pancreatitis. Br J Surg 80: 1583–6PubMedCrossRefGoogle Scholar
  12. 12.
    Stastna R, Karasova L, Svacek J, Petrasek R, Winkler L, Lanska V, Skala I (1990) Endocrine pancreatic secretion in patients after acute pancreatitis. Pancreas 5: 358–60PubMedCrossRefGoogle Scholar
  13. 13.
    Otsuki M, Nakano S, Tachibana I (1994) Treatment with cholecystokinin receptor antagonist loxiglumide enhances insulin response to intravenous glucose stimulation in postpancreatitic rats. Regul Pept 52: 85–95PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • J. E. Domínguez-Muñoz
  • P. di Sebastiano
  • P. Malfertheiner

There are no affiliations available

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