Skip to main content
SpringerLink
Log in

Pancreatitis in childhood

  • Published:
Current Gastroenterology Reports Aims and scope Submit manuscript

Abstract

Inflammatory disease of the pancreas falls into two major classifications: acute and chronic. Acute pancreatitis is a reversible process, whereas chronic pancreatitis produces irreversible changes in the architecture and function of the pancreas. The recent finding that mutations in the gene encoding cationic trypsinogen are associated with hereditary pancreatitis, the identification of genes that increase the risk for developing chronic pancreatitis, and advances in cell biology have contributed greatly to our understanding of the molecular mechanisms leading to pancreatitis. Although pancreatitis is less common in children than in adults, it still occurs with regularity and should be considered in any child with acute or chronic abdominal pain. The major difference between pancreatitis in children and adults lies in the etiologies and outcome of acute pancreatitis and in the etiology of chronic pancreatitis. The treatment of acute and chronic pancreatitis is similar at all ages.

This is a preview of subscription content, log in via an institution to check access.

Access this article

Log in via an institution

Price excludes VAT (USA)
Tax calculation will be finalised during checkout.

Instant access to the full article PDF.

Institutional subscriptions

Similar content being viewed by others

References and Recommended Reading

  1. Werlin SL, Kugathasan S, Frautschy BC: Pancreatitis in children. J Pediatr Gastroenterol Nutr 2003, 37:591–595. This paper describes the incidence, causes, and outcome of pancreatitis at a regional children’s hospital. Two hundred fourteen episodes in 180 patients were analyzed.

    Article  PubMed  Google Scholar 

  2. Lopez MJ: The changing incidence of acute pancreatitis in children: a single-institution perspective. J Pediatr 2002, 140:622–624. Two hundred seventy-four cases of pancreatitis were analyzed for etiology. This study provides the first evidence of rising incidence of acute pancreatitis in childhood.

    Article  PubMed  Google Scholar 

  3. DeBanto JR, Goday PS, Pedroso MR, et al.: Acute pancreatitis in children. Am J Gastroenterol 2002, 97:1726–1731. This multicenter study describes the incidence, causes, and outcomes in 301 cases of pancreatitis. It also develops and validates a pediatric scoring system for acute pancreatitis.

    Article  PubMed  Google Scholar 

  4. Steer ML: Frank Brooks Memorial Lecture: The early intraacinar cell events which occur during acute pancreatitis. Pancreas 1998, 17:31–37. The text of an address by Dr. Steer provides an excellent overview of current theories of the pathogenesis of acute pancreatitis.

    Article  PubMed  CAS  Google Scholar 

  5. Sakorafas GH, Tsiotou AG: Etiology and pathogenesis of acute pancreatitis: current concepts. J Clin Gastroenterol 2000, 30:343–356.

    Article  PubMed  CAS  Google Scholar 

  6. Choi BH, Lim YJ, Yoon CH, et al.: Acute pancreatitis associated with biliary disease in children. J Gastroenterol Hepatol 2003, 18:915–921.

    Article  PubMed  Google Scholar 

  7. Otani T, Chepilko SM, Grendell JH, et al.: Codistribution of TAP and the granule membrane protein GRAMP-92 in rat caeruleininduced pancreatitis. Am J Physiol 1998, 275:G999-G1009.

    PubMed  CAS  Google Scholar 

  8. Cavallini G, Frulloni L: Antiproteasic agents in the prevention of post-ERCP pancreatitis: rationale for use and clinical results. JOP 2003, 4:75–82.

    PubMed  Google Scholar 

  9. Whitcomb DC: Genetic predispositions to acute and chronic pancreatitis. Med Clin North Am 2000, 84:531–547. This review covers the evidence for the role of genetic mutations and polymorphisms in acute and chronic pancreatitis.

    Article  PubMed  CAS  Google Scholar 

  10. Frossard JL, Past CM: Experimental acute pancreatitis: new insights into the pathophysiology. Front Biosci 2002, 7:275–287.

    Article  Google Scholar 

  11. Halangk W, Lerch MM, Brandt-Nedelev B, et al.: Role of cathepsin B in intracellular trypsinogen activation and the onset of acute pancreatitis. J Clin Invest 2000, 106:773–781.

    Article  PubMed  CAS  Google Scholar 

  12. Schneider A, Whitcomb DC: Hereditary pancreatitis: a model for inflammatory diseases of the pancreas. Best Pract Res Clin Gastroenterol 2002, 16:347–363. This review highlights the genetic studies on kindreds with hereditary pancreatitis, reviews a risk classification scheme, and reviews the major independent theories on the development of chronic pancreatitis.

    Article  PubMed  Google Scholar 

  13. Whitcomb DC, Gorry MC, Preston RA, et al.: Hereditary pancreatitis is caused by a mutation in the cationic trypsinogen gene. Nat Genet 1996, 14:141–145. This paper is the original description of the association of a mutation in cationic trypsinogen with hereditary pancreatitis.

    Article  PubMed  CAS  Google Scholar 

  14. Etemad B, Whitcomb DC: Chronic pancreatitis: diagnosis, classification, and new genetic developments. Gastroenterology 2001, 120:682–707.

    Article  PubMed  CAS  Google Scholar 

  15. Kukor Z, Toth M, Pal G, et al.: Human cationic trypsinogen. Arg(117) is the reactive site of an inhibitory surface loop that controls spontaneous zymogen activation. J Biol Chem 2002, 277:6111–6117.

    Article  PubMed  CAS  Google Scholar 

  16. Sahin-Toth M: Human cationic trypsinogen: role of Asn-21 in zymogen activation and implications in hereditary pancreatitis. J Biol Chem 2000, 275:22750–22755.

    Article  PubMed  CAS  Google Scholar 

  17. Sanfey H, Sarr MG, Bulkley GB, et al.: Oxygen-derived free radicals and acute pancreatitis: a review. Acta Physiol Scand Suppl 1986, 548:109–118.

    PubMed  CAS  Google Scholar 

  18. Guice KS, Miller DE, Oldham KT, et al.: Superoxide dismutase and catalase: a possible role in established pancreatitis. Am J Surg 1986, 151:163–169.

    Article  PubMed  CAS  Google Scholar 

  19. Anderson MC, Schoenfeld FB, Iams WB, et al.: Circulatory changes in acute pancreatitis. Surg Clin North Am 1967, 47:127–140.

    PubMed  CAS  Google Scholar 

  20. Demols A, Le Moine O, Desalle F, et al.: CD4(+)T cells play an important role in acute experimental pancreatitis in mice. Gastroenterology 2000, 118:582–590.

    Article  PubMed  CAS  Google Scholar 

  21. Gloor B, Todd KE, Lane JS, et al.: Hepatic Kupffer cell blockade reduces mortality of acute hemorrhagic pancreatitis in mice. J Gastrointest Surg 1998, 2:430–435.

    Article  PubMed  CAS  Google Scholar 

  22. Pezzilli R, Billi P, Beltrandi E, et al.: Impaired lymphocyte proliferation in human acute pancreatitis. Digestion 1997, 58:431–436.

    Article  PubMed  CAS  Google Scholar 

  23. Bhatia M, Brady M, Shokuhi S, et al.: Inflammatory mediators in acute pancreatitis. J Pathol 2000, 190:117–125.

    Article  PubMed  CAS  Google Scholar 

  24. Bhatia M, Neoptolemos JP, Slavin J: Inflammatory mediators as therapeutic targets in acute pancreatitis. Curr Opin Investig Drugs 2001, 2:496–501.

    PubMed  CAS  Google Scholar 

  25. Abou-Assi S, Craig K, O’Keefe SJ: Hypocaloric jejunal feeding is better than total parenteral nutrition in acute pancreatitis: results of a randomized comparative study. Am J Gastroenterol 2002, 97:2255–2262.

    Article  PubMed  Google Scholar 

  26. Ranson JH: Etiological and prognostic factors in human acute pancreatitis: a review. Am J Gastroenterol 1982, 77:633–638.

    PubMed  CAS  Google Scholar 

  27. Blamey SL, Imrie CW, O’Neill J, et al.: Prognostic factors in acute pancreatitis. Gut 1984, 25:1340–1346.

    PubMed  CAS  Google Scholar 

  28. Knaus WA, Draper EA, Wagner DP, et al.: APACHE II: a severity of disease classification system. Crit Care Med 1985, 13:818–829.

    Article  PubMed  CAS  Google Scholar 

  29. Whitcomb DC: Hereditary pancreatitis: new insights into acute and chronic pancreatitis. Gut 1999, 45:317–322.

    Article  PubMed  CAS  Google Scholar 

  30. Applebaum-Shapiro SE, Finch R, Pfutzer RH, et al.: Hereditary pancreatitis in North America: the Pittsburgh-Midwest Multi-Center Pancreatic Study Group Study. Pancreatology 2001, 1:439–443.

    Article  PubMed  CAS  Google Scholar 

  31. Witt H, Luck W, Hennies HC, et al.: Mutations in the gene encoding the serine protease inhibitor, Kazal type 1 are associated with chronic pancreatitis. Nat Genet 2000, 25:213–216.

    Article  PubMed  CAS  Google Scholar 

  32. Naruse S, Kitagawa M, Ishiguro H, et al.: Cystic fibrosis and related diseases of the pancreas. Best Pract Res Clin Gastroenterol 2002, 16:511–526.

    Article  PubMed  CAS  Google Scholar 

  33. Noone PG, Zhou Z, Silverman LM, et al.: Cystic fibrosis gene mutations and pancreatitis risk: relation to epithelial ion transport and trypsin inhibitor gene mutations. Gastroenterology 2001, 121:1310–1319.

    Article  PubMed  CAS  Google Scholar 

  34. Sharer N, Schwarz M, Malone G, et al.: Mutations of the cystic fibrosis gene in patients with chronic pancreatitis. N Engl J Med 1998, 339:645–652.

    Article  PubMed  CAS  Google Scholar 

  35. Cohn JA, Bornstein JD, Jowell PS: Cystic fibrosis mutations and genetic predisposition to idiopathic chronic pancreatitis. Med Clin North Am 2000, 84:621–631.

    Article  PubMed  CAS  Google Scholar 

  36. Whitcomb DC: Value of genetic testing in management of pancreatitis. Gut 2004, in press.

  37. Ellis I, Lerch MM, Whitcomb DC: Genetic testing for hereditary pancreatitis: guidelines for indications, counselling, consent and privacy issues. Pancreatology 2001, 1:405–415. The paper provides a good synopsis of the many issues related to genetic testing.

    Article  PubMed  CAS  Google Scholar 

  38. Applebaum-Shapiro SE, Peters JA, O’Connell JA, et al.: Motivations and concerns of patients with access to genetic testing for hereditary pancreatitis. Am J Gastroenterol 2001, 96:1610–1617.

    Article  PubMed  CAS  Google Scholar 

  39. Applebaum SE, Kant JA, Whitcomb DC, et al.: Genetic testing. Counseling, laboratory, and regulatory issues and the EUROPAC protocol for ethical research in multicenter studies of inherited pancreatic diseases. Med Clin North Am 2000, 84:575–588.

    Article  PubMed  CAS  Google Scholar 

  40. Lowenfels AB, Maisonneuve P, Whitcomb DC, et al.: Cigarette smoking as a risk factor for pancreatic cancer in patients with hereditary pancreatitis. JAMA 2001, 286:169–170.

    Article  PubMed  CAS  Google Scholar 

  41. Whitcomb DC: Motion-genetic testing is useful in the diagnosis of nonhereditary pancreatic conditions: arguments for the motion. Can J Gastroenterol 2003, 17:47–52.

    PubMed  Google Scholar 

  42. Cohn JA: Motion-genetic testing is useful in the diagnosis of nonhereditary pancreatic conditions: arguments against the motion. Can J Gastroenterol 2003, 17:53–55.

    PubMed  Google Scholar 

  43. Pfutzer RH, Barmada MM, Brunskill AP, et al.: SPINK1/PSTI polymorphisms act as disease modifiers in familial and idiopathic chronic pancreatitis. Gastroenterology 2000, 119:615–623.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Division of Pediatric Gastroenterology, Children’s Hospital of Pittsburgh and the University of Pittsburgh Medical Center, 3705 Fifth Avenue, 15213, Pittsburgh, PA, USA

    Mark E. Lowe MD, PhD

Authors
  1. Mark E. Lowe MD, PhD
    View author publications

    You can also search for this author in PubMed Google Scholar

Rights and permissions

Reprints and permissions

About this article

Cite this article

Lowe, M.E. Pancreatitis in childhood. Curr Gastroenterol Rep 6, 240–246 (2004). https://doi.org/10.1007/s11894-004-0014-5

Download citation

  • Issue Date:

  • DOI: https://doi.org/10.1007/s11894-004-0014-5

Keywords

Search

Navigation