Chronic pancreatitis

Current Opinion in Gastroenterology

Volumn 27, Issue 5, 2011, Pages 452-459

  DiMagno, Matthew J ^a   DiMagno, Eugene P ^b  

^a UNIVERSITY OF MICHIGAN MEDICAL SCHOOL   (United States)

^b MAYO CLINIC   (United States)

Author keywords

chronic pancreatitis; cystic fibrosis; exocrine pancreatic insufficiency

Indexed keywords

ALCOHOL; ANABOLIC AGENT; BUPIVACAINE; CORTICOSTEROID; ELASTASE; METANDROSTENDIOL; NARCOTIC ANALGESIC AGENT; OCTREOTIDE; SERINE PROTEASE INHIBITOR KAZAL TYPE 1; SERINE PROTEINASE INHIBITOR; TRANSMEMBRANE CONDUCTANCE REGULATOR; UNCLASSIFIED DRUG;

ANALGESIA; AUTOIMMUNE PANCREATITIS; CELIAC PLEXUS; CHRONIC PANCREATITIS; DIAGNOSTIC TEST; ENDOSCOPIC ECHOGRAPHY; ENVIRONMENTAL FACTOR; FECES ANALYSIS; GENE LOCATION; GENE MUTATION; GENETIC ASSOCIATION; HUMAN; IRRITABLE COLON; KIDNEY DISEASE; NERVE BLOCK; NEUROPATHIC PAIN; NONHUMAN; PANCREAS DISEASE; PANCREAS EXOCRINE INSUFFICIENCY; PANCREATIC HYPERENZYMEMIA; REVIEW; RISK FACTOR; TROPICAL PANCREATITIS;

AUTOIMMUNE DISEASES; EXOCRINE PANCREATIC INSUFFICIENCY; HUMANS; PAIN MANAGEMENT; PANCREATITIS, CHRONIC;

EID: 80051709605     PISSN: 02671379     EISSN: 15317056     Source Type: Journal    
DOI: 10.1097/MOG.0b013e328349e333     Document Type: Review

References (83)

1. DiMagno MJ, DiMagno EP. Chronic pancreatitis. Curr Opin Gastroenterol 2010; 26:490-498.
2. Cote GA, Yadav D, Slivka A, et al. Alcohol and smoking as risk factors in an epidemiology study of patients with chronic pancreatitis. Clin Gastroenterol Hepatol 2011; 9:266-273. The North American Pancreatitis Study Group reports that the current epidemiologic profile of chronic pancreatitis in the United States differs from historical data by showing that less than half (44%) were assigned as having heavy alcohol consumption as a cause of chronic pancreatitis, 27% had nonalcoholic chronic pancreatitis and 29% had an idiopathic cause.
3. Law R, Parsi M, Lopez R, et al. Cigarette smoking is independently associated with chronic pancreatitis. Pancreatology 2010; 10:54-59.
4. Andriulli A, Botteri E, Almasio PL, et al. Smoking as a cofactor for causation of chronic pancreatitis: A meta-analysis. Pancreas 2010; 39:1205-1210.
5. Lowenfels AB, Maisonneuve P. Defining the role of smoking in chronic pancreatitis. Clin Gastroenterol Hepatol 2011; 9:196-197. An editorial to the study by Cote et al. [2'] that emphasizes the individual contribution of smoking as a risk factor for chronic pancreatitis and what data are available to understand the pathophysiological basis for this relationship.
6. DiMagno MJ, DiMagno EP. Chronic pancreatitis. Curr Opin Gastroenterol 2003; 19:451-457.
7. Bhatia E, Choudhuri G, Sikora SS, et al. Tropical calcific pancreatitis: Strong association with SPINK1 trypsin inhibitor mutations. Gastroenterology 2002; 123:1020-1025.
8. Rossi L, Pfutzer RH, Parvin S, et al. SPINK1/PSTI mutations are associated with tropical pancreatitis in Bangladesh. A preliminary report. Pancreatology 2001; 1:242-245.
9. Mohan V, Premalatha G, Pitchumoni CS. Tropical chronic pancreatitis: An update. J Clin Gastroenterol 2003; 36:337-346.
10. Schneider A, Suman A, Rossi L, et al. SPINK1/PSTI mutations are associated with tropical pancreatitis and type II diabetes mellitus in Bangladesh. Gastroenterology 2002; 123:1026-1030.
11. Chandak GR, IdrisMM, Reddy DN, et al. Mutations in the pancreatic secretory trypsin inhibitor gene (PSTI/SPINK1) rather than the cationic trypsinogen gene (PRSS1) are significantly associated with tropical calcific pancreatitis. J Med Genet 2002; 39:347-351.
12. Hassan Z, Mohan V, Ali L, et al. SPINK1 is a susceptibility gene for fibrocalculous pancreatic diabetes in subjects from the Indian subcontinent. Am J Hum Genet 2002; 71:964-968.
13. Midha S, Khajuria R, Shastri S, et al. Idiopathic chronic pancreatitis in India: Phenotypic characterisation and strong genetic susceptibility due to SPINK1 and CFTR gene mutations. Gut 2010; 59:800-807. A referral center in India investigated the genetic profile of patients with idiopathic chronic pancreatitis by reporting the frequency of SPINK1 mutations in 113 patients andCFTRmutations andpolymorphisms in100. Patientscommonly hadtheSPINK1 N34S gene mutation (42 vs. 4% in controls) and CFTR gene polymorphisms (50 vs. 10% in controls) but not CFTR mutations. Malnutrition and cassava were not risk factors for idiopathic chronic pancreatitis. The authors propose that the observed strong genetic susceptibility of idiopathic chronic pancreatitis in India warrants consideration of whether the term 'tropical calcific pancreatitis' is a misnomer.
14. 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.
15. DiMagno EP. Gene mutations and idiopathic chronic pancreatitis: Clinical implications and testing. Gastroenterology 2001; 121:1508-1512.
16. Bishop MD, Freedman SD, Zielenski J, et al. The cystic fibrosis transmembrane conductance regulator gene and ion channel function in patients with idiopathic pancreatitis. Hum Genet 2005; 1-10.
17. Ramesh H. Idiopathic chronic pancreatitis in India. Gut 2010. [Epub ahead of print]
18. Balakrishnan V. Tropical chronic pancreatitis: A historical perspective. Gut 2010. [Epub ahead of print]
19. Paliwal S, Bhaskar S, Rao GV, et al. What's there in a name: Tropical calcific pancreatitis and idiopathic chronic pancreatitis in India. Gut 2010. [Epub ahead of print]
20. Ko SB, Mizuno N, Yatabe Y, et al. Corticosteroids correct aberrant CFTR localization in the duct and regenerate acinar cells in autoimmune pancreatitis. Gastroenterology 2010; 138:1988-1996. The investigators performed serial pancreatic biopsy and secretin stimulated direct pancreatic function testing on 21 patients with AIP and found that corticosteroids reduced pancreatic fibrosis and tissue inflammation, triggered regeneration of acinar tissue and increased secretin evoked pancreatic juice bicarbonate and amylase concentrations, particularly after 12 months. They attributed improved bicarbonate secretion to restoration of the mislocalized CFTR protein in the ductal cytoplasm to the apical ductal membrane. Interestingly, ductal CFTR mislocalization was present in pancreas from 11 patients with other forms of chronic pancreatitis, which raises the possibility that mislocalization of CFTR (and a variant CF phenotype) may explain aberrant pancreatic bicarbonate secretion in other forms of chronic pancreatitis.
21. Forcione DG, Brugge WR. New kid on the block? Autoimmune pancreatitis. Best Pract Res Clin Gastroenterol 2010; 24:361-378.
22. Kamisawa T, Takuma K, Egawa N, et al. Autoimmune pancreatitis and IgG4- related sclerosing disease. Nat Rev Gastroenterol Hepatol 2010; 7:401-409.
23. Chari ST, Kloeppel G, Zhang L, et al. Histopathologic and clinical subtypes of autoimmune pancreatitis: The Honolulu consensus document. Pancreas 2010; 39:549-554. An international consensus group describes two separate forms of AIP (types 1 and 2). Each has a similar clinical presentation but distinctly different histopathology [lymphoplasmacytic sclerosing pancreatitis (LPSP) and idiopathic duct centric pancreatitis (IDCP)], demography, serological characteristics, extrapancreatic organ involvement, and disease relapse. Based on these differences, there is controversy whether type 2 AIP is an autoimmune disease [25].
24. Sah RP, Chari ST, Pannala R, et al. Differences in clinical profile and relapse rate of type 1 versus type 2 autoimmune pancreatitis. Gastroenterology 2010; 139:140-148. Investigators describe two distinct forms of AIP (types 1 and 2), as described in the Honolulu consensus document [23]. The authors emphasize that only type 1 AIP has a high relapse rate and neither affects long-term survival.
25. Kamisawa T, Notohara K, Shimosegawa T. Two clinicopathologic subtypes of autoimmune pancreatitis: LPSP and IDCP. Gastroenterology 2010; 139:22- In an editorial to the study by Sah et al. [2-], authors raise concern that type 2 AIP is not an autoimmune disease based on a number of differences between type 1 and 2 AIP. In contrast to type 1 AIP, type 2 AIP lacks serological characteristics and extrapancreatic lesions and has a neutrophilic rather than lymphocytic pancreatic inflammatory infiltrate. This controversy is addressed also in the Honolulu consensus document [23].
26. Lohr JM, Faissner R, Koczan D, et al. Autoantibodies against the exocrine pancreas in autoimmune pancreatitis: Gene and protein expression profiling and immunoassays identify pancreatic enzymes as a major target of the inflammatory process. Am J Gastroenterol 2010; 105:2060-2071. Investigators report acinar cells are involved in the autoimmune process in AIP. They found reduced gene and protein expression of trypsinogen isoforms in pancreatic tissue from 12 patients with AIP compared to eight patients with non-AIP chronic pancreatitis. AIP patients also had autoantibodies against the trypsin inhibitor PSTI and two of three trypsinogen isoforms, raising the possibility that trypsinogen autoantibodies may help to diagnose AIP.
27. Moon SH, Kim MH, Park do H, et al. IgG4 immunostaining of duodenal papillary biopsy specimens may be useful for supporting a diagnosis of autoimmune pancreatitis. Gastrointest Endosc 2010; 71:960-966.
28. Kamisawa T, Takuma K, Anjiki H, et al. Differentiation of autoimmune pancreatitis from pancreatic cancer by diffusion-weighted MRI. Am J Gastroenterol 2010; 105:1870-1875.
29. Kamisawa T, Egawa N, Inokuma S, et al. Pancreatic endocrine and exocrine function and salivary gland function in autoimmune pancreatitis before and after steroid therapy. Pancreas 2003; 27:235-238.
30. Song MH, Kim MH, Lee SK, et al. Regression of pancreatic fibrosis after steroid therapy in patients with autoimmune chronic pancreatitis. Pancreas 2005; 30:83-86.
31. Groman JD, Meyer ME, Wilmott RW, et al. Variant cystic fibrosis phenotypes in the absence of CFTR mutations. N Engl J Med 2002; 347:401-407.
32. Knowles MR, Durie PR. What is cystic fibrosis? N Engl J Med 2002; 347:439-442.
33. Abasov IT, Gidayatov AA. The functional state of adrenal cortex in patients with chronic relapsing pancreatitis. Gastroenterol Jpn 1986; 21:374-378.
34. Tuzhilin SA, Dreiling DA. On the appearance, levels and regulation of pancreatic enzyme serum concentrations. Am J Gastroenterol 1978; 69:428-435.
35. Gomez G, Townsend CM Jr, Green D, et al. Involvement of cholecystokinin receptors in the adverse effect of glucocorticoids on diet-induced necrotizing pancreatitis. Surgery 1989; 106:230-236.
36. Pescador R, Manso MA, Rebollo AJ, et al. Effect of chronic administration of hydrocortisone on the induction and evolution of acute pancreatitis induced by cerulein. Pancreas 1995; 11:165-172.
37. Tuzhilin SA, Shaternikov VA, Petrova AA, et al. Treatment of chronic pancreatitis with anabolic steroid preparations. Vrach Delo 1968; 10:36-39.
38. Bank S, Marks IN, Barbezat GO. Treatment of acute and chronic pancreatitis. Drugs 1977; 13:373-381.
39. Gullo L. Chronic nonpathological hyperamylasemia of pancreatic origin. Gastroenterology 1996; 110:1905-1908.
40. Gullo L. Familial pancreatic hyperenzymemia. Pancreas 2000; 20:158-160.
41. Donati F, Boraschi P, Gigoni R, et al. Secretin-stimulated MR cholangiopancreatography in the evaluation of asymptomatic patients with nonspecific pancreatic hyperenzymemia. Eur J Radiol 2010; 75:e38-e44. Investigators defined asymptomatic hyperenzymemia as less than three-fold increase in lipase and/or amylase for at least 6 months and reported that 71% of affected patients (57/80) have pancreatic abnormalities by MRCP. Others emphasize (see ref. [43]) that this and similar data are difficult to interpret because the abnormal pancreatic imaging findings in patients with asymptomatic hyperenzymemia are 'nonspecific and/or of unknown clinical significance, and do not benefit the patient because there are no immediate diagnostic or therapeutic consequences'.
42. Testoni PA, Mariani A, Curioni S, et al. Pancreatic ductal abnormalities documented by secretin-enhanced MRCP in asymptomatic subjects with chronic pancreatic hyperenzymemia. Am J Gastroenterol 2009; 104:1780-1786.
43. Lankisch PG. Pancreatic ductal abnormalities documented by secretin-enhanced MRCP in asymptomatic subjects with chronic pancreatic hyperenzymemia. Am J Gastroenterol 2010; 105:703-705. An editorial to the study by Testoni et al. [42] but also applicable to the study by Donati et al. [41-] emphasizing that abnormal pancreatic imaging findings in patients with asymptomatic hyperenzymemia are 'nonspecific and/or of unknown clinical significance, and do not benefit the patient because there are no immediate diagnostic or therapeutic consequences'.
44. Griesche-Philippi J, Otto J, Schworer H, et al. Exocrine pancreatic function in patients with end-stage renal disease. Clin Nephrol 2010; 74:457-464.
45. Leeds JS, Hopper AD, Sidhu R, et al. Some patients with irritable bowel syndrome may have exocrine pancreatic insufficiency. Clin Gastroenterol Hepatol 2010; 8:433-438. Investigators used the fecal elastase test to assess exocrine pancreatic insufficiency (EPI) and reported that EPI was present in 19 of 314 (6.1%) patients who fulfilled the Rome II criteria for IBS-D. The data are difficult to interpret because fecal elastase is inaccurate to diagnose EPI and definite pancreatic disease was present (by CT) in only four of the 19 with a low fecal elastase (21%), or four of 314 with IBS-D (1%).
46. Owyang C, Miller LJ, DiMagno EP, et al. Pancreatic exocrine function in severe human chronic renal failure. Gut 1982; 23:357-361.
47. Hahn JU, Bochnig S, Kerner W, et al. A new fecal elastase 1 test using polyclonal antibodies for the detection of exocrine pancreatic insufficiency. Pancreas 2005; 30:189-191.
48. Beharry S, Ellis L, Corey M, et al. How useful is fecal pancreatic elastase 1 as a marker of exocrine pancreatic disease? J Pediatr 2002; 141:84-90.
49. Schappi MG, Smith VV, Cubitt D, et al. Faecal elastase 1 concentration is a marker of duodenal enteropathy. Arch Dis Child 2002; 86:50-53.
50. Nousia-Arvanitakis S. Fecal elastase-1 concentration: An indirect test of exocrine pancreatic function and a marker of an enteropathy regardless of cause. J Pediatr Gastroenterol Nutr 2003; 36:314-315.
51. Carroccio A, Verghi F, Santini B, et al. Diagnostic accuracy of fecal elastase 1 assay in patients with pancreatic maldigestion or intestinal malabsorption: A collaborative study of the Italian Society of Pediatric Gastroenterology and Hepatology. Dig Dis Sci 2001; 46:1335-1342.
52. Salvatore S, Finazzi S, Barassi A, et al. Low fecal elastase: Potentially related to transient small bowel damage resulting from enteric pathogens. J Pediatr Gastroenterol Nutr 2003; 36:392-396.
53. Hardt PD, Krauss A, Bretz L, et al. Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus. Acta Diabetol 2000; 37:105-110.
54. Rathmann W, Haastert B, Icks A, et al. Low faecal elastase 1 concentrations in type 2 diabetes mellitus. Scand J Gastroenterol 2001; 36:1056-1061.
55. Nunes AC, Pontes JM, Rosa A, et al. Screening for pancreatic exocrine insufficiency in patients with diabetes mellitus. Am J Gastroenterol 2003; 98:2672-2675.
56. Hahn JU, Kerner W, Maisonneuve P, et al. Low fecal elastase 1 levels do not indicate exocrine pancreatic insufficiency in type-1 diabetes mellitus. Pancreas 2008; 36:274-278.
57. Afzalpurkar RG, Schiller LR, Little KH, et al. The self-limited nature of chronic idiopathic diarrhea. N Engl J Med 1992; 327:1849-1852.
58. Wollaeger EE, Comfort MW, Osterberg AE. Total solids, fat and nitrogen in the feces: III. A study of normal persons taking a test diet containing a moderate amount of fat; comparison with results obtained with normal persons taking a test diet containing a large amount of fat. Gastroenterology 1947; 9:272-283.
59. Wollaeger EE, Comfort MW, Weir JF, et al. The total solids, fat and nitrogen in the feces: I. A study of normal persons and of patients with duodenal ulcer and a test diet containing large amounts of fat. Gastroenterology 1946; 6:83-92.
60. Wollaeger EE, Comfort MW, Clagett OT, et al. Efficiency of gastrointestinal tract after resection of head of pancreas. J Am Med Assoc 1948; 137:838-848.
61. Regan PT, Malagelada JR, DiMagno EP, et al. Comparative effects of antacids, cimetidine and enteric coating on the therapeutic response to oral enzymes in severe pancreatic insufficiency. N Engl J Med 1977; 297:854-858.
62. Catalano MF, Sahai A, Levy M, et al. EUS-based criteria for the diagnosis of chronic pancreatitis: The Rosemont classification. Gastrointest Endosc 2009; 69:1251-1261.
63. Gardner TB, Levy MJ. EUS diagnosis of chronic pancreatitis. Gastrointest Endosc 2010; 71:1280-1289. A very balanced review of the EUS diagnosis of chronic pancreatitis.
64. Lieb JG 2nd, Palma DT, Garvan CW, et al. Intraobserver agreement among endosonographers for endoscopic ultrasound features of chronic pancreatitis: A blinded multicenter study. Pancreas 2011; 40:177-180.
65. Stevens T, Dumot JA, Parsi MA, et al. Combined endoscopic ultrasound and secretin endoscopic pancreatic function test in patients evaluated for chronic pancreatitis. Dig Dis Sci 2010; 55:2681-2687.
66. Albashir S, Bronner MP, Parsi MA, et al. Endoscopic ultrasound, secretin endoscopic pancreatic function test, and histology: Correlation in chronic pancreatitis. Am J Gastroenterol 2010; 105:2498-2503. Aretrospective study reported sensitivity and specificity ofEUSand ePFT for chronic pancreatitis using histology (>2 fibrosis scale) as the gold standard. EUS had 84% sensitivity and 100% specificity and ePFT had 86% sensitivity and 67% specificity. By combining results of both tests the sensitivity was 100%. Limitations of the study are the inclusion of a very select group of patients who all had surgery and observations that four patients (16%) were submitted to surgery unnecessarily [all four had no significant fibrosis and only one of four had any abnormal test (ePFT)].
67. Treede RD, Jensen TS, Campbell JN, et al. Neuropathic pain: Redefinition and a grading system for clinical and research purposes. Neurology 2008; 70:1630-1635.
68. Demir IE, Tieftrunk E, Maak M, et al. Pain mechanisms in chronic pancreatitis: Of a master and his fire. Langenbecks Arch Surg 2011; 396:151-160.
69. Kuner R. Central mechanisms of pathological pain. Nat Med 2010; 16:1258-1266.
70. Olesen SS, Brock C, Krarup AL, et al. Descending inhibitory pain modulation is impaired in patients with chronic pancreatitis. Clin Gastroenterol Hepatol 2010; 8:724-730.
71. Czakanski P, Ness TJ. Impaired diffuse noxious inhibitory controls: An additional mechanism of pain in chronic pancreatitis? Clin Gastroenterol Hepatol 2010; 8:647-648.
72. Demir IE, Ceyhan GO, Rauch U, et al. The microenvironment in chronic pancreatitis and pancreatic cancer induces neuronal plasticity. Neurogastroenterol Motil 2010; 22:480-490.
73. Feng QX, Wang W, Feng XY, et al. Astrocytic activation in thoracic spinal cord contributes to persistent pain in rat model of chronic pancreatitis. Neuroscience 2010; 167:501-509.
74. Brock C, Andresen T, Frokjaer JB, et al. Central pain mechanisms following combined acid and capsaicin perfusion of the human oesophagus. Eur J Pain 2010; 14:273-281.
75. Bradley EL 3rd, Bem J. Nerve blocks and neuroablative surgery for chronic pancreatitis. World J Surg 2003; 27:1241-1248.
76. Guarner L, Navalpotro B, Molero X, et al. Management of painful chronic pancreatitis with single-dose radiotherapy. Am J Gastroenterol 2009; 104:349-355.
77. Volkova LP, Sharova LA. Experience with radiotherapy of chronic painful recurrent pancreatitis. Ter Arkh 1964; 36:21-24.
78. Gress F, Schmitt C, Sherman S, et al. A prospective randomized comparison of endoscopic ultrasound- and computed tomography-guided celiac plexus block for managing chronic pancreatitis pain. Am J Gastroenterol 1999; 94:900-905.
79. Madsen P, Hansen E. Coeliac plexus block versus pancreaticogastrostomy for pain in chronic pancreatitis. A controlled randomized trial. Scand J Gastroenterol 1985; 20:1217-1220.
80. Santosh D, Lakhtakia S, Gupta R, et al. Clinical trial: A randomized trial comparing fluoroscopy guided percutaneous technique vs. endoscopic ultrasound guided technique of coeliac plexus block for treatment of pain in chronic pancreatitis. Aliment Pharmacol Ther 2009; 29:979-984.
81. Puli SR, Reddy JB, Bechtold ML, et al. EUS-guided celiac plexus neurolysis for pain due to chronic pancreatitis or pancreatic cancer pain: A meta-analysis and systematic review. Dig Dis Sci 2009; 54:2330-2337.
82. Kaufman M, Singh G, Das S, et al. Efficacy of endoscopic ultrasound-guided celiac plexus block and celiac plexus neurolysis for managing abdominal pain associated with chronic pancreatitis and pancreatic cancer. J Clin Gastroenterol 2010; 44:127-134. Investigators performed a systematic review of six studies of EUS-guided CPB for painful chronic pancreatitis (n=221 patients) and five studies of EUS-guided CPN for painful pancreatic cancer (n=119 patients) and reported alleviation of pain by CPB in 51% (95% CI 33-100) and by CPN in 73% (95%CI 51-100). Similar to prior studies, EUS-guided CPB and CPN appear effective and well tolerated in treating patients with pain due to chronic pancreatitis or pancreatic cancer, respectively, but identification of predictors for response to CPB would greatly improve selecting appropriate patients for this therapy in painful chronic pancreatitis.
83. Baghdadi S, Abbas MH, Albouz F, et al. Systematic review of the role of thoracoscopic splanchnicectomy in palliating the pain of patients with chronic pancreatitis. Surg Endosc 2008; 22:580-588.