Correspondence
Acute Pancreatitis
N Engl J Med 1994; 331:948-949October 6, 1994
- Article
To the Editor:
In their excellent review of acute pancreatitis (April 28 issue),1 Steinberg and Tenner address, among other aspects of the disease, the pathophysiologic features of gallstone-induced pancreatitis. They suggest that the argument about whether or not Opie's common-channel theory of 19012 explains pancreatitis in humans has not been settled. After nearly a century of research, however, the evidence that the common-channel theory is invalid appears overwhelming. The common terminal conduit between the pancreatic duct and the bile duct is, if present at all, much too short in most humans to allow for communication between the two ducts (Opie's common channel) when a gallstone is impacted at the papilla3. Even if such a common channel were created not by the stone itself but instead by the sphincter stenosis arising from the passage of the stone, the pancreatic secretory pressure would still exceed the pressure of the bile duct4. As a consequence, reflux of pancreatic juice into the biliary tract would result, rather than reflux of bile into the pancreas. Even if we assume that bile could somehow be regurgitated into the pancreas, it would still remain a harmless event. At pressures below those required for the experimental disruption of intercellular junctions, bile can be perfused through the pancreatic duct without damage to the organ5. The final arguments are provided by recent studies showing that pancreatic outflow obstruction is the triggering event for gallstone-induced pancreatitis and that reflux of bile through a common channel is neither required for the onset of the disease nor likely to occur6.
6 ReferencesMarkus M. Lerch, M.D.
Ulm University, D-89070 Ulm, GermanyCarlos A. Hernandez, M.D.
Universidad Nacional de Cordoba, Cordoba 5000, ArgentinaGuido Adler, M.D.
Ulm University, D-89070 Ulm, Germany1
Steinberg W ,Tenner S . Acute pancreatitis. N Engl J Med 1994;330:1198-1210
Full Text | Web of Science | Medline2
Opie EL . The etiology of acute hemorrhagic pancreatitis. Bull Johns Hopkins Hosp 1901;12:182-188
Web of Science3
DiMagno EP ,Shorter RG ,Taylor WF ,Go VL . Relationship between pancreaticobiliary ductal anatomy and pancreatic ductal and parenchymal histology. Cancer 1982;49:361-368
CrossRef | Web of Science | Medline4
Carr-Locke DL ,Gregg JA . Endoscopic manometry of pancreatic and biliary sphincter zones in man: basal results in healthy volunteers. Dig Dis Sci 1981;26:7-15
CrossRef | Web of Science | Medline5
Robinson TM ,Dunphy JE . Continuous perfusion of bile and protease activators through the pancreas. JAMA 1963;183:530-533
Web of Science | Medline6
Lerch MM, Weidenbach H, Hernandez CA, Preclik G, Adler G. Pancreatic outflow obstruction as the critical event for human gallstone-induced pancreatitis. Gut (in press).
To the Editor:
The excellent review of acute pancreatitis by Steinberg and Tenner contained an erroneous statement about cystic fibrosis and pancreatitis. This complication of cystic fibrosis is not limited to children. In fact, it is probably more likely to occur in adolescents and young adults, as reported by Shwachman et al. in 19751.
It is important not to label pancreatitis as “idiopathic” in an adult or child before the diagnosis of cystic fibrosis is excluded, since pancreatitis may be the presenting problem, especially in older patients with mild cystic fibrosis2,3. As patients with “mild genotypes” are discovered,4 such as R117H compound heterozygotes, this may become a more commonly recognized adult disease.
4 ReferencesJohn L. Colombo, M.D.
University of Nebraska Medical Center, Omaha, NE 68105-10651
Shwachman H ,Lebenthal E ,Khaw KT . Recurrent acute pancreatitis in patients with cystic fibrosis with normal pancreatic enzymes. Pediatrics 1975;55:86-95
Web of Science | Medline2
O'Connor KW ,Brashear RE . Cystic fibrosis: an adult perspective. Arch Intern Med 1985;145:153-154
CrossRef | Web of Science | Medline3
Masaryk TJ ,Achkar E . Pancreatitis as initial presentation of cystic fibrosis in young adults: a report of two cases. Dig Dis Sci 1983;28:874-878
CrossRef | Web of Science | Medline4
The Cystic Fibrosis Genotype-Phenotype Consortium
Full Text | Web of Science | Medline
To the Editor:
The review by Steinberg and Tenner1 provides a comprehensive overview of medical progress in acute pancreatitis. However, the authors misstate the use of adjunctive total parenteral nutrition in persons who are critically ill, because the subjects in the cited study were unselected people with relatively mild pancreatitis2. Nutritional support remains an important adjunctive therapy in highly selected subjects with acute pancreatitis who have critical illness3-5. Since nearly 25 percent of all attacks of pancreatitis are severe1 and overall mortality approaches 9 percent,1 it is appropriate to consider nutritional support in those who are critically ill with complications that dictate a protracted period of no oral feeding. The goal of nutritional-support therapy is to reduce morbidity and mortality by preventing the loss of body cell mass and promoting wound healing and immunocompetence.
5 ReferencesGordon L. Jensen, M.D., Ph.D.
Geisinger Medical Center, Danville, PA 17822George L. Blackburn, M.D., Ph.D.
New England Deaconess Hospital, Boston, MA 022151
Steinberg W ,Tenner S . Acute pancreatitis. N Engl J Med 1994;330:1198-1210
Full Text | Web of Science | Medline2
Sax HC ,Warner BW ,Talamini MA , et al. Early total parenteral nutrition in acute pancreatitis: lack of beneficial effects. Am J Surg 1987;153:117-124
CrossRef | Web of Science | Medline3
Blackburn GL ,Williams LF ,Bistrian BR , et al. New approaches to the management of severe acute pancreatitis. Am J Surg 1976;131:114-124
CrossRef | Web of Science | Medline4
Pisters PW ,Ranson JH . Nutrition support for acute pancreatitis. Surg Gynecol Obstet 1992;175:275-284
Web of Science | Medline5
Kirby BF, Delegge MH. Gut disease (pancreatitis). In: Zaloga GP, ed. Nutrition and critical care. St. Louis: Mosby Press, 1994:618-22.
To the Editor:
Steinberg and Tenner provide an interesting review of acute pancreatitis. We would add that amanita poisoning is a potentially important cause of this disease. Alpha-amanitin, the cyclopeptide toxin present in some mushrooms such as Amanita phalloides, may cause clinical or biochemical pancreatitis in up to 50 percent of the poisoned patients1. Amanita poisoning is an increasingly frequent medical emergency in the United States and a common problem in Europe2. We think that it is necessary to include this alimentary poisoning as a cause of acute pancreatitis.
2 ReferencesAgustin Castiella, M.D.
Angel Cosme, M.D.
Juan I. Arenas, M.D.
Nuestra Senora de Aranzazu Hospital, 20080 San Sebastian, Spain1
Klein AS ,Hart J ,Brems JJ ,Goldstein L ,Lewin K ,Busuttil RW . Amanita poisoning: treatment and the role of liver transplantation. Am J Med 1989;86:187-193
CrossRef | Web of Science | Medline2
Pinson CW ,Daya MR ,Benner KG , et al. Liver transplantation for severe Amanita phalloides mushroom poisoning. Am J Surg 1990;159:493-499
CrossRef | Web of Science | Medline
- Citing Articles (4)
Citing Articles
1
Laura Iris Cosen-Binker, Marcelo Gustavo Binker, Rodica Cosen, Gustavo Negri, Osvaldo Tiscornia. (2006) Influence of Hydrocortisone, Prednisolone, and NO Association on the Evolution of Acute Pancreatitis. Digestive Diseases and Sciences 51:5, 915-925
CrossRef2
Ali Fazel, Joseph E Geenen, Koorosh MoezArdalan, Marc F Catalano. (2005) Intrapancreatic Ductal Pressure in Sphincter of Oddi Dysfunction. Pancreas 30:4, 359-362
CrossRef3
George H. Sakorafas, Adelais G. Tsiotou. (2000) Etiology and Pathogenesis of Acute Pancreatitis. Journal of Clinical Gastroenterology 30:4, 343-356
CrossRef4
M. M. Lerch, R. Schmid. (1995) Klinik der akuten Pankreatitis. European Surgery 27:4, 186-189
CrossRef
