- Email: [email protected]
Pain in chronic pancreatitis
July
CORRESPONDENCE
1985
is easily detectable
by histochemical staining of stool (7,8). To establish the diagnosis of mild pancreatic insufficiency, we SUSpect that it is going to be better to carry out a Lundh test meal and measure enzyme concentrations in the jejunal aspirates (91, or to perform the usual cholecystokinin-stimulation test (10). Several new noninvasive tests for assessment of pancreatic exocrine function have recently been reported (ll-131, and it will be of interest to compare these tests with not only results from invasive procedures, but also with FFC measurement in patients with varying degrees of pancreatic exocrine hypofunction. In the meantime, if fecal fat measurements are made to quantitate the degree of steatorrhea in a patient with malabsorption (who does not have hepatobiliary disease or previous gastrointestinal surgery), the astute clinician who observes an elevated FFC (>lO%) in the lab report may immediately make a presumptive diagnosis of pancreatic insufficiency with some confidence.
ALAN F. HOFMANN,
M.D. Division of Gastroenterology Department of Medicine University of California, San 225 Dickinson Street San Diego, California 92103
2.
3.
4.
5.
6. 7. 8.
Dear Sir: It does not surprise us that operations and medication designed to reduce gastric activity and thus hormonal stimulation of the pancreas are not very successful in relieving the pain of chronic pancreatitis. It is evident now that even during prolonged fasting the gland is spontaneously active at 100-min intervals. In dogs we obtain half-maximal protein secretion and about one-eighth maximal juice volume at spontaneous peak activity. Spontaneous peaking is completely abolished by ganglion blocking agents (1,2) and our evidence is that cholecystokinin and secretin release are abolished also (3,4). Might not a long-acting blocker, like pentolinium tartrate, be worth a trial in the disease? The argument that these agents cause hypotension is not really relevant as the orthostatic hypotension that can result is of little consequence to patients in bed. Creighton
Diego
Bo-Linn GW, Fordtran JS. Fecal fat concentration in patients with steatorrhea. Gastroenterology 1984;87:319-22. Hofmann AF. The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy. Gastroenterology 1967:52:752-7. Hofmann AF, Poley JR. Role of bile acid malabsorption in pathogenesis of diarrhea and steatorrhea in patients with ileal resection. I. Response to cholestyramine or replacement of dietary long chain triglyceride by medium chain triglyceride. Gastroenterology 1972;62:1191-9. Ammon HV, Phillips SF. Inhibition of colonic water and electrolyte secretion by fatty acids in man. Gastroenterology 1973;65:744-9. Dornberger GR, Comfort MW, Wollaeger EE, Power MH. Total fecal solids, fat and nitrogen: study of patients with chronic relapsing pancreatitis. Gastroenterology 1948;11:691-700. Bliss CM, Small DM. A comparison of ileal and fecal lipid in pancreatic steatorrhea (abstr). Gastroenterology 1970;58:928. Luk CD. Screening for steatorrhea (letter). Gastroenterology 1979;77:205-6. Newcomer AD, Hofmann AF, DiMagno EP, Thomas PJ. Carl-
son CL. Triolein breath test: a sensitive and specific test for fat malabsorption. Gastroenterology 1979;76:6-13. 9. Braganza JM. Herman K, Hine P, Kay G, Sandle GI. Pancreatic enzymes in human duodenal juice-a comparison of responses in secretin pancreocymin and Lundh Borgstrom tests. Gut 1978;19:358-66. 10.
Pain in Chronic Pancreatitis
D. F. MAGEE, M.D., Ph.D
JAMES W. MANIER Lovelace Medical Center Albuquerque, New Mexico 1.
233
DiMagno EP, Go VLW, Summerskill WHJ. Relations between pancreatic enzyme outputs and malabsorption in severe pancreatic insufficiency. N Engl J Med 1973;288:813-5. 11. Braganza JM, Kay GH, Tetlow VA, Herman KJ. Observations on the BT PABAIl%-PABA tubeless test of pancreatic function. Clin Chim Acta 1983:130:339-47. 12. Lankisch PG, Schreiber A, Otto J. Pancreolauryl test. Evaluation of a tubeless pancreatic function test in comparison with other indirect and direct tests for exocrine pancreatic function. Dig Dis Sci 1983;28:490-3. 13. Cole S, Rossi S, Stern A, Hofmann AF, Mundlos S. A cholesterol octanoate breath test for pancreatic exocrine function: feasibility studies (abstr). Am J Gastroenterol (in press).
University
School of Medicine 2500 California Street Omaha, Nebraska 68178 S. NARUSE. M.D. National Institute
for Physiological
Sciences
Department of Molecular Physiology Laboratory of Cellular Metabolism Myodaiji, Okazaki, 444 Japan Magee DF, Naruse S. Neural control of periodic secretion of the pancreas and the stomach in fasting dogs. J Physiol 1983; 344:153-60. Magee DF, Naruse S. Characteristics of secretin stimulated pancreatic secretion in dogs. J Physiol 1983;346:115P. Hong SS, Magee DF, Crewdson F. The physiological regulation of gallbladder evacuation. Gastroenterology 1956;30:625-30. Hong SS, Magee DF. Pharmacological studies on the regulation of pancreatic secretion in pigs. Ann Surg 1970;172:41-8.
Diagnosis of IBS Dear Sir: We enjoyed reading the excellent editorial by Drossman (1) that summarized the difficulties encountered in the diagnostic workup and classification of patients suspected to suffer from irritable bowel syndrome (IBS). It was mentioned that the determination of whether a patient has either IBS or organic disease cannot always be made in clinical practice. We would like to add some further information. The protocol of our study (2) was designed to develop a weighted score for the diagnosis of IBS and to test the diagnostic accuracy of this scoring system in two patient groups to be defined as precisely as possible. Thus, we created the scoring system using the data of patients with symptoms of IBS but without any recognizable organic disease and of other patients also with symptoms compatible with IBS, but with some organic disease diagnosed. Patients with organic disease but with the additional diagnosis of IBS were excluded from all calculations. In this group, IBS was diagnosed because the complaints seemed not to be fully explained by the organic disease and were typical of IBS. This may appear arbitrary because the symptoms complained about by patients classified into the group “organic disease” may also not necessarily be related to the underlying organic disease. However, in the absence of a “gold” standard for the diagnosis of IBS, as discussed in the editorial, arbitrary decisions cannot be eliminated completely.
CORRESPONDENCE
1985
is easily detectable
by histochemical staining of stool (7,8). To establish the diagnosis of mild pancreatic insufficiency, we SUSpect that it is going to be better to carry out a Lundh test meal and measure enzyme concentrations in the jejunal aspirates (91, or to perform the usual cholecystokinin-stimulation test (10). Several new noninvasive tests for assessment of pancreatic exocrine function have recently been reported (ll-131, and it will be of interest to compare these tests with not only results from invasive procedures, but also with FFC measurement in patients with varying degrees of pancreatic exocrine hypofunction. In the meantime, if fecal fat measurements are made to quantitate the degree of steatorrhea in a patient with malabsorption (who does not have hepatobiliary disease or previous gastrointestinal surgery), the astute clinician who observes an elevated FFC (>lO%) in the lab report may immediately make a presumptive diagnosis of pancreatic insufficiency with some confidence.
ALAN F. HOFMANN,
M.D. Division of Gastroenterology Department of Medicine University of California, San 225 Dickinson Street San Diego, California 92103
2.
3.
4.
5.
6. 7. 8.
Dear Sir: It does not surprise us that operations and medication designed to reduce gastric activity and thus hormonal stimulation of the pancreas are not very successful in relieving the pain of chronic pancreatitis. It is evident now that even during prolonged fasting the gland is spontaneously active at 100-min intervals. In dogs we obtain half-maximal protein secretion and about one-eighth maximal juice volume at spontaneous peak activity. Spontaneous peaking is completely abolished by ganglion blocking agents (1,2) and our evidence is that cholecystokinin and secretin release are abolished also (3,4). Might not a long-acting blocker, like pentolinium tartrate, be worth a trial in the disease? The argument that these agents cause hypotension is not really relevant as the orthostatic hypotension that can result is of little consequence to patients in bed. Creighton
Diego
Bo-Linn GW, Fordtran JS. Fecal fat concentration in patients with steatorrhea. Gastroenterology 1984;87:319-22. Hofmann AF. The syndrome of ileal disease and the broken enterohepatic circulation: cholerheic enteropathy. Gastroenterology 1967:52:752-7. Hofmann AF, Poley JR. Role of bile acid malabsorption in pathogenesis of diarrhea and steatorrhea in patients with ileal resection. I. Response to cholestyramine or replacement of dietary long chain triglyceride by medium chain triglyceride. Gastroenterology 1972;62:1191-9. Ammon HV, Phillips SF. Inhibition of colonic water and electrolyte secretion by fatty acids in man. Gastroenterology 1973;65:744-9. Dornberger GR, Comfort MW, Wollaeger EE, Power MH. Total fecal solids, fat and nitrogen: study of patients with chronic relapsing pancreatitis. Gastroenterology 1948;11:691-700. Bliss CM, Small DM. A comparison of ileal and fecal lipid in pancreatic steatorrhea (abstr). Gastroenterology 1970;58:928. Luk CD. Screening for steatorrhea (letter). Gastroenterology 1979;77:205-6. Newcomer AD, Hofmann AF, DiMagno EP, Thomas PJ. Carl-
son CL. Triolein breath test: a sensitive and specific test for fat malabsorption. Gastroenterology 1979;76:6-13. 9. Braganza JM. Herman K, Hine P, Kay G, Sandle GI. Pancreatic enzymes in human duodenal juice-a comparison of responses in secretin pancreocymin and Lundh Borgstrom tests. Gut 1978;19:358-66. 10.
Pain in Chronic Pancreatitis
D. F. MAGEE, M.D., Ph.D
JAMES W. MANIER Lovelace Medical Center Albuquerque, New Mexico 1.
233
DiMagno EP, Go VLW, Summerskill WHJ. Relations between pancreatic enzyme outputs and malabsorption in severe pancreatic insufficiency. N Engl J Med 1973;288:813-5. 11. Braganza JM, Kay GH, Tetlow VA, Herman KJ. Observations on the BT PABAIl%-PABA tubeless test of pancreatic function. Clin Chim Acta 1983:130:339-47. 12. Lankisch PG, Schreiber A, Otto J. Pancreolauryl test. Evaluation of a tubeless pancreatic function test in comparison with other indirect and direct tests for exocrine pancreatic function. Dig Dis Sci 1983;28:490-3. 13. Cole S, Rossi S, Stern A, Hofmann AF, Mundlos S. A cholesterol octanoate breath test for pancreatic exocrine function: feasibility studies (abstr). Am J Gastroenterol (in press).
University
School of Medicine 2500 California Street Omaha, Nebraska 68178 S. NARUSE. M.D. National Institute
for Physiological
Sciences
Department of Molecular Physiology Laboratory of Cellular Metabolism Myodaiji, Okazaki, 444 Japan Magee DF, Naruse S. Neural control of periodic secretion of the pancreas and the stomach in fasting dogs. J Physiol 1983; 344:153-60. Magee DF, Naruse S. Characteristics of secretin stimulated pancreatic secretion in dogs. J Physiol 1983;346:115P. Hong SS, Magee DF, Crewdson F. The physiological regulation of gallbladder evacuation. Gastroenterology 1956;30:625-30. Hong SS, Magee DF. Pharmacological studies on the regulation of pancreatic secretion in pigs. Ann Surg 1970;172:41-8.
Diagnosis of IBS Dear Sir: We enjoyed reading the excellent editorial by Drossman (1) that summarized the difficulties encountered in the diagnostic workup and classification of patients suspected to suffer from irritable bowel syndrome (IBS). It was mentioned that the determination of whether a patient has either IBS or organic disease cannot always be made in clinical practice. We would like to add some further information. The protocol of our study (2) was designed to develop a weighted score for the diagnosis of IBS and to test the diagnostic accuracy of this scoring system in two patient groups to be defined as precisely as possible. Thus, we created the scoring system using the data of patients with symptoms of IBS but without any recognizable organic disease and of other patients also with symptoms compatible with IBS, but with some organic disease diagnosed. Patients with organic disease but with the additional diagnosis of IBS were excluded from all calculations. In this group, IBS was diagnosed because the complaints seemed not to be fully explained by the organic disease and were typical of IBS. This may appear arbitrary because the symptoms complained about by patients classified into the group “organic disease” may also not necessarily be related to the underlying organic disease. However, in the absence of a “gold” standard for the diagnosis of IBS, as discussed in the editorial, arbitrary decisions cannot be eliminated completely.