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Prospective evaluation of serum trypsin levels in patients with chronic abdominal pain
A368
AGA ABSTRACTS
GASTROENTEROLOGY, VOl. 108, NO,.4
HYPERGLYCEMIA REDUCES CEPHALIC STIMULATED EXOCRINE: PANCREATIC SECRETION. W.F. Lain, A.A.M: Masclee, M. Lindeboom, C.B.H.W. Lamers. Dept. Gastroenterelogy-Hepatology, University Hospital Leiden, The Netherlands.
• INTRAVENOUS CONTRAST DOES NOT EFFECT THE SEVERITY OF EXPERIMENTAL ACUTE HEMORRHAGIC PANCREATITIS AM Kusske_, AG Patel, MT Toyama, PLr'Reber, SW Ashley, HA Reber. Depts of Surgery, UCLA and Sepulveda VAMC, Los Angeles, Ca.
In healthy subjects acute hyperglycemia inhibits gastrointestinal motility, possibly through vagal cholinergic mechanisms. We have investigated whether hyperglycemia influences exocrine pancreatic secretion during cephalic stimulation which is vagal-cholinergically mediated. Six healthy subjects (age24-32 yr) were studied twice, in random order, during normoglycemia (5 mmol/I) oracute hyperglycemia (15 mmol/I) using a glucose clamp technique. Duodenal juice was collected in 10 min portions through a 4-lumen tube using PEG as recovery marker. Pancreatic and biliary secretion were measured unstimulated for 90 rain and for 90 rain after cephalic stimulation with modified sham feeding (MSF) of a meal (hamburger, bread, butter, tea).
Recent studies have been interpreted to suggest that contrastenhanced computerized tomography employed early in the course of acute pancreatitis (AP) may be detrimental. Contrast infusion within 6 hr of the induction of AP in rats was associated with an increase in acinar necrosis and mortality. To evaluate this further, we examined the effects of intravenous contrast in a feline model of acute hemorrhagic pancreatitis (AHP). Methods: AHP was induced using the permeable duct-low pressure perfusion model At 24 hr after induction; tO more realistically simulate the clinical situation, cats received either saline as a control, iodinated or noniodinated .contrast. Pancreatic mierovascular blood flow (PBF) was measured by H2 gas clearance before, immediately after, and 24 hr after contrast !njection. Serum amylase and lipase, pancreatic wet/dry weight, and histology were compared in the three groups. Results: Control Iodinated Noniodinated Basal PBF 90±8 133_+7 107±9 45rain post injection 94±5 127-+16 84±7* 90min post injection 98±6 84+_21" 110+9.4 24 hrs post injection 90-+10 104±5 -93±4 (PBF ml.min'a.100g-~, *p<0 05 vs. basal) Although both iodinated .and noniodinated contrast reduced PBF initially, this returned to normal by 24 hr after injection. In contrast, there were no significant differences in serum amylase or lipase, wet/dry weight, or histologic injury in the three groulgs. Conclusions: These results suggest that, although intravenous contrast injection is associated with a transient reduction in PBF in the setting of AHP, if administered at 24 hr after induction, the severity of the pancreatitis is unaffected.
PROSPECTIVE EVALUATION OF SERUM TRYPSIN LEVELS IN PATIENTS WITH CHRONIC ABDOMINAL PAIN Department of Medicine, Tulane University School of Medicine, New Orleans, LA. Chronic abdominal pain is one of the most frequent complaints presenting to gastroenterologists. While chronic pancreatitis (CP) is a frequent cause of the abdominal pain it is often difficult to diagnose. Low serum trypsin (ST) has been proposed as an easy relatively speeifte means of diagnosing CP. Aim: This study prospectively evaluates the accuracy of ST in patients with chronic abdominal pain in whom CP is suspected. Methods: From August of 1993 to November 1994 18 patients presented with chronic abdominal pain suggestive of CP. All patients had serum assayed for cathodic trypsinogen by radioimmtmoassy. The patients then underwent diagnostic testing. All had computed tomography (CT). Endoscopic retrograde pancreatography (ERP) motility studies or other diagnostic tests were added as needed. If a diagnosis was established for their abdominal pain (CP or other) no further testing was done. In 8 patients in whom the diagnosis was not clear a secretin test was performed. Results: Eighteen patients initially had ST levels assayed, 8 (44%) had CP either by imaging or a positive secretin test. The remaining 10 (56%) had either a non CP diagnosis (i.e., urethral stone, pancreatic eystadenoma) or had a negative secretin test. The mean ST level in CP patients was 23.5 ng/ml (+7.7 SEM). The mean in non'CP patients was 31.9 ng/ml (+6.9 SEM). A receiver operator characteristic curve determined the best cutoff for the diagnosis of CP is a level below 20 ng/ml; Using this cutoff ST has a sensitivity of 63% and a specificity of 90%. the positive predictive value of a ST below 20 ng/ml for CP is 83% and the negative predictive value is 75%. Conclusion: These data suggest that a ST level below 20 ng/ml is a good indicator of CP in patients with chronic abdominal pain.
Results: (mean+SEM) (Output/30 min)
Basal
MSF 5 mmol/I
MSF 15 mmol/I
Bilirubin (gmol)
2+1
165:4"
4+_2A
Trypsin (U)
9+3
26t-6"
7+4A
Lipase (KU) HCO3 (mmol)
14+5
36-J:9"
15:L-5A
0.6:L~0.1
0.8t-0.1
0.6:L-0.1
p<0.05 vs basal; A p<0.05 vs MSF 5 mmol/I Compared to normoglycemia, during hyperglycemia pancreatic polypeptide (PP) secretion, as an indirect measure of vagal-cholinergic tone, was significantly (p<0.05) reduced in response to MSF (56:1:23 vs 172.t:41 pM30 min). Conclusions: MSF significantly increases biliary and pancreatic enzyme secretion (PES) dunng normoglycemia. During hyperglycemia MSF stimulated PES is significantly reduced. Since the cephalic phase of digestion is vagal-cholinergic dependent, these results suggest that hyperglycemia reduces MSF induced PES by inhibition of vagalcholinergic activity.
'0
LATE POSTPRANDIAL MOTILITY CHANGES IN CHRONIC PANCREATITIS: PATHOGENETIC ROLE OF MALABSORPTION. P. Laver, M. v.d.Ohe, G. Grtger, D. Grandt; M. Rtinzi, H. Goebell. Div Gastroenterology, University of Essen Essen Germany Background: Intraluminal nutrients modulate human gastrointestinal motil{ty in health, but if postprandial motility is altered in pancreatic insufficiency with maldigestion is unknown. Aims: To compare postprandial motor responses in healthy subjects and patients either with untreated or enzyme-treated pancreatic insufficiency, and to correlate them with proximal and distal intestinal nutrient exposure, Methods: After placement of a multilumen tube for duodenal, jejunal, and distal ileal sampling, marker perfusion, and manometric motility recording, 14 normal subjects and 12 patients with chronic pancreatitis and Severe exocfine insufficiency received a labeled standard meal (1257 kJ) on two occasions, either without or with pancreatic enzyme supplementation. We determined postprandial luminal nutrients, gastric emptyihg, small intestinal transit, and duration of fed motor pattern Results: Compared with normal subjects, untreated patients had accelerated gastric emptying and small intestinal transit, and a shorter fed motility response. These changes were associated with increased intraluminal nutrient loads, and reversed by enzyme treatment. NORMAL CHRONIC PANCREATITIS no enzymes Iwith enzymes Nutrient delivery (cumulative) to duodenum (kJ) 318±67 639±222* ] 381±149t to ileum (Id) 69±21 487±232* 227±115+ Gastric emptying (90%, rain) 163±12 128±10" 148±14t Smallintestinal transit (rain), 86±9 44± 6* 62± 6* Duodenal nutrient flow at end of fed oeriod (J/rain) 486 ± 62 1796± 417" 984±518¢ Mean values + SE; *p<0.001vs normal; ~'p<0.01 vs no enzymes Conclusions: (1) Patients with chronic pancreatitis and pancreatic insufficiency-have a shorter digesuve motor response; this may partly be explained, by accelerated gastric emptying and intestinal transit. (2) However. in untreated patients termination of digestive motility occurred in the presence of large duodenal nutrient flow rates, i.e., endogenous stimulation which should maintain a fed motor pattern. This suggests that in patients, additional inhibitory mechanisms, such as increased ileal nutrient delivery (Am.J. Physiol.1990;258:G196), may be involved in the premature conversion of fed into interdigestive pattern.
AGA ABSTRACTS
GASTROENTEROLOGY, VOl. 108, NO,.4
HYPERGLYCEMIA REDUCES CEPHALIC STIMULATED EXOCRINE: PANCREATIC SECRETION. W.F. Lain, A.A.M: Masclee, M. Lindeboom, C.B.H.W. Lamers. Dept. Gastroenterelogy-Hepatology, University Hospital Leiden, The Netherlands.
• INTRAVENOUS CONTRAST DOES NOT EFFECT THE SEVERITY OF EXPERIMENTAL ACUTE HEMORRHAGIC PANCREATITIS AM Kusske_, AG Patel, MT Toyama, PLr'Reber, SW Ashley, HA Reber. Depts of Surgery, UCLA and Sepulveda VAMC, Los Angeles, Ca.
In healthy subjects acute hyperglycemia inhibits gastrointestinal motility, possibly through vagal cholinergic mechanisms. We have investigated whether hyperglycemia influences exocrine pancreatic secretion during cephalic stimulation which is vagal-cholinergically mediated. Six healthy subjects (age24-32 yr) were studied twice, in random order, during normoglycemia (5 mmol/I) oracute hyperglycemia (15 mmol/I) using a glucose clamp technique. Duodenal juice was collected in 10 min portions through a 4-lumen tube using PEG as recovery marker. Pancreatic and biliary secretion were measured unstimulated for 90 rain and for 90 rain after cephalic stimulation with modified sham feeding (MSF) of a meal (hamburger, bread, butter, tea).
Recent studies have been interpreted to suggest that contrastenhanced computerized tomography employed early in the course of acute pancreatitis (AP) may be detrimental. Contrast infusion within 6 hr of the induction of AP in rats was associated with an increase in acinar necrosis and mortality. To evaluate this further, we examined the effects of intravenous contrast in a feline model of acute hemorrhagic pancreatitis (AHP). Methods: AHP was induced using the permeable duct-low pressure perfusion model At 24 hr after induction; tO more realistically simulate the clinical situation, cats received either saline as a control, iodinated or noniodinated .contrast. Pancreatic mierovascular blood flow (PBF) was measured by H2 gas clearance before, immediately after, and 24 hr after contrast !njection. Serum amylase and lipase, pancreatic wet/dry weight, and histology were compared in the three groups. Results: Control Iodinated Noniodinated Basal PBF 90±8 133_+7 107±9 45rain post injection 94±5 127-+16 84±7* 90min post injection 98±6 84+_21" 110+9.4 24 hrs post injection 90-+10 104±5 -93±4 (PBF ml.min'a.100g-~, *p<0 05 vs. basal) Although both iodinated .and noniodinated contrast reduced PBF initially, this returned to normal by 24 hr after injection. In contrast, there were no significant differences in serum amylase or lipase, wet/dry weight, or histologic injury in the three groulgs. Conclusions: These results suggest that, although intravenous contrast injection is associated with a transient reduction in PBF in the setting of AHP, if administered at 24 hr after induction, the severity of the pancreatitis is unaffected.
PROSPECTIVE EVALUATION OF SERUM TRYPSIN LEVELS IN PATIENTS WITH CHRONIC ABDOMINAL PAIN Department of Medicine, Tulane University School of Medicine, New Orleans, LA. Chronic abdominal pain is one of the most frequent complaints presenting to gastroenterologists. While chronic pancreatitis (CP) is a frequent cause of the abdominal pain it is often difficult to diagnose. Low serum trypsin (ST) has been proposed as an easy relatively speeifte means of diagnosing CP. Aim: This study prospectively evaluates the accuracy of ST in patients with chronic abdominal pain in whom CP is suspected. Methods: From August of 1993 to November 1994 18 patients presented with chronic abdominal pain suggestive of CP. All patients had serum assayed for cathodic trypsinogen by radioimmtmoassy. The patients then underwent diagnostic testing. All had computed tomography (CT). Endoscopic retrograde pancreatography (ERP) motility studies or other diagnostic tests were added as needed. If a diagnosis was established for their abdominal pain (CP or other) no further testing was done. In 8 patients in whom the diagnosis was not clear a secretin test was performed. Results: Eighteen patients initially had ST levels assayed, 8 (44%) had CP either by imaging or a positive secretin test. The remaining 10 (56%) had either a non CP diagnosis (i.e., urethral stone, pancreatic eystadenoma) or had a negative secretin test. The mean ST level in CP patients was 23.5 ng/ml (+7.7 SEM). The mean in non'CP patients was 31.9 ng/ml (+6.9 SEM). A receiver operator characteristic curve determined the best cutoff for the diagnosis of CP is a level below 20 ng/ml; Using this cutoff ST has a sensitivity of 63% and a specificity of 90%. the positive predictive value of a ST below 20 ng/ml for CP is 83% and the negative predictive value is 75%. Conclusion: These data suggest that a ST level below 20 ng/ml is a good indicator of CP in patients with chronic abdominal pain.
Results: (mean+SEM) (Output/30 min)
Basal
MSF 5 mmol/I
MSF 15 mmol/I
Bilirubin (gmol)
2+1
165:4"
4+_2A
Trypsin (U)
9+3
26t-6"
7+4A
Lipase (KU) HCO3 (mmol)
14+5
36-J:9"
15:L-5A
0.6:L~0.1
0.8t-0.1
0.6:L-0.1
p<0.05 vs basal; A p<0.05 vs MSF 5 mmol/I Compared to normoglycemia, during hyperglycemia pancreatic polypeptide (PP) secretion, as an indirect measure of vagal-cholinergic tone, was significantly (p<0.05) reduced in response to MSF (56:1:23 vs 172.t:41 pM30 min). Conclusions: MSF significantly increases biliary and pancreatic enzyme secretion (PES) dunng normoglycemia. During hyperglycemia MSF stimulated PES is significantly reduced. Since the cephalic phase of digestion is vagal-cholinergic dependent, these results suggest that hyperglycemia reduces MSF induced PES by inhibition of vagalcholinergic activity.
'0
LATE POSTPRANDIAL MOTILITY CHANGES IN CHRONIC PANCREATITIS: PATHOGENETIC ROLE OF MALABSORPTION. P. Laver, M. v.d.Ohe, G. Grtger, D. Grandt; M. Rtinzi, H. Goebell. Div Gastroenterology, University of Essen Essen Germany Background: Intraluminal nutrients modulate human gastrointestinal motil{ty in health, but if postprandial motility is altered in pancreatic insufficiency with maldigestion is unknown. Aims: To compare postprandial motor responses in healthy subjects and patients either with untreated or enzyme-treated pancreatic insufficiency, and to correlate them with proximal and distal intestinal nutrient exposure, Methods: After placement of a multilumen tube for duodenal, jejunal, and distal ileal sampling, marker perfusion, and manometric motility recording, 14 normal subjects and 12 patients with chronic pancreatitis and Severe exocfine insufficiency received a labeled standard meal (1257 kJ) on two occasions, either without or with pancreatic enzyme supplementation. We determined postprandial luminal nutrients, gastric emptyihg, small intestinal transit, and duration of fed motor pattern Results: Compared with normal subjects, untreated patients had accelerated gastric emptying and small intestinal transit, and a shorter fed motility response. These changes were associated with increased intraluminal nutrient loads, and reversed by enzyme treatment. NORMAL CHRONIC PANCREATITIS no enzymes Iwith enzymes Nutrient delivery (cumulative) to duodenum (kJ) 318±67 639±222* ] 381±149t to ileum (Id) 69±21 487±232* 227±115+ Gastric emptying (90%, rain) 163±12 128±10" 148±14t Smallintestinal transit (rain), 86±9 44± 6* 62± 6* Duodenal nutrient flow at end of fed oeriod (J/rain) 486 ± 62 1796± 417" 984±518¢ Mean values + SE; *p<0.001vs normal; ~'p<0.01 vs no enzymes Conclusions: (1) Patients with chronic pancreatitis and pancreatic insufficiency-have a shorter digesuve motor response; this may partly be explained, by accelerated gastric emptying and intestinal transit. (2) However. in untreated patients termination of digestive motility occurred in the presence of large duodenal nutrient flow rates, i.e., endogenous stimulation which should maintain a fed motor pattern. This suggests that in patients, additional inhibitory mechanisms, such as increased ileal nutrient delivery (Am.J. Physiol.1990;258:G196), may be involved in the premature conversion of fed into interdigestive pattern.