Biomedical subjects

J B Jansen

Publications and source records attributed to J B Jansen.

At least 73 records · Page 4Linked to original sources

PubMed1997

Plasma glutathione S-transferase alpha 1-1 levels in patients with chronic liver disorders.

Recent data suggest that plasma levels of the phase II detoxification enzyme glutathione S-transferase alpha may be a sensitive indicator of hepatocellular integrity in acute liver disorders but little information is available in chronic hepatic disorders. Using a newly developed enzyme linked immunosorbent assay, glutathione S-transferase A1-1 (GSTA1-1) levels were measured in 279 plasma samples from patients with chronic liver disorders. Results were categorized as normal or elevated plasma GSTA1-1 and normal or elevated plasma aspartate aminotransferase (AST) levels. In 24 patients with alcoholic liver cirrhosis, plasma GSTA1-1 levels were not significantly different from a group of 350 healthy controls and only one patient (4%) had an elevated GSTA1-1 level while 10 (42%) patients had elevated AST activities. In samples from patients with primary biliary cirrhosis (n = 150), primary sclerosing cholangitis (n = 26) or chronic hepatitis (n = 79) significantly (P < 0.0001) elevated plasma GSTA1-1 concentrations were detected in 25 (17%), 7 (27%) and 17 (22%) of the samples, respectively. AST activities were increased in a higher percentage of samples in all three disorders: 89%, 88%, and 57%, respectively. Plasma GSTA1-1 and AST levels were significantly correlated (P < 0.005) in the above mentioned disorders but not in alcoholic liver cirrhosis. It is concluded that plasma GSTA1-1 is not a sensitive parameter for the detection of hepatocellular damage in chronic liver disorders.

Alanine Transaminase↗

PubMed1997

Inhibition of pancreaticobiliary secretion by loperamide in humans.

Loperamide, a peripherally acting opiate receptor agonist with antidiarrheal action, inhibits ileal and colonic motor function. It was determined whether loperamide also affects gallbladder emptying and pancreatic enzyme secretion in humans. Plasma cholecystokinin (radioimmunoassay), gallbladder volume (ultrasonography), and intraduodenal bilirubin and amylase output (spot sampling) were measured at regular intervals before and during intraduodenal perfusion of an amino acid meal in 8 healthy subjects: once without and once with pretreatment of 8 mg loperamide, ingested 13 and 4 hours before the start of the meal. Loperamide decreased basal amylase output from 3.2 +/- 0.5 to 1.0 +/- 0.5 kU/h (P < .005) and abolished basal bilirubin output (21 +/- 5 vs. 0 +/- 0 micromol/h; P < .005) into the duodenum. Loperamide increased basal gallbladder volume from 28 +/- 4 to 39 +/- 4 mL (P < .0001) but was without effect on basal plasma cholecystokinin (2.7 +/- 0.3 vs. 3.0 +/- 0.3 pmol/L). During the amino acid meal, pretreatment with loperamide inhibited amylase output from 5.1 +/- 0.8 to 1.6 +/- 0.4 kU/h (P < .001), bilirubin output from 39 +/- 6 to 18 +/- 6 micromol/h (P < .0005) and gallbladder contraction from 47% +/- 3% to 26% +/- 6% (P < .05), whereas loperamide enhanced amino acid-stimulated plasma cholecystokinin from 4.5 +/- 1.6 to 7.6 +/- 1.0 pmol/L (P < .05). It is concluded that loperamide inhibits basal and amino acid-stimulated gallbladder motility and intraduodenal output of bilirubin and amylase, despite an enhanced postprandial cholecystokinin release.

Adult↗

PubMed1997

Altered postprandial motility in chronic pancreatitis: role of malabsorption.

BACKGROUND & AIMS: Intraileal nutrients modulate gastrointestinal motility, but effects of maldigestion on postprandial motility are unknown. The aim of this study was to compare motor responses with ileal nutrient exposure in health and pancreatic insufficiency after a meal or intraluminal perfusion. METHODS: After oroileal multilumen intubation for duodeno-jejuno-ileal sampling, marker perfusion, and motility recording, 14 normal subjects and 12 patients with severe pancreatic insufficiency received a labeled liquid meal twice, either with placebo or pancreatin. Effects of intraileal nutrient perfusion on fed motility induced by duodenal amino acid perfusion were also investigated. RESULTS: Compared with normals, untreated patients had greater cumulative ileal nutrient delivery (69 +/- 21 vs. 487 +/- 232 kJ), shorter fed pattern (196 +/- 22 vs. 131 +/- 14 minutes), greater 90% gastric emptying (163 +/- 12 vs. 128 +/- 10 minutes), and faster small intestinal transit (86 +/- 9 vs. 44 +/- 6 minutes). Pancreatin reversed these changes. Ileal nutrient perfusion converted fed into interdigestive-like motility in normals (7 of 8) and patients (4 of 5). CONCLUSIONS: In subjects with pancreatic insufficiency, a low-energy liquid meal induces shorter fed motor pattern associated with accelerated gastric emptying and intestinal transit compared with healthy subjects. Because changes responded to enzyme treatment and could be reproduced by ileal nutrient perfusion, ileal delivery of malabsorbed chyme may be involved as a mechanism.

Adult↗

PubMed1997

Sucrose polyester does not inhibit gastric acid secretion or stimulate cholecystokinin release in men.

Replacement of dietary fat by sucrose polyester reduces fat intake. However, little is known about the effects of sucrose polyester on gastrointestinal function. To investigate the effect on gastric acid secretion and on release of cholecystokinin into plasma, we perfused eight healthy male volunteers intraduodenally with sucrose polyester, digestible fat, or saline on separate days in random order. Intraduodenal perfusion of sucrose polyester did not suppress gastrin-stimulated gastric acid secretion (-1.8 +/- 6.8%) whereas digestible fat suppressed gastric acid secretion by 64 +/- 9% (P = 0.001) compared with saline. Sucrose polyester did not affect plasma cholecystokinin concentrations (-12.8 +/- 9.3 pmol.30 min/L) whereas perfusion with digestible fat resulted in a significant increase (31.7 +/- 9.3 pmol.30 min/L, P = 0.017) compared with saline. We conclude that sucrose polyester, in contrast with digestible fat, does not inhibit gastrin-stimulated gastric acid secretion or stimulate release of cholecystokinin.

Adult↗

PubMed1997

Effects of nonsteroidal anti-inflammatory drugs on glutathione S-transferases of the rat digestive tract.

Nonsteroidal anti-inflammatory drugs (NSAIDs) have been demonstrated to reduce cancer rates in oesophagus, stomach and colon of humans and animals. Earlier, we showed that high human gastrointestinal tissue levels of glutathione S-transferase (GST), a family of detoxification enzymes consisting of class alpha, mu, pi and theta isoforms, were inversely correlated with cancer risk. We investigated whether the NSAIDs indomethacin, ibuprofen, piroxicam, acetyl salicylic acid (ASA), and sulindac, supplemented in the diet for 2 weeks at 25, 400, 400, 400, and 320 ppm, respectively, influenced gastrointestinal GSTs in male Wistar rats. In cytosolic fractions of oesophagus, stomach, intestine and liver, GST activity towards 1-chloro-2,4-dinitrobenzene was measured, GST isozyme levels were determined by densitometrical analysis of Western blots after immunodetection with monoclonal antibodies, and glutathione levels were determined by HPLC. GST activity and GST mu levels were increased (1.2-1.8 x) in oesophagus and small intestine by indomethacin, ibuprofen, piroxicam and sulindac. GST alpha levels were induced (1.2-2.8 x) in stomach by piroxicam, in small intestine by indomethacin, ibuprofen, piroxicam and sulindac, and in liver by piroxicam. GST pi levels were raised (1.9-3.6 x) in stomach by ibuprofen, ASA, and sulindac, and in small intestine by indomethacin, piroxicam, ASA, and sulindac. Glutathione levels were raised (1.2-2.3 x) by indomethacin and ASA in small intestine and by piroxicam in oesophagus. Enhancement of GSTs in the upper part of the digestive tract, resulting in a more efficient detoxification, may explain in part the anticarcinogenic properties of NSAIDs.

Animals↗

PubMed1997

Management in general practice of patients with persistent dyspepsia. A decision analysis.

To determine whether an empirical drug treatment strategy (empirical group) instead of upper gastrointestinal endoscopy followed by treatment (conventional group) in patients with persistent dyspepsia increases appropriate use of endoscopy facilities, we did a decision analysis based on data found in the literature. We estimated the percentage of patients having an upper gastrointestinal endoscopy in 1 year, the percentage of patients with symptom relief, and the average medical costs per patient for both groups. In the empirical group, fewer patients (38%) had upper gastrointestinal endoscopies compared with the conventional group. Furthermore, an additional 5% of patients in the empirical group experienced symptom relief, and the average medical costs per patient were estimated to be 8% less in this group when compared with the patients in the conventional treatment group. The proposed empirical drug treatment strategy for patients with persistent dyspepsia results in the performance of fewer diagnostic upper gastrointestinal endoscopies per year with greater effectiveness compared with upper gastrointestinal endoscopy followed by treatment.

Decision Trees↗

PubMed1997

Pancreatic secretory response to intrajejunal tryptophan: studies in dogs with an autotransplanted entire jejunoileum.

In two sets of dogs with gastric, duodenal, and jejunal fistulas, we studied the effect of atropine (14 nmol/ kg/h) on the pancreatic secretory response to intrajejunal tryptophan (0.12-10.0 mmol/h; given against a secretin background) before (n = 7) and after extrinsic denervation of the jejunoileum (orthotopical autotransplantation; n = 6). Plasma levels of cholecystokinin were determined by radioimmunoassay. The incremental bicarbonate response to tryptophan was not significantly different between the two sets of dogs. Atropine had no effect on the incremental bicarbonate response to tryptophan. In both sets of dogs, intrajejunal tryptophan caused a dose-dependent increase in pancreatic protein output, which was reduced by atropine. The tryptophan-stimulated levels of plasma cholecystokinin were not significantly altered by denervation and or atropine. We conclude that in dogs (1) intrajejunal tryptophan stimulates pancreatic bicarbonate and protein secretion via release of hormones, (2) extrinsic denervation of the jejunoileum does not significantly alter the incremental bicarbonate and protein responses to intrajejunal tryptophan, (3) the cholinergic intrinsic nerves of the jejunoileum and the hormone cholecystokinin are probably involved in control of the pancreatic protein response to tryptophan, and (4) the release of cholecystokinin by intrajejunal tryptophan does not depend on the extrinsic and intrinsic cholinergic nerves of the jejunoileum.

Animals↗

PubMed1997

The effect of octreotide on gastric emptying at a dosage used to prevent complications after pancreatic surgery: a randomised, placebo controlled study in volunteers.

BACKGROUND: Octreotide is used in many centres to prevent complications after pancreatic surgery. Delayed gastric emptying is a another complication occurring in around 30% of patients after pancreatoduodenectomy (PD) and causes prolonged hospital stay. The influence of octreotide on this complication is doubtful. AIMS: To assess the effect of octreotide, at the clinical dosage used after pancreatic surgery, on gastric emptying in healthy volunteers. SUBJECTS AND METHODS: Eight healthy male volunteers (mean age 22.5 years) participated in this double blind, placebo controlled study. On day 1 subjects received 100 micrograms of octreotide or placebo subcutaneously, three times daily and on day 2, one hour after the fourth injection, gastric emptying, postprandial cholecystokinin (CCK) release, and mouth to caecum transit time (MCTT) were measured. This protocol was repeated after one week, in a crossover design. On the test day subjects received a liquid test meal (1.57 MJ/300 ml) and gastric emptying measurements were performed with applied potential tomography, an non-invasive, validated technique which measures gastric emptying through impedance differences. From the gastric emptying curves, lag time, t50, and postlag emptying rate were measured. MCTT was measured using the hydrogen breath test. RESULTS: Lag time decreased from 29.6 (6.3) (mean (SEM)) to 12.2 (4.6) minutes (p < 0.05) during octretide treatment; t50 decreased from 87.8 (12.0) to 47.5 (8.2) minutes (p < 0.02) and there was a trend towards an increased postlag emptying rate (0.8 to 1.6% per minute; p = 0.07). MCTT increased from 150 (12.7) to 229 (17.9) minutes during octreotide treatment (p < 0.01). Octreotide suppressed postprandial CCK release (p < 0.05). CONCLUSIONS: MCTT was delayed by octreotide, suggesting impairment of small bowl treatment. Octreotide administered at the clinical dosage for pancreatic surgery accelerates gastric emptying, mainly by shortening the lag time. Suppression of postprandial CCK release may be involved in this process. Octreotide administration is therefore not a contributing factor in the pathogenesis of delayed postoperative gastric emptying after PD and might even play a role in preventing this complication.

Adult↗

PubMed1997

Regulation of gastric and pancreatic lipase secretion by CCK and cholinergic mechanisms in humans.

Gastric lipase (HGL) contributes significantly to fat digestion. However, little is known about its neurohormonal regulation in humans. We studied the role of CCK and cholinergic mechanisms in the postprandial regulation of HGL and pancreatic lipase (HPL) secretion in six healthy subjects. Gastric emptying of a mixed meal and outputs of HGL, pepsin, acid, and HPL were determined with a double-indicator technique. Three experiments were performed in random order: intravenous infusion of 1) placebo, 2) low-dose atropine (5 micrograms.kg-.h-1), and 3) the CCK-A receptor antagonist loxiglumide (22 mumol.kg-.h-1). Atropine decreased postprandial outputs of HGL, pepsin, gastric acid, and HPL (P < 0.03) while slowing gastric emptying (P < 0.05). Loxiglumide markedly increased the secretion of HGL, pepsin, and acid while distinctly reducing HPL outputs and accelerating gastric emptying (P < 0.03). Plasma CCK and gastrin levels increased during loxiglumide infusion (P < 0.03). Atropine enhanced gastrin but not CCK release. Postprandial HGL, pepsin, and acid secretion are under positive cholinergic but negative CCK control, whereas HPL is stimulated by cholinergic and CCK mechanisms. We conclude that CCK and cholinergic mechanisms have an important role in the coordination of HGL and HPL secretion to optimize digestion of dietary lipids in humans.

Adult↗

PubMed1997

Cholestyramine influences meal-stimulated pancreaticobiliary function and plasma cholecystokinin independent of gastric emptying and food digestion.

BACKGROUND: Cholestyramine enhances gallbladder emptying and plasma cholecystokinin responses to oral ingestion of a mixed meal. It is not known whether this effect occurs independently of alterations in gastric emptying or maldigestion of nutrients. METHODS: We perfused 15 g of an amino acid meal intraduodenally for 60 min in seven healthy volunteers, once with and once without cholestyramine. Intraduodenal perfusion of saline with or without cholestyramine (6 g/h) was started 60 min before the amino acid meal and continued for 2 h. RESULTS: Cholestyramine markedly enhanced the incremental plasma cholecystokinin response to the meal from 36 +/- 12 to 139 +/- 25 pmol/l x 60 min (P < 0.005), incremental amylase output from 2.4 +/- 0.7 to 5.7 +/- 0.7 kU/h (P < 0.05), and incremental integrated gallbladder contraction from 1948 +/- 235 to 2840 +/- 189% x 60 min (P < 0.05). CONCLUSION: The enhancing effect of cholestyramine on postprandial gallbladder contraction, pancreatic enzyme secretion, and plasma cholecystokinin release is not dependent on gastric emptying rates or appropriate digestion of nutrients.

Adult↗

PubMed1996

Inhibition of gastrin-stimulated gastric acid secretion by medium-chain triglycerides and long-chain triglycerides in healthy young men.

Long-chain triglycerides inhibit gastric acid secretion, but the effect of medium-chain triglycerides in humans is unknown. We compared the effects of intraduodenally perfused saline, medium-chain and long-chain triglycerides on gastrin-stimulated gastric acid secretion and cholecystokinin release. Eight healthy male volunteers participated in this study. Gastrin-stimulated gastric acid output was 9.4 +/- 1.1 mmol/30 min during saline perfusion. It was suppressed by medium-chain triglycerides by 43 +/- 9% (P = 0.04 vs. saline) and by long-chain triglycerides by 74 +/- 6% (P = 0.0003 vs. saline). Thus medium-chain triglycerides inhibited gastrin-stimulated gastric acid secretion but less so than long-chain triglycerides. When compared to saline perfusion (73 +/- 6 pM x 30 min) integrated plasma cholecystokinin concentrations were significantly elevated by long-chain triglycerides (96 +/- 5 pM x 30 min, P < 0.004) but not by medium-chain triglycerides perfusion (65 +/- 7 pM x 30 min). We also investigated the role of cholecystokinin infusion on gastrin stimulated gastric acid secretion. Higher concentrations (191.4 +/- 4.5 pM x 30 min) of CCK than released in the long-chain triglycerides perfusion experiment, did not suppress gastric acid secretion. Thus, circulating cholecystokinin appears not responsible for the inhibition of gastrin-stimulated gastric acid secretion by dietary fat.

Adult↗

PubMed1996

[Intrathecal administration of morphine and bupivacaine in the treatment of severe pain in chronic pancreatitis].

A 25-year-old male with idiopathic chronic pancreatitis suffered from severe pain not reacting to medical therapy. Intractable pain persisted after the following procedures: subtotal resection of the pancreas, interpleural administration of bupivacaine, epidural administration of bupivacaine, and thoracoscopic sympathectomy. Eventually, adequate pain relief was achieved with intrathecal administration of morphine and bupivacaine. An infusion pump, externally controlled by radiotelemetry, was implanted subcutaneously for intrathecal drug administration. With this pump the patient was fully ambulant. Intrathecal administration of morphine and bupivacaine through an implanted pump is a possible new technique for pain management in chronic pancreatitis.

Adult↗

PubMed1996

Serum alkaline phosphatase activity during zinc deficiency and long-term inflammatory stress.

A decrease in serum zinc can be caused by a real zinc deficiency but can also be caused by an apparent zinc deficiency, e.g. in inflammatory stress. The aim of this study was to evaluate the diagnostic power of serum alkaline phosphatase (AP) activity in the discrimination between pathophysiologic states of "real" and "apparent" zinc deficiency. A decrease in serum zinc was induced in growing and adult rats, by providing a diet low in zinc and by causing inflammatory stress. AP activity was determined using reagents low or enriched in zinc. Serum AP was decreased in zinc-deficient adult rats (P < 0.01). In zinc-deficient growing rats AP activity was not different from normal rats but AP activity decreased rapidly. In the same growing rats a significant difference was found in AP activities determined using buffers low and enriched in zinc (P < 0.001) between both groups of rats. After inducing inflammatory stress a decrease in AP activity (P < 0.01) and serum zinc (P < 0.001) was seen during the first few days. After the initial phase of inflammation AP activity normalized, serum zinc showed a rise which after correction for the decrease in serum albumin reached the level of the control rats. A difference in AP activity in buffers low and enriched in zinc was observed only during the first few days after induction of inflammatory stress (P < 0.001). Probably the method of measurement of the difference in enzyme activity, using buffers low and enriched in zinc, can be used as an indication for zinc deficiency in situations with changing AP enzyme concentrations. AP activity is decreased during the initial phase of inflammatory stress due to a decrease in serum zinc.

Alkaline Phosphatase↗

PubMed1996

Atrophic gastritis and Helicobacter pylori infection in patients with reflux esophagitis treated with omeprazole or fundoplication.

BACKGROUND: Helicobacter pylori infection plays an important part in the development of atrophic gastritis and intestinal metaplasia, conditions that predispose patients gastric cancer. Profound suppression of gastric acid is associated with increased severity of gastritis caused by H. pylori, but it is not known whether acid suppression increases the risk of atrophic gastritis. METHODS: We studied patients from two separate cohorts who were being treated for reflux esophagitis: 72 patients treated with fundoplication in Sweden and 105 treated with omeprazole (20 to 40 mg once daily) in the Netherlands. In both cohorts, the patients were followed for an average of five years (range, three to eight). After fundoplication, the patients did not receive acid-suppressive therapy. The presence of H. pylori was assessed at the first visit by histologic evaluation in the fundoplication group and by histologic and serologic evaluation in the omeprazole group. The patients were not treated for H. pylori infection. Before treatment and during follow-up, the patients underwent repeated gastroscopy, with biopsy sampling for histologic evaluation. RESULTS: Among the patients treated with fundoplication, atrophic gastritis did not develop in any of the 31 who were infected with H. pylori at base line or the 41 who were not infected; 1 patient infected with H. pylori had atrophic gastritis before treatment that persisted after treatment. Among the patients treated with omeprazole, none of whom had atrophic gastritis at base line, atrophic gastritis developed in 18 of the 59 infected with H. pylori(P<0.001) and 2 of the 46 who were not infected (P=0.62). CONCLUSIONS: Patients with reflux esophagitis and H. pylori infection who are treated with omeprazole are at increased risk of atrophic gastritis.

Adolescent↗

PubMed1996

Function and survival of intrasplenic islet autografts in dogs.

Successful transplantation of isolated islets of Langerhans has been reported in large mammals, including man, but metabolic control has not been well-established. We studied the glucose and islet hormone response to fasting, i.v. glucose bolus infusion, i.v. arginine bolus infusion during a 35-mmol/l hyperglycaemic clamp, mixed meals, and i.v. insulin-induced hypoglycaemia up to 3 years after intrasplenic islet autotransplantation in six pancreatectomised dogs. The individual postprandial insulinogenic index (ratio of 2-h postprandial insulin to glucose levels) at 1 month post-transplant, predicted (r = 0.99) the time to functional graft failure (6-175 weeks). Metabolic studies at 6 months post-transplant in four dogs demonstrated normal fasting glucose and hormone levels, except for reduced pancreatic polypeptide levels. Intravenous glucose and arginine-stimulated insulin were reduced to 15% of preoperative values. In contrast, postprandial normoinsulinaemia was observed--albeit with moderate hyperglycaemia (approximately 10 mmol/l). Postprandial glucagon and glucose-dependent insulinotropic polypeptide (GIP) had increased. Comparison of the post-transplant insulin responses to a meal and to intravenous challenges demonstrated maximal stimulation of the graft by the meal. Post-transplant pancreatic polypeptide responses to a meal and i.v. arginine were severely reduced, and no pancreatic polypeptide response to i.v. insulin-induced hypoglycaemia was observed--indicating absence of cholinergic reinnervation. Thus, glucose regulation and both the insulin secretory capacity and life expectancy of islet grafts were best documented by meal testing. Tentatively, a postprandial hyperglycaemia-enhanced incretin effect of glucose-dependent insulinotropic polypeptide and other gut hormones may account for the difference in the insulin response to i.v. glucose and a meal. Aside from the reduced insulin secretory capacity, both a deranged pulsatile delivery of insulin, hyperglucagonaemia, and pancreatic polypeptide deficiency may have been conducive to glucose intolerance.

Animals↗

PubMed1996

Influence of orlistat on the regulation of gallbladder contraction in man: a randomized double-blind placebo-controlled crossover study.

Orlistat (tetrahydrolipstatin) is a potent inhibitor of gastric and pancreatic lipase activity causing a diminution of free fatty acids in the intestinal lumen. The release of cholecystokinin (CCK) critically depends on the presence of free fatty acids in the small intestine. Postprandial CCK release and gallbladder contraction might be decreased by orlistat, potentially resulting in an increased risk of gallstone formation. In this double-blind, placebo-controlled, six-way crossover study, six healthy volunteers ingested in a randomized order three isocaloric test meals (250 ml) of identical osmolality with either orlistat (200 mg) or placebo: (a) a pure-fat meal (25 g triglycerides), (b) a mixed meal containing fat (8 g; 29% of caloric content), protein (10 g; 17%), and dextrose (32 g; 54%), and (c) a fat-free meal containing albumin (25 g; 46%) and dextrose (32 g; 54%). Gallbladder volumes were determined by ultrasonography, and plasma CCK, pancreatic polypeptide and gastrin levels by RIA. Gall-bladder contraction (AUC, % x 90 min; difference of means +/- 95% CI) in subjects receiving orlistat or placebo did not significantly differ after intake of the pure-fat meal (443+/-1174), the mixed meal (313+/-1170), or the fat-free-meal (-760+/-1180). The release of CCK (AUC; pM x 90 min; difference of means +/- 95% CI) was not different between orlistat and placebo after ingestion of the pure-fat meal (-18+/-64), the mixed meal (-45+/-62), and the fat-free meal (27+/-63). Likewise, the release of pancreatic polypeptide and gastrin was similar after intake of the meals with either orlistat or placebo. A single dose of orlistat did not reduce gallbladder motility after ingestion of meals with differing fat contents. The safety of long-term treatment with orlistat with respect to gallstone formation remains to be determined.

Adult↗

PubMed1996

Review article: symptom improvement through eradication of Helicobacter pylori in patients with non-ulcer dyspepsia.

The aim of this article is to determine, by reviewing the literature, whether treatment of Helicobacter pylori infection in patients with non-ulcer dyspepsia affects symptoms. Ten publications were identified through a computerized and manual literature search, and the percentage of patients with symptom improvement after successful or unsuccessful eradication therapy for H. pylori infection was calculated. In the 10 studies, symptom improvement after treatment was found in 73% of the patients that became H. pylori-negative and 45% of the patients that remained H. pylori-positive. Symptom improvement was modified by various clinical features and methodological aspects. If eradication of H. pylori failed, symptoms only improved over a short period. Symptom improvement was more pronounced in dyspeptic patients in whom H. pylori was eradicated than in those in whom H. pylori infection persisted.

Dyspepsia↗

PubMed1996

Role of intraduodenal proteases in plasma cholecystokinin and pancreaticobiliary responses to protein and amino acids.

BACKGROUND & AIMS: The role of small intestinal proteolytic activity in the regulation of upper gastrointestinal function in humans is poorly understood. The aim of this study was to determine the importance of proteolytic activity for protein- or amino acid-induced cholecystokinin release and pancreaticobiliary secretion. METHODS: In 9 healthy subjects, saline was perfused intraduodenally for 3 hours either with or without the synthetic protease inhibitor camostate. During the last hour, albumin or amino acids in the same molecular composition as albumin were also perfused. RESULTS: Perfusion with camostate, in concentrations that abolished intraduodenal proteolytic activity, had no effect on unstimulated plasma cholecystokinin concentrations or gallbladder emptying, but markedly (P < 0.05) increased unstimulated pancreatic enzyme output. Perfusion with protein distinctly stimulated cholecystokinin release, gallbladder emptying, and pancreatic enzyme output (P < 0.05). Perfusion with camostate resulted in significantly lower protein-stimulated plasma cholecystokinin, gallbladder, and pancreatic enzyme responses (P < 0.05). Perfusion with amino acids also stimulated plasma cholecystokinin, gallbladder emptying, and pancreatic enzyme output (P < 0.05). Camostate did not inhibit these values. CONCLUSIONS: This study shows that appropriate digestion of protein is required to stimulate plasma cholecystokinin release, gallbladder emptying, and pancreatic enzyme secretion in humans.

Adult↗