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M Ledeboer

Publications and source records attributed to M Ledeboer.

15 recordsLinked to original sources

[The use of a self-expanding stent as palliation or before elective surgery in patients with obstructive colorectal carcinoma].

OBJECTIVE: To evaluate the use of colorectal stents. DESIGN: Retrospective. METHOD: Data were collected on all patients treated at the Deventer Hospital, the Netherlands, between 1 April 1996 and 31 December 2003 in whom the placement of a self-expanding colorectal stent was attempted. Each patient's physician was contacted to inquire about the patient's status, including quality of life with the stent in situ. RESULTS: Stent placement was attempted in 57 patients as palliation (n = 45) or before elective surgery (n = 12). Of the 57 patients, 29 were men and 28 were women, and the mean age was 71 years (range: 46-94). All patients had colorectal carcinoma, except 1 patient with stenosis following ischaemic colitis. Passage of air and faeces occurred immediately after stent expansion in 55 of the 57 patients (96%). Perforation during stent placement occurred in 2 patients, who subsequently underwent colostomy. 4 additional patients required a colostomy due to stent migration within a few hours or days after placement (n = 3) or obstruction by tumor growth after 65 days (n = 1). Patients in the palliative group had an acceptable quality of life. Those who received a stent before elective surgery were able to undergo resection, did not require colostomy, and had no postoperative complications. One patient did not undergo surgery because of extensive metastases. CONCLUSION: A colorectal stent can be used in the palliative treatment of terminal patients with colorectal carcinoma before colostomy is considered. Experiences with stents before elective surgery were also positive.

Aged↗

Chronic pancreatitis: relation between function and morphology.

BACKGROUND: In our department, we routinely use a combined exocrine-endocrine function test to evaluate the pancreatic function in chronic pancreatitis i.e. urinary para amino benzoic acid (PABA) recovery and pancreatic polypeptide secretion in response to a meal and glucose tolerance test. AIM: To study the relationship between changes in morphology and exocrine/endocrine function in patients with chronic pancreatitis. PATIENTS AND METHODS: In 103 patients with chronic pancreatitis seen by our department for evaluation of pancreatic function between 1989 and 1999, we retrospectively analysed the correlation between morphology (Cambridge-score) and function. Furthermore the differences in presentation, function and morphology between patients with alcohol-induced chronic pancreatitis and idiopathic chronic pancreatitis were evaluated. RESULTS: Significant correlation were found for both PABA recovery and pancreatic polypeptide secretion with morphologic score, respectively r = -0.205 (P = 0.037) and r = -0.209 (P = 0.031), but not with endocrine function. The correlation between morphology and PABA recovery or pancreatic polypeptide secretion was observed in the subgroup with alcohol-induced chronic pancreatitis but not in those with idiopathic chronic pancreatitis. Pain is a prominent symptom of chronic pancreatitis. Pain was more frequent and more severe in patients suffering from chronic pancreatitis caused by alcohol or idiopathy. CONCLUSIONS: Morphology and exocrine function correlate in patients with alcohol-induced chronic pancreatitis but not in patients with chronic pancreatitis. When compared to patients with chronic pancreatitis of idiopathic origin, patients with alcoholic origin show differences in presentation and morphology but not in function.

4-Aminobenzoic Acid↗

Gall bladder dysmotility: a risk factor for gall stone formation in hypertriglyceridaemia and reversal on triglyceride lowering therapy by bezafibrate and fish oil.

BACKGROUND AND AIM: The aim of this study was to unravel the mechanisms responsible for the increased risk of gall stone disease in hypertriglyceridaemia (HTG) and to compare the effects of triglyceride lowering therapy by bezafibrate and fish oil on determinants of cholelithiasis (biliary lipid composition and gall bladder motility) in HTG patients. PATIENTS AND METHODS: Gall bladder motility (ultrasonography) was studied postprandially and during infusion of cholecystokinin (CCK). Determinants of cholelithiasis and serum lipids were compared between nine HTG patients and 10 age, sex, and body mass index matched normolipidaemic controls. The effects of bezafibrate and fish oil in HTG patients were studied in a randomised cross over trial. RESULTS: HTG patients showed 14-fold higher serum triglyceride (TG) levels than controls. Biliary lipid composition, fasting gall bladder volumes, and CCK levels did not differ between HTG patients and controls. Gall bladder emptying was reduced in HTG patients compared with controls during CCK infusion (-22%) as well as in response to a meal (-37%; both p<0.001). Postprandial CCK levels were significantly higher in HTG patients. Both bezafibrate and fish oil reduced serum TG levels (-68% and -51% v baseline, respectively; both p<0.01). Fasting CCK levels were not affected whereas CCK induced gall bladder emptying increased during bezafibrate (+29%; p<0.001) and tended to increase on fish oil therapy (+13%; p=0.07). Postprandial gall bladder motility improved on bezafibrate and fish oil (+47 and +25% v baseline, respectively; both p<0.02) at least partly due to increased gall bladder sensitivity to CCK (both p<0.05 v baseline). Bezafibrate but not fish oil increased the molar ratio of cholesterol to bile acids (+40%; p</=0.05) but no effects on cholesterol saturation index were seen with either treatment. CONCLUSIONS: We suggest that impaired gall bladder motility occurs in HTG patients due to decreased sensitivity to CCK, which may add to the enhanced risk of gall stone disease in HTG patients. Triglyceride lowering therapy by both fish oil and bezafibrate improve gall bladder dysmotility without adversely affecting biliary cholesterol saturation.

Analysis of Variance↗

Effects of very long chain versus long chain triglycerides on gastrointestinal motility and hormone release in humans.

Fish oil (a very long chain triglycerides, VLCT) has received much attention because of its favorable metabolic properties; however, its effect on gastrointestinal function has not been studied. We investigated the effects of intraduodenally administered VLCT on gut-hormone release [cholecystokinin (CCK), neurotensin, peptide YY (PYY)], gallbladder emptying, antroduodenal motility, and small bowel transit time (SBTT) in comparison to intraduodenal administration of saline and long chain triglycerides (LCT, corn oil) in nine healthy volunteers. Gallbladder contraction duration was significantly shorter after VLCT than after LCT (138 +/- 16 min vs 233 +/- 38 min, P < 0.05). Both fats induced a fed motility pattern, while SBTT was not significantly altered. CCK secretion was significantly reduced after VLCT compared to LCT (36 +/- 12 pM x 120 min vs 78 +/- 15 pM x 120 min, P < 0.05), whereas PYY and neurotensin release were not significantly different. In conclusion, effects of triglycerides on CCK and gallbladder motility appear to be chain-length dependent, in contrast to the effects on distal gut-hormone release and intestinal motility and transit, which appear to be chain-length independent.

Adolescent↗

Antroduodenal motility and small bowel transit during continuous intraduodenal or intragastric administration of enteral nutrition.

BACKGROUND: Gastrointestinal intolerance is observed more frequently during intraduodenal (ID) tube feeding than during intragastric (IG) feeding, possibly because it evokes a stronger gastrointestinal response and accelerates small bowel transit. We have investigated whether the accelerated small bowel transit during ID feeding results from alterations in antroduodenal motility pattern. DESIGN: The effect of IG and ID infusion of a polymeric diet (Nutrison, 125 kcal h-1) on antroduodenal motility, small bowel transit time (SBTT) and gastrointestinal hormone release was studied in nine healthy subjects. These subjects were studied on three occasions for 6 h during fasting, continuous IG or ID feeding. RESULTS: Phase III recurrence time was significantly prolonged during IG feeding compared with fasting (240 +/- 51 vs. 136 +/- 24 min; P < 0.05). None of the subjects had recurrence of phase III during ID feeding; the fed motor pattern remained present. Parameters of fed motility (mean amplitude and motility index) were not significantly different between IG and ID feeding, although the frequency of antral and duodenal contractions was lower during ID than during IG feeding. SBTT was significantly accelerated during ID compared with IG feeding and with fasting (58 +/- 8 vs. 73 +/- 9 and 83 +/- 10 min respectively; P < 0.05). Plasma cholecystokinin (CCK) and pancreatic polypeptide (PP) levels were significantly higher during ID than during IG feeding. Peptide YY (PYY) levels were significantly higher during ID than during fasting, but not during IG feeding CONCLUSIONS: During intraduodenal feeding, a fed motility pattern is preserved, whereas during intragastric feeding transition from a fed to a fasting motor pattern is observed in over 50% of the subjects. These differences may be related to augmented hormone release during intraduodenal feeding.

Adult↗

Prospective study of the effect of the Belsey Mark-IV fundoplication on reflux mechanisms.

BACKGROUND: Transient lower esophageal sphincter relaxations (TLESRs) are the major mechanism permitting gastroesophageal reflux (GER). Little information is available on how anti-reflux surgery affects reflux mechanisms, especially TLESRs. We evaluated the effects of partial fundoplication (Belsey Mark IV) on reflux mechanisms. METHODS: Sixteen patients were prospectively studied before and after Belsey Mark-IV operation by endoscopy, 24-h esophageal pH-metry, and simultaneous recording of pH and lower esophageal sphincter (LES) characteristics by sleeve manometry. RESULTS: The operation was successful in 14 of 16 patients (87%). Fasting and postprandial reflux decreased significantly (P < 0.01) after the operation. Partial fundoplication significantly (P < 0.05) decreased the number of TLESRs per hour in the fasting and postprandial period from 3.2+/-0.4 and 5.6+/-0.5 to 1.7+/-0.3 and 2.8+/-0.4, respectively. The percentage of TLESRs associated with reflux also decreased significantly (P < 0.05). Basal LES pressure increased from 14.7+/-2.1 mmHg to 17.9+/-2.6 mmHg (not significant). CONCLUSIONS: Partial fundoplication controls GER through a reduction in the number of TLESRs and by decreasing the number of relaxations associated with reflux.

Adult↗

Effect of intragastric or intraduodenal administration of a polymeric diet on gallbladder motility, small-bowel transit time, and hormone release.

OBJECTIVE: During postpyloric tube feeding, GI intolerance is observed more frequently than during prepyloric feeding, possibly by evoking a stronger GI response. METHODS: We investigated the effect of intragastric and intraduodenal administration of a polymeric diet (125 kcal/h) on gallbladder motility (by ultrasonography), duodeno-cecal transit time (by lactulose H2 breath test), and GI hormone release (including cholecystokinin, pancreatic polypeptide, and gastrin). Six healthy subjects (two male, four female; mean age 22 yr, range 18-27 yr) were studied on two separate occasions in random order during 6 h of continuous administration of the diet through either the gastric or duodenal port of a two-lumen tube. RESULTS: Intraduodenal feeding resulted in a more rapid contraction of the gallbladder, from 32 +/- 4 to 23 +/- 4 cm3 at 10 min (p < 0.05), reaching a minimum of 6 +/- 1 cm3, in contrast to intragastric feeding (31 +/- 4 to 19 +/- 3 cm3 at 60 min, p < 0.05; minimum 14 +/- 1 cm3). The gallbladder remained contracted during the 6-h study period during both intraduodenal and intragastric feeding. Small-bowel transit time was significantly accelerated during intraduodenal compared with intragastric feeding (51 +/- 12 vs 81 +/- 9 min; p = 0.003). Plasma cholecystokinin secretion was significantly (p < 0.05) increased during intraduodenal compared with intragastric feeding (848 +/- 107 vs 279 +/- 89 pmol x L(-1) x 360 min). The same was true for pancreatic polypeptide secretion. However, gastrin release was significantly (p < 0.05) higher during intragastric feeding. CONCLUSIONS: Intraduodenal feeding elicited a stronger GI response than intragastric feeding, as demonstrated by accelerated small-bowel transit time, more rapid and stronger gallbladder contractions, and increased cholecystokinin and pancreatic polypeptide release. Gastrin release, on the other hand, was stronger during intragastric feeding.

Adolescent↗

Effect of medium- and long-chain triglycerides on lower esophageal sphincter pressure: role of CCK.

Fat meals are known to decrease lower esophageal sphincter (LES) pressure, possibly through postprandial CCK release. Dietary fat consists mainly of long-chain triglycerides (LCT), which potently stimulate CCK secretion. This effect contrasts with that of medium-chain triglycerides (MCT), which do not induce CCK release. We recorded LES pressure and gallbladder volume in six healthy subjects on five separate occasions during intraduodenal administration of 1) saline control, 2) LCT, 3) MCT, 4) LCT during intravenous infusion of the CCK receptor antagonist loxiglumide, and 5) MCT together with loxiglumide. LES pressure decreased significantly during administration of both LCT and MCT. Loxiglumide completely prevented the reduction in LES pressure during intraduodenal LCT, but not during intraduodenal MCT. Gallbladder volume decreased during LCT, but not during MCT. It is concluded that intraduodenal administration of equimolar amounts of both LCT and MCT significantly reduces LES pressure. The effect of LCT on LES pressure is mediated by CCK. The effect of MCT is not dependent on CCK, since MCT does not release CCK and loxiglumide does not prevent the MCT-induced reduction in LES pressure.

Adult↗

Do patients with systemic sclerosis have abnormal gallbladder function?

OBJECTIVE: To determine gallbladder motility in patients with systemic sclerosis. DESIGN: Case control study. SETTING: University hospital, out-patient department of rheumatology. PATIENTS: Ten patients with systemic sclerosis according to the criteria of the American Rheumatism Association with documented involvement of the gastrointestinal tract and 10 healthy controls matched for age, sex and body mass index. INTERVENTION: Cephalic vagal cholinergic simulation by modified sham feeding and hormonal stimulation by infusion of cholecystokinin. MEASUREMENTS: Gallbladder volume obtained by ultrasonography and determination of plasma cholecystokinin concentrations. RESULTS: Fasting gallbladder volumes were not significantly different between patients with systemic sclerosis and controls (19.6 +/- 1.9 cm3 and 23.3 +/- 2.9 cm3, respectively, mean plus or minus standard error of the mean). Neither were there significant differences in reduction of gallbladder volume in response to modified sham feeding (35 +/- 4% and 33 +/- 4%, respectively) nor during cholecystokinin infusion (56 +/- 4% and 60 +/- 6%, respectively). The increase in plasma cholecystokinin levels during infusion was not different in the two groups. CONCLUSION: Gallbladder motility in patients with systemic sclerosis is preserved in response to both cholinergic and hormonal stimulation, even when other gastrointestinal motor disturbances are present. These results suggest that patients with systemic sclerosis are not at increased risk for cholelithiasis because of gallbladder dysmotility.

Case-Control Studies↗

Gallbladder motility and cholecystokinin secretion during continuous enteral nutrition.

OBJECTIVES: During total parenteral nutrition, gallbladder motility is impaired, resulting in sludge and stone formation. Little is known about gallbladder motility during prolonged enteral nutrition. METHODS: We studied gallbladder motility during continuous enteral nutrition (CEN) in nine hospitalized patients with active inflammatory bowel disease. The patients received a polymeric diet (2000 kcal/24 h) by CEN through a nasogastric tube for a prolonged period. Gallbladder volumes were obtained daily by ultrasonography, starting from day 0 (before CEN) and on 7 consecutive days during CEN. At days 0, 1, 4, and 7, the gallbladder response to i.v. cholecystokinin (CCK-33; 0.5 Ivy Dog unit/kg/h) was studied. Plasma CCK levels were determined at regular intervals by radioimmunoassay. RESULTS: No significant differences were observed on day 0 between patients and a group of nine healthy control subjects in fasting gallbladder volumes (19.4 +/- 2.3 and 19.6 +/- 2.4 cm3, respectively) and gallbladder contraction during CCK infusion (56 +/- 14% and 69 +/- 7%, respectively). During CEN, from day 1 to day 7, mean gallbladder volume remained significantly (p < 0.05) reduced compared with fasting gallbladder volume, and mean plasma CCK levels remained significantly (p < 0.05) increased compared with fasting levels. Although gallbladder volume was significantly reduced during CEN, the gallbladder contractile response to CCK was not affected; at days 1, 4, and 7, gallbladder contraction was 36-57%. CONCLUSIONS: During CEN, 1) gallbladder volume is significantly reduced and plasma CCK levels are significantly increased, 2) these effects are sustained over time (7 days), and 3) the gallbladder remains responsive to exogenous CCK. These results indicate that gallbladder contractility and gallbladder responsiveness to CCK are preserved during prolonged CEN in patients with inflammatory bowel disease.

Adult↗

Effect of cholecystokinin on lower oesophageal sphincter pressure and transient lower oesophageal sphincter relaxations in humans.

The effect of cholecystokinin (CCK) on the lower oesophageal sphincter (LOS) pressure, frequency of transient LOS relaxations, and the number of reflux episodes was investigated in six healthy subjects. LOS pressure was recorded on four separate occasions during continuous intravenous infusion of either saline or CCK-33 in doses of 0.25, 0.5, or 1.0 Ivy Dog units per kg body weight per hour (IDU.kg-1.h-1) for 90 minutes. Plasma CCK concentrations did not change during saline infusion, but increased significantly from 2.5 (0.3) pmol/l to steady state levels of 4.0 (0.4) pmol/l, 6.1 (0.4) pmol/l, and 9.3 (0.9) pmol/l respectively starting from 30 minutes. LOS pressure did not change significantly during infusion of saline or of CCK-33 at doses of 0.25 or 0.5 IDU.kg-1.h-1. However, a significant (p < 0.05) reduction in LOS pressure to a minimum level of 12 (4) mm Hg at 30 minutes compared with basal level (18 (4) mm Hg) and compared with saline was observed during infusion of CCK-33 at a dose of 1.0 IDU.kg-1.h-1. In addition, oesophageal motility and pH were recorded simultaneously in these six subjects on two separate occasions one hour before (fasting) and three hours during administration of a gastric load (dextrose 5%, pH 3) combined with continuous intravenous infusion of saline or CCK-33 at a dose of 1.0 IDU,kg-1.h-1. Plasma CCK concentrations did not change during the gastric load combined with saline, but increased significantly to a steady state level of 10.8 (0.8) pmol/l during intravenous infusion of CCK. The number of transient LOS relaxations increased significantly in the first hour during administration of the gastric load compared with fasting levels, both during saline infusion (fasting: 1.7 (0.6)/h, 1st hour: 4.3 (1.2)/h) and during CCK infusion (fasting: 1.7 (0.5)/h, 1st hour: 3.8 (0.7)/h). In the second and third hours the number of transient LOS relaxations fell to fasting levels in both experiments. No significant differences were observed in the number and type of transient LOS relaxations, mechanism of gastro-oesophageal reflux, or duration of acid exposure between the two experiments. It is concluded that in healthy subjects infusion of CCK-33 in a dose of 1.0 IDU.kg-1.h-1 significantly reduces LOS pressure but does not affect the frequency of transient LOS relaxations or acid exposure time during a continuous liquid gastric load.

Adult↗

'The tropics in our bathroom': chronic diarrhoea after return from the tropics.

Interest in imported tropical diseases has increased with the rising number of travellers to the tropics. This is especially true in the case of tropical gastroenterologic disorders. The causative organisms of chronic diarrhoea are different from those causing acute diarrhoea. Bacteria are relatively unusual; parasites, e.g. Entamoeba histolytica or Giardia lamblia or an opportunistic parasitic infestation associated with an HIV infection are more likely. Furthermore, non-infectious causes, such as postinfective tropical malabsorption, lactase deficiency or coeliac disease have to be considered. Today, elderly people often undertake a journey to the tropics; in these cases the diarrhoea may be associated not only with an increased susceptibility to tropical bowel infections but also with causes previously present, such as diverticulosis, carcinoma or inflammatory bowel disease. The classification of chronic diarrhoea following a visit to the tropics is essentially the same as that for acute diarrhoea: diarrhoea with and without fever and with and without blood. In addition, malabsorption is an important feature of chronic diarrhoea.

Adult↗

Effect of equimolar amounts of long-chain triglycerides and medium-chain triglycerides on small-bowel transit time in humans.

BACKGROUND: The use of medium-chain triglycerides in diets is limited by the frequent occurrence of diarrhea or crampy abdominal pain. Because these symptoms may result from an accelerated transit time induced by medium-chain triglycerides, we investigated the effect of equimolar amounts of long-chain triglycerides and medium-chain triglycerides on small-bowel transit time in 10 healthy subjects. METHODS: Small-bowel transit time was measured by the lactulose hydrogen breath test after intraduodenal administration of lactulose. RESULTS: Intraduodenal administration of 20 mmol of long-chain triglycerides per hour for 90 minutes did not alter small-bowel transit time compared with control (77 +/- 11 minutes vs 77 +/- 10 minutes, respectively), whereas intraduodenal infusion of an equimolar dose of medium-chain triglycerides significantly accelerated small-bowel transit time (59 +/- 6 minutes) compared with long-chain triglycerides and control (p < .05). In six individuals, small-bowel transit time was shorter during the administration of medium-chain triglycerides compared with control, and three of these subjects experienced abdominal symptoms. Plasma cholecystokinin levels increased significantly (p < .05) during the administration of long-chain triglycerides, from 2.6 +/- 0.3 pmol/L to a maximum of 4.3 +/- 0.6 pmol/L. No significant alterations were observed in plasma cholecystokinin levels during administration of medium-chain triglycerides or in the control experiment. CONCLUSIONS: Although it significantly increases cholecystokinin secretion, the intraduodenal infusion of long-chain triglycerides does not affect small-bowel transit time, whereas the infusion of medium-chain triglycerides accelerates small-bowel transit time, independent of cholecystokinin.

Adult↗

Differences in cholecystokinin release and gallbladder contraction between emulsified and nonemulsified long-chain triglycerides.

BACKGROUND: Fat is a potent stimulus of cholecystokinin (CCK) release. Apart from lipolysis, fatty acid chain length, and saturation, emulsification may also determine the magnitude of CCK release. METHODS: We have studied the effect of emulsification of soybean oil on CCK and pancreatic polypeptide (PP) release (radioimmunoassay [RIA]) and gallbladder motility (ultrasonography). Six healthy subjects were studied on three separate occasions in random order during (1) intraduodenal administration of emulsified long-chain triglycerides (LCT) (6 mmol/h for 120 minutes); (2) equimolar amounts of nonemulsified LCT with addition of emulsifier; and (3) saline with emulsifier (control). RESULTS: Intraduodenal administration of both nonemulsified LCT and emulsified LCT induced significant (p < .05) increases in plasma CCK and PP levels and reductions in gallbladder volume. However, compared with nonemulsified LCT, emulsified LCT resulted in a readier and significantly stronger CCK release (212+/-62 pmol/L per 120 minutes vs 36+/-7 pmol/L per 120 minutes; p < .05); PP release (2034+/-461 pmol/L per 120 minutes vs 671+/-106 pmol/L per 120 minutes; p < .05); and gallbladder contraction (77%+/-2% vs 41%+/-7%; p < .05). No significant alterations were observed in plasma CCK or PP levels and gallbladder volume during administration of saline with emulsifier. CONCLUSIONS: Intraduodenal administration of a low-dose emulsified LCT more potently stimulates CCK and PP release and gallbladder contraction in comparison to equimolar amounts of nonemulsified LCT. These findings point to an important role for solubilization of LCT in determining the magnitude of CCK release from the intestine.

Adolescent↗