[Nontraumatic rhabdomyolysis with acute kidney insufficiency].
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Acute Kidney Injury↗
Biomedical subjects
A A Masclee
Publications and source records attributed to A A Masclee.
Hyperglycemia reduces pancreaticobiliary secretion in response to modified sham feeding in humans.
BACKGROUND/AIMS: We have investigated the effect of acute hyperglycemia on pancreaticobiliary secretion and pancreatic polypeptide (PP) release. METHODS: Duodenal outputs of bilirubin, trypsin, lipase, amylase and bicarbonate were measured using a recovery marker under basal conditions and in response to modified sham feeding (MSF) in 6 healthy subjects on two separate occasions: during normoglycemia and during acute hyperglycemia (15 mmol/l). RESULTS: During hyperglycemia the basal pancreaticobiliary output was significantly (p < 0.05) reduced. During normoglycemia MSF significantly (p < 0.05) increased the output of bilirubin and pancreatic enzymes; during hyperglycemia only the output of pancreatic enzymes increased significantly (p < 0.05) over basal. During MSF the outputs of bilirubin (16 +/- 4 vs. 4 +/- 2 micromol/30 min), trypsin (26 +/- 7 vs. 7 +/- 4 U/30 min), lipase (36 +/- 11 vs. 15 +/- 6 kU/30 min), amylase (3.4 +/- 0.7 vs. 1.4 +/- 0.7 kU/30 min) and bicarbonate (0.8 +/- 0.1 vs. 0.5 +/- 0.1 mmol/30 min) were significantly (p < 0.05) reduced during hyperglycemia compared to normoglycemia. During hyperglycemia basal and MSF-stimulated PP levels were significantly (p < 0.05) reduced compared to normoglycemia. MSF did not significantly influence plasma cholecystokinin levels in both experiments. CONCLUSIONS: This study indicates (1) that the blood glucose levels affect basal and cephalic stimulated pancreaticobiliary secretion and (2) that the PP secretion during hyperglycemia is reduced, suggesting impaired vagal cholinergic activity during hyperglycemia.
Adult↗
Effect of intravenous fat on cholecystokinin secretion and gallbladder motility in man.
During total parenteral nutrition (TPN) gallbladder bile stasis and hypomotility have been well documented. Little is known, however, about the effect of the separate components of TPN on gallbladder motor function. Inasmuch as fat, administered intraduodenally, is a potent stimulus of cholecystokinin (CCK) secretion and gallbladder contraction we have investigated whether intravenous (IV) fat affects gallbladder motility. Six healthy volunteers were studied on two separate occasions, during infusion of Intralipid 10%, 200 mL/h or saline infusion (control) for 3 hours, to evaluate the effect of IV infusion of fat on (1) plasma CCK concentration and gallbladder volume and (2) CCK-induced gallbladder emptying. Intravenous infusion of Intralipid resulted in significant increases in serum triglycerides from 0.9 +/- 0.1 to 5.1 +/- 1.3 mmol/L (at 90 min). During fat infusion no significant changes in plasma CCK and gallbladder volume were noted when compared with basal values or to the control experiment. During IV fat, concomitant infusion of 0.25, 0.5, and 1.0 Ivy dog unit (IDU) per kilogram per hour of CCK-33 resulted in a significant reduction in gallbladder volume from 26 +/- 6 cm3 (basal) to 15 +/- 4 cm3 (p less than .05), 6 +/- 2 cm3 (p less than .05) and 2.5 +/- 1 cm3 (p less than .05), respectively. No significant differences in CCK-induced gallbladder emptying were observed between IV fat and saline infusion (control). It is concluded that, in contrast to intraduodenal fat, IV infusion of fat does not affect (1) basal plasma CCK and gallbladder volume and (2) CCK-induced gallbladder contraction.
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↗
Effect of i.v. amino acids on satiety in humans.
BACKGROUND: Parenteral nutrients suppress oral food intake. Separate i.v. infusion of amino acids (IVAA) at high doses affects gastrointestinal motility and secretion. However, little is known on the effects of separate i.v. infusion of amino acids at these high doses on satiety. Therefore, we have studied the effect of two different doses of a commercially available mixed amino acids solution on satiety and food intake. METHODS: Six healthy volunteers (ages 20 to 34 years) were studied on three separate occasions in random order during (a) i.v. saline (control), (b) low-dose IVAA ([LDA] 125 mg protein/kg/h, Vamin 18EF; Kabi Pharmacia BV, Woerden, The Netherlands), or (c) high-dose IVAA ([HDA] 250 mg protein/kg/h) for 360 minutes. Subjective criteria such as wish to eat, prospective feeding intentions, and feelings of hunger and fullness were scored on 100-mm visual analog scales at 30-minute intervals. Food preference also was measured every 60 minutes with food selection lists. At the end of the experiment a meal was presented. RESULTS: Feelings of fullness were significantly (p < .05) increased during both LDA and HDA. The wish to eat was significantly (p < .05) decreased during HDA compared with control and LDA. Prospective feeding intentions also tended to be reduced during HDA (not significant). Feelings of hunger were not significantly different between the three experiments. Total food selection was significantly (p < .05) decreased during LDA and HDA, mainly because of a significantly (p < .05) decreased preference for fat-rich items. However, the total amount of food consumed at the end of the experiment was not significantly different between the three experiments. CONCLUSIONS: The present study shows that in healthy volunteers, IVAA (1) increase satiety ratings, (2) increase feelings of fullness, (3) decrease preprandial food selection, and (4) have no effect on subsequent oral food intake.
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↗
Limited influence of pouch function on quality of life after ileal pouch-anal anastomosis.
BACKGROUND/AIMS: Despite a high frequency of pouch function disorders, most patients are satisfied with the outcome of ileo-anal pouch surgery. Aims of this study were: 1) To assess the influence of pouch function on quality of life and, 2) to determine which aspects of pouch dysfunction affect quality of life the most. METHODOLOGY: Questionnaires, addressing current pouch function and quality of life (Rand-36, GIQLI), were sent to all (53) patients with intact ileo-anal pouches, operated on between 1987 and 1997 in our center. RESULTS: Thirty-six of 53 patients responded. Compared to reference data, Rand-36 scores for role-limitations based on a physical problem, vitality and general health perception were significantly diminished (P < 0.01). Physical and social functioning were normal. The GIQLI score was slightly decreased (111.7 vs. 125.8, P < 0.01). Overall pouch function did not correlate with the overall Rand-36 score, but correlated well with the overall GIQLI score (r = -0.47). Both quality of life scores were diminished mainly by the night-time stool frequency. CONCLUSIONS: 1) Quality of life after IPAA, as measured with validated questionnaires, is only slightly decreased; 2) the GIQLI questionnaire is more sensitive to pouch dysfunction than the Rand-36; 3) night-time stool frequency influences quality of life the most.
Adolescent↗
The role of cholecystokinin in appetite control.
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Appetite↗
Gallbladder sensitivity to CCK in duodenal ulcer disease, highly selective and truncal vagotomy.
BACKGROUND/AIMS: Following truncal vagotomy, a heightened contractile response of the gallbladder to cholecystokinin (CCK) has been reported in patients. We investigated whether the gallbladder responsiveness to the CCK analog cerulein is also affected in patients with a highly selective vagotomy (HSV) and in duodenal ulcer patients, since most patients had truncal vagotomy for recurrent peptic ulcer disease. MATERIALS AND METHODS: Gallbladder emptying (cholescintigraphy) and plasma cholecystokinin like immunoreactivity (CCK-LI) levels were studied during infusion of graded doses of the CCK analog cerulein. RESULTS: In duodenal ulcer patients (n = 9), patients with HSV (n = 9), patients with truncal vagotomy (n = 9) and control subjects (n = 9), infusion of stepwise increasing doses of cerulein (1-16 ng.kg-1.h-1) induced dose related changes in plasma CCK-LI. In patients with truncal vagotomy, the gallbladder contraction in response to 1, 2 and 4 ng.kg-1.h-1 of cerulein was significantly increased over controls; whereas the gallbladder contraction to cerulein in duodenal ulcer patients and patients with HSV was not significantly different from controls. CONCLUSIONS: Thus, in patients with truncal vagotomy, gallbladder contractile response to CCK is significantly enhanced, possibly due to denervation of hepatic vagal branches since gallbladder contraction after CCK infusion shows no difference between post HSV or duodenal ulcer patients and the controls.
Adult↗
Therapy and prevention of gastric ulcer.
After establishing the benign nature of a gastric ulcer, the treatment is primarily medical. This medical therapy is aimed to alleviate symptoms, to heal the ulcer and to prevent relapses. Based on the history of non-steroidal anti-inflammatory drugs (NSAIDs) and the Helicobacter pylori-status, gastric ulcer patients can be divided into four categories (1) H. pylori positive plus NSAID-use, (2) H. pylori positive without NSAID use, (3) NSAID use with negative H. pylori-status, (4) Negative H. pylori-status and no NSAID use. Patients taking NSAIDs should stop this therapy if possible. Patients with gastric H. pylori infection should be treated by a regimen of a proton pump inhibitor with at least two appropriate antibiotics. This treatment will result in early alleviation of symptoms, rapid healing of the ulcer and prophylaxis of ulcer relapse. In patients with gastric ulcer who cannot stop NSAIDs, maintenance therapy with prostaglandins or potent antisecretory drugs should be considered. The few patients with gastric ulcer who do not take NSAIDs and do not have gastric H. pylori infection should be treated by antisecretory drugs, and they should be carefully followed endoscopically to exclude malignant (carcinoma, lymphoma) or non-peptic (Crohn's disease) disease. All patients with gastric ulcer should be re-endoscoped to verify complete ulcer healing. Surgery may be considered in gastric ulcer patients with complications, in those with severe dysplasia of the gastric mucosa, and in those who are not able or willing to take the medication.
Anti-Inflammatory Agents, Non-Steroidal↗