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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Alimentary pharmacology & therapeutics 11 (1997), S. 0 
    ISSN: 1365-2036
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: H. pylori eradication usually involves treatment with three or four drugs for at least 7 days. Possible advantages of short treatment regimens are better patient compliance and tolerability, and less adverse effects. Recently two reports have shown a cure rate of 〉 90% using a 4-day quadruple therapy.〈section xml:id="abs1-2"〉〈title type="main"〉Aim:To confirm these data and to evaluate the efficacy and tolerability of 4-day quadruple therapy in a single centre.〈section xml:id="abs1-3"〉〈title type="main"〉Methods:Thirty-eight consecutive patients with non-ulcer dyspepsia or peptic ulcer disease, and proven H. pylori infection, received 4 days of quadruple therapy (bismuth, tetracycline, metronidazole, lansoprazole). At least 6 weeks after treatment, endoscopy was repeated with six biopsies of antrum and corpus for histology and culture.〈section xml:id="abs1-4"〉〈title type="main"〉Results:The intention-to-treat cure rate was 34/38 (89.5%, 95% CI: 79.7–99.2%). In the per protocol analysis the cure rate was 34/37 (91.9%, 95% CI: 83.1–100%). Primary metronidazole resistance was observed in two patients; both were cured. Metronidazole resistance induction was observed in one patient in whom therapy failed. The treatment was generally well tolerated.〈section xml:id="abs1-5"〉〈title type="main"〉Conclusion:Routine use of 4-day quadruple anti-H. pylori treatment is effective and well tolerated.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Gallbladder emptying ; hyperglycaemia ; cholecystokinin ; Type 1 (insulin-dependent) diabetes mellitus ; autonomic neuropathy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with diabetes mellitus are at increased risk of developing gallstones. This has been attributed, among other factors, to alterations in gallbladder motility in the presence of autonomic neuropathy. Since high blood glucose concentrations impair gastric emptying in diabetic patients, we have investigated the effect of acute hyperglycaemia on gallbladder motility. Seven Type 1 (insulin-dependent) diabetic patients were studied twice during euglycaemia (blood glucose 5 mmol/l) and hyperglycaemia (blood glucose 15 mmol/l) using a clamp technique. In addition, seven healthy volunteers were studied during euglycaemia and hyperglycaemia. Gallbladder volumes, measured with ultrasonography, were studied before and during infusion of step-wise increasing doses of cholecystokinin-33, 0.25, 0.5 and 1.0 Ivy Dog Unit · kg−1 · h−1, each dose for 30 min. Mean basal gallbladder volumes were not significantly different in the four experiments. Administration of cholecystokinin resulted in significant (p〈0.05) dose-dependent reductions in gallbladder volume in all experiments. During euglycaemia the gallbladder contraction in diabetic patients was not significantly different from the control subjects. During hyperglycaemia the gallbladder contraction in the diabetic patients was significantly (p〈0.05) reduced compared to euglycaemia only during infusion of 0.25 Ivy Dog Unit · kg−1 · h−1 of cholecystokinin (19±6% vs 33±6%). Compared to euglycaemia, during hyperglycaemia the gallbladder contraction in the control subjects was significantly (p〈0.05) reduced during infusion of 0.25, 0.5 and 1.0 Ivy Dog Unit · kg−1 · h−1 of cholecystokinin (14±4% vs 31±3%; 42±6% vs 65±5%; 74±4% vs 90±3%, respectively). It is concluded that during euglycaemia the gallbladder contraction in response to cholecystokinin in Type 1 diabetic patients is not significantly different from control subjects. During hyperglycaemia the gallbladder contraction in response to 0.25 Ivy Dog Unit · kg−1 · h−1 cholecystokinin, leading to cholecystokinin levels as observed after ingestion of a light meal, is significantly reduced in Type 1 diabetic patients.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Key words Gallbladder emptying, hyperglycaemia, cholecystokinin, Type 1 (insulin-dependent) diabetes mellitus, autonomic neuropathy.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with diabetes mellitus are at increased risk of developing gallstones. This has been attributed, among other factors, to alterations in gallbladder motility in the presence of autonomic neuropathy. Since high blood glucose concentrations impair gastric emptying in diabetic patients, we have investigated the effect of acute hyperglycaemia on gallbladder motility. Seven Type 1 (insulin-dependent) diabetic patients were studied twice during euglycaemia (blood glucose 5 mmol/l) and hyperglycaemia (blood glucose 15 mmol/l) using a clamp technique. In addition, seven healthy volunteers were studied during euglycaemia and hyperglycaemia. Gallbladder volumes, measured with ultrasonography, were studied before and during infusion of step-wise increasing doses of cholecystokinin-33, 0.25, 0.5 and 1.0 Ivy Dog Unit·kg−1·h−1, each dose for 30 min. Mean basal gallbladder volumes were not significantly different in the four experiments. Administration of cholecystokinin resulted in significant (p 〈0.05) dose-dependent reductions in gallbladder volume in all experiments. During euglycaemia the gallbladder contraction in diabetic patients was not significantly different from the control subjects. During hyperglycaemia the gallbladder contraction in the diabetic patients was significantly (p 〈0.05) reduced compared to euglycaemia only during infusion of 0.25 Ivy Dog Unit·kg−1·h−1 of cholecystokinin (19±6 % vs 33±6 %). Compared to euglycaemia, during hyperglycaemia the gallbladder contraction in the control subjects was significantly (p 〈0.05) reduced during infusion of 0.25, 0.5 and 1.0 Ivy Dog Unit·kg−1·h−1 of cholecystokinin (14±4 % vs 31±3 %; 42±6 % vs 65±5 %; 74±4 % vs 90±3 %, respectively). It is concluded that during euglycaemia the gallbladder contraction in response to cholecystokinin in Type 1 diabetic patients is not significantly different from control subjects. During hyperglycaemia the gallbladder contraction in response to 0.25 Ivy Dog Unit·kg−1·h−1 cholecystokinin, leading to cholecystokinin levels as observed after ingestion of a light meal, is significantly reduced in Type 1 diabetic patients. [Diabetologia (1994) 37: 75–81]
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  • 4
    ISSN: 1573-2568
    Keywords: hyperglycemia ; gallbladder ; intestinal transit ; pancreatic polypeptide ; cholecystokinin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The aim of the present study was to investigate the effect of acute hyperglycemia on (1) the intestinal phase of gallbladder contraction induced by the intraduodenal administration of emulsified fat, and (2) the small intestinal transit time measured by the lactulose breath hydrogen test. Six healthy volunteers were studied in random order during normoglycemia and hyperglycemia (blood glucose levels 15 mmol/liter). Gallbladder volumes were measured with ultrasonography. Administration of 1 and 2 g/hr of fat resulted in significant reductions in gallbladder volumes from 24±2 cm3 to 11±1 cm3 (P〈0.05) and 8±1 cm3 (P〈0.05), respectively during normoglycemia, and from 24±2 cm3 to 21±2 cm3 (P〈0.05) and 16±2 cm3, respectively (P〈0.05) during hyperglycemia. Compared to normoglycemia, the gallbladder contraction was significantly (P〈0.05) reduced during hyperglycemia. No significant differences in CCK secretion were observed between experiments. Small intestinal transit time during hyperglycemia (101±12 min) was significantly (P〈0.05) prolonged compared to normoglycemia (57±12 min). During hyperglycemia, basal PP levels and PP secretion in response to intraduodenal fat were significantly (P〈0.05) reduced compared to normoglycemia. It is concluded that (1) low doses of intraduodenal emulsified fat result in significant gallbladder contraction and CCK secretion, (2) acute hyperglycemia inhibits intraduodenal fat induced gallbladder contraction, (3) acute hyperglycemia does not affect the intraduodenal fat induced CCK secretion, (4) small intestinal transit is significantly prolonged during acute hyperglycemia, and (5) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1573-2568
    Keywords: hyperglycemia ; amino acids ; parenteral nutrition ; gallbladder motility ; cholecystokinin ; pancreatic polypeptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The present study was undertaken to investigate the effect of acute hyperglycemia on the gallbladder contraction induced by intravenous administration of high doses of amino acids (Vamin 18, 250 mg protein/kg/hr). Six healthy volunteers were studied in random order on two occasions during normoglycemia and hyperglycemia with blood glucose levels stabilized at 15 mmol/liter. Gallbladder volumes, measured with ultrasonography, were studied for 60 min before and for 120 min during intravenous infusion of amino acids (IVAA). Administration of IVAA resulted in a significant reduction (P〈0.05) in gallbladder volume from 32±5 cm3 to 17±2 cm3 during normolgycemia. During hyperglycemia no significant changes in gallbladder volume were observed in response to IVAA. No significant changes in plasma CCK concentration, the major hormonal stimulus for gallbladder contraction, occurred in response to IVAA. During hyperglycemia, pancreatic polypeptide (PP) secretion, as an indirect measure of vagal cholinergic tone, in response to IVAA was significantly (P〈0.05) reduced compared to normoglycemia. It is concluded that: (1) administration of high doses of IVAA results in significant gallbladder contraction, (2) high doses of IVAA do not stimulate CCK secretion, (3) acute hyperglycemia inhibits IVAA-induced gallbladder contraction, and (4) acute hyperglycemia inhibits basal and stimulated plasma PP secretion, suggesting impaired vagal-cholinergic tone during hyperglycemia.
    Type of Medium: Electronic Resource
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