Digestive diseases and sciences
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Randomized Controlled Trial Clinical Trial
Erythromycin enhances solid-phase gastric emptying in induced-hyperglycemia in patients with truncal vagotomy and pyloroplasty.
Erythromycin has been found to be a gastrointestinal prokinetic agent while acute hyperglycemia has been associated with delayed gastric emptying in healthy controls and diabetics. The aim of this study was to investigate whether hyperglycemia, per se, alters gastric motility, during erythromycin-induced acceleration of gastric emptying of solids in patients with truncal vagotomy and pyloroplasty (TVP) and the role of vagus nerves. Eight TVP patients and six controls underwent scintigraphic measurement of gastric emptying of a solid meal, during placebo in normoglycemia (5-8.9 mmol/liter glucose) or 200 mg intravenous erythromycin lactobionate in normo- or hyperglycemia (16-19 mmol/liter glucose) induced by intravenous glucose infusion, on separate days in random order. ⋯ A significant increase in the delay of gastric emptying was achieved in TVP patients compared to controls after giving erythromycin in hyperglycemia and after placebo. Despite the inhibitory effect of induced hyperglycemia on gastric emptying, erythromycin is still able to accelerate the emptying rate and could prove to be a useful prokinetic agent under hyperglycemic conditions. Hyperglycemia may indicate a cholinergic-antagonist pathway that delays the erythromycin-induced acceleration of gastric emptying of solids and is more evident in vagotomized patients than controls, who retain the functional integrity of the vagus nerves.
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Randomized Controlled Trial Clinical Trial
A randomized, controlled study of thymosin-alpha1 therapy in patients with anti-HBe, HBV-DNA-positive chronic hepatitis B.
No consistently effective therapy is yet available for the treatment of chronic HBsAg, anti-HBe, HBV-DNA-positive hepatitis. A multicenter trial has shown that the response rates are not significantly different when patients with anti-HBe-positive hepatitis are treated with six-month course of thymosin-alpha1 or of interferon-alpha. However, since among these patients, interferon's real efficacy is still debated, with sustained biochemical response achieved in only a few of the treated patients, we conducted this controlled study to investigate the safety and efficacy of thymosin-alpha1 as compared with no treatment. ⋯ Among the treated patients, median IgM anti-HBc levels were low with respect to baseline values 4-10 months after treatment started. None became HBsAg negative. In conclusion, these results indicate that, in anti-HBe, HBV-DNA-positive chronic hepatitis B, thymosin-alpha1 therapy alone does not increase the response rate, but may contribute to reduce the immune-mediated liver cell necrosis as indirectly assessed by ALT and IgM anti-HBc levels.
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Randomized Controlled Trial Clinical Trial
Gastric PCO2 tonometry is independent of carbonic anhydrase inhibition.
Tonometric measurement of an elevated intragastric Pco2 and a decreased calculated gastric intramucosal pH can be used to detect gastric mucosal ischemia, provided that intraluminal production of CO2 through acid buffering by bicarbonate is avoided by adequate acid secretion suppression. If the diffusion rate is known, steady state Pco2 can be calculated when measurement intervals are used that are shorter than needed for complete equilibration. The CO2 diffusion might be influenced by the choice of acid-suppressive drugs, since some of them inhibit gastric carbonic anhydrase (CA) and CA facilitates diffusion of CO2/bicarbonate over the gastrointestinal mucosa. ⋯ Measurement intervals were 10, 20, 30 and 60 min. Neither the diffusion rate of CO2 (k = 0.13 +/- 0.02/min in group I and 0.11 +/- 0.02/min in group II), nor the steady-state Pco2 (38 +/- 3 mm Hg in group I and 40 +/- 4 mm Hg in group II), nor the gastric-blood differences in Pco2 and pH differed between groups. These results indicate that diffusion of CO2 into the tonometer balloon is independent of CA and thus of the type of gastric acid secretion inhibition.
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Randomized Controlled Trial Comparative Study Clinical Trial
Response to intraluminal gas in irritable bowel syndrome. Motility versus perception.
Our aim was to evaluate the response to intraluminal gas in irritable bowel syndrome and to determine whether this response was consequent upon disordered motility or altered perception. We evaluated 10 patients who satisfied the clinical criteria for the diagnosis of irritable bowel syndrome and 10 healthy controls. An eight-lumen perfused catheter assembly was positioned to monitor motor activity in the duodenum and proximal jejunum; a separate side port in the distal duodenum permitted gas infusion. ⋯ Patients with irritable bowel syndrome described more pain (score, mean +/- SE, control versus irritable bowel: 0.22 +/- 0.16 vs 1.65 +/- 0.5, P < 0.01) and nausea (0.25 +/- 0.21 vs 1.45 +/- 0.64, P < 0.04) during sham gas; motility indices were similar in both groups. During active gas, irritable bowel syndrome patients reported more pain (0.40 +/- 0.39 vs 2.94 +/- 1.16, P < 0.03); motility indices at all sites were similar in both groups. Symptom severity in irritable bowel syndrome subjects randomized to receive atropine was similar to control subjects during active gas infusion; motility indices were similar.(ABSTRACT TRUNCATED AT 250 WORDS)
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Randomized Controlled Trial Clinical Trial
Oral naloxone antagonizes loperamide-induced delay of orocecal transit.
Orocecal transit time was determined by the lactulose hydrogen breath test in nine healthy volunteers after administration of placebo, loperamide (16 mg per os), and loperamide (16 mg per os) followed by oral naloxone at doses of 16 and 32 mg. The four tests were performed in double-blind conditions and in random sequences. Transit time (mean, SD) after loperamide (128.8 min, 32.9) was significantly increased (P less than 0.05) compared with placebo (85.5 min, 35.7), loperamide followed by naloxone 16 mg (88.8 min, 46.2), and loperamide followed by naloxone 32 mg (84.4 min, 40.6). These results show that the peripheral opioid agonist loperamide delays orocecal transit in healthy subjects and that naloxone per os at adequate doses antagonizes this effect.