Abstract: Background: The relative potency of prokinetics in patients with gastroparesis has not been systematically studied. This study, therefore, aimed to assess the available data and to

Abstract: Acute pancreatitis is an inflammatory disease, which varies in severity from mild to severe. Factors determining the severity of pancreatitis are not known. It is generally believed that the earliest events in the evolution of acute pancreatitis lead to premature intra-acinar cell activation of digestive zymogens and that those enzymes, once activated cause acinar cell injury. Recent studies have suggested that the ultimate severity of resulting pancreatitis may be determined by events which occur subsequent to acinar cell injury. These include inflammatory cell recruitment and activation as well as the generation and release of cytokines and other chemical mediators of inflammation. Recently, we have undertaken studies to elucidate the role of various inflammatory agents in determining the severity of pancreatitis. Results from these ongoing studies indicate that substance P acting via neurokinin-1 (NK1) receptors, chemokines interacting with CCR1 receptors and platelet activating factor play an important pro-inflammatory role in regulating the severity of pancreatitis and associated lung injury. On the other hand, complement factor 5a (C5a) acts as an anti-inflammatory agent during the development of pancreatitis.

Abstract: Clostridium difficile is the most common nosocomial pathogen of the gastrointestinal tract and has increased in frequency over time. Typical symptoms of C. difficile infection include diarrhea, which is usually nonbloody, or colitis associated with severe abdominal pain, fever and/or gross or occult blood in the stools. Pseudomembranous colitis (PMC), the severest form of this disease, occurs as a result of a severe inflammatory response to the C. difficile toxins. This review focuses on PMC, as this severe form is associated with the greatest medical concern. Diagnosis rests on detection of C. difficile in the stool, either by culture, tissue culture assay for cytotoxin B or detection of antigens in the stool by rapid enzyme immunoassays. Oral therapy with metronidazole 250 mg 4 times a day for 10 days is the recommended first-line therapy. Vancomycin is also effective, but its use must be limited to decrease the development of vancomycin-resistant organisms such as enterococci. Vancomycin (125-500 mg 4 times a day for 10 days) should be limited to those who cannot tolerate or have not responded to metronidazole, or when metronidazole use is contraindicated, as in the first trimester of pregnancy. A therapeutic response within a few days is usual. Recurrence of symptoms after antibiotics occurs in 20% of cases and is associated with persistence of C. difficile in the stools. Further recurrences then become more likely. Therapy with antibiotics in a pulsed or tapered regimen is often effective as are efforts to normalize the fecal flora. The yeast Saccharomyces boulardii has been proven in controlled trials to reduce recurrences when given as an adjunct to antibiotic therapy. Careful hand washing and environmental decontamination are necessary to prevent epidemics.

Abstract: The objective of this study is to validate the Spanish translation of the Inflammatory Bowel Disease Questionnaire (SIBDQ) on ulcerative colitis and Crohn's disease by assessing its convergence validity, discriminatory power, reliability and sensitivity to change. For that purpose, 211 patients with inflammatory bowel disease (116 with ulcerative colitis and 95 with Crohn's disease) completed the SIBDQ, the Psychological General Well-Being Index and the EuroQol. SIBDQ was repeated in those patients who remained in stable remission and in those with changes in clinical activity. Clinical activity was assessed by the Rachmilewitz and Harvey-Bradshaw indices. Correlations among scores of SIBDQ, EuroQol, Psychological General Well-Being Index and clinical indices of activity were all positive and comparable for both diseases (r = -0. 50 to r = -0.70, p < 0.01). Analysis of variance showed that SIBDQ discriminates between different clinical degrees of activity. Cronbach's alpha was 0.96 in ulcerative colitis and Crohn's disease. SIBDQ was also highly reliable when it was repeated in clinically stable patients with ulcerative colitis (intraclass correlation coefficient = 0.82) and Crohn's disease (intraclass correlation coefficient = 0.86). SIBDQ was sensitive to clinical changes in ulcerative colitis and in Crohn's disease, whether patients entered remission (effect size -1.88 and -1.81, respectively) or relapsed (effect size 1.70 and 8.04, respectively). In conclusion, the Spanish version of the IBDQ has proven to be a valid, reliable and sensitive instrument to detect clinical changes in patients with ulcerative colitis and Crohn's disease.

Abstract: Aims: Previous studies have found a positive association between Helicobacter pylori infection and colorectal adenomas. The aim of the present study was to examin

Abstract: Background/Aim: Mutations of the adenomatous polyposis coli (APC) tumor suppressor gene have been described in a subset of pancreatic carcinomas. The APC gene modulates the β-cateni

Abstract: Regardless of whether the initiating event is alcohol, gallstones or some other less common cause, acute pancreatitis progresses in a predictable manner eventually leading to failure of multiple unrelated organs. Very quickly following the inciting event, a local inflammatory process is initiated which results in the local production of inflammatory mediators. Virtually all patients with acute pancreatitis will experience some symptoms related to this local inflammation, with some resolving completely at this point. Most patients will go on to develop a systemic hyperinflammatory state expressed as the development of fever, tachycardia, tachypnea, and mild acid-base disturbances. Although this systemic hyperinflammatory state is usually mild, occasionally it may be very severe resulting in overt distant organ failure. With a more thorough understanding of the inflammatory mediators responsible for this hyperinflammatory state, many new therapeutic approaches are on the horizon.

Abstract: Acute pancreatitis may follow a mild or a severe course. Whereas mild or edematous pancreatitis is a self-limiting disease with a low complication rate and low death rate, morbidity and mortality in s

Abstract: Background: Chronic constipation is a frequent symptom among the general population, and a minority of cases do not respond to any therapeutic measures, except surgery. The purpose

Abstract: Twenty-two healthy teetotal volunteers underwent gastroscopy during which biopsy samples from the antrum and body were taken for chemiluminescence assay, routine histology, and for malonyldialdehyde, xanthine oxidase and glutathione determination. Subjects were divided into 2 groups which, in a double-blind fashion, were randomly and orally given either (a) Bionormalizer 9 g at bedtime and 3 h prior examination, or (b) flavored sugar 9 g as placebo. During the second gastroscopy 40 ml of 80% ethanol were sprayed perendoscopically. Gastroscopy with biopsy was repeated 60 min later. As compared to the placebo group, subjects given Bionormalizer showed significantly reduced gastric mucosal damage at endoscopy and the histological level. When considering the placebo group, ethanol administration brought about a significant increase in the luminol-amplified chemiluminescence response in gastric mucosa as compared to the baseline value which was correlated with the histological score. The mean chemiluminescence value in the Bionormalizer group was significantly lower than in the placebo group. Ethanol ingestion brought about a significant increase in xanthine oxidase and malonyldialdehyde together with a decreased glutathione concentration. Bionormalizer significantly prevented such changes. The present data suggest that the natural antioxidant Bionormalizer when given orally promotes an effective protection against ethanol-induced gastric mucosal damage.

Abstract: Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive loss of motor neurons However, ALS has been recognized to also involve non-motor systems Subclinical involvement of the autonomic system in ALS has been described The recently developed (13)C-octanoic acid breath test allows the noninvasive measurement of gastric emptying With this new technique we investigated 18 patients with ALS and 14 healthy volunteers None of the patients had diabetes mellitus or other disorders known to cause autonomic dysfunction The participants received a solid standard test meal labeled with (13)C-octanoic acid Breath samples were taken at 15-min intervals for 5 h and were analyzed for (13)CO(2) by isotope selective nondispersive infrared spectrometry Gastric emptying peak time (t(peak)) and emptying half time (t(1/2)) were determined All healthy volunteers displayed normal gastric emptying with a mean emptying t(1/2) of 138 +/- 34 (range 68-172) min Gastric emptying was delayed (t(1/2) > 160 min) in 15 of 18 patients with ALS Emptying t(1/2) in ALS patients was 218 +/- 48 (range 126-278) min (p < 0001) These results are compatible with autonomic involvement in patients with ALS, causing delayed gastric emptying of solids and encouraging the theory that ALS is a multisystem disease rather than a disease of the motor neurons only

Abstract: Background: The pathophysiology of pancreatitis and the pancreatic stress response are not well understood. In the pancreas, mitogen-activated protein kinase (MAPK) and stress-activated protein kinase (SAPK) are reportedly regulated by secretagogue stimulation and hyperstimulation. However, no data exist on the expression and regulation of pancreatic p38 Map kinase. Aims: Pancreatic expression of p38 Map kinase and MAPK, SAPK and p38 regulation during pancreatic stress were investigated. Methods: For hyperstimulation and secretory stress, cerulein was given intravenously, while hyperthermia preconditioning stress was induced by whole body hyperthermia (42°C). Results: In addition to MAPK and SAPK, p38 Map kinase was found to be expressed in the rat pancreas. Cerulein regulated all kinases time- and dose-dependently. MAPK and p38 Map kinase showed basal activity and were further activated at low cerulein doses. SAPK had no basal activity and its activation required maximal secretory to supramaximal amounts of cerulein. Cerulein hyperstimulation, inducing pancreatitis, activated p38 more rapidly than SAPK and more strongly than MAPK. In contrast to cerulein hyperstimulation stress, hyperthermia stress only activated p38 Map kinase. Conclusions: p38 Map kinase is expressed in the pancreas and is most rapidly activated following cerulein hyperstimulation. Both SAPK and p38 Map kinase are possibly important regulators during the onset of cerulein pancreatitis.

Abstract: It has been speculated that impaired salivary flow contributes to abnormal acid clearance of the esophagus in gastroesophageal reflux and results in reflux esophagitis (RE). To test this hypothesis, salivary functions were measured by quantitative salivary scintigraphies in patients with RE and in age- and sex-matched controls for comparison. Nineteen patients with RE and 36 healthy volunteers were enrolled in the study. After an intravenous injection of 5 mCi Tc-99m pertechnetate, sequential images of 1 min/frame were acquired for 30 min. The 1- and 15-min uptake ratios (UR) of the tracer in the four major salivary glands over the backgrounds were calculated. Saliva excretion was stimulated by 1 tablet of 200 mg ascorbic acid given orally 15 min after injection of the tracer, then the maximal excretion ratios (ER) of the four major salivary glands were calculated for the sialagogue stimulation. RE patients had lower values of 1st and 15th min UR and maximal ER than controls in the 4 major salivary glands. Poor salivary functions which represented a decrease in both UR and ER for patients with RE have been confirmed by quantitative salivary scintigraphy in this study.

Abstract: Somatostatin, a naturally occurring peptide, displays a wide range of biological actions, mainly inhibitory ones, that can make it an appropriate drug for the treatment of a variety of digestive diseases. The marked effect of the peptide on splanchnic hemodynamics together with its inhibitory action on acid-peptic and pancreatic exocrine secretions represent the rationale for the use in upper gastrointestinal (GI) bleeding and surgical conditions of the pancreas. Besides the hemodynamic effects, other pharmacological actions of somatostatin may contribute to its therapeutic efficacy in active variceal bleeding. The peptide indeed increases lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood into the submucous venous plexus of the esophagus and hence into the esophageal varices. Through its inhibitory action on acid-peptic secretion, somatostatin may also inhibit peptic digestion of the clot at the site of hemostasis on the varix itself. In addition, the natural peptide was shown to enhance human platelet aggregation in vitro, whose stimulation can activate the hemostatic process. Since its short half-life makes continuous intravenous infusion mandatory, several long-acting analogs have been synthesized. Amongst the hundreds of cyclic peptides synthesised, octreotide (which binds mainly to SSTR-2 and SSTR-5 receptor subtypes) has been the most extensively investigated. A thorough analysis of the pharmacological activities and therapeutic efficacy of the native somatostatin and the synthetic analogs reveals that the biological actions of these peptides are not always identical. These differences appear to be related to the different affinities of the natural hormone and synthetic derivatives for the different receptor subtypes. The fading of the pharmacological effect, which has yet been observed only with analogs, has never been reported with the natural peptide and may be due to down-regulation of specific receptor subtypes. The safety profile of both natural somatostatin and synthetic analogs is today well established. Most adverse reactions to these peptides are merely a consequence of their pharmacological activity and consist mainly of gastrointestinal complaints and effects on glucose metabolism. They are often of little clinical relevance, especially in the short term. Native somatostatin and its synthetic analogs are therefore safe and effective drugs for the treatment of a variety of GI disorders. While the native peptide is the drug of choice in the acute hospital setting, the synthetic derivatives are better indicated, on outpatient basis, for the long-term management of chronic conditions.

Abstract: Background/Aim: Several diagnostic tests are available for evaluating Helicobacter pylori (Hp) infection: histological examination, culture of gastric biopsy spec

Abstract: Intestinal fistulae usually arise as a complication of abdominal surgery. Its treatment is complex and intestinal fistula-related morbidity and mortality is high. Fistula closure rates under conservative medical treatment vary between 24 and 72%. Octreotide and somatostatin reduce gastrointestinal, biliary and pancreatic secretion and increase intestinal water and electrolyte absorption. In recent years, octreotide and somatostatin have been associated with conservative medical treatment for patients with intestinal fistulae. Four placebo-controlled studies have been published within the past 6 years. The interpretation of their results is difficult because patient collectives were small and heterogeneous. In one study, somatostatin decreased fistula-related complications when compared to placebo, and in another study, octreotide decreased the healing time of intestinal fistulae and the time patients required total parenteral nutrition when compared to placebo. In contrast, the fistula closure rate, hospitalization time and mortality were not influenced by the use of octreotide or somatostatin in conservative medical treatment. In conclusion, octreotide and somatostatin actually cannot be recommended in the treatment of intestinal fistulae in settings outside of controlled trials.

Abstract: The distribution of tryptophan hydroxylase, the rate-limiting enzyme in the biosynthesis of serotonin, was investigated immunohistochemically in various organs of the gastrointestinal tract and compared with that of neuroendocrine markers. While immunoreactivity for serotonin and chromogranin A was restricted to enterochromaffin cells, positive staining for tryptophan hydroxylase was detected in normal enterocytes lining the epithelium of the small intestine. Tryptophan hydroxylase was localized in the supranuclear cytoplasm of absorptive cells, and was absent from the terminal web. The enterocytes of the exfoliation zone at the tips of the villi demonstrated a strong immunoreactivity similar to those at the slope of the villi. Mucus-containing Goblet cells, Paneth cells and stromal cells of the lamina propria remained unlabelled. The duodenal glands of Brunner revealed only sporadically a weak immunostaining for tryptophan hydroxylase. The monooxygenase was also detected in numerous secretory tubules of the pyloric mucosa, where the proportion of positive cells decreased progressively from the crypts towards the upper parts of the gastric glands. No significant immunoreactivity was demonstrated in colon, adrenal cortex, liver, pancreas, and mesenteric lymph nodes. The demonstration of tryptophan hydroxylase in normal enterocytes suggested that epithelial cells of the small intestine are able to synthesize 5-hydroxytryptophan.

Abstract: Background/Aims: It has been suggested that the distal portion of the dorsal pancreatic duct and the ventral pancreatic duct usually merge into the main pancreatic duct, and the pro

Abstract: Background: The rationale for medical therapy of initial achalasia and the results obtained over the last 20 years in our laboratory are presented. Methods: Achal

Abstract: Aim: To assess whether patients with misdiagnoses of chronic pancreatitis (CP), followed at an early stage by a diagnosis of pancreatic cancer (PCr), present different epidemiologic

Abstract: Helicobacter pylori colonises the gastric mucosa, but can also be found within the oral cavity. The presence of H. pylori was monitored in the oral cavity of 22 patients with duodenal ulcer, before and after antibiotic treatment and of 24 hospital employees who were or were not professionally exposed to H. pylori. Gastric infection was determined by breath test. Bacteria in the oral cavity were detected by nested PCR of samples containing saliva and dental plaque, using primers specific for 16S rRNA and ureC genes. Before treatment, 9 out of 22 infected ulcer patients harbored H. pylori in their oral cavity. Bacteria disappeared from the oral cavity of 3 of 7 cured patients. Twelve of 17 exposed subjects harbored H. pylori in their oral cavity, while no bacteria could be detected in the mouths of the 7 nonexposed subjects. Presence of bacteria in the oral cavity reflects handling of contaminants; it does not correlate with gastric infection and does not seem to promote it.

Abstract: The aim of the present work was to examine in pigs the effect of a dietary supplementation with the flavor enhancer monosodium glutamate (MSG) on intestinal amino acid metabolism. For this purpose, pi

Abstract: Hospitalization for nonvariceal upper gastrointestinal hemorrhage (UGIH) is still common with an incidence of 100/100,000 adults/year. Mortality rates range between 8 and 14%. The most common etiologi

Abstract: Background/Aims: Primary hepatic neuroendocrine tumor represents an extremely rare clinical entity with only very few cases having been reported to date. Methods:

Abstract: Immunocytochemical studies demonstrate that S-14 is

Abstract: Nine hundred and seven polyps (mean size 3.7 mm; range 2–8) from 460 patients (mean age 67 years; range 34–94) were removed with monopolar electrocoagulation forceps (‘hot biopsy forceps’). Sixty-thre

Abstract: Epidermal growth factor (EGF) exhibits gastroprotective and ulcer-healing action. These observations prompted us to determine the influence of EGF on cerulein-induced pancreatitis (CIP) in the rat. Ac

Abstract: Background/Aims: Matrix metalloproteinases (MMPs) are endopeptidases that degrade extracellular matrix and are involved in the pathogenesis of gastrointestinal ulcer and cancer along with tissue inhibitors of metalloproteinases (TIMPs). The purpose of this study is to examine their localization and functions in the normal stomach. Methods: We examined the localization of MMP-1, MMP-2, MMP-9 and TIMP-2 in normal human and rabbit stomachs by light- and electron-microscopic immunohistochemistry and Western blotting, and the enzymatic activities of MMP-2 and MMP-9 by gelatin zymography. Results: Immunohistochemistry revealed their localization in parietal cells, and surface and foveolar epithelial cells. Electron-microscopic immunohistochemistry of parietal cells showed immunolabeling of MMP-2 and TIMP-2 in the cisternae of the rough endoplasmic reticulum, and that of MMP-1 and MMP-9 in tubular structures in their cytoplasm. Western blotting revealed that the densities of MMP-2 and MMP-9 bands were higher for the fundic gland region than for the pyloric gland region. Gelatin zymography revealed that tissue extracts of the fundic gland region exhibited higher enzymatic activity of MMP-2 and MMP-9 than those of the pyloric gland region. Conclusion: Normal rabbit and human stomachs contain MMP-1, MMP-2, MMP-9, and TIMP-2 and these are mainly localized in, and synthesized by parietal cells.

Abstract: Expressions of the cholecystokinin (CCK)-A and -B receptor genes in human duodenum, pancreas and gallbladder were examined by Northern blot analysis and reverse transcriptase polymerase chain reaction (RT-PCR) followed by Southern blot hybridization. The autoradiographic study of CCK-A and -B receptors in the human duodenum and pancreas was examined in vitro. To determine the subtypes to CCK receptors in the pancreas or duodenum, we studied the abilities of CCK-A and -B receptor agonists (CCK-8 and gastrin) and antagonists (loxiglumide, L-364,718 and L-365,260) to inhibit binding of 125I-CCK-8. CCK-A receptor mRNA was not expressed in the human pancreas, but was expressed in the gallbladder and duodenum, although it was expressed in the pancreas by RT-PCR. CCK-B receptor mRNA was expressed in the pancreas, but not in gallbladder and duodenum. Using autoradiography, high concentrations of CCK-A receptors were detected in the duodenal mucosa, although in the pancreas only CCK-B receptors were detected by this method. These results suggest that localization of CCK-A receptor in human duodenum provides a biochemical and morphological basis for some physiological functions of CCK.