Intact Stomach Research Articles

Esophageal cancer in patients with a history of distal gastrectomy.

There is an association between a history of distal gastrectomy and the development of esophageal cancer. Surgical treatment of esophageal cancer in patients with a history of gastrectomy is more complicated but will not result in increased mortality in an experienced center. Case-control study. Tertiary care center for the treatment of esophageal cancer. Forty patients with a history of gastrectomy and 1266 patients with intact stomachs who underwent esophagectomy for cancer. Patients' demographic characteristics, tumor characteristics, operative morbidity, mortality, and long-term survival. There were more squamous tumors located in the lower third of the esophagus in those who had a history of gastrectomy compared with those with intact stomachs (16 [41%] of 40 patients vs 318 [25%] of 1266 patients; P=.04). This difference was more pronounced after Billroth I vs Billroth II gastrectomy (8 [73%] of 11 patients vs 8 [29%] of 28 patients; P=.03). Twenty-four patients (60%) in the gastrectomy group and 738 (58%) in the nongastrectomy group underwent surgical resection (P=.87). The operative time (300 [160-465] vs 220 [90-520] minutes; P<.001) was longer and more blood loss (1000 [300-2500] vs 700 [150-7000] mL;P<.001) was encountered for esophagectomy after previous gastrectomy (data are given as median [range]). A colon interposition was the substitute conduit of choice in the gastrectomy group (20 [83%] of 24 patients), and the stomach was the preferred loop in those with intact stomachs (729 [99%] of 738 patients). Postoperative complication rates were similar. In-hospital mortality rates also did not differ for those with a history of gastrectomy vs those without such a history (12% for both,P>.99). Median survival after resection was 13.8 and 12.5 months for patients who did and did not undergo prior gastrectomy, respectively (P=.62). A history of gastrectomy (especially the Billroth I type) is associated with more lower-third squamous cell esophageal carcinomas. Surgical resections in patients with such a history were more complicated but resulted in similar outcomes.

Endogenous cyclo-oxygenase activity regulates mouse gastric surface pH.

In the stomach, production of prostaglandins by cyclo-oxygenase (COX) is believed to be important in mucosal defence. We tested the hypothesis that endogenous COX activity is required for protective gastric surface pH control. Intact stomachs of anaesthetized mice were perfused with a weakly buffered solution (150 mM NaCl + 4 mM Homopipes) at pH values from 2.5 to 7.0. Gastric effluents were collected to measure pH and estimate amounts of acid or alkali secretion in nanomoles secreted per minute. A switch from net acid to net alkali secretion was seen in response to acidifying luminal pH with an apparent 'set point' between pH 4 and 5. At luminal pH 3, the net alkali secretion (12.7 +/- 2.8 nmol OH(-) equivalents min(-1)) was abolished (2.2 +/- 1.7 nmol OH(-) min(-1)) by the non-specific COX inhibitor indomethacin (5 mg kg(-1) I.P.). Similar inhibition was observed using a COX-1 inhibitor (SC-560; 10 mg kg(-1) I.P.), but not a COX-2 inhibitor (NS-398; 10 mg kg(-1) I.P.). Subsequent treatment with 16,16-dimethyl prostaglandin E(2) (dm-PGE(2); 1 mg kg(-1) I.P.) rescued the alkali secretion (21.8 +/- 2.7 nmol OH(-) min(-1)). In either the absence or presence of the H(+),K(+)-ATPase inhibitor omeprazole (60 mg kg(-1) I.P.), indomethacin blocked similar amounts of net alkali secretion (10.5 +/- 2.7 and 16.4 +/- 3.4 nmol OH(-) min(-1), respectively). We also used in vivo confocal microscopy to examine pH near the mucosal surface. The gastric mucosal surface of anaesthetized mice was exposed and mucosal surface pH was imaged using the fluorescence intensity ratio of Cl-NERF as a pH indicator. Results showed a switch from a continuous net acid to net alkali secretion by the stomach in response to changing superfusate pH from 5 to 3. At luminal pH 3, the relatively alkaline surface pH (4.3 +/- 0.1) was acidified (3.6 +/- 0.2) by indomethacin, and subsequent dm-PGE(2) restored surface pH (4.2 +/- 0.2). We conclude that the pre-epithelial alkaline layer is regulated by endogenous COX activity.

Intraduodenal capsaicin inhibits gastric migrating motor complex via an extrinsic neural reflex in conscious dogs.

The aim was to study the effect of intraduodenal capsaicin on interdigestive gastric contractions. Mongrel dogs were equipped with strain-gauge force transducers to measure gastroduodenal motility. The effects of intraduodenal capsaicin with or without pharmacological antagonists on spontaneous and motilin-induced interdigestive gastric contractions and on plasma motilin were studied in dogs with intact stomachs. The effect of intraduodenal capsaicin on gastric contractions was also studied in vagally denervated gastric (Heidenhain) pouch and vagally innervated antral pouch. Intraduodenal capsaicin inhibited spontaneous and motilin-induced gastric contractions. The spontaneous peak in plasma motilin was inhibited by intraduodenal capsaicin. The effect of intraduodenal capsaicin on motilin-induced gastric contractions was not affected by blockade of nitric oxide synthase, or by beta-adrenoceptor antagonist. Administration of alpha-adrenergic blocker inhibited basal interdigestive gastric motility. Intraduodenal capsaicin had no effect on contractions in the Heidenhain pouch but inhibited those in vagally innervated antral pouch. Duodenal afferent fibres stimulated by capsaicin inhibit gastric contractions via a nitric oxide-independent extrinsic neural reflex.

5-Fluorouracil-induced colitis--a review based upon consideration of 6 cases

At increasing use of high-dose 5-fluorouracil-based chemotherapy for metastatic colorectal and gastric cancer complicated drug-induced colitis is observed more frequently. From May 1998 to November 2000 we observed 6 cases of 5-fluorouracil-induced colitis, in which we looked for involvement of small intestine. We report summing up on the 6 cases including both endoscopic and histological findings in both sites of the gut. In 2 men and 4 women (age 49-78 years) with advanced colon (n = 2), gastric (n = 3 ) and gallbladder (n = 1) cancer a palliative weekly high-dose infusional 5-fluorouracil (2,6 g/m(2)/24 h) and folinic acid (500 mg/m(2)/2 h) chemotherapy was performed. Few days after 1-5 chemotherapy courses the patients were admitted to our hospital with abdominal pain and partly severe watery diarrhea (up to 20 times evacuations/per day). The stool cultures were negative and there were no proof both of clostridium difficile and his toxin A and B. In 4 patients colonoscopy showed different grades of colitis up to diffuse erythema and microlesions, 2 patients had no visible lesions. In 4 patients endoscopy of the upper GI-tract showed a severe inflammation (n = 1) and a fibrinopurulent exsudate, severe edema and isolated ulcerations (n = 3) of jejunum after gastrectomy or duodenum with intact stomach. In the histological assessment different grades of 5-FU-induced colitis without (n = 2) or with (n = 4) involvement of the upper small intestine destruction of the superficial mucosa and crypts (epitheliumapoptosis) were found. 5 patients were treated by antibiotics (vancomycin n = 2, metronidazole n = 3), glucocorticoids (n = 5) and Saccaromyces cerevisiae (n = 3). After 8-10 days the patients were complete free of symptoms. One patient died due to the enterocolitis. The present cases demonstrate that high-dose 5-fluorouracil-based chemotherapy not only induces a colitis but also may involve the upper small intestine tract. Consequently, it represents an increasing and serious adverse event of high-dose chemotherapy. The etiology of the enterocolitis (drug- or bacterial-induced) needs further investigations in order to find a causal therapy and/or prophylaxis.

Effect of glucagon, GLP-1, GLP-2 and glicentin on interdigestive gastroduodesal motility in dogs with extrinsically denervated gastric pouches

Aims of the present study were to study the effect of equal molar doses of glucagon, glucagonlike peptide (GLP)-I, -2, and glicentin on gastroduodenal contractile activity, and the role of extrinsic nerves, nitric oxide (NO), and adrenoceptors in the inhibitory effect of these peptides. METHODS: Five mongrel dogs equipped with 4 strain gauge force transducers on the extrinsically denervated gastric pouch, gastric body, gastric antrum, and duodenum were used. We studied the effect of glucagon, GLP-1, -2, and glicentin at 0.01,0.1, and 1 nmol/kg on motilitn (0.4/~/kg-h)-induced interdigestive phase Ill contractions as well as the effect of L-NAME (a NO synthesis inhibitor; 10 mg/kg) and phentolamine + propranolol (adrenergic blockers; 0.5 + 0.5 mg/kg) on motor inhibition induced by the peptides. RESULTS: Glucagon at 1 nmol/kg inhibited contractions in the pouch, body, and antrum, but did not affect duodenal motility. GLP-1 at 0.1 nmol/kg inhibited contractions in the body and antrum, and contractile activity at all sites was suppressed by GLP-1 at 1 nmol/kg. GLP-2 at 1 nmol/kg inhibited contractions in the pouch but had no effect on the body, antrum and duodenum. Glicentin did not affect motility at any site. Pretreatment with L-NAME and phentolamine + propranolol abolished the inhibitory effect of glucagon, GLP-1, and GLP-2 on contractions in the pouch, but did alter the inhibitory effect of glucagon and GLP-1 on gastric body, antrum, and duodenum. SUMMARY: Inhibitory effects of glucagon, GLP-1, and GLP-2 on contra~ons in the extrinsically denervated gastric pouch was mediated via NO and adrenoceptors, which were not involved in inhibitory effect of glucagon and GLP-1 on neurally intact gastroduodenum. CONCLUSIONS: Glucagon, GLP-1 and 2 can exert their inhibitory effects on contractile activity even in extrinsically denrevated stomach. Certain changes in innervation of enteric nervous system after chronic surgical extrinsic denervation must lead to involvement of pathways in the stomach different from those in the neurally intact stomach.

Gastric corpus mucin expression after partial gastrectomy, in relation to colonization with Helicobacter pylori.

Twelve different genes for mucin have been described. MUC5AC and MUC6 encode the secreted apomucins of the stomach. A gradient from the surface epithelium (foveola) to the glands is typical for MUC5AC synthesis, whereas a gradient in the opposite direction was found for MUC6. Our goal was to determine the distribution of MUC5AC and MUC6 in the postoperative stomach, with relation to the H. pylori status. Gastric corpus biopsy specimens from patients who underwent partial gastrectomy were examined by immunohistochemistry for mucin gene (MUC5AC and MUC6) apoproteins. We used polyclonal antibodies for amino acid tandem repeats of both proteins. A scoring system (0-3) was used to assess staining intensity at four sites: the lumen, the foveola, the mucous neck cells, and the glands. Helicobacter pylori status was determined by histology and rapid urease test and was considered positive or negative when both tests were positive or negative, respectively. We studied 19 H. pylori-positive and 32 H. pylori-negative patients. No significant change in MUC5AC or MUC6 synthesis and secretion was demonstrated between H. pylori-positive or -negative patients. A gradient similar to that shown for the intact stomach (from the surface epithelium to the glands) for MUC5AC protein and an increase of MUC6 protein presentation from the mucous neck cell to the glands were demonstrated. The pattern of MUC5AC protein synthesis was not different between H. pylori-positive and -negative patients in the postoperative stomach. MUC6 expression was higher in the foveola in H. pylori-positive patients, whereas there was no difference in the other cell layers.

Effect of Glucagon, Glicentin, Glucagon-like Peptide-1 and-2 on Interdigestive Gastroduodenal Motility in Dogs with a Vagally Denervated Gastric Pouch

Background: We previously reported that inhibition of gastric motility and hypertrophy of the small intestinal mucosa were observed after ileo-jejunal transposition which induced hypersecretion of enteroglucagon. Our aim was to study the effect of four enteroglucagon-related peptides (glucagon, glucagon-like peptide (GLP)-1, -2 and glicentin) on gastroduodenal motility and their mechanisms of action. Methods: The effect of these four peptides on motilin-induced interdigestive contractions was studied in dogs with vagally denervated gastric pouches equipped with four strain gauge force transducers on the pouch, gastric body, antrum and duodenum. Whether or not nitric oxide synthase inhibitor or phentolamine and propranolol reverses the inhibitory effect of those peptides was also studied. Results: Glucagon inhibited contractions in the pouch and stomach but had no effect on duodenal contractility. GLP-1 inhibited contractions at all sites. GLP-2 inhibited contractions in the pouch but did not affect motility in the neurally intact gastroduodenum. Glicentin had no effect on contractions at any site. Pretreatment with either a nitric oxide synthase inhibitor or phentolamine and propranolol reversed the inhibitory effect of glucagon, GLP-1 and GLP-2 on contractions in the pouch, but did not alter the inhibitory effect of glucagon and GLP-1 on motility in the neurally intact stomach and duodenum. Conclusions: These results suggest that the effects of four peptides on gastroduodenal motility differ, and changes occur in the enteric neural modulation of motor activity after chronic surgical extrinsic denervation.

Carcinogenic potential of duodenal reflux juice from patients with long-standing postgastrectomy.

To determine whether study on the carcinogenic potential of reflux juice from patients with remote gastrectomy could clarify the inherent relationship between duodenal reflux and gastric stump cancer. A total of 37 reflux juice samples (13 Billroth I, 24 Billroth II) were employed in the present study. A two-stage transformation assay using BALB/c 3T3 cells was carried out to test the initiating or promoting activity of these samples. Two of 18 (11.1%) reflux samples exerted initiating activities, whereas 9/19 (47.4%) samples enhanced the MNNG-initiating cell transformation, suggesting the duodenal reflux juice might more frequently possess the tumor-promoter activity (P = 0.029). In addition, there was no difference in initiating activities of the samples irrespective of surgical procedures (P = 0.488), while Billroth II samples exhibited stronger tumor-promoter activity than Billroth I samples (P = 0.027). Furthermore, the promoter activities were well correlated with the histological changes of the stomas (r(s) = 0.625, P = 0.004), but neither their cytotoxicities nor initiating activities had this correlation (Probabilities were 0.523 and 0.085, respectively). The duodenal reflux juice from patients with remote postgastrectomy did have carcinogenic potential, and suggested that tumor-promoting activity should principally account for the high incidence of gastric cancer in gastrectomy patients. In contrast, it is difficult to explain the high stump-cancer incidence with the N-nitroso compounds theory-a popular theory for the intact stomach carcinogenesis, and it seemed to be justified to focus chemo-prevention of this cancer on the tumor-promoting potential of reflux juice.

Cell proliferation in type C gastritis affecting the intact stomach

Aims—Type C gastritis caused by bile reflux has a characteristic appearance, similar to that seen in other forms of chemical gastritis, such as those associated with NSAIDs or alcohol. An...

3499 Therapeutic ercp in the setting of long limb surgical bypass: improved success and outcome of therapeutic procedures.

INTRODUCTION: We reported initial ERCP experience in 18 long-limb surgical bypasses (Gastrointest Endosc 1998;47: 62-7). Only 6 had intact papillas and only 3 required sphincterotomy (ES). We report additional experience. PATIENTS & METHODS: From 4/93-8/99, 47 pts (male 18, female 29, age 24-80) were referred for consideration of therapeutic ERCP with long-limb surgical bypasses: 8 with gastric bypass; 16 with Whipple's, 11 with hepatojejunostomy; and 12 with post-gastrectomy Roux-en-Ys. Indications: pain (n=26), jaundice (n=17), recurrent or chronic pancreatitis (n=11), suspected CD stones (n=7), and anastomotic bleeding (n=1). An enteroscope was used in 13, a pediatric colonoscope in 17 and a duodenoscope in 17. RESULTS: The papilla or pancreaticobiliary anastomosis was reached in 41 of 47 (87%). The overtube was used with 5 and only in the setting of an intact stomach. 6 failures were due to inability to pass into the afferent limb. 2 failures were due to inability to locate the PD anastomoses. 20 patients had intact papillas (12 with Roux-en-Ys, 8 with gastric bypass). Cannulation failed in 4 of these 20 (20%) due to an inability to align the long front viewing instruments. 7 pts with intact papillas needed ES; 3 methods were used: (1) Following guidewire and temporary stent placement, a stent guided needle-knife ES was used when alignment could be achieved (n=4); (2) A wire-guided B-II type sphinctertome was used (n=1). (3) One patient failing guidewire placement underwent successful needle knife ES only. The final patient required a combined procedure with PTC guidewire placement followed by B-II type ES at a second ERCP. Among the 35 cannulated patients, successful Rx followed in 34: stents in 16 (10 biliary plastic stents, 2 PD stents, 4 Wallstents); biliary dilatation in 6; stone extraction 3; tissue sampling 3; pancreatic dilatation 1; duodenal dilatation 1. In 1 patient, coagulation of a visible vessel required surgical treatment for recurrence. No post-ERCP pancreatitis, bleeding, or perforation was noted. CONCLUSION: Although technically difficult, successful therapeutic ERCP is generally possible with long limb surgical bypasses with a high success rate and a low complication rate. The intact papilla greatly exacerbates these difficulties and occasionally requires percutaneous wire placement for assistance. The development of a colonoscope length, oblique-viewing enteroscope with an elevator should greatly enhance therapeutic ERCP in these patients.

Interstitial Cells of Cajal Mediate Cholinergic Neurotransmission from Enteric Motor Neurons

Interstitial cells of Cajal (ICC) are interposed between enteric neurons and smooth muscle cells in gastrointestinal muscles. The role of intramuscular ICC (IC-IM) in mediating enteric excitatory neural inputs was studied using gastric fundus muscles of wild-type animals and W/W(v) mutant mice, which lack IC-IM. Excitatory motor neurons, labeled with antibodies to vesicular acetylcholine transporter or substance-P, were closely associated with IC-IM. Immunocytochemistry showed close contacts between enteric neurons and IC-IM. IC-IM also formed gap junctions with smooth muscle cells. Electrical field stimulation yielded fast excitatory junction potentials in the smooth muscle that were blocked by atropine. Neural responses were greatly reduced in muscles of W/W(v) animals. Loss of cholinergic responses in W/W(v) muscles seemed to be caused by the loss of close synaptic contacts between motor neurons and IC-IM, because these muscles were not less responsive to exogenous acetylcholine than were wild-type muscles. W/W(v) muscles also responded to excitatory nerve stimulation when the breakdown of acetylcholine was blocked by neostigmine. The density of cholinergic nerve bundles within the muscles was not significantly different in wild-type and W/W(v) muscles, and similar amounts of (14)[C]choline were released from preloaded wild-type and W/W(v) muscles in response to nerve stimulation. The impact of losing IC-IM on gastric compliance was also evaluated in intact stomachs. Pressure increased as a function of fluid volume and infusion rate in wild-type animals, but W/W(v) animals showed little basal tone and minimal increases in pressure with fluid infusions. These data suggest that IC-IM play a major role in receiving cholinergic excitatory inputs from the enteric nervous system in the murine fundus.

Investigation of Gastro-oesophageal Reflux in Patients with an Intact Stomach: Is Oesophageal Bilirubin Monitoring a Useful Addition to pH Monitoring?

Objectives: Ambulatory bilirubin monitoring has helped to establish the role of duodenal contents in gastro-oesophageal reflux disease. This study aims to define the clinical role of oesophageal bilirubin monitoring in reflux patients with an intact stomach. Methods: In total, 113 consecutive patients with reflux symptoms were prospectively studied using combined ambulatory oesophageal pH and bilirubin monitoring. Patients were categorized as follows: no pathological reflux, isolated acid reflux, isolated bilirubin reflux, combined acid and bilirubin reflux. Results: Thirty-eight patients (33%) had no pathological reflux, 49 patients (44%) had combined pathological acid and bilirubin reflux, and 17 patients (15%) had isolated pathological acid reflux. Only nine patients (8%) had isolated pathological bilirubin reflux. In these nine, the extent of pathological bilirubin reflux was small (median total bilirubin exposure time 12.2%, range 6.5%-20.7%) and mucosal damage was minimal (five had grade 1 oesophagitis, four had a normal oesophagus). In one patient, symptoms were temporally related to acid reflux, and in none were symptoms temporally related to bilirubin reflux. Conclusions: Isolated oesophageal bilirubin reflux in patients with an intact stomach is uncommon. In these patients mucosal injury is minimal, and reflux symptoms are not related to bilirubin reflux episodes. Further work is needed to define the role for oesophageal bilirubin monitoring in the investigation of reflux disease in patients with an intact stomach.

Intact smooth muscle metabolism: its responses to cyanide poisoning and pyruvate stimulation.

Smooth muscle mitochondria are unique in their compartmentalization of metabolism with the contractile proteins and putative role in cell fate choice. In this study we examine the relative and quantitative differences that smooth muscle mitochondria have with regard to cyanide inhibition. The effect of cyanide poisoning in the mitochondria of smooth muscle was examined in the intact porcine carotid artery and intact guinea pig stomach. The respiratory responses of these tissues were monitored in the presence of cyanide and following the addition of various metabolites. In HEPES buffer with 10 mM glucose as the substrate, it was found that the EC50 for cyanide inhibition was 0.11+/-0.02 and 0.14+/-0.02 mM in the pig carotid and guinea stomach respectively. We also found that the signaling metabolite, pyruvate could partially reverse this inhibition. With pyruvate (10 mM) as the substrate, the EC50 increased significantly to 6.52+/-0.11 (carotid artery) and 1.95+/-0. 30 (stomach) mM as well as being significantly different between the tissues. This apparent resistance to cyanide inhibition caused by pyruvate was lost when sodium bicarbonate buffer was used (EC50 in the presence of pyruvate of 0.13+/-0.04 and 0.25+/-0.04 for carotid and stomach respectively). HEPES buffer permitted pyruvate's protection from cyanide poisoning whereas bicarbonate buffer did not. The rate of respiration caused by pyruvate re-stimulation was not significantly different than control in the stomach (2.63+/-0.77 and 2.69+/-0.3??Mol O2/min/g dw respectively) but was significantly greater in the carotid artery. Therefore, smooth muscle with 10 mM pyruvate and 1 mM cyanide had a rate or respiration significantly greater than with 10 mM glucose alone (0.90+/-0.2 and 0.59+/-0. 06??Mol O2/min/g dw respectively). Using 31P NMR spectroscopy, we observed a complete normalisation of high energy phosphates and pH in the guinea pig stomach smooth muscle caused by pyruvate after cyanide poisoning. These results suggest that cyanide's toxicity of smooth muscle oxidative metabolism is affected by the buffer (HEPES versus Bicarbonate) and metabolic signalling molecules or substrates (pyruvate versus glucose) in which the tissues are exposed to as well as tissue to tissue variations.

Gastritis and gastropathy of childhood.

Gastritis and gastropathy of childhood.

Inter-relationship between Gasterophilus larvae and the horse’s gastric and duodenal wall with special reference to penetration

The degree of penetration into the stomach and duodenum of the horse by bot fly larvae, Gasterophilus intestinalis (De Geer) and G. nasalis (Linnaeus) (Diptera : Gasterophilidae) was evaluated. Evidence of larval perforation of the stomach or duodenum was not found on gross inspection. Palpation of the intact stomach and duodenum was not effective in establishing the existence of Gasterophilus larvae within the organs. Findings suggest that larvae of both species produce an ulcer of similar depth within the gastrointestinal wall. The ulcer depth produced by larvae did not correlate with the normal, unaffected thickness of the particular stomach or duodenum. Tissue proliferation beneath ulcers of the stomach and duodenum was not correlated with the depth of the ulcer. Proliferation of the tissue beneath the ulcers of the stomach generally exceeded that found under duodenal ulcers. Gastric wall beneath the G. intestinalis ulcer frequently attained a thickness equal to or greater than the normal stomach wall. Histopathological examinations below the ulcer revealed intense fibrosis. Duodenal thickness below the G. nasalis ulcer was typically less than normal and resulted in an attenuated wall. Histopathological analysis of the affected duodenum revealed severe loss of submucosal glands in a sharply demarcated area below and surrounding the lesion. Fibrosis of the underlying lamina propria mucosae and tunica submucosa was appreciable but failed to restore the original thickness of the duodenal wall. Host tissue response and moderation of the parasite’s behavior reduce the chances of direct perforation of the gastrointestinal tissue.

Gastric symptoms and duodenogastric reflux in patients referred for gastroesophageal reflux symptoms and endoscopic esophagitis

Background: The role of excessive duodenogastric reflux (DRG) in the genesis of gastric symptoms in patients primarily referred for both gastroesophageal reflux (GER) symptoms and esophagitis is poorly understood. Methods: The study is based on the clinical, endoscopic, histologic, and 24-hour gastric data from the Bilitec optoelectronic device (Prodotec, Florence, Italy, licensed by Synectics Medical, Stockholm, Sweden) from 49 patients having both typical GER symptoms and gastric symptoms suggestive of excessive DGR (ie, epigastric pain, nausea, or bilious vomiting) in the absence of previous esophageal or gastric surgery (group I). Helicobacter pylori organisms were searched for on antral biopsy specimens with use of the Giemsa method. The percentages of total, upright, and supine time during which absorbance exceeded various thresholds through all the working range of the Bilitec device were calculated. Bilitec data from group 1 were compared with those from 16 patients with endoscopic esophagitis and GER symptoms only (group 2) and 25 healthy subjects (group 3). Results: The prevalence of an abnormal Bilitec test result in group 1 increased from 27% (13/49) at the 0.25 absorbance threshold to 36% (18/49) at thresholds ranging from 0.40 to 0.60 and to 41% (20/49) when multiple thresholds ranging from 0.25 to 0.60 were considered. In group 2 one patient had an abnormal Bilitec test result at the 0.25 to 0.30 threshold, whereas the other 15 patients had a normal test result. H pylori antral infection was present in 14 group 1 patients. None of these had an abnormal Bilitec test result, whereas the test was positive in 40% of the H pylori–negative patients without endoscopic gastritis and in 70% of H pylori–negative patients with endoscopic gastritis ( P = .001). Conclusions: Twenty-four-hour intragastric bile monitoring provides the clinician with unequivocal evidence of excessive DGR in 41% of patients with an intact stomach having endoscopic esophagitis, GER symptoms, and gastric symptoms suggestive of DGR. The most dependable data are obtained when absorbance thresholds higher than 0.40 are considered. H pylori antral infection and excessive DGR at 24-hour intragastric bile monitoring are mutually exclusive. (Surgery 1999;125:480-6.)

Helicobacter pylori and Epstein-Barr virus infection and the p53 tumour suppressor pathway in gastric stump cancer compared with carcinoma in the non-operated stomach.

AIM: To evaluate similarities and differences between gastric stump cancer and conventional carcinoma in the non-operated stomach. METHODS: 26 stump carcinomas were compared with 24 conventional stomach cancers. Stage, histological...

Acetylcholine as pruritugenic mediator

To explore the mechanisms of the effects of sucralfate on the stomach, we investigated the action of sucrose octasulfate (SOS), a constituent of sucralfate, on the function of canine gastric parietal cells and somatostatin cells and in the isolated perfused intact rat stomach. Somatostatin cells from the canine gastric fundus were isolated by EDTA-collagenase dispersion and counterflow elutriation, and somatostatin-like immunoreactivity (SLI) release in response to SOS was measured by radioimmunoassay. Similar methods were used to isolate gastric parietal cells, in which gastric acid secretion was measured by uptake of a radiolabeled weak base, [14C]aminopyrine. SLI release by the intact rat stomach was examined in an isolated vascularly perfused rat stomach model. SOS, either alone or co-administered with epinephrine or gastrin heptadecapeptide (G17), dose-dependently stimulated SLI release by isolated canine fundic D-cells. At the highest doses, SOS potentiated the effect of epinephrine but not G17. Similarly, SOS potentiated the stimulating effect of dibutyryl cyclic adenosine 3′,5′-monophosphate (DBcAMP), but not 12-O-tetradecanoylphorbol 13-acetate (TPA). The effect of SOS on SLI release could be inhibited by octreotide, a somatostatin analogue. SOS did not alter acid secretion by cultured canine parietal cells either in the basal state or when coadministered with acid secretagogues. In isolated perfused rat stomach studies, SOS produced a significant (60% greater than basal) increase in SLI secretion. There was a similar effect when SOS was perfused against a background of isoproterenol. SOS stimulates SLI release from gastric somatostatin cells and from the isolated perfused stomach but has no direct effect on gastric parietal cells. These actions of SOS may mediate in part the apparent ability of sucralfate to enhance gastric mucosal defense.

Multiple early gastric stump carcinomas after gastrectomy for peptic ulcer

The remnant stomach after partial gastrectomy is considered to have a predilection for the development of primary gastric carcinoma. However, early gastric stump carcinomas are uncommon because the diagnosis of gastric stump carcinoma is more difficult than that of carcinoma in the intact stomach. Triple early gastric stump carcinomas, as in the present case, are exceedingly rare and may provide some clues for further investigation of carcinogenesis in the gastric stump. We studied about the histological appearance, genetic alterations (P-53 gene, c-erbB-2 gene and K-ras gene), and expression of tumor-associated antigens (carcinoembryonic antigen, carbohydrate antigen 19-9, and sialyl-Tn) in this rare case. The three carcinomas differed from each other histologically. With respect to genetic alterations, c-erbB-2 was amplified in one lesion, but no mutations of K-ras and P-53 gene were detected. The three carcinomas also differed from each other on the expression of tumor-associated antigens. In noncancerous mucosal epithelium at the anastomosis showing hyperplasia and cystic formation of glandular epithelial cells, no genetic alterations were detected, but sialyl-Tn and carbohydrate antigen 19-9 were expressed. These results suggest that there may be different processes of carcinogenesis of the three carcinomas even though they occurred under identical environmental conditions to those that have increased cancer risk.

Colonization of H. Pylori in the stomach of rats with acetic acid-induced ulcers: Effects of antibiotics and acid pump inhibitors

It is generally believed that H. pylori cannot colonize the stomachs of normal rats. We examined the potential H. pylori colonization in the stomachs of rats with or without chronic ulcers and the effects of antibiotic drugs and acid pump inhibitors on H. pylori viability and ulcer healing. [Methods] Ulcers were produced by acetic acid (20%, 0.04ml) injection into the stomachs of male Donryu rats (7-wk-old). All rats were orally inoculated once with H. pylori (ATCC43504, 3 X 108CFU/rat). 2, 4, 6, 8 and 10 wk after the inoculation, the animals were killed and then H. pylori viability, ulcerated area, and rnyeloperoxidase (MPO) activity in the gastric mucosa were determined. Clarithromycin (CAM, 20, 40, 80mg/kg), amoxiciUin (AMX, 1, 3, 5mg/kg), metronidazole (MTR, 5 mg/kg), omeprazole (OME, 30mg/kg), leminoprazole (LEM, 80mg/kg), CAM+OME or CAM+LEM was orally administered for 1 or 2 wk. [Results] A single inoculation of 1-1, pylori could not colonize the intact rat stomach, ie., no ulcers. Even under complete suppression of gastric acid with omeprazole, no colonizatin was observed in the normal rats. In contrast, H. pylori did colonize the ulcerated stomach for up to 10 wk at an incidence > 80%; 1.2 x 105CFU/rat. MPO activity was significantly elevated in the gastric mucosa with ulcer (608.1 +-81.0 vs. 364.9 +46.4 pMH202/min in the 1-1. pylori non-infected group). CAM (2wk), AMX and MTR (lwk) significantly and dose-dependently eradicated H. pylori. While AMX and MTR had insignificant effect on ulcer healing, CAM at > 40mgkg significantly delayed ulcer healing. In contrast, OME and LEM tended to enhance ulcer healing. However, they significantly prevented the delay in ulcer healing caused by CAM. [Conclusion] H. pylori was unable to colonize the intact stomach of rats, but did colonize the stomach with ulcers. CAM significantly eradicated H. pylori, but delayed ulcer healing which was significantly prevented with acid pump inhibitors.