Gastric Acid Levels Research Articles

Association of gastric acid and mucus secretion level with low-dose aspirin-induced gastropathy

Low-dose aspirin is known to cause upper gastrointestinal complications. The mechanism by which the aspirin disrupts gastric mucosal integrity remains to be clarified. In this study we investigated the temporal association of gastric secretory parameters (acid and mucus) with aspirin-induced gastropathy. In 42 long-term low-dose aspirin-takers and the same number of sex- and age-matched controls, pentagastrin-stimulated gastric juice was collected for 10 min during endoscopic examination. The collected gastric juice was divided and half was submitted to analysis for gastric acid (mEq/10 min) and the other half was analyzed for mucin (mg hexose/10 min) output. The grade of gastric mucosal injury was assessed endoscopically according to the modified Lanza score, and a score of more than 4 was defined as the presence of severe gastropathy. While gastric acid secretion did not differ significantly between aspirin-takers and controls, gastric mucus secretion, in terms of mucin output, was significantly increased in aspirin-takers compared to controls (4.1 (SD 4.8) vs. 2.3 (1.4) mg hexose/10 min, P < 0.05). Consequently, the acid/mucin ratio was significantly decreased in aspirin-takers compared to controls (1.2 (1.0) vs. 1.7 (1.4), P < 0.05). In the subanalysis of 25 aspirin-takers without severe gastropathy, gastric mucus secretion was increased and the acid/mucus ratio was decreased compared with controls, but there was no such association in the remaining 17 aspirin-takers with severe gastropathy. Overall, gastric mucus secretion is increased in aspirin-takers, suggesting a functional adaptive response to long-term administration of the drug. However, it is possible that the adaptive response is impaired in some aspirin takers, who might be susceptible to severe upper gastrointestinal complication.

The Effects of Female Sex Steroids on Gastric Secretory Responses of Rat Following Traumatic Brain Injury

Objective(s) Gastric ulceration is induced by various forms of stress like surgery, ischemia and trauma. The female sex has more resistance to stress and the gastrointestinal lesions happen fewer than male sex. The purpose of this study was to evaluate the role of estradiol and progesterone on the gastric acid and pepsin levels following traumatic brain injury (TBI) induction. Materials and Methods Diffuse TBI was induced by Marmarou method in female rats. Rats randomly assigned into 9 groups: intact, OVX (ovarectomized rat), Sham+OVX, TBI (intact rats under TBI), TBI+OVX (ovarectomized rats under TBI) and treated OVX rats with vehicle (sesame oil), E2 (estradiol), P4 (progesterone) or E2+P4 combination. The acid content and pepsin levels of each gastric washout sample were measured 5 days after the TBI induction. Results There was no significant difference in gastric acid output between groups either after TBI induction or after treatment with E2 or P4 or E2+P4. Gastric pepsin levels were increased in Sham+OVX, TBI (P< 0.001) and TBI+OVX (P< 0.05) compared to intact group. Gastric pepsin levels were significantly lower in E2 and E2+ P4 treated rats than vehicle treated group (P< 0.01). P4 treatment increased gastric pepsin level compared to TBI+OVX group (P< 0.05) and this increment was higher than rats that were treated with the E2 and E2+P4 (P< 0.01). Conclusion These results suggest that protective effect of estradiol and E2+P4 combination against mucosal damage after TBI, might be mediated by inhibition of pepsin secretion.

Association of Gastric Acid and Mucus Secretion Level With Low-Dose Aspirin Induced Gastropathy

Association of Gastric Acid and Mucus Secretion Level With Low-Dose Aspirin Induced Gastropathy

Maternal supplementation of omega 3 fatty acids to micronutrient-imbalanced diet improves lactation in rat

The present study aims to examine the effect of maternal supplementation of omega 3 fatty acids to a micronutrient (folic acid and vitamin B(12))-imbalanced diet on gastric milk volume and long-chain polyunsaturated fatty acid composition. Pregnant female rats were divided into 6 groups at 2 levels of folic acid in both the presence and absence of vitamin B(12). Both vitamin B(12)-deficient groups were supplemented with omega 3 fatty acid. Gastric milk volume and long-chain polyunsaturated fatty acids were analyzed. Our results for the first time indicate that imbalance in maternal micronutrients reduces gastric milk volume and milk docosahexaenoic acid levels (P < .01 for both) as compared with control. Supplementation with omega 3 fatty acids to this diet imbalanced in micronutrients increases (P < .01) milk docosahexaenoic acid level as compared with control. Imbalance in maternal micronutrients during pregnancy can alter milk fatty acid composition, which may ultimately affect infant growth and development.

Why is the coexistence of gastric cancer and duodenal ulcer rare? Examination of factors related to both gastric cancer and duodenal ulcer

The coexistence of gastric cancer with duodenal ulcer has been found empirically to be rare, but why it is rare is difficult to explain satisfactorily. To elucidate this question, we carried out a literature review of the subject. The frequency with which the two diseases coexist is 0.1-1.7%, and the main factor associated with both gastric cancer and duodenal ulcer is Helicobacter pylori infection. However, there are marked differences between the disorders of hyperchlorhydria in duodenal ulcer, and hypochlorhydria in gastric cancer. The most acceptable view of the reason for the difference may be that the acquisition of H. pylori infection occurs mainly in childhood, so that the time of acquisition of atrophic gastritis may be the most important, and if atrophic gastritis is not acquired early, high levels of gastric acid may occur, and consequently acute antral gastritis and duodenal ulcer may occur in youth, whereas, in elderly individuals, persistent H. pylori infections and the early appearance of atrophic gastritis may be the causes of low gastric acid, and consequently gastric cancer may occur. In patients with duodenal ulcer, factors such as nonsteroidal anti-inflammatory drugs (NSAIDs) and dupA-H. pylori strains may contribute to preventing the early acquisition of atrophic gastritis, while acid-suppressive therapy and vascular endothelial growth factor and other entities may inhibit atrophic gastritis. In contrast, in gastric cancer, factors such as excessive salt intake, acid-suppressive therapy, polymorphisms of inflammatory cytokines, and the homB-H. pylori strain may contribute to the early acquisition of atrophic gastritis, while factors such as NSAIDs; fruits and vegetables; vitamins A, C, and E; and good nutrition may inhibit it.

Anti‐acid medication as a risk factor for food allergy

An important feature for oral allergens is their digestion-resistance during gastrointestinal transit. For some oral allergens, digestion stability is an innate feature, whereas digestion-labile antigens may only persist in times of impairment of the digestive system. In this review, we collect evidence from mouse and human studies that besides the inherent molecular characteristics of a food protein, the stomach function is decisive for the allergenic potential. Gastric acid levels determine the activation of gastric pepsin and also the release of pancreatic enzymes. When anti-ulcer drugs inhibit or neutralize gastric acid, they allow persistence of intact food allergens and protein-bound oral drugs with enhanced capacity to sensitize and elicit allergic reactions via the oral route. Mouse studies further suggest that maternal food allergy arising from co-application of a food protein with anti-acid drugs results in a Th2-biased immune response in the offspring. Especially, anti-ulcer drugs containing aluminum compounds act as Th2 adjuvants. Proton pump inhibitors act on proton secretion but also on expression of the morphogen Sonic hedgehog, which has been related to the development of atrophic gastritis. On the other hand, atrophic gastritis and resulting hypoacidity have previously been correlated with enhanced sensitization risk to food allergens in elderly patients. In summary, impairment of gastric function is a documented risk factor for sensitization against oral proteins and drugs.

Diagnosis and surgical management of functional pancreatic endocrine tumors: a report of 45 cases

Objective To investigate the diagnosis and treatment of functional pancreatic endocrine tumors (PETs). Methods The clinical data of 45 patients with functional PETs who were admitted to the Southwest Hospital from January 1998 to December 2008 were retrospectively analyzed. Etiologic and localization diagnosis were made preoperatively according to the manifestation and the results of color doppler ultrasound and computed tomography, respectively. Eight patients received resection of the body and tail of the pancreas and spleen, 32 received tumor enucleation, one received resection of the pancreaticobiliary junction and four received pancreaticoduodenectomy. All patients received chemotherapy after the operation. Results Thirty-four cases of the PETs were benign and the rest eleven cases were malignant. Eight cases of the PETs were in the head of the pancreas,26 in the tail of the pancreas, seven in the body of the pancreas and four cases were with multiple PETs. The diameters of the PETs were 0. 3-5.0 cm, and the diameters of the PETs in 19 cases were above 2.0 cm. Eight patients were complicated with pancreatic leakage, two with incision infection and one with abdominal infection. Of the 33 patients with insulinoma, the blood glucose of five patients with multiple PETs was still abnormal after the operation, three patients underwent reoperation and the other two were treated by diazoxide to control the blood glucose in the normal range. The clinical symptoms of the seven patients with gastrinoma disappeared after the operation, and the gastric ulcer was healed, the 12-hour gastric juice volume and the level of the gastric acid were in the normal range after a continuous treatment with proton pump inhibition agents for 6 months. Necrotizing or migratory rash and diabetes of the four patients with glucagonoma were cured three weeks later, and the level of the amino acid was back to normal. Diarrhea and electronic disturbance of one patient with vasoactive intestinal peptide tumor were alleviated after the operation. Thirty-nine patients were followed up for 20-120 months. Of the 32 patients with benign PETs, two patients had tumor recurrence, and three patients died of other diseases. Of the seven patients with malignant PETs, two patients survived, and three patients died of hepatic metastasis or tumor recurrence, two patients died of other diseases. Conclusions Surgical treatment is effective for the treatment of functional PETs. Palliative resection of the tumor also can obviously improve the life quality of patients with fuctional PETs. Key words: Pancreas; Endocrine tumors; Diagnosis; Therapy

Intracellular Calcium Release and Protein Kinase C Activation Stimulate Sonic Hedgehog Gene Expression During Gastric Acid Secretion

Hypochlorhydria during Helicobacter pylori infection inhibits gastric Sonic Hedgehog (Shh) expression. We investigated whether acid-secretory mechanisms regulate Shh gene expression through intracellular calcium (Ca2(+)(i))-dependent protein kinase C (PKC) or cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) activation. We blocked Hedgehog signaling by transgenically overexpressing a secreted form of the Hedgehog interacting protein-1, a natural inhibitor of hedgehog ligands, which induced hypochlorhydria. Gadolinium, ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) + 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA), PKC-overexpressing adenoviruses, and PKC inhibitors were used to modulate Ca(2+)(i)-release, PKC activity, and Shh gene expression in primary gastric cell, organ, and AGS cell line cultures. PKA hyperactivity was induced in the H(+)/K(+)-β-cholera-toxin-overexpressing mice. Mice that expressed secreted hedgehog-interacting protein-1 had lower levels of gastric acid (hypochlorhydria), reduced production of somatostatin, and increased gastrin gene expression. Hypochlorhydria in these mice repressed Shh gene expression, similar to the levels obtained with omeprazole treatment of wild-type mice. However, Shh expression also was repressed in the hyperchlorhydric H(+)/K(+)-β-cholera-toxin model with increased cAMP, suggesting that the regulation of Shh was not solely acid-dependent, but pertained to specific acid-stimulatory signaling pathways. Based on previous reports that Ca(2+)(i) release also stimulates acid secretion in parietal cells, we showed that gadolinium-, thapsigargin-, and carbachol-mediated release of Ca(2+)(i) induced Shh expression. Ca(2+)-chelation with BAPTA + EGTA reduced Shh expression. Overexpression of PKC-α, -β, and -δ (but not PKC-ϵ) induced an Shh gene expression. In addition, phorbol esters induced a Shh-regulated reporter gene. Secretagogues that stimulate gastric acid secretion induce Shh gene expression through increased Ca(2+)(i)-release and PKC activation. Shh might be the ligand transducing changes in gastric acidity to the regulation of G-cell secretion of gastrin.

Deficient aldehyde dehydrogenase 2 is associated with increased risk for esophageal squamous cell carcinoma in the presence of gastric hypochlorhydria

Objective. In Orientals, deficient aldehyde dehydrogenase 2 (ALDH2) is associated with an increased risk for esophageal squamous cell carcinoma (ESCC). The local metabolism of carcinogenic acetaldehyde in the upper gastrointestinal tract could be involved in the association, but the underlying mechanism has not been fully elucidated. Since an anacidic stomach can promote bacteria-catalyzed local acetaldehyde production, the gastric acid level could also affect acetaldehyde metabolism. This study investigated whether ALDH2-related susceptibility to ESCC differs depending on the gastric secretion level. Material and methods. Sixty-two patients with ESCC and sex- and age-matched normal controls were enrolled in this study. ALDH2 polymorphism was analyzed by polymerase chain-restriction fragment length polymorphism, and those with an inactive allele (ALDH2-1/2-2 or ALDH2-2/2-2) were defined as ALDH2 deficient. Gastrin-stimulated acid output was assessed by endoscopic gastrin test and hypochlorhydria was defined as 0.6 mEq/10 min or lower. Multiple logistic regression analyses were used to adjust for other potential confounders. Results. ALDH2 deficiency or hypochlorhydria was more prevalent in ESCC compared with controls and both showed increased independent associations with ESCC in multivariate analysis. Stratified analysis by the gastric acid secretion level revealed that the associations between the ALDH2 genotype and ESCC differed according to the individual gastric acid secretion levels and that ALDH2 deficiency was a significant risk factor for ESCC exclusively in individuals with hypochlorhydria with an odds ratio (95% confidence interval): 5.0 (1.2–21.2). Conclusion. Microbial production of carcinogen acetaldehyde in the presence of gastric hypochlorhydria is most probably involved in the mechanism of ALDH2-related susceptibility to ESCC.

A DIRECT ROLE FOR SECRETORY PHOSPHOLIPASE A2 AND LYSOPHOSPHATIDYLCHOLINE IN THE MEDIATION OF LPS-INDUCED GASTRIC INJURY

Endotoxemia from sepsis can injure the gastrointestinal tract through mechanisms that have not been fully elucidated. We have shown that LPS induces an increase in gastric permeability in parallel with the luminal appearance of secretory phospholipase A2 (sPLA2) and its product, lysophosphatidylcholine (lyso-PC). We proposed that sPLA2 acted on the gastric hydrophobic barrier, composed primarily of phosphatidylcholine (PC), to degrade it and produce lyso-PC, an agent that is damaging to the mucosa. In the present study, we have tested whether lyso-PC and/or sPLA2 have direct damaging effects on the hydrophobic barriers of synthetic and mucosal surfaces. Rats were administered LPS (5 mg/kg, i.p.), and gastric contents were collected 5 h later for analysis of sPLA2 and lyso-PC content. Using these measured concentrations, direct effects of sPLA2 and lyso-PC were determined on (a) surface hydrophobicity as detected with an artificial PC surface and with intact gastric mucosa (contact angle analysis) and (b) cell membrane disruption of gastric epithelial cells (AGS). Both lyso-PC and sPLA2 increased significantly in the collected gastric juice of LPS-treated rats. Using similar concentrations to the levels in gastric juice, the contact angle of PC-coated slides declined after incubation with either pancreatic sPLA2 or lyso-PC. Similarly, gastric contact angles seen in control rats were significantly decreased in sPLA2 and lyso-PC-treated rats. In addition, we observed dose-dependent injurious effects of both lyso-PC and sPLA2 in gastric AGS cells. An LPS-induced increase in sPLA2 activity in the gastric lumen and its product, lyso-PC, are capable of directly disrupting the gastric hydrophobic layer and may contribute to gastric barrier disruption and subsequent inflammation.

Scientific Opinion on the substantiation of health claims related to sodium bicarbonate and reducing gastric acid levels (ID 1653) pursuant to Article 13(1) of Regulation (EC) No 1924/2006

Scientific Opinion on the substantiation of health claims related to sodium bicarbonate and reducing gastric acid levels (ID 1653) pursuant to Article 13(1) of Regulation (EC) No 1924/2006

Histamine 3 receptor activation mediates inhibition of acid secretion duringHelicobacter-induced gastritis

To test the hypothesis that histamine 3 receptor (H3R) activation during Helicobacter infection inhibits gastric acid secretion in vivo and in vitro. Helicobacter felis (H. felis) infected and uninfected C57Bl/6 mice were infused with either PBS or the H3 receptor antagonist thioperamide (THIO) for 12 wk. After treatment, mice were analyzed for morphological changes and gastric acid content. Total RNA was prepared from the stomachs of each group and analyzed for changes in somatostatin and gastrin mRNA abundance by real time-polymerase chain reaction (RT-PCR). Location of H3 receptors in the stomach was analyzed by co-localization using antibodies specific for the H3 receptor and parietal cell marker H(+), K(+)-ATPase β subunit. Inflammation and parietal cell atrophy was observed after 12 wk of H. felis infection. Interestingly, treatment with the H3R antagonist thioperamide (THIO) prior to and during infection prevented H. felis-induced inflammation and atrophy. Compared to the uninfected controls, infected mice also had significantly decreased gastric acid. After eradication of H. felis with THIO treatment, gastric acidity was restored. Compared to the control mice, somatostatin mRNA abundance was decreased while gastrin gene expression was elevated during infection. Despite elevated gastric acid levels, after eradication of H. felis with THIO, somatostatin mRNA was elevated whereas gastrin mRNA was suppressed. Immunofluorescence revealed the presence of H3 receptors on the parietal cells, somatostatin-secreting D-cells as well as the inflammatory cells. This study shows that during H. felis infection, gastric acidity is suppressed as a consequence of an inhibitory effect on the parietal cell by H3R activation. The stimulation of gastric mucosal H3Rs increases gastrin expression and release by inhibiting release of somatostatin.

Tetra-probe, 24-hour pH monitoring for laryngopharyngeal reflux: a technique for simultaneous study of hypopharynx, oesophagus and stomach

This study aimed to introduce the technique of tetra-probe, 24-hour pH monitoring for laryngopharyngeal reflux disease. Tetra-probe, 24-hour pH monitoring was performed for 30 suspected cases of laryngopharyngeal reflux. The proximal probe was placed in the hypopharynx, just above the upper oesophageal sphincter, the second probe was placed in the middle oesophagus, the third probe was placed a few centimetres above the lower oesophageal sphincter, and the distal probe was placed in the stomach. As the pH at the four sensor sites could be monitored simultaneously, gastric acid levels and gastroesophageal and laryngopharyngeal reflux could be examined. This pH monitoring technique enabled the pH relationship between the four sensor locations to be well documented, enabling gastric acid levels and patterns of reflux to be assessed. This procedure was also able to be used as a functional examination to evaluate anti-reflux medication efficacy. Tetra-probe, 24-hour pH monitoring is a reliable functional examination for laryngopharyngeal reflux.

The Aggravatory Effect of Nicotine on Helicobacter pylori-induced Gastric Mucosa Injury

Nitric oxide (NO) is a well-known gastric mucosa protection factor. Recently, it has been reported that methylated arginine compound such as asymmetric dimethylarginine (ADMA), which inhibits nitric oxide synthesis, may be related to the development of gastric mucosa injury in patients with Helicobacter pylori infection. In the present study, we tested the relationship between endogenous ADMA and gastric mucosa injury in H. pylor- infected patients and cultured gastric epithelial cells. One hundred and fifty subjects with gastric diseases were entered in this study. The levels of ADMA in gastric juice and plasma were measured in both H. pylori+ and H. pylori- patients. We analyzed independent risk factors that contribute to ADMA levels by multiple linear regression analyses. Mucosal epithelium cells were treated with nicotine (10 microM) for 24 hours in the presence or absence of H. pylori. The concentrations of ADMA in the culture medium and the rate of cell apoptosis were determined. The ADMA level in gastric juice was significantly increased in H. pylori+ patients (P<0.05), whereas there were no differences in the content of ADMA in the plasma between H. pylori+ patients and H. pylori- patients. Smoking and H. pylori infection were 2 independent risk factors contributing to ADMA levels, and in the population of H. pylori+ patients, the level of ADMA in smokers was higher compared with nonsmokers. Incubation of nicotine (10 microM) with epithelial cells for 24 hours further increased the elevated level of ADMA and the rate of cell apoptosis owing to H. pylori infection. H. pylori infection caused an increase of ADMA levels in gastric juice, which was aggravated by smoking. Endogenous ADMA may be an important factor contributing to gastric mucosa injury.

Risks of proton‐pump inhibitors: what every doctor should know

Medical Journal of AustraliaVolume 190, Issue 3 p. 109-110 Editorial Risks of proton-pump inhibitors: what every doctor should know Nicholas J Talley MD, PhD, FRACP, Corresponding Author Nicholas J Talley MD, PhD, FRACP Professor of Medicine and Epidemiology, and Chair of Department of Medicine talley.nicholas@mayo.edu Mayo Clinic, Jacksonville, Fla, USA.Correspondence: talley.nicholas@mayo.eduSearch for more papers by this author Nicholas J Talley MD, PhD, FRACP, Corresponding Author Nicholas J Talley MD, PhD, FRACP Professor of Medicine and Epidemiology, and Chair of Department of Medicine talley.nicholas@mayo.edu Mayo Clinic, Jacksonville, Fla, USA.Correspondence: talley.nicholas@mayo.eduSearch for more papers by this author First published: 02 February 2009 https://doi.org/10.5694/j.1326-5377.2009.tb02305.xCitations: 10Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article.Citing Literature Volume190, Issue3February 2009Pages 109-110 RelatedInformation

Fatty acid composition of subcutaneous adipose tissue and gastric mucosa: is there a relation with gastric ulceration?

BackgroundBoth in vitro and epidemiological studies indicate that dietary polyunsaturated fatty acids may play a protective role against peptic ulcer in humans. Adipose tissue fatty acid composition is thought to reflect dietary fatty acid intake. The aim of the present study is to investigate adipose and gastric mucosa fatty acid levels in relation to gastric ulceration status.MethodsFifty two adult outpatients undergoing upper gastrointestinal tract endoscopy participated in the study. Adipose tissue samples were taken from the abdomen and buttock during the endoscopy procedure and samples from gastric tissue were taken from a subsample of 30 subjects. The presence of Helicobacter pylori was determined using the CLO test. Capillary gas chromatography was used for the extraction of 36 and 42 adipose tissue and gastric mucosa lipids respectively.ResultsThe monounsaturated fatty acids (MUFAs) C18:1n-12c, C16:1n-5, C16:4n-1 and the polyunsaturated fatty acids (PUFAs) C16:3n-4, C20:3n-3, C20:4n-6, C21:5n-3 and C18:2n-9c,12t of the gastric mucosa were present in higher proportions in ulcer negative patients. These unsaturated fatty acids, however, each contributed less than 1% on average to total fatty acid content. In addition, higher average levels of eicosapentaenoic acid (EPA) C20:5n-3 and docosahexaenoic acid (DHA) C22:6n-3 were detected in abdominal and buttock samples in CLO negative controls, compared to CLO positive controls. Adipose tissue and gastric mucosa n-6 and trans fatty acid levels were positively linearly correlated (r = 0.37 and 0.41 for n-6 and trans fatty acids respectively).ConclusionCertain minor MUFAs and PUFAs of the gastric mucosa appear to be present in higher proportions in ulcer negative patients. Overall, the findings provide only weak evidence of an association between the gastric mucosal fatty acids and the presence of gastric ulceration. The higher average levels of EPA and DHA in abdominal and buttock adipose tissue in CLO negative controls could be an indicator that dietary FAs inhibit Helicobacter pylori growth. Larger studies are necessary to provide evidence of a biologically relevant effect.

Role of Helicobacter pylori in refractory iron deficiency anaemia

The role of Helicobacter pylori infection in the development of iron deficiency anaemia has been the focus of attention over the past decade. However, confirmation of a relationship has not confirmed the pathophysiological mechanisms involved in the phenomenon. The aim of the present work is to study the levels of fasting gastric acidity (free and total) as well as the level of tumour necrosis factor-α (TNFα) in male refractory iron deficiency anaemia patients seropositive for H. pylori infection versus those who are seronegative. Thirty adult patients with iron deficiency anaemia and gastroduodenitis were subdivided into two groups of matched age and haemoglobin value. Group l was H. pylori-seropositive for infection and these patients did not receive prior treatment for eradication of H. pylori infection. Group 2 comprised patients seronegative for H. pylori infection (control group). Patients with active bleeding or previous medical problems were excluded from the study. All patients and controls were subjected to the following at presentation: history taking and thorough clinical examination, complete blood picture, reticulocytes (%), assessment of serum iron, total iron binding capacity, serum ferritin, IgG anti-Helicobacter antibody and TNFα, stool for occult blood and measurement of gastric acidity (total and free). Upper endoscopy was performed and multiple biopsies were taken and tested for expression of cytotoxin-associated gene A (cagA) by the polymerase chain reaction (PCR). Results showed significantly higher values of free and total gastric acidity as well as TNFα levels in Group 1 compared to controls (Group 2). Among those in Group 1, higher TNFα levels were seen in seven H. pylori cagA-positive patients than in eight cagA-negative patients. Haemoglobin values were inversely correlated with TNFα levels. Thus, elevated serum TNFα in the H. pylori-seropositive group may be one of the underlying pathophysiological mechanism for iron deficiency anaemia observed in these patients.

The Effect of Helicobacter pylori Eradication Treatment on the MUC 1 and Lewis Antigens Level in Human Gastric Juice: Preliminary Study

Helicobacter pylori is considered as a causative agent of gastritis, duodenal and gastric ulcers, and gastric cancer. During inflammation, association of the pathogen of gastric epithelial cells and mucins is considered important. It was postulated that Lewis b structures of secretory MUC 5AC mucin can be a receptor for the bacterium. Some authors also suggest that epithelial MUC 1 mucin may be implicated in the mechanism of infection. The main aim of our work was to support this last suggestion by evaluation of the possible changes in MUC 1 and Lewis a and b levels in gastric juice before and at the end of eradication treatment. The gastric juices of ten examined patients were chromatographed on a Sepharose 4 B column, electrotransferred on Immobilon P membranes, and assessed for MUC 1 and Lewis a and b structures using monoclonal antibodies. In 90% of examined patients, higher amounts of MUC 1 mucin were observed at the end of eradication treatment. Similar results for Lewis a and b structures were found. In the case of MUC 1 and Lewis b, the differences were statistically significant. Helicobacter pylori influences expression of the soluble form of MUC 1 mucin and Lewis a and b structures present in gastric juice.

Leptin and Ghrelin in Relation toHelicobacter pyloriStatus in Adult Males

Leptin and ghrelin, hormones involved in human energy homeostasis, are both produced in the stomach. We sought to determine whether the presence of Helicobacter pylori affects gastric and systemic levels of leptin and ghrelin. We consecutively enrolled 256 patients referred for upper endoscopy at a Veterans Affairs outpatient endoscopy center. We obtained fasting serum, fundic and antral biopsies, and gastric juice. Based on histological, biochemical, and serological assays, patients were categorized as H. pylori+ or H. pylori-. Leptin and total ghrelin levels in serum, gastric biopsies, and gastric juice were determined by specific ELISAs. Of the 256 subjects, 120 were H. pylori+ and 96 were H. pylori-; 40 patients of indeterminate status were excluded. Serum and fundic leptin levels correlated with body mass index in the H. pylori+ (r = 0.35; P < 0.0001 and r = 0.35; P < 0.0001, respectively) and H. pylori- (r = 0.65; P < 0.0001 and r = 0.41; P < 0.0001, respectively) groups, but H. pylori+ subjects had significantly lower serum leptin levels [median 2.2 ng/ml (interquartile range 0.9-4.6) vs. 4.0 ng/ml (1.7-7.2); P = 0.0003]. Serum ghrelin levels were similar in the H. pylori+ and H. pylori- groups [median 1651 pg/ml (interquartile range 845-2247) vs. 1629 pg/ml (992-2886); P = 0.23]. H. pylori status did not significantly affect gastric biopsy leptin and ghrelin levels. Ghrelin levels in gastric juice varied over 4 log(10) (<80-776,000 pg/ml) and correlated with gastric juice pH in the H. pylori+ group (r = 0.68; P < 0.0001). These findings provide evidence that H. pylori status affects leptin and ghrelin homeostasis, presumably via intragastric interactions.

Development of Ethanol‐induced Chronic Gastric Ulcer Model and the Effect of Protein Sources and their Hydrolysates on the Model of adult rats

This study was aimed to establish chronic gastric ulcer model and compare the healing effects of protein sources and their hydrolysates using Sprague‐Dawley(SD) adult rats. We administrated 50 to 80% ethanol for inducing acute ulcer and then 10 to 20% ethanol to maintain gastric ulcer for 3 to 11 days. From the result, chronic gastric ulcer model was developed with oral administration of 70% ethanol followed by 15% ethanol solution(15 ml EtOH/dl D.W.) for 5 days; apparent gastric lesions were not observed after 7 days. With this model, the rats were divided into 5 groups and fed with AIN 93M diet containing various protein sources; 20% of casein, whey protein (WP), whey protein hydrolysate(WPH), gluten protein(GP), and gluten protein hydrolysate(GPH), respectively, for 5 days. Weight gains were significantly low and the severe lesions in gastric tissue were observed in GP and GPH groups. However, there was no significant difference in gastric acid(pH) and glutathione level as an antioxidant among groups. The results indicate that chronic gastric ulcer can be maintained with continuous provision of 15% ethanol for 5 days after the oral feeding of 70% ethanol for once. Whey protein may have positive impacts on ethanol‐induced chronic gastric ulcer while gluten may not. Besides, protein hydrolysates are more desirable for healing chronic gastric ulcer than intact proteins. The details of biochemical data will be discussed.