Is duodenal gastric metaplasia a consequence of Helicobacter pylori infection in children?

BACKGROUND: Duodenal gastric metaplasia (DGM) is commonly found in association with Helicobacter pylori (Hp)-associated gastritis in adults. DGM is also considered a risk factor for duodenal ulcer development. The prevalence of DGM in children and its association with gastritis, duodenitis, or the presence of Hp organisms is not clear. We investigated the prevalence of DGM in children and explore its association with several possible risk factors, including age, gender, gastritis, duodenitis, or Hp presence in the gastric antrum. METHODS: A retrospective analysis of 173 upper endoscopy procedures performed between 1993 and 1995 at Cabell Huntington Hospital, Huntington, WV, was done. Gastric and duodenal biopsies were stained with Giemsa for Hp detection, periodic acid-Schiff for DGM, and hematoxylin and eosin for histologic assessment. Gastric mucosal inflammation was graded according to Sydney criteria. RESULTS: Duodenal gastric metaplasia was identified in 23 of 173 (13%) patients. Duodenitis but not age, gender, gastritis, or the presence of Hp in the gastric antrum was associated with DGM development. In 4 of 23 DGM foci, Hp was identified. CONCLUSIONS: In children, DGM is not the consequence of Hp infection.     

Gastric acidity in a double ulcer (of the stomach and duodenum)

Gastric salt-acid secretion was studied in three comparative patient groups with gastric ulcer, endoscopically confirmed, combination of gastric and duodenal ulcers. In the patients with double localization of the ulcer (stomach and duodenum) - hyperacidity was determined after pentagastrin stimulation. Acid-salt secretion was higher than that of the patients with gastric ulcer and was close to the secretion of those with duodenal ulcer, being but with a high standard deviation, necessitates consideration to be given to each concrete case of treatment. No discrepancy in the volume of gastric secretion before meals was established, thus impugning the role of pylor stasis in the genesis of secondary gastric ulceration. The incidence of atrophic gastritis in case of gastric and double ulcer is almost identical, hence attention is paid to the duodeno-gastric reflux as an eventual cause for damaging gastric mucosa with its successive ulceration in the patients with duodenal ulcer of many years. That is the reason, drugs enhancing the resistance of gastric mucosa as well as methoclopramid intake are proposed additionally to the drugs, neutralizing or blocking the gastric acid-salt secretion.     

Circadian gastric acidity in Helicobacter pylori positive ulcer patients with and without gastric metaplasia in the duodenum

BACKGROUND: The presence of gastric metaplasia allows helicobacter pylori to colonise the duodenum and this condition is thought to be acquired as a response to acid hypersecretion. This functional disorder, however, is present only in a subgroup of duodenal ulcer patients and, in addition, surface gastric metaplasia has been frequently found in the proximal duodenum of normal subjects and patients with non-ulcer dyspepsia, who cannot be certainly considered as acid hypersecretors. AIMS: To clarify the role of acid in inducing gastric type epithelium in the duodenum. This study aimed at assessing whether the pattern of circadian gastric acidity differs between H pylori positive duodenal ulcer patients with and without duodenal gastric metaplasia. PATIENTS: Seventy one patients with duodenal ulcer confirmed by endoscopy and who were found to be positive for H pylori infection by histology on antrum biopsy specimens were enrolled into this study. METHODS: Gastric type epithelium in the duodenum was found in 49 of 71 ulcer patients (69%). Continuous 24 hour gastric pH metry was performed in 50 healthy subjects and in the two subgroups of duodenal ulcer patients with and without gastric metaplasia in the duodenum. Gastric acidity was calculated for 24 hours (1700-1659), night (2000-0759) and day-time (0800-1959). RESULTS: Ulcer patients without gastric metaplasia showed a significantly higher gastric acidity (p < 0.001) than controls for every time interval considered, while the ulcer subgroup with gastric metaplasia was more acid than healthy subjects (p < 0.001) during the whole 24 hour period and the daytime. There was no difference between the two subgroups of duodenal ulcer patients with and without gastric metaplasia during the various time segments analysed. CONCLUSION: The findings confirm that the circadian gastric acidity of duodenal ulcer patients is higher than that of controls. As there is no difference in gastric pH between duodenal ulcer patients with and without gastric metaplasia, gastric hyperacidity is not specific to patients with duodenal gastric metaplasia. It is probable that this histological change is a non-specific response to mucosal injury resulting from various factors and not exclusively to acid.     

Isolation and structure elucidation of cirensenosides O and P from the leaves of Oplopanax elatus Nakai

Among 1470 patients over 65-year-old who were treated for various diseases, 50 had gastric ulcer and 10 had duodenal ulcer. About half the gastric ulcers were located in the body and fundus (n = 24, 48.0%). One third of the patients with gastric or duodenal ulcers had as their chief complaints hematemesis and hematochezia (n = 20, 33.3%), and a greater number had atypical gastrointestinal complaints (general malaise, fever etc, n = 25, 41.7%). In 10 patients (16.7%) the ulcers were due to non-steroidal anti-inflammatory drugs, in 5 (8.3%) they were due to steroid hormones, both of which had been given to treat other conditions; in 45 (75.0%) the origin of the ulcers was unknown. Complications of gastric and duodenal ulcers were hematemesis and hematochezia (n = 20, 33.3%), and perforation (n = 2, 3.3%). Duodenal ulcers tended to be severe, and were associated with death due to bleeding and peritonitis.     

Helicobacter pylori infection in a randomly selected population, healthy volunteers, and patients with gastric ulcer and gastric adenocarcinoma. A seroprevalence study in Taiwan

To investigate the association of Helicobacter pylori and gastric ulcer and adenocarcinoma, IgG antibodies against H. pylori were examined in 823 randomly selected subjects, 92 healthy volunteers, 117 patients with gastric ulcer, and 148 with gastric adenocarcinomas in Taiwan, where the prevalence of gastric adenocarcinoma is high. The seropositivity of this population in Taiwan was 54.4%. Gastric ulcer patients had a higher seropositivity (83.8%) than healthy volunteers (62.0%) and gastric adenocarcinoma patients (62.2%) (P < 0.001). Gender difference, blood type, and habit of smoking were not associated with the seroprevalence in any study groups. Gastric ulcer coexistent with duodenal ulcer had a higher seropositivity (94.7%) (P < 0.05). The seropositivity of H. pylori in gastric adenocarcinoma patients was higher than in healthy volunteers only in younger age and was not associated with histologic type, invasion, and location of major tumors. The results reemphasize the association of H. pylori infection with gastric ulcer but not with gastric adenocarcinoma in Taiwan.     

Cytotoxin genes of Helicobacter pylori in chronic gastritis, gastroduodenal ulcer and gastric cancer: an age and gender matched case-control study

Helicobacter pylori (H. pylori) infection is involved in many gastrointestinal diseases, such as chronic gastritis (CAG), peptic ulcer and gastric cancer (GCA). Both host factors and H. pylori strain differences may contribute to differences in the diseases. Thus, we conducted an age and gender matched case-control study of 35 patients each with CAG, gastric ulcer (GUL), duodenal ulcer (DUL) and gastric cancer (GCA) to examine the role of strain differences of the H. pylori cytotoxin genes cagA and vacA in these diseases. We employed polymerase chain reaction to examine the gastric juice for H. pylori DNA. The test was positive for 26 (74.3%) CAG, 29 (82.9%) GUL, 28 (80.0%) DUL and 27 (77.1%) GCA patients, showing no statistically significant difference among the diseases (P = 0.84). cagA and vacA genes (picked up by using a vacA1 + vacA2 primer pair which detected non-variable regions of the vacA gene) were detected by PCR in the H. pylori DNA-positive cases as follows: CAG, 92.3% and 76.9%; GUL, 100% and 86.2%; DUL, 89.3% and 89.3%; GCA, 92.6% and 85.2%, respectively. No statistically significant differences were found in the frequencies of these cytotoxin genes in H. pylori-positive cases among the various gastric diseases (P = 0.39 for cagA and P = 0.64 for vacA).     

Zollinger-Ellison syndrome and antral G-cell hyperfunction in patients with resistant duodenal ulcer disease

We measured basal and pentagastrin-stimulated acid secretion, as well as basal and meal-stimulated plasma gastrin concentration to determine, in 67 patients affected by resistant duodenal ulcer, whether their condition could be related to gastric acid secretion and/or gastrin-related syndromes. We then compared them to 46 duodenal ulcer control patients. The outpatients were investigated consecutively. The resistant duodenal ulcer patients differed from the controls only in their higher complication rates (bleeding or perforation, P < 0.05). We identified five patients in the resistant duodenal ulcer group with Zollinger-Ellison syndrome and 12 with antral G cell hyperfunction, whereas in the control group only one patient was affected by antral G cell hyperfunction. IgG anti-Helicobacter pylori antibodies were positive for the presence of infection in 7 of the hypergastrinaemic patients. When Zollinger-Ellison syndrome or antral G cell hyperfunction were excluded, no differences could be found in gastric acid secretion, or basal and meal-stimulated plasma gastrin levels, between the resistant and control duodenal ulcer patients, except for basal acid hypersecretion (resistant duodenal ulcer 16% vs duodenal ulcer 2% P = 0.0144). In the presence of duodenal ulcer disease resistant to H2-blockers, it is mandatory to measure basal plasma gastrin concentration since it was possible to diagnose the gastrin-related syndromes, Zollinger-Ellison syndrome and antral G cell hyperfunction, in 26% of this group of patients.     

Vagal and hormonal influences on gastric secretion in duodenal ulcer disease

Current concepts on the pathophysiology of gastric hypersecretion in duodenal ulcer disease have been presented and the role of vagal nerves and gastrointestinal hormones particularly gastrin has been discussed. Duodenal ulcer patients form a heterogenous group with regard to the gastric acid and pepsin secretion and gastrin release. They may differ from healthy subjects by several wall defined defects including an increased mass of parietal and peptic cells, increased capacity to secrete acid and pepsin, increased vagal drive to the parietal cells, hyperreactivity of antrum, decreased effectiveness of antral and duodenal autoregulatory mechanisms, defective release of secretin, increased gastric emptying and defective removal of gastric acid load from the duodenum. Very little is known what proportion of duodenal ulcer patients suffer from various pathologic disturbences and what are the mechanisms underlying these changes.     

Non-verbal communication: evaluation of a computer-assisted learning package

To assess the effect of 4 weeks' therapy with ranitidine 150 mg twice daily on the healing of symptomatic NSAID-associated gastric and duodenal ulcers, 149 arthritic patients were randomly allocated to one of three treatment groups: ranitidine with NSAID continued, ranitidine with NSAID discontinued, and placebo with NSAID discontinued. The healing frequency in patients with gastric ulceration was 67, 68 and 47%, and in those with duodenal ulceration 61, 81 and 42%, respectively. Only the difference between the duodenal ulcer healing rates for ranitidine with NSAID discontinued and placebo was statistically significant (P = 0.02). Healing rates were uninfluenced by gender, age, smoking habits, alcohol consumption, ulcer frequency or size, arthritic disease, or participating country.     

Dynamic phenotypic restructuring of the CD4 and CD8 T-cell subsets with age in healthy humans: a compartmental model analysis

The incidence of ulcer perforation in 1480 patients treated in the Bergen area of Norway between 1935 and 1990 was analyzed for daily (circadian), weekly (circaseptan), and yearly (circannual) time effects. A circadian rhythm was found overall that was reproducible and fairly stable across seasons, decades, and days of the week. After subgrouping, a circadian rhythm was found in younger patients, males, and duodenal perforations, while a 12 h (circasemidian) rhythm characterized ulcer perforation for women and for gastric ulcers. Duodenal perforations showed highest incidence in the afternoon, while gastric perforations showed a major peak around noon and a secondary peak near midnight. For duodenal ulcer perforation, the circannual pattern was characterized by a 6-month rhythm, with significantly higher incidence in May-June-July and in November-December in most subgroups. A circaseptan rhythm was not found, but there was a significantly higher incidence on Thursday-Friday as compared to Sunday-Monday. The pathophysiological mechanisms underlying the perforation of an ulcer thus seemed to show pronounced circadian and 6-month rhythmic variations, much less so circaseptan or circannual rhythms. While it is likely that exogenous environmental and/or societal factors play a significant role, variations in ulcer perforation may be related to endogenous biological rhythms in pathophysiological factors since the circadian pattern of duodenal perforation follows that for gastric acidity. Knowledge of the temporal patterns in peptic ulcer perforation and associated pathophysiologic factors should prove useful in optimizing the chronotherapeutic management of ulcer disease.     

Isolation and characterization of cDNA clones encoding a 32-kDa dense-granule antigen of Sarcocystis muris (Apicomplexa)

BACKGROUND AND STUDY AIMS: A second-look endoscopy is often performed to evaluate the efficacy of a prior injection therapy in patients with bleeding peptic gastric or duodenal ulcers. Although this strategy is widely established, it does not rely on unequivocal data from controlled studies. In a prospective, randomized, controlled multicenter trial we assessed the effect of programmed endoscopic follow-up examinations with eventual retreatment on the outcome of bleeding ulcers in these patients. PATIENTS AND METHODS: One hundred and five patients with gastric or duodenal peptic ulcers presenting with active (Forrest type I) or recent (Forrest type IIa and IIb) bleeding upon endoscopy within four hours after admission were included in the study. Emergency treatment consisted of the sequential injection of both epinephrine (1:10,000 v/v) and up to 2 ml of fibrin/thrombin around the ulcer base. Fifty-two patients were randomized to receive programmed endoscopic monitoring with eventual retreatment in cases of Forrest type I, IIa, or IIb ulcers beginning within 16-24 hours after the index bleed. Follow-up endoscopies were continued until the macroscopic appearance revealed a Forrest type IIc or III ulcer. Fifty-three patients in the control group were closely monitored, and only received a second endoscopy when there was clinical or biochemical evidence of recurrent bleeding. The groups did not differ with respect to age, sex, site and severity of bleeding. RESULTS: The numbers of patients with recurrent bleeding were similar whether they were endoscopically monitored or not (21% versus 17%, P=0.80 chi-squared test). In addition, there was no statistically significant difference between the two groups with respect to the number of blood units transfused, need for surgical intervention, hospital stay or number of deaths (Mann-Whitney U-test). Improving local ulcer stigmata was not related to a better outcome. CONCLUSIONS: Programmed endoscopic follow-up examinations with eventual retreatment in patients locally injected for an acute or recent hemorrhage from a gastric or duodenal ulcer did not influence their outcome when compared to patients receiving only a second endoscopic intervention upon evidence for recurrent hemorrhage. Scheduled control endoscopies cannot be recommended after an initial successful endoscopic treatment of peptic ulcer bleeding when selection of the patients for second-look endoscopy is directed by the Forrest criteria.     

Diurnal variation in intragastric pH in children with and without peptic ulcers

Diurnal variation in intragastric pH in children with peptic ulcers has not been previously reported. Therefore, we monitored intragastric pH during a 24-h period in 82 subjects (10 children with gastric ulcers, 9 children with duodenal ulcers, 58 non-ulcer (comparison group) children, and 5 healthy adults) using a monopolar glass pH electrode. The percent of readings below pH 2, 3, 4, and 5 for each subject was calculated and compared between the comparison group and the two ulcer groups using means and slopes (i.e. changes in percent with age for each group) of percent readings for each pH analysis. In the comparison group children, gastric acidity increased with age and reached adult levels by 14 y. Mean readings for all pH analyses in gastric ulcer children were lower than those in age-adjusted comparison children (p < 0.05). The slopes of the relationships between age and the percent time below any pH for the gastric ulcer group were different from those in the comparison group (p < 0.05) and were negative for all pH analyses. The mean time below pH 2 in children with duodenal ulcers was greater than that in age-adjusted comparison children (p = 0.002). The slope of the relationship between age and the percent time below pH 2 in the duodenal ulcer group was different from that in the comparison group (p < 0.05). Gastric acidity in children with primary gastric ulcers was reduced during childhood, but in children with primary duodenal ulcer, gastric acidity was at or above adult levels.     

Effect of chronic duodenal ulceration and its treatment with lanzoprazole or sucralfate on gastroduodenal mucosal protein turnover and TGF-alpha, bFGF, and EGF receptor expression in humans

In order to investigate whether chronic duodenal ulcer disease is a consequence of disturbed mucosal turnover and growth factor expression, we studied 16 patients with duodenal ulcers before, during, and after endoscopic healing with lansoprazole or sucralfate. Before treatment, gastric fundal and antral mucosal protein turnover rates were higher in patients than controls, without parallel increases in growth factors. Both forms of therapy produced similar changes, with overall increases in duodenal mucosal turnover and transforming growth factor-alpha (TGF-alpha) and epidermal growth factor receptor (EGF-r) levels. Measurements after healing showed persistent elevations of mucosal turnover in the antrum and duodenum and depressions of basic fibroblast growth factor (bFGF) in gastric fundal and duodenal mucosa. We conclude that mucosal turnover is abnormally high in patients with chronic duodenal ulcer disease and is not easily explained by growth factor changes. The failure of lansoprazole and sucralfate to normalize rates, despite endoscopic healing, may explain the high ulcer relapse rates in non-HP-eradicated patients.     

Clinical observation of the temporal association between crack cocaine and duodenal ulcer perforation

HYPOTHESIS: To determine if a cause-effect relationship exists between crack cocaine use and duodenal ulcer perforation (DUP). PATIENTS AND METHODS: A retrospective study was conducted of all patients undergoing emergency surgical management for peptic ulcer disease over a 6-year period at a large inner-city municipal teaching hospital. The hospital records of 78 consecutive patients presenting with complications of peptic ulcer disease between April 1990 and April 1996 were reviewed. Group A (n = 24) consisted of patients with confirmation of crack cocaine usage within 8 hours of clinical presentation; group B (n = 54) consisted of patients with no antecedent history of crack cocaine use. Demographic data, timing of drug use, clinical presentation, laboratory and radiographic findings, toxicology screening, operative findings, and postoperative course were compared between the two groups. RESULTS: Both groups revealed a similar gender distribution, tobacco use, prior peptic ulcer symptoms, and laboratory findings. Group A patients were younger (t test, P = 0.01) and more likely to present with perforation, whereas patients in group B presented with a combination of symptoms (chi square, P = 0.03). Duodenal ulcer perforation was present in 75% of patients in group A compared with 46% of patients in group B (chi square, P = 0.04). Group B patients had a significantly longer hospital stay compared with those in group A (t test, P = 0.01). Both crack cocaine and alcohol are independent predictors of duodenal ulcer perforation. CONCLUSIONS: Patients with recent use of crack cocaine and/or alcohol are more likely to present with duodenal perforations. Although a temporal association between crack cocaine use and duodenal ulcer perforation was demonstrated, this study does not confirm a cause-effect relationship. A prospective cohort study is needed to clarify the pathogenesis of this potential cause-effect relationship.     

Virulence-associated genes as markers of strain diversity in Helicobacter pylori infection

To establish a marker of strain diversity of Helicobacter pylori, a genetic examination was performed based on the detection rates by PCR of cagA and vacA, which are known to be virulence-associated genes. The test strains were obtained from 70 patients suffering from gastric ulcer (GU), 82 patients with duodenal ulcer (DU) and 48 patients with gastritis (GS). Fragments located in the three different regions of vacA were amplified; V1 being the upstream portion, V2 the mid-portion and V3 the downstream portion. For cagA, the detection rates were 70% for GU, 79% for DU and 50% for GS, showing a significantly higher rate for DU than for GS (P = 0.0005). With V1, the detection rates were 90% for GU, 90% for DU and 69% for GS, giving a significantly higher rate for GU than for GS (P = 0.0036) and also giving a significantly higher rate for DU than for GS (P = 0.0019). With V2, the detection rates were 60% for GU, 70% for DU and 44% for GS, giving a significantly higher rate for DU than for GS (P = 0.0024). The differences in vacA gene polymorphism were closely related to the evidence of gastroduodenal ulcers in H. pylori infection. Furthermore, the detection rates of cagA and polymorphisms of vacA by PCR could be used as markers of strain diversity in H. pylori-induced gastroduodenal ulcer.     

Protein and RNA synthesis in larvae of the yellow mealworm beetle (Tenebrio molitor) during cooling and cold acclimatization

Adult patients with symptoms of gastric disease were randomly assigned to two treatment groups (roxatidine group, n = 115; famotidine group, n = 113) or untreated control group (placebo, n = 111). The treatment groups randomly received 75 mg of roxatidine or 20 mg of famotidine at 9 pm, and 12 - 13 h later gastric juice secretion was measured with gastric X-ray films in both groups. Mean gastric juice secretion was significantly lower in the treated groups (roxatidine, 16.1 ml/12 h; famotidine, 19.9 ml/12 h) than in the untreated controls (placebo, 49.5 ml/12 h). Gastric juice suppression by roxatidine and by famotidine, respectively, was 82% and 37% in patients with gastric ulcer; 71% and 39% in patients with duodenal ulcer; 70% and 64% in patients with gastritis; and 68% and 86% in patients with no evidence of disease. It is concluded that roxatidine was more effective than famotidine for gastric juice suppression in patients with peptic ulcer. In patients with no evidence of gastric disease, however, famotidine was more effective than roxatidine.     

Helicobacter pylori eradication as a surrogate marker for the reduction of duodenal ulcer recurrence

OBJECTIVES: An abundance of data exists documenting the association of H. pylori eradication with the reduction in duodenal ulcer recurrence. AIM: To evaluate the validity of using H. pylori eradication as a surrogate marker for the reduction in duodenal ulcer recurrence using rigorously controlled studies. METHODS: Three controlled clinical trials were conducted in patients with uncomplicated, active duodenal ulcers. Patients were treated with various combinations of omeprazole and amoxycillin. Ulcer healing and H. pylori eradication were assessed. For patients whose duodenal ulcer healed, duodenal ulcer recurrence was determined over a 6-month period in patients with H. pylori eradication and those remaining positive for H. pylori at least 4 weeks after treatment. To support the data obtained from these clinical trials, a search of the medical literature was conducted to identify additional human clinical trials in which duodenal ulcer recurrence rates were measured and categorized by H. pylori status at least 1 month post-treatment. RESULTS: In 11 controlled trials, the overall 6-18-month duodenal ulcer recurrence rate was 54% among patients remaining positive for H. pylori at least 4 weeks after treatment compared to 6% among patients with H. pylori eradication following treatment. This finding was corroborated by the uncontrolled trials, in which the duodenal ulcer recurrence rate was 64% among patients found to be H. pylori-positive and 6% for patients found to be H. pylori-negative at least 4 weeks after treatment. A time course of duodenal ulcer recurrence rates using pooled data from both controlled and uncontrolled studies demonstrated that duodenal ulcer recurrence rates for H. pylori-negative patients persisted for up to 4 years following treatment. Duodenal ulcer recurrence rates for H. pylori-positive patients increased for the first year, then levelled off. A comparison of the duodenal ulcer recurrence rates for different treatment regimens revealed that eradication regimens based on omeprazole plus antibiotics and bismuth plus antibiotics exhibited similar duodenal ulcer recurrence rates for H. pylori-positive and -negative patients. CONCLUSION: Regardless of treatment regimens, H. pylori eradication produced a consistent and significant reduction in duodenal ulcer recurrence. Therefore H. pylori eradication, 4 weeks post-therapy, can be used as a surrogate marker for reduced duodenal ulcer recurrence in investigational clinical trials.     

Helicobacter pylori detection by polymerase chain reaction in gastric juice and its correlation with the histology (Giemsa)]

HP infection is involved in the pathogenesis of several gastroduodenal diseases, as type B chronic gastritis, duodenal and gastric ulcer, MALT lymphoma and gastric cancer. The recent availability of molecular techniques, specifically the PCR, allow us to detect very low amounts of the bacterium. The aim of the study is to evaluate the presence of HP in gastric juice by PCR technique and to correlate this findings with histology (Giemsa) of gastric mucosa. Gastric juice PCR positive findings were found in 10/31 (32.3%) HP positive patients at histology. We concluded that HP in gastric juice is possible to detect by molecular techniques. In our study 32.3% of the patients showed the presence of HP in gastric juice.     

Genetico-mathematical analysis of the inheritance pattern of peptic ulcer disease. II. Method of simple registration. Assessment of the direct methods of Weinberg

The inheritance pattern of ulcer disease was analyzed by means of the method of simple registration. We also studied comparatively and assessed all direct methods of Weinberg using the coefficients of genetic proportion calculated by them as a criterion at complete inclusion of the investigated groups. 351 probands' families were studied: 57 with type II and 27 with type III gastric ulcer disease and 267 with duodenal ulcer disease. Gastric ulcer types were determined according to the classification of H. Johnson. The coefficient of genetic proportion in the cases of duodenal ulcer disease was additionally calculated according to the type of patients' familial pre-disposition. The coefficient of genetic proportion was found to acquire identical values for all groups studied without exception when calculated on the basis of one proband in a family (y = 1) both by the method of probands and the method of simple registration. The segregation coefficient values obtained using the direct methods of Weinberg do not support the hypothesis of monogenic transmission pattern either of the ulcer disease as a whole or of its different varieties.     

Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure

BACKGROUND: How Helicobacter pylori infection affects gastric acid secretion is still unclear. METHODS: Gastric juice pH, ammonia concentration in gastric juice, serum gastrin level, and grade of gastritis in accordance with the Sydney System were determined for patients with gastric ulcer (GU) and duodenal ulcer (DU) before and after treatment with lansoprazole and amoxicillin, and results were compared with those of H. pylori-negative controls. RESULTS: Scores for H. pylori density, atrophy, metaplasia, and activity of gastritis in the corpus were higher in patients with GU, especially those with proximally located GU, than in those with DU. Gastric juice pH was significantly higher in GU patients than in DU patients and controls. After H. pylori eradication, gastric juice pH and serum gastrin levels in both GU and DU patients were significantly decreased to control levels. In patients without eradication, no significant changes in these factors were observed. CONCLUSIONS: These findings suggest that H. pylori infection and gastritis in the corpus suppress acid secretion and increase gastric juice pH, resulting in hypergastrinemia, and that eradication of H. pylori normalizes acid secretion and serum gastrin levels.