Helicobacter pylori infection and duodenal ulcer in children and adolescents

To investigate the relationship between H. pylori infection and duodenal ulcer in children and adolescents, the markers of H. pylori infection were studied in 22 children and adolescents who had duodenal ulcers and were followed prospectively (Group A). Another 36 patients with gastrointestinal symptoms, but without ulcer, were also studied for comparison (Group B). Antral and duodenal tissues were biopsied and analyzed for the presence of H. pylori using three standard methods: urease test, culture and histology. The specific IgG antibody against H. pylori positivity using the ELISA method were also analysed. By these three methods, H. pylori positivity in the antral tissues, chronic active antral gastritis, and seroprevalence rate were found to be much higher in Group A than Group B. However, a similar trend was not found in the duodenal tissues. H. pylori was found in four of five patients during postoperative follow-up for duodenal ulcer. Among the four patients, no duodenal ulcer but chronic active gastritis was detected endoscopically in three who received vagotomy. Only the one who received simple closure of the perforated duodenal ulcer had a recurrent duodenal ulcer. It was concluded that a close relationship among duodenal ulcer, chronic active gastritis and H. pylori is present in children and adolescents.     

Developing a critical pathway for orientation

In an attempt to establish the etiologic role of Helicobacter pylori (H. pylori) in gastric and/or duodenal pathology, 169 patients were tested and compared with a control group of 25 healthy subjects, for a total of 194 subjects. Data on sex, age, familiarity, smoking, coffee and alcohol habits were collected and each patient underwent histological, microbiological and immunological tests. 80 (41.2%) subjects were found positive to H. pylori. This bacterium was detected in 53.3% of patients with gastric ulcer while IgG were found in 86.7%; in 50% of patients with chronic atrophic gastritis while IgG were detected in 80%; in 48.5% of patients with duodenal ulcer while IgG were found in 87.9%; in 41.8% of patients with superficial chronic gastritis while IgG were detected in 80.2%. In the control group of healthy patients H. pylori was found in 28% of patients while IgG were detected in 62.5%. The results do not confirm a direct clear-cut correlation between this microorganism and the pathologies studied.     

Histamine and peptic ulcer: a prospective study of mucosal histamine concentration in duodenal ulcer patients and in control subjects suffering from various gastrointestinal diseases

In a prospective study the histamine content of the mucosa of the body of the stomach was measured in 100 patients consisting of control subjects, patients with duodenal ulcer and patients suffering from various gastrointestinal diseases. The histamine content was found to be 43 mug/g in male control subjects (median) while in duodenal ulcer patients levels attained were significantly lower by about 30 per cent. In all the other groups of patients histamine concentrations in gastric mucosa were found to be "normal". Since in most species it is extremely diffcult to alter the mucosal histamine concentration by any form of treatment, the diminished histamine content of the gastric mucosa in patients with duodenal ulcer seems remarkable. Among several possible explanations offered for this finding we think the most likely is that histamine release is increased in duodenal ulcer disease.     

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.     

Seasonal behaviour of healed duodenal ulcer

Incidence of peptic ulcer is more in people living at higher altitude and similarly relapse of healed duodenal ulcer is more in winter season. Seasonal behaviour of healed duodenal ulcer with or without maintenance therapy with H2 blockers was studied among subjects residing around Shimla (approximate altitude 7000 feet above mean sea level). Sixty-four subjects of endoscopically healed duodenal ulcer were alternatively advised placebo (32 subjects) and ranitidine 150 mg (32 subjects) at bed time as maintenance therapy for period of one year. Subjects were reviewed endoscopically and evaluated for H pylori by rapid urease test, every months or earlier if symptomatic. Relapse rate was analysed among 60 subjects at the end of one year. Cumulative relapse rate was found 60% in ranitidine group and 100% in placebo group. In ranitidine group percentage of relapse to number of endoscopic examinations was 21.4% throughout the year, but in placebo group during winter and spring season relapse was 87.5% of endoscopic examination whereas 57.2% during summer and fall season. Incidence of duodenal ulcer relapse without maintenance therapy was more in winter and spring season (October to March) as compared to summer and fall (April to September), whereas intermittent seasonal treatment is efficacious in prevention of duodenal ulcer relapse and also improves cost benefit ratio of ulcer treatment.     

The antibiotic sensitivity of Staphylococcus aureus--the causative agent of chronic tonsillitis and pharyngitis--in gastroenterology patients]

Sensitivity was studied to fifteen antibiotics of different members of Staphylococcus aureus group of bacteria recovered from the mucous coats of the palatine tonsils, throat, in twenty seven patients with gastroduodenitis, 21 those with duodenal ulcer, 12 patients with other gastroenterological disorders, and 17 essentially healthy carriers of above micro-organisms. The pathogens causing tonsillopharyngitis in the patients appeared to be significantly less sensitive to seven antibiotics than they were in controls. Polyresistance to antibiotics is a sign of a higher virulence. It is conceivable that staphylococcus has a part in the pathogenesis of harmful changes in the tissues of the gastroduodenal zone.     

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.     

Helicobacter pylori infection in the etiopathogenesis of duodenal ulcer in children

The study evaluates the frequency of Helicobacter pylori (H. pylori) infection, as well as systemic cellular immune response to H. pylori in children with duodenal ulcer (DU). The study group comprised 47 children with DU, aged 6-17 (mean 13, 1 +/- 4, 2). H. pylori detection was based on urease test, histology, culture and serologic tests. Endoscopic and morphologic findings were analysed according to Sydney System criteria. In 12 children from the overmentioned group subsets of blood lymphocytes B and T (CD3, CD4, CD8, CD3/DR, CD19) and NK cells, some neutrophils functions (phagocytosis, chemiluminescence) and phagocytes receptors before and one month after H. pylori triple treatment were investigated. H. pylori infection was detected in 44 of the investigated children. In addition, pathologic examination revealed chronic gastritis in 44 children and chronic duodenitis in 42 of them. In immunosystemic examination decreased percentage of CD8 lymphocytes and NK cells, increased CD4/CD8 ratio, decreased mitogen-induced response and changes of function and receptor expression of neutrophils were found. After H. pylori treatment in follow-up endoscopy no ulcers were found and histologic examination did not reveal chronic active gastroduodenitis, while the rate of nonactive gastritis was increased. Eradication of H. pylori infection in 41 children and normalisation of immune parameters in 11 children were obtained. The results of our investigation indicate, that H. pylori infection plays an important role in the pathogenesis of DU in children.     

Differential north to south gastric cancer-duodenal ulcer gradient in China. China Ulcer Study Group

There are suggestions that duodenal ulcer protects individuals from gastric cancer and that rice is ulcerogenic while wheat is gastro-protective. We aimed to examine the relationship of gastric cancer, duodenal and gastric ulcers in different geographical regions in China and identified dietary risk factors for duodenal ulcer and gastric cancer. The prevalence of peptic ulcer and gastric cancer among symptomatic patients in eight major cities, four each from the north and the south representing all the six defined regions of China were studied. Endoscopy and case records over a 10 year period were reviewed and cases of confirmed duodenal and gastric ulcer and gastric cancer, together with the total number of endoscopies performed per year, were recorded. Rates were expressed as cases/1000 endoscopies. Results were compared to another epidemiological study on diet and mortality in the same regions in China conducted at the same time. Duodenal ulcer rates were 2.4-fold higher in southern China than northern China, whereas gastric cancer rates were 1.6-fold higher in the north than in the south. Correlation studies showed for the first time an inverse linear relationship between the gastric cancer rates and the duodenal ulcer rates (r=-0.8076, P=0.015), as well as the duodenal ulcer: gastric ulcer ratios (r=-0.9133, P=0.002). Gastric ulcer rates were higher in southern China but did not correlate with the gastric cancer rates (r=0.1455, P=0.731). Duodenal ulcer rates were found to be related to daily rice intake (r=0.8554, P=0.029) and inversely related to daily wheat flour intake (r=-0.8472, P=0.033). Gastric cancer rates were not related to any dietary risk factors tested. We concluded there was an inverse relationship between gastric cancer rates and duodenal ulcer rates. Although duodenal ulceration and gastric cancer are both linked to Helicobacter pylori infection, the findings of this study indicate independent additional aetiological factors for the pathogenesis of these conditions. Dietary factors such as rice or wheat intake may play a role.     

Gastric emptying in control subjects and patients with duodenal ulcer before and after vagotomy

The emptying of a solid meal labelled with Indium 113mDTPA from the stomach was studied with a gamma camera in 26 normal subjects, 27 patients with duodenal ulcer, on 41 occasions after truncal vagotomy and pyloroplasty and 38 times after highly selective vagotomy. Applying the method of principal component analysis to the results, differences were detected between control and duodenal ulcer subjects and two probable subgroups of duodenal ulcer were observed. Half emptying times did not reveal these patterns. After vagotomy, delayed emptying was general at one week. At one month, patients after highly selective vagotomy had a more normal result than those with truncal vagotomy and pyloroplasty (TV), but by six months no significant difference in overall emptying rate was found, although changes in the pattern of gastric emptying persisted in some patients after TV.     

Helicobacter pylori infection in patients with chronic pancreatitis and duodenal ulcer

BACKGROUND: The prevalence of duodenal ulcer is high in patients with chronic pancreatitis. Patients with simple duodenal ulcer without chronic pancreatitis are mostly Helicobacter pylori-infected, and the prevalence of IgG seropositivity is > 95%. The prevalence of H. pylori infection in patients with chronic pancreatitis is not known. METHODS: IgG antibodies against H. pylori were measured in a cross-sectional survey of consecutive patients who had their exocrine pancreas function examined with a Lundh meal test in the period 1988-95 and in a control group of patients with simple duodenal ulcer. RESULTS: Twenty-seven per cent of the patients with chronic pancreatitis had duodenal ulcer during the observation period. The prevalence of IgG antibodies against H. pylori was 22% in patients with chronic pancreatitis without duodenal ulcer as compared with 27% with non-organic abdominal pain. The prevalence of IgG antibodies against H. pylori was 60% in patients with chronic pancreatitis complicated by duodenal ulcer as compared with 86% in controls with simple duodenal ulcer. CONCLUSIONS: H. pylori infection contributes but may not be the only cause of duodenal ulcer in patients with chronic pancreatitis.     

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.     

Nonsteroidal anti-inflammatory drug-associated upper gastrointestinal lesions in rheumatoid arthritis patients. Relationships to gastric histology, Helicobacter pylori infection, and other risk factors for peptic ulcer

BACKGROUND: Nonsteroidal anti-inflammatory drugs (NSAIDs) are risk factors for peptic ulcer in rheumatoid arthritis (RA) patients, but the contribution of reactive gastritis, concomitant Helicobacter pylori infection, or RA activity to NSAID ulcer pathogenesis is unknown. METHODS: Ninety-six RA patients taking NSAIDs and dyspeptic sex- and age-matched control patients without NSAID use or an RA diagnosis were enrolled in the study. RESULTS: Gastric ulcer (GU) was detected in 29 (30%) RA patients and 3 control patients (P < 0.001). Sixteen RA patients and no control patient had an H. pylori-negative GU. The GUs of the RA patients were mainly located in the prepyloric region (28%) and antrum (62%). Nine of the 29 RA patients (31%) with GU had more than 1 ulcer. Erosive gastropathy was detected in 34 (71% H. pylori-negative) RA patients and in 13 (62% H. pylori-negative) control subjects (P < 0.001). Chronic gastritis was observed in 65 RA patients (48% H. pylori-negative) and in 58 control subjects (43% H. pylori-negative) (NS). whereas reactive gastritis was found in only 2 RA patients and in none of the controls. Corticosteroid use was the only independent risk factor for GU: odds ratio was 6.8 (95% confidence interval, 1.3-36.0). The prevalences of duodenal ulcer or esophagitis were not increased in RA patients. CONCLUSIONS: RA patients using NSAIDs continuously are at a greatly increased risk of developing both H. pylori-negative and -positive GUs, and corticosteroid use is an independent risk factor for ulcer development. Most RA patients have chronic gastritis, whereas reactive gastritis is rarely associated with continuous NSAID use in RA patients.     

Duodenal bicarbonate secretion: eradication of Helicobacter pylori and duodenal structure and function in humans

BACKGROUND & AIMS: Eradication of Helicobacter pylori expedites duodenal ulcer healing and prevents recurrences. Most patients with duodenal ulcers have impaired proximal duodenal mucosal bicarbonate secretion (DMBS). In patients with inactive, healed duodenal ulcers and normal subjects, the effect of H. pylori infection on DMBS and proximal duodenal secretory function and structure were examined. METHODS: DMBS was quantitated before and after eradication of H. pylori. Mucosal structure (duodenal bulb histopathology) and function (DMBS at rest and stimulated, effect of active vs. healed ulcer and of age) were determined in patients with duodenal ulcers and normal subjects. RESULTS: In patients with duodenal ulcers, H. pylori eradication normalized proximal DMBS. Histological examination of duodenal biopsy samples was comparable in patients with duodenal ulcers and normal subjects without apparent relationship between inflammation and DMBS. Significantly impaired DMBS occurred in response to all agonists tested (luminal acid, prostaglandin E2, and cephalic-vagal stimulation) in patients with duodenal ulcers, suggesting a generalized secretory defect. Neither the presence of active (vs.inactive) ulcer nor age significantly affected bicarbonate secretion. CONCLUSIONS: In patients with duodenal ulcers, eradication of H. pylori normalized proximal DMBS and may thereby reduce ulcer recurrences. Altered DMBS in patients with duodenal ulcers was unrelated to histopathologic abnormalities. Impaired bicarbonate secretion in patients with duodenal ulcers could be caused by a cellular and/or physiological regulatory transport defect possibly related to H. pylori.     

Ventricular premature beats. When is drug treatment justified?

Histological investigations were carried out upon the state of the gastric and duodena mucosa in 27 young patients with duodenal ulcer, seven out of them being in the state of exaverbation of the ulcer and 20-in remission. While the duodenal mucosa in the majority of the cases (88.9%) was established to be affected, in 85.2 percent of the patients the gastric mucosa remained intact. The chronic duodenitis observe n 24 of the cases have no atrophic character. The changes in the mucous secretion of duodenal mucosa are in direct correlation with the state of exacerbation or remission of the ulcer process. Similar correlation was not established in gastric mucosa.     

The effect of H. pylori in perforation of duodenal ulcer

BACKGROUND/AIMS: H. pylori has been described as an opportunistic pathogen attracted by changes in the gastric mucosa caused by inflammation and ulceration. However, the role of H. pylori infection in the perforation of duodenal ulcers has not yet been clearly determined. The aim of this study was to assess the prevalence of H. pylori infection in patients undergoing laparotomy for repair of a perforated duodenal ulcer. METHODOLOGY: Patients who underwent surgery for a perforated duodenal ulcer in our Surgical Unit between January 1994 and July 1996 were included in this study. The study population consisted of eighteen patients with a mean age of 32.7 (21-48) years. All of the patients were male. Patients with chronic duodenal ulcer perforation and with no contraindications for definitive surgery, such as peritonitis, shock (blood pressure <90 mm Hg), age >60 years, or more than a 12-hour elapse from the time of perforation, were treated by bilateral truncal vagotomy and Weinberg pyloroplasty. The ulcer was excised with the pyloric ring. The cut was then extented by about 2 cm on both the gastric and duodenal sides. Two biopsies were taken from the antral mucosa by endoscopic biopsy forceps. The defect was closed transversely. The ulcer specimen and the antral biopsies were fixed separately in 10% formalin solution and sent to the department of Histopathology. The specimens were stained with Hematoxylin-Eosin and examined for H. pylori . Sections of the ulcer specimen were especially investigated for the presence of H. pylori through all layers of the ulcer. RESULTS: H. pylori was found in the antral biopsies of 16 patients (88.8%). In seven of the ulcer specimens (38.8%), H. pylori was present in the mucosa and also extended through the wall of the ulcer. H. pylori was positive in the antral biopsies of all patients with H. pylori present in the ulcer wall. CONCLUSIONS: In our study, H. pylori was present at a high ratio in the antral biopsies of patients with duodenal ulcer perforation. The presence of H. pylori throughout the ulcer wall to a considerable extent emphasizes the fact that eradication of H. pylori is important in the treatment of perforated duodenal ulcer.     

Pain syndrome in gastroenterological practice: potentialities of evaluation

Qualitative and quantitative characteristics of chronic pain syndrome and their possible use in assessing analgetic effects of treatment were studied in 16, 49, 26 and 17 patients with gastric ulcer, duodenal ulcer, chronic pancreatitis, chronic colitis, respectively. Pain was measured with the use of McHill's questionnaire modification and visual-verbal-analog scale. In addition to routine analysis of the data from the respondents, graphic mean profiles of pain for each group have been devised. There were differences in quantitative parameters of pain syndrome depending on nosological unity and profiles of patients. The questionnaire proved rather informative in evaluation and gradation of analgetic effects of therapeutic factors in ulcer patients.     

Causes of death in duodenal and gastric ulcer

An analysis has been made of 235 deaths that occurred among 1905 patients with peptic ulcer who constituted a random sample of the occurrence of ulcer disease in an area of Denmark comprising half a million inhabitants. The disease itself, according to the death certificate, was considered the primary cause of death in 10% of the cases; half of these had been operated on immediately before death. The other patients died more frequently than expected from the following causes: chronic bronchitis, pulmonary emphysema, cancer of the lung, cirrhosis of the liver, and cancer of the pancreas. Although the comorbidity with chronic bronchitis and emphysema was especially pronounced in patients with gastric ulcer, the association with liver cirrhosis and cancer of the pancreas occurred only in patients with duodenal ulcer. In women the mortality rate attributable to cardiac and vascular diseases was lower than expected. No excess coincidence of suicide was found. Berkson's fallacy is considered to be of much less importance as a possible explanation of the comorbidity found in the present study than in the majority of publications concerned with this question.     

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.