Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection may not be the primary cause of duodenal ulceration in cases not associated with non-steroidal anti-inflammatory drugs, but may be a secondary complication. In developing countries with a uniformly high prevalence of H. pylori infection there are marked regional differences in the prevalence of duodenal ulcer (DU). In some countries, especially those with a low prevalence of H. pylori, 30-40% or more patients with DU may be H. pylori negative. The absence of H. pylori infection in early cases of DU is also reported. In DU patients with antral H. pylori infection, duodenal colonization by H. pylori may often be absent. After complete H. pylori eradication, recurrence of DU within 6 months in some reports is as high as 20%. The evidence suggests that high acidity and reduced duodenal mucosal resistance remain the primary causes of DU and that H. pylori infection, when present, results in chronicity. Reduced mucosal resistance results in duodenal gastric metaplasia which permits colonization of the duodenum with H. pylori from the antrum. Therefore, whatever causes reduced mucosal resistance may be the primary factor and evidence suggests that this cause may be diet related. This would explain the enigma of regional variations in DU prevalence unrelated to H. pylori prevalence.
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PMID:Is Helicobacter pylori the primary cause of duodenal ulceration? 1057 30

The objective of the present study was to evaluate seasonal periodicity in the prevalence of Helicobacter pylori. A prospective study was performed on 1076 consecutive patients who were investigated in our hospital over a 3-year span because of epigastric complaints. Our findings indicate a significant accumulation of positive Helicobacter pylori tests in October. Gastric acidity, gender, and age did not influence Helicobacter pylori infection significantly. There was no significant correlation between potential seasonal influence on the diagnosis of ulcer disease and the seasonal fluctuation of Helicobacter pylori infection. The seasonality was confirmed by cosinor analysis for the absolute frequencies of H. pylori infections and also for the number of cases positive for H. pylori per number of presenting patients per month. A seasonal concept of a sensitivity threshold for positive Helicobacter pylori testing is introduced, taking into account such factors as immune system, nutrition, and medication status.
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PMID:Is there seasonal periodicity in the prevalence of Helicobacter pylori? 1058 80

The association of Helicobacter pylori with gastritis, peptic ulcers, and gastric neoplasia has led to fundamental changes in the understanding of gastric disease in humans. The relationship of Helicobacter spp. infection to gastric disease in dogs is unclear. The objective of this study was to determine if Helicobacter infection affects the gastric secretory axis of dogs. Eight Beagle dogs with naturally acquired Helicobacter spp. infection were studied before and after (4 and 29 days) the attempted eradication of Helicobacter spp. with a combination of amoxicillin, metronidazole, and famotidine (AMF). Six specific-pathogen-free, Helicobacter-free Beagle dogs served as controls. The electron microscopic appearance of spiral organisms in infected dogs indicated coinfection with Helicobacter felis- and H bizzozeronii-like organisms. Unstimulated gastric pH and fasting, postprandial, and bombesin-stimulated plasma gastrin were similar in both infected and uninfected dogs, although a trend (P = .09) toward higher meal-stimulated gastrin was observed in infected dogs at 60 minutes. Pentagastrin-stimulated maximal acid output (mmol HCI/kg0.75/hour) and titratable acidity (mmol HCl/mL) were similar in both infected and uninfected dogs, but gastric pH during maximal acid output was lower (P < .01) in uninfected dogs. Mild gastric inflammation was present in both infected and uninfected dogs. Gastric spiral organisms were undetectable in 6/8 infected dogs 4 days after AMF but had recurred in 8/8 dogs 29 days after AMF. Analysis of gastric DNA with Helicobacter-specific primers indicated persistence of Helicobacter DNA at 4 and 29 days after antibiotic therapy. Acid secretion, plasma gastrin, and mucosal inflammation were not affected by the transient suppression of Helicobacter spp. by AMF. These findings suggest that gastric secretory function in dogs is not markedly perturbed by naturally acquired Helicobacter spp. infection and that treatment with amoxicillin, metronidazole, and famotidine causes suppression rather than eradication of gastric Helicobacter spp. in dogs.
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PMID:Gastric function in dogs with naturally acquired gastric Helicobacter spp. infection. 1058 48

The effects of Helicobacter pylori infection on gastric acid secretion has not been clarified. The aim of this study was to elucidate the effects of H. pylori infection on gastric juice pH in relation to gene expression of interleukin-1beta (IL-1beta), which is reported to inhibit gastric acid secretion. Gastric juice pH and serum gastrin levels were measured in patients with peptic ulcer disease. The amount of IL-1beta mRNA in gastric fundic gland mucosa was also measured by a competitive reverse transcription-polymerase chain reaction method. These parameters were determined before and after treatment with lansoprazole and amoxicillin. Before treatment a significant positive relation was observed between the amount of IL-1beta mRNA in gastric fundic gland mucosa and gastric juice pH. After treatment significant decreases in the amount of IL-1beta mRNA, gastric juice pH, and serum gastrin levels were observed in patients with eradication of H. pylori, whereas no significant changes were observed in patients without eradication. These results suggest that H. pylori infection induces IL-1beta and suppresses acid secretion, resulting in increases in gastric juice pH and serum gastrin levels. Eradication of H. pylori decreases IL-1beta induction, resulting in an increase in gastric juice acidity and normalization of serum gastrin levels.
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PMID:Relation between interleukin-1beta messenger RNA in gastric fundic mucosa and gastric juice pH in patients infected with Helicobacter pylori. 1061 59

Published data on the regression of the extent of duodenal gastric metaplasia (DGM) after the eradication of Helicobacter pylori infection and the normalization of the organism-induced alterations in gastric physiology are scanty and controversial. Therefore, we decided to assess the circadian pattern of gastric acidity and the degree of DGM before and one year after H. pylori eradication in a group of duodenal ulcer patients. Fifteen consecutive H. pylori-positive patients with endoscopically proven duodenal ulcer were recruited for this study. The diagnosis of H. pylori infection was based on CLO-test and histology, and DGM was assessed on four bulb biopsies taken before and one year after H. pylori eradication. At the same time, gastric pH was measured by 24-hr continuous intraluminal recording. H. pylori eradication was ascertained by means of concomitant negative CLO-test and histology performed both four weeks after the end of the eradicating treatment and at the one-year endoscopic control. After successful cure, all patients discontinued any antiulcer medication. The mean 24-hr gastric pH was 1.7 +/- 0.4 before and 1.6 +/- 0.4 after one year of H. pylori eradication (P = 0.75). DGM improved in three cases, worsened in four cases, and was unchanged in eight cases at the one-year control (P = 0.87). No correlation was found between 24-hr gastric pH and DGM (P = NS) both at baseline and one year after eradication. Our results show that neither circadian gastric acidity nor DGM change significantly one year after H. pylori eradication in duodenal ulcer patients. Thus, the disappearance of H. pylori infection does not determine any increase in gastric pH and any reversal of gastric-type epithelium in the duodenum.
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PMID:Effect of Helicobacter pylori eradication on 24-hour gastric pH and duodenal gastric metaplasia. 1096 9

The hypergastrinemia and hyperacidity associated with Helicobacter pylori infection has been explained by either a primary excess of gastrin or a lack of inhibitory influence by somatostatin (SOM). The objective of the present study was to compare the concentrations of fundic and antral SOM- and antral progastrin-derived peptides in nonulcer dyspepsia (NUD) subjects with and without H. pylori infection. Antral and fundic mucosal biopsies were extracted and assayed for SOM and gastrin amide, glycine-extended gastrin (gastrin gly), progastrin, and total gastrin. There was a significant sixfold reduction in antral SOM but no change in fundic SOM content in H. pylori-infected subjects compared to uninfected subjects. Antral gastrin amide concentrations were significantly higher in infected subjects. However, the concentrations of the nonamidated gastrin forms (progastrin and glycine-extended gastrin) were significantly lower in the infected subjects, indicating an increased conversion of the precursor forms of gastrin to amidated gastrin, the type known to stimulate gastric acidity. The present study demonstrates that the elevated gastrin concentrations associated with H. pylori infection may be due to a reduction in the paracrine inhibitory effect of SOM on antral gastrin release. In addition, the posttranslational processing of gastrin to the amidated forms is increased in infected subjects, explaining why the elevation in antral gastrin is confined to the amidated form.
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PMID:Expression of progastrin-derived peptides and somatostatin in fundus and antrum of nonulcer dyspepsia subjects with and without Helicobacter pylori infection. 1111 84

We present a case with extremely high serum gastrin induced by atrophic gastritis and Helicobacter pylori infection. The patient, a 95-year-old male, was diagnosed with idiopathic chronic diarrhea. During diagnostic work-up, his fasting serum gastrin was up to 2078 pg/mL. The secretin test was negative for gastrinoma. Octreotide scan showed no suspicious lesion except for diffuse faint uptake over the gastric antrum on the 48-hour-delay film. Gastric acidity test revealed achlorhydria. On histology examination, atrophic gastritis with Helicobacter pylori infection was found in the gastric body, but the antral mucus was normal with a slight increase in gastrin-secreting cells. To our knowledge, such extremely high serum gastrin induced by atrophic gastritis and Helicobacter pylori infection has never been reported before.
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PMID:Extreme hypergastrinemia caused by atrophic gastritis and Helicobacter pylori infection--a case report. 1149 Aug 38

The prevalence of Helicobacter pylori infection is steadily decreasing in developing countries, and this has been paralleled by an increasing incidence of gastroesophageal reflux disease (GERD) and adenocarcinomas of the esophagus and of the esophagogastric junction. The prevalence of H. pylori infection, which is on the decline in Europe and in the United States, is probably related to improvements in sanitary conditions and socioeconomic status. These epidemiological data do not support a role for H. pylori in the pathogenesis of GERD, but at the same time suggest a negative association with the rising incidence in esophageal diseases. While H. pylori infection clearly does not cause GERD, it may protect certain susceptible individuals from the development of GERD and its complications. There are conflicting reports that GERD can develop after H. pylori eradication and that proton pump inhibitors are less effective in suppressing intragastric acidity in H. pylori negative patients--reasons not to eradicate H. pylori in GERD patients. On the contrary, other data suggest an increase in the development of atrophic gastritis in GERD patients (H. pylori positive) on long-term proton pump inhibitor therapy - a reason to eradicate H. pylori. Preexisting lower esophageal sphincter dysfunction, susceptibility to GERD, unmasking of latent GERD, and patterns and severity of gastritis may be important factors contributing to the development of GERD rather than just the presence or absence of infection with H. pylori.
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PMID:Helicobacter pylori: a debated factor in gastroesophageal reflux disease. 1154 22

Endoscopic and morphological examinations of the upper gastrointestinal tract (GIT) were made in 80 patients with nonspecific ulcerative colitis (NUC). Tests for Helicobacter pylori infection and gastric juice acidity were also conducted. It was found that in many patients NUC was associated with development of nonspecific esophagitis, gastritis and duodenitis. The endoscopic examination revealed erosions of the abdominal esophagus in 13.8% cases, erosive-ulcerative alterations in the stomach and duodenum in 27.5% of NUC patients. The most marked changes occurred in patients with severe NUC. Alterations in the upper GIT were not related with either Hp or the acidity. Morphological examinations of the biopsies from the esophagus, stomach and duodenum demonstrated changes similar to those in biopsy material from the colon. The same type of morphological changes in mucosa from the upper GIT and the colon in NUC indicates that their pathogenesis is also the same.
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PMID:[Upper gastrointestinal tract lesions in patients with nonspecific ulcerative colitis]. 1285 68

Epidemiological studies demonstrate a negative association between Helicobacter pylori infection and gastro-oesophageal reflux disease and its complications. This might represent a protective effect because of the tendency for H. pylori infection to lower gastric acid secretion with advancing age. However, studies of the effect of H. pylori eradication on gastro-oesophageal reflux disease have failed to show any worsening of gastro-oesophageal reflux disease symptoms. Several interactions between H. pylori and proton-pump inhibitor therapy used to treat gastro-oesophageal reflux disease need to be considered. Helicobacter pylori infection improves the control of gastric acidity by proton-pump inhibitors and this produces a small advantage in clinical control of reflux disease. The infection prevents rebound acid hypersecretion occurring when proton-pump inhibitor therapy is discontinued. However, concerns have been expressed that the body gastritis induced by proton-pump inhibitor therapy in H. pylori-infected subjects might increase the risk of gastric cancer. At present, it is unclear whether H. pylori should be eradicated in gastro-oesophageal reflux disease patients.
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PMID:Review article: Helicobacter pylori and gastro-oesophageal reflux disease. 1604 57


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