Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Helicobacter pylori infection of the gastric mucosa can be found in approximately 50% of the world's population and is associated with a range of pathology, including peptic ulcer, atrophic gastritis, and gastric cancer. To explore immunization as a strategy for preventing and treating H. pylori-associated disease, we assessed the safety and immunogenicity in healthy adults of a formalin-inactivated, oral H. pylori whole-cell (HWC) vaccine, administered with or without mutant Escherichia coli heat-labile toxin (LT(R192G)) as a mucosal adjuvant. In a dose-response study, 23 subjects with or without H. pylori infection were vaccinated with either 2.5 x 10(6) HWC, 2.5 x 10(8) HWC, or 2.5 x 10(10) HWC, plus 25 microg of LT(R192G). Thereafter, a randomized study was conducted in which 18 H. pylori-infected subjects were assigned, in a double-blind fashion, to receive either 2.5 x 10(10) HWC plus placebo-adjuvant, placebo-vaccine plus 25 microg of LT(R192G), placebo-vaccine plus placebo-adjuvant, or 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Diarrhea (six subjects), low-grade fever (five subjects), and vomiting (two subjects) were observed, usually after the first dose. Significant rises in geometric mean mucosal (fecal and salivary) anti-HWC immunoglobulin A antibodies occurred among H. pylori-infected and uninfected subjects following inoculation with 2.5 x 10(10) HWC plus 25 microg of LT(R192G). Moreover, among H. pylori-negative volunteers, this regimen induced significant lymphoproliferative responses in 5 of 10 subjects and gamma interferon production responses to H. pylori sonicate in 7 of 10 subjects. There was no evidence that vaccination eradicated H. pylori in infected volunteers. These results suggest that it is possible to stimulate mucosal and systemic immune responses in humans to H. pylori antigens by using an HWC vaccine.
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PMID:Safety and immunogenicity of oral inactivated whole-cell Helicobacter pylori vaccine with adjuvant among volunteers with or without subclinical infection. 1134 17

Dyspepsia can describe a subset of children with episodic or persistent abdominal symptoms--often related to feeding--that are thought to be caused by disorders of the proximal part of the digestive tract. Symptoms, such as vomiting, early satiety, postprandial epigastric abdominal pain, heartburn, abdominal fullness, poor weight gain, and/or anorexia, have been incorporated into the definition of dyspepsia. Unfortunately, presenting signs and symptoms in children with dyspepsia are nonspecific and can occur as a result of many diseases, such as parasitic infections, esophagitis, eosinophilic gastroenteritis, Helicobacter pylori infection, Crohn's disease, biliary tract or hepatic disease, pancreatitis, and lactose intolerance. This lack of specificity makes the evaluation of dyspepsia more difficult. Here, we describe an approach for the evaluation of dyspepsia that correlates in part with the child's presenting symptoms.
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PMID:Techniques for the evaluation of dyspepsia in children. 1141 83

In institutionalized adults with intellectual disability (ID), Helicobacter pylori infection occurs at approximately twice the rate it appears in the general population, and it may be responsible for the twofold higher rates of peptic ulcer disease and gastric cancer in this population. Medical, behavioural and additional environmental factors, as well as level of ID, may be related to the risk of infection with H. pylori. One hundred and sixty-eight adults with ID who were currently, had previously been or had never been institutionalized underwent a biopsychosocial evaluation. This included assessment of: level of ID using the Adaptive Behaviour Scale (ABS) Part I; levels of maladaptive behaviour using the ABS Part II; demographic, medical and environmental factors; as well as H. pylori tests using serology and faecal antigen. The overall rates of past or current infection with H. pylori in institutionalized and previously institutionalized participants were about twice that of the overall group of never-institutionalized participants, i.e. 87% and 79% compared to 44%, respectively (P < 0.001). The rates of H. pylori infection appeared to increase with age in the never-institutionalized group, but were consistently high across all ages in the other groups. The rate of infection was higher in those institutionalized for more than 5 years (95% versus 76%, P=0.02), in those with flatmates with excessive oral secretions (65% versus 21%, P < 0.001) or faecal incontinence (67% versus 27%, P < 0.001), and in those with more chronic illness and medications. All mean domain scores of the ABS Part I (Intellectual Disability) were significantly lower (indicating more severe ID) in the group currently infected with H. pylori compared to their non-infected counterparts. The majority of mean domain scores of the ABS Part II (Behaviour) were also worse, with half of these score differences reaching statistical significance in the currently infected group. The presence of alarm symptoms (e.g. vomiting, weight loss, haematemesis and melena), iron deficiency and body mass index were not significantly different in currently infected subjects. Adults with ID appear to be particularly at risk of infection with H. pylori. Environmental associations with infection include past or current institutionalization, a longer period of institutionalization, living with flatmates with excessive oral secretions and faecal incontinence. Medical associations include chronic disease and more medications, but not alarm symptoms or body mass index. Demographic associations may include increasing age in never-institutionalized adults, but no age effect in currently or previously institutionalized individuals. Psychosocial associations include more severe ID and maladaptive behaviour with current infection.
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PMID:Environmental, medical, behavioural and disability factors associated with Helicobacter pylori infection in adults with intellectual disability. 1185 56

It is estimated that by 2020, >16% of people in the United States will be > or =65 years of age and that nearly 20 million will be >85 years of age. Aging imparts a variety of physiologic changes in the oropharynx, esophagus, and stomach that increase the risk for esophageal and gastrointestinal disorders. Older individuals also tend to have a higher prevalence of comorbid factors, such as Helicobacter pylori infection, smoking, presence of other diseases, or use of medications (e.g., nonsteroidal anti-inflammatory drugs [NSAIDs]) that increase their risk for acid-related disorders. Given these physiologic and comorbidity factors, the elderly are at higher risk for gastroesophageal reflux disease (GERD), pill-induced esophagitis, peptic ulcer disease, and complications related to the use of NSAIDs. Unfortunately, in the elderly patient with these disorders--even those with severe disease or complications--symptom presentation may be subtle or atypical, resulting in a delayed diagnosis. Endoscopy remains the "gold standard" for the identification of mucosal disease and should be performed in all patients with "new-onset" or persistent symptoms who are >45 years of age, as well as in individuals of any age who present with alarm symptoms, such as weight loss, vomiting, anemia, dysphagia, or evidence of gastrointestinal bleeding. In general, the treatment of older individuals with peptic ulcer or GERD and its complications is similar to that of younger individuals. Proton pump inhibitors are the mainstay of therapy for symptom relief, healing of erosive esophagitis, resolution of peptic ulceration, reduction of the risk for NSAID-induced mucosal damage, and prevention of disease recurrence.
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PMID:Aging, the gastrointestinal tract, and risk of acid-related disease. 1547 47

Collagenous gastritis, a counterpart of collagenous colitis, is an extremely rare disorder. The first case of collagenous gastritis in a Korean boy in his pre-teens who had been receiving treatment for refractory iron deficiency anemia has been reported. The patient had been suffering from intermittent abdominal pain, recurrent blood-tinged vomiting and poor oral intake. The gastric endoscopy revealed diffuse cobblestone appearance of the mucosa with easy touch bleeding throughout the stomach but no abnormalities in the esophagus, duodenum, and colon. Pathologic examination of the gastric biopsies from the antrum, body and cardia showed a subepithelial collagen deposition with entrapped dilated capillaries, moderate infiltrates of lympho-plasma cells and eosinophils of the lamina propria, and marked hypertrophy of the muscularis mucosa. The collagen deposition appeared as discontinuous bands with focally irregular extension into the deeper part of the antral mucosa. It measured up to 150 microm. Helicobacter pylori infection was not detected. The biopsies from the duodenum, esophagus and colon revealed no pathologic abnormalities.
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PMID:Collagenous gastritis in a Korean child: a case report. 1571 21

Idiopathic dyspepsia refers to pain and/or discomfort perceived in the epigastrium that is not secondary to organic, systemic, or metabolic diseases. Symptoms may overlap with those of gastroesophageal reflux disease and irritable bowel syndrome. Gastrointestinal motor disorders, hypersensitivity to mechanical or chemical stimuli, and psychosocial factors can act individually or in concert to induce the symptoms of dyspepsia. Accordingly, there is no single therapy, and treatment must be individualized. Eradication of Helicobacter pylori infection rarely achieves symptom improvement. Treatment of idiopathic dyspepsia should begin by reassuring the patient about the benign nature of the syndrome and educating them on the knowledge that has been achieved in recent years regarding potential causes of the syndrome. Both prokinetic and antisecretory drugs have been reported to improve dyspeptic symptoms, but results are not completely convincing. Although well-designed studies demonstrate superiority of proton pump inhibitors over placebo, it should be noted that patients with nonerosive gastroesophageal reflux disease were invariably included; when these patients are excluded, the benefit of antisecretory medications is questionable. We suggest that patients with idiopathic dyspepsia be initially treated according to the predominant symptom. Those with epigastric pain/burning should receive a trial with standard doses of proton pump inhibitors for 4 to 8 weeks, whereas prokinetic patients should be prescribed at recommended doses for similar periods of time to patients with nonpainful dyspeptic symptoms such as posprandial fullness, early satiety, nausea, or vomiting. Nonresponders may benefit from combination therapies or short trials with higher doses of drugs. Visceral analgesics and antidepressants can also be prescribed alone or in combinations with other therapeutic strategies. Recent studies demonstrate utility for psychologic therapy and hypnotherapy, although truly controlled studies are difficult in this area. Herbal medicines deserve further evaluation.
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PMID:Idiopathic Dyspepsia. 1576 39

Disorders of the stomach represent a significant portion of the practice of pediatric gastroenterology. Controversy still exists in the appropriate management of children with abdominal pain and vomiting and large gaps remain in our understanding of the physiology and pathophysiology of the stomach in children. Nevertheless, we have made significant progress in understanding Helicobacter pylori infection and gastric motility in the pediatric population.
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PMID:Pediatric disorders of the stomach. 1703 48

A 6-year-old boy was hospitalized because of dark feces and facial pallor of 1 weeks duration. Other gastrointestinal symptoms, including vomiting and abdominal pain, were absent, but he felt dizziness when standing and fatigue on effort. Hematologic studies revealed iron-deficiency anemia, and endoscopy showed gastric erosions and a duodenal ulcer. All test results for Helicobacter pylori infection, including H. pylori antigen in stool, anti-H. pylori IgG immunoassay in serum, and the (13)C-urea breath test, were positive. Because an H. pylori-associated gastric ulcer had been diagnosed with endoscopy in the patients father 3 years earlier, father-son transmission was suspected. The patient was treated with triple-agent eradication therapy (proton pump inhibitor [lansoprazol], amoxicillin, and clarithromycin) for 2 weeks. One month after therapy was completed, eradication of H. pylori was confirmed by negative results on the stool antigen test. Peptic ulcer disease can occur in young children, as in this case. The stool antigen test kit is a useful and reliable method that can be used even in preschool children to diagnose H. pylori infection.
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PMID:Helicobacter pylori infection with a duodenal ulcer in a 6-year-old boy. 1710 82

The mode of transmission of Helicobacter pylori infection is poorly characterized. In northern California, 2,752 household members were tested for H. pylori infection in serum or stool at a baseline visit and 3 months later. Among 1,752 person considered uninfected at baseline, 30 new infections (7 definite, 7 probable, and 16 possible) occurred, for an annual incidence of 7% overall and 21% in children <2 years of age. Exposure to an infected household member with gastroenteritis was associated with a 4.8-fold (95% confidence interval [CI] 1.4-17.1) increased risk for definite or probable new infection, with vomiting a greater risk factor (adjusted odds ratio [AOR] 6.3, CI 1.6-24.5) than diarrhea only (AOR 3.0, p = 0.65). Of probable or definite new infections, 75% were attributable to exposure to an infected person with gastroenteritis. Exposure to an H. pylori-infected person with gastroenteritis, particularly vomiting, markedly increased risk for new infection.
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PMID:Gastroenteritis and transmission of Helicobacter pylori infection in households. 1728 20

Gastric hyperplastic polyps in organ transplant recipients have been recently described; however, the clinical significance of hyperplastic polyps in this setting remains unclear. The aim of this study is to further characterize the clinical presentation and histopathology of gastric hyperplastic polyps in organ transplant recipients as compared to hyperplastic polyps in non-transplant individuals. All gastric hyperplastic polyps diagnosed in our institute from 1999 to 2005 were retrieved. Clinical data including endoscopic findings were reviewed. Twenty cases without history of transplantation were randomly selected for a control population. Hematoxylin and eosin and Genta stains were reviewed. 104 cases of gastric hyperplastic polyps were identified. Sixteen (15%) had a history of solid organ (one liver/kidney, four livers, one lung, one kidney, one kidney/pancreas, three hearts) or bone marrow transplantation (five). The average time after transplantation was 28 months. Signs/symptoms leading to endoscopy were more frequently nausea/vomiting in transplant patients as compared to bleeding/hematemesis/anemia in non-transplant patients. The transplant patients tended to be younger with a reversed M:F ratio, but age was the only demographic factor that was statistically significant. There was no difference in polyp size, location and number. Histologically, no difference was observed in the frequency of active inflammation, Helicobacter pylori infection or intestinal metaplasia. Dysplasia was not present in any of the cases. None of the patients had a history of polyposis syndrome. In conclusion, a significant percentage of gastric hyperplastic polyps (15%) were from organ transplant patients, further suggesting a strong association of gastric hyperplastic polyps with transplantation. The younger age in the transplant group may be explained by the nature of the cohort qualified for transplantation. While no statistically significant differences in histopathologic features were found between transplant and non-transplant groups, analysis was limited by small case numbers. Overall, gastric hyperplastic polyps in the post transplant setting is a common, but under-recognized entity and merits further clinicopathologic analysis.
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PMID:Gastric hyperplastic polyps in post transplant patients: a clinicopathologic study. 1850 Feb 62


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