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Query: UMLS:C0024623 (gastric cancer)
 36,219 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Working Party Report on the Management of Helicobacter pylori serves as a clinical practice guideline for Malaysian doctors. H. pylori is not uncommon in the Malaysian population. Marked racial differences and the consistently low prevalence rates amongst Malays are noted. The working party recommends that if endoscopy is to be performed, a rapid urease test should be used for diagnosis. Where suspicion of the infection is strong and the urease test is negative, histology should be performed on gastric biopsies. Culture should be used to monitor resistance patterns to antibiotics and regional laboratories should assume this responsibility. The urea breath tests are highly accurate tests for diagnosis of H. pylori but is as yet not widely available in Malaysia. The working party strongly recommends that all peptic ulcer patients infected with H. pylori whether active, in remission and complicated ulcers should be treated for the infection. Patients with low-grade gastric mucosal lymphoid tissue lymphoma should also be treated for H. pylori infection. It is considered advisable that patients on long term nonsteroidal antinflammatory drug (NSAID) treatment with a history of peptic ulcers or dyspepsia and patients following resection of early gastric cancer or those with a family history of gastric cancer should also be tested and treated for H. pylori. The working party recommends, as first line treatment a 7-day combination therapy of a proton pump inhibitor, clarithromycin and metronidazole or amoxicillin. High metronidazole resistance rates locally may adversely affect regimens containing the antibiotic. It should also be noted that regimens that yield lower eradication rates may result in higher long term expenditure.
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PMID:Management of Helicobacter pylori infection--a Working Party Report of the Malaysian Society of Gastroenterology and Hepatology. 1096 73

Since the causative role of Helicobacter pylori in peptic ulcer and gastritis was established, a number of advances have been made. Helicobacter virulence factors have been identified, the changes it causes in gastric acid secretion has been elucidated, and the entire genome of H. pylori has been mapped. Multiple lines of evidence indicate a strong link between the bacterium and noncardia gastric cancer. The infection can be confidently diagnosed by noninvasive serologic tests and the urea breath test. Triple therapy is almost always curative, and the infection almost never recurs in Canadian adults, but eradicating the bacteria in the absence of peptic ulcer only rarely leads to resolution of dyspepsia. New studies suggest that treating Helicobacter may increase the risk of peptic esophagitis and adenocarcinoma of the esophagus and cardia.
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PMID:Helicobacter and disease: still more questions than answers. 1104 91

AIM:To investigate the expression of multiple genes and the behavior of cellular biology in gastric cancer (GC) and other gastric mucosal lesions and their relations to Helicobacter pylori (H. pylori) infection, tumor staging and histological subtypes.METHODS:Three hundred and twenty seven specimens of gastric mucosa obtained via endoscopy or surgical resection, and ABC immunohistochemical staining were used to detect the expression of p53, p16, Bcl-2 and COX-2 proteins.H. pylori was determined by rapid urea test combined with patholo-gical staining or 14 Curea breath test. Cellular image analysis was performed in 66 patients with intestinal metaplasia (IM) and/or dysplasia (Dys). In 30 of them, both cancer and the paracancerous tissues were obtained at the time of surgery. Histolo-gical pattern, tumor staging, lymph node metastasis, grading of differentiation and other clinical data were studied in the medical records.RESULTS:p16 expression of IM or Dys was significantly lower in positive H. pylori chronic atrophic gastritis (CAG) than those with negative H. pylori (CAG: 54.8% vs 88.0%, IM:34.4% vs 69.6%, Dys: 23.8% vs 53.6%, all P < 0.05), Bcl-2 or COX-2 expression of IM or Dys in positive H. pylori cases was signi-ficantly higher than that without H. pylori (Bcl-2: 68.8% vs 23.9%, 90.5% vs 60.7%; COX-2: 50.0% vs 10.8%, 61.8% vs 17.8%; all P <0.05). The mean number of most parame-ters of cellular image analysis in positive H. pylori group was significantly higher than that in negative H. pylori group (Ellipser: 53 plus minus 14, 40 plus minus 12&mgr;m, Area(1): 748 plus minus 572, 302 plus minus 202&mgr;m(2), Area(2): 3050 plus minus 1661, 1681 plus minus 1990&mgr;m(2), all P< 0.05; Ellipseb: 79 plus minus 23, 58 plus minus 15&mgr;m, Ratio-1: 22% plus minus5%,13% plus minus4%,Ratio-2:79% plus minus17%,53% plus minus20%,all P<0.01). There was significant correl-ation between Bcl-2 and histologic pattern of gastric carcinoma, and between COX-2 and tumor staging or lymph node metasta sis (Bcl-2: 75.0% vs16.7%; COX-2: 76.0% vs 20.0%, 79.2% vs 16.7%; all P< 0.05).CONCLUSION:p16, Bcl-2, and COX-2 but not p53 gene may play a role in the early genesis/progression of gastric carcinoma and are associated with H. pylori infection. p53 gene is relatively late event in gastric tumorigenesis and mainly relates to its progression. There is more cellular-biological behavior of malignant tumor in gastric mucosal lesions with H. pylori infec-tion. Aberrant Bcl-2 protein expression appears to be preferentially associated with the intestinal type cancer. COX-2 seems to be related to tumor staging and lymph node metastasis.
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PMID:Multiple genetic alterations and behavior of cellular biology in gastric cancer and other gastric mucosal lesions:H.pylori infection, histological types and staging. 1181 7

Significant progress and new insights have been gained in the 4 years since the first Maastricht Consensus Report, necessitating an update of the original guidelines. To achieve this, the European Helicobacter Pylori Study Group organized a meeting of specialists and experts from around the world, representatives from National Gastroenterology Societies and general practitioners from Europe to establish updated guidelines on the current management of Helicobacter pylori infection. The meeting took place on 21-22 September 2000. A "test and treat" approach is recommended in adult patients under the age of 45 years (the age cut-off may vary locally) presenting in primary care with persistent dyspepsia, having excluded those with predominantly gastro-oesophageal reflux disease symptoms, non-steroidal anti-inflammatory drug users and those with alarm symptoms. Diagnosis of infection should be by urea breath test or stool antigen test. As in the previous guidelines, the eradication of H. pylori is strongly recommended in all patients with peptic ulcer, including those with complications, in those with low-grade gastric mucosa-associated lymphoid tissue lymphoma, in those with atrophic gastritis and following gastric cancer resection. It is also strongly recommended in patients who are first-degree relatives of gastric cancer patients and according to patients' wishes after full consultation. It is advised that H. pylori eradication is considered to be an appropriate option in infected patients with functional dyspepsia, as it leads to long-term symptom improvement in a subset of patients. There was consensus that the eradication of H. pylori is not associated with the development of gastro-oesophageal reflux disease in most cases, and does not exacerbate existing gastro-oesophageal reflux disease. It was agreed that the eradication of H. pylori prior to the use of non-steroidal anti-inflammatory drugs reduces the incidence of peptic ulcer, but does not enhance the healing of gastric or duodenal ulcer in patients receiving antisecretory therapy who continue to take non-steroidal anti-inflammatory drugs. Treatment should be thought of as a package which considers first- and second-line eradication therapies together. First-line therapy should be with triple therapy using a proton pump inhibitor or ranitidine bismuth citrate, combined with clarithromycin and amoxicillin or metronidazole. Second-line therapy should use quadruple therapy with a proton pump inhibitor, bismuth, metronidazole and tetracycline. Where bismuth is not available, second-line therapy should be with proton pump inhibitor-based triple therapy. If second-line quadruple therapy fails in primary care, patients should be referred to a specialist. Subsequent failures should be handled on a case-by-case basis by the specialist. In patients with uncomplicated duodenal ulcer, eradication therapy does not need to be followed by further antisecretory treatment. Successful eradication should always be confirmed by urea breath test or an endoscopy-based test if endoscopy is clinically indicated. Stool antigen test is the alternative if urea breath test is not available.
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PMID:Current concepts in the management of Helicobacter pylori infection--the Maastricht 2-2000 Consensus Report. 1186 Mar 99

Helicobacters are a new genus of bacteria, inhabiting the interface between mucosa and lumen of the gut. Microaerophilic, spiral, flagellated and urease positive, they possess features necessary for colonisation of the juxtamucosal mucus environment. Helicobacter pylori is the major pathogenic species. Once attached to the gastric epithelial cells, it incites an immune response characterised histologically by the development of active gastritis and immunologically by the presence of specific IgG. Persistence of infection is ensured by attachment to tissue antigens (eg Lewis B), a vacuolating toxin (VacA) which assists the free passage of urea through epithelial cells, and a cytotoxin (CagA) which is actually injected into the epithelial cells via a Type IV secretion system. Finally, during the typical lifelong chronic infection, two important diseases occur. H. pylori alters gastric physiology to cause acid hypersecretion and peptic ulcer. Secondly, it damages the acid secreting mucosa leading to atrophic gastritis and gastric cancer risk.
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PMID:Helicobacter pylori: 20 years on. 1199 Oct 99

Helicobacter pylori is the cause of most peptic ulcer disease and a primary risk factor for gastric cancer. Eradication of the organism results in ulcer healing and reduces the risk of ulcer recurrence and complications. Testing and treatment have no clear value in patients with documented nonulcer dyspepsia; however, a test-and-treat strategy is recommended but for patients with undifferentiated dyspepsia who have not undergone endoscopy. In the office setting, initial serology testing is practical and affordable, with endoscopy reserved for use in patients with alarm symptoms for ulcer complications or cancer, or those who do not respond to treatment. Treatment involves 10- to 14-day multidrug regimens including antibiotics and acid suppressants, combined with education about avoidance of other ulcer-causing factors and the need for close follow-up. Follow-up testing (i.e., urea breath or stool antigen test) is recommended for patients who do not respond to therapy or those with a history of ulcer complications or cancer.
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PMID:Management of Helicobacter pylori infection. 1240 15

Treatment recommendations for H. pylori infection are peptic ulcer disease, MALT lymphoma, atrophic gastritis and following gastric cancer resection as well as first degree relatives of gastric cancer patients. Advisable situations are functional dyspepsia, before introduction of NSAID's or intended long-term proton-pump inhibitor treatment. It is thought that eradication therapy is not associated with gastro-esophageal reflux disease and does not enhance NSAID induced peptic ulcer healing. Therapy should be given as a package which considers first and second line eradication therapies together; in uncomplicated duodenal ulcer patients, eradication therapy does not need to be followed by further antisecretory treatment. First line therapy should be with triple therapy using a proton pump inhibitor (PPI), combined with clarithromycin and amoxycilline or metronidazole. Second-line therapy should use a quadruple therapy with a PPI, bismuth, metronidazole and tetracycline. Where bismuth is not available, second line therapy should be with a PPI triple therapy. If second line quadruple therapy fails in primary care, patients should be referred to the specialist and handled on a case by case basis. Successful eradication should always be confirmed by urea breath test (UBT), or endoscopy-based tests if endoscopy is clinically indicated. Stool antigen test is the alternative if UBT is not available. A 'test and treat' approach based on non-invasive testing can be offered to adult patients presenting in primary care with persistent dyspepsia under the age of 45 years (the age cut-off may vary locally), having excluded those with predominantly gastroesophageal reflux disease (GERD) symptoms, NSAID users, and patients with alarm symptoms.
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PMID:[Helicobacter pylori--2002]. 1207 Oct 78

Infection with Helicobacter pylori(H. pylori) is thought to be an important factor in the pathogenesis of gastritis, peptic ulcer and gastric cancer, and the 13C-urea breath test (13C-UBT) is a convenient and non-invasive method for the detection of H. pylori in the stomach. We have examined the sensitivity, specificity and accuracy of 13C-UBT, comparing it with histology. The 13CO2/12CO2 ratio was measured by using infra-red spectroscopy(IR) and gas chromatography/mass spectrometry(GC-MS). The IR analyzer should be particularly useful for the diagnostic test of H. pylori infection using 13C-UBT.
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PMID:[13C-urea breath test]. 1260 18

The INK4a/ARF locus encodes two cell cycle-regulatory proteins, p16INK4a and p14ARF. These share an exon using different reading frames, and act through Rb and p53 pathways. Recently, it has been found that silencing of p16INK4a and p14ARF expressions by aberrant methylation of the CpG islands in the promoter regions is an alternative mechanism that inactivates possible tumor suppressor functions in various tumors. To clarify the features of gastric cancers with promoter methylation of p16INK4a and p14ARF, we investigated the methylation status in gastric cancer cell lines and primary gastric cancers using methylation-specific PCR (MSP), and correlated the methylation status with microsatellite instability (MSI), DNA ploidy pattern, p53 immunohistochemistry, and various clinicopathologic factors, paying attention to the correlations with the histologic types. Of 10 cell lines studied, silencing of the expression of p16INK4a and p14ARF due to promoter methylation was detected by MSP and RT-PCR in six (60%) and two (20%) cell lines, respectively. p14ARF silencing was detected only in cell lines derived from gastric cancer of the diffuse type, while p16INK4a silencing was found in cell lines derived from both diffuse and intestinal types. In 59 primary gastric cancers, promoter methylation of p16INK4a and p14ARF was found in 10 (17%) and 14 (24%) of the tumors independently, there being an association with DNA diploidy, but not with p53 immunohistochemistry. p16INK4a methylation was found irrespective of tumor stages and histology. Whereas p14ARF methylation was found more frequently in intestinal type cancers in an early stage and in diffuse type cancers in an advanced stage, MSI tended to be related especially to p14ARF methylation in cancers of the intestinal type. Thus, the significance of p14ARF methylation differed between intestinal and diffuse types, while such a difference was not observed in p16INK4a methylation.
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PMID:Promoter methylations of p16INK4a and p14ARF genes in early and advanced gastric cancer. Correlations of the modes of their occurrence with histologic type. 1260 55

H. pylori (Hp) -induced atrophic gastritis is a well-known risk factor for the development of gastric cancer. Whether Hp eradication can prevent or retard the progress of atrophy and metaplasia has been the topic of numerous studies but the subject remains controversial. Recently, the increased expression of ornithine decarboxylase (ODC), gastrin and cyclooxygenase (COX)-2 has been shown to be increased in premalignant lesions in gastric mucosa and to play an essential role in the malignant transformation. The aim of the study is to assess the effect of eradication therapy on atrophic gastritis and analyze the gene expression for ODC, COX-2 and gastrin in gastric mucosa after succesful eradication in patients with atrophic gastritis. Twenty patients with chronic atrophic gastritis including both corpus and antrum of the stomach were included in this study. Four antral mucosal biopsy specimens were obtained from antrum and four from corpus. The histopathologic evaluation of gastritis was based on Sydney classification of gastritis. All patients were Hp positive based on the [13C] urea breath test (UBT) and the presence of anti-Hp IgG and anti-CagA-antibodies detected by ELISA. The patients were then eradicated with triple therapy consiting of omeprazol (2 x 20 mg), amoxycillin (2 x 1 g) and clarithromycin (2 x 500 mg) for seven days and vitamin C 1 g/day for three months. In gastric mucosal samples obtained from the antrum and corpus before and after eradication, the mRNA expression for ODC, COX-2, and gastrin was assessed by reverse-transcription polymerase chain reaction (RT-PCR). In all patients the gastric secretory analysis was performed by measuring gastric acid output and serum gastrin levels. After triple therapy the successful eradication assessed by UBT was observed in 95% of patients. In 45% of patients the infection with CagA-positive Hp strain was observed. Three months after eradication a significant reduction in the gastric activity (neutrophilic infiltrate) and severity (mononuclear infiltrate) of gastritis was observed. The atrophy score improved in both antrum and corpus after eradication. The expression of COX-2 and ODC was significantly up-regulated in the gastric mucosa of patients with atrophic gastritis and significantly reduced after eradication therapy. In all successfully eradicated patients with atrophic gastritis a significant increase in gastric acid secretion and decrease in serum gastrin were observed. We conclude that: (1) Hp eradication leads to the decrease in ODC and COX-2 gene expression in the gastric mucosa, and this may be relevant for the prevention of the Hp-associated gastric carcinogenesis; and (2) gastric atrophy ameliorates upon successful Hp eradication therapy.
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PMID:Gene expression of ornithine decarboxylase, cyclooxygenase-2, and gastrin in atrophic gastric mucosa infected with Helicobacter pylori before and after eradication therapy. 1264 88


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