Stomach is the most common site of primary extranodal lymphoma. Mucosa-associated lymphoid tissue (MALT) lymphoma is a unique type of extranodal lymphoma which is associated with Helicobacter pylori (H. pylori). The development of low-grade MALT lymphoma of stomach is dependent on H. pylori. A transformed clone carrying the translocation t(11;18)(q21;q21) forms a MALT lymphoma, the growth of which is independent of H. pylori and will not respond to bacterial eradication. And inactivation of the tumor suppressor genes, p53 can lead to high-grade transformation. Endoscopic ultrasound (EUS) is essential to document the extent of disease and is superior to CT scan in the detection of spread to perigastric lymph nodes and follow-up EUS may determine the response to therapy and detect the relapse in early phase. Lesions that are confined to the mucosa or submucosa of gastric wall can be successfully treated with H. pylori eradication. Those low-grade MALT lymphomas that are not H. pylori positive or do not respond to antibiotic therapy can be treated with surgery, radiation, or chemotherapy. Follow-up is critical in all patients who have been treated with H. pylori eradication and consists of multiple endoscopic biopsies and EUS.
Helicobacter Infections/complications ; Helicobacter pylori ; Humans ; *Lymphoma, B-Cell, Marginal Zone/microbiology/pathology ; Stomach Diseases/complications ; *Stomach Neoplasms/microbiology/pathology

Both lymphocytic gastritis and gastric mucosa associated lymphoid tissue (MALT) lymphoma are associated with Helicobacter pylori (H. pylori) infection. However, this association has not been fully elucidated. We report two cases of lymphocytic gastritis in 57-year-old male and 47-year-old female patients which were diagnosed after the H. pylori eradication to treat gastric MALT lymphoma. MALT lymphoma was successfully treated in case 1, but residual MALT lymphoma remained in case 2. During the follow-up endoscopic examinations, several elevated erosions in case 1 and irregular mucosal atrophy in case 2 were newly detected. Biopsy specimens showed marked infiltration of lymphocytes in the surface epithelium (56.6+/-15.9 intraepithelial lymphocytes (IELs)/100 epithelial cells in case 1 and 40.5+/-9.3 IELs/100 epithelial cells in case 2), which were exclusively CD8-positive T lymphocytes. These findings suggest that H. pylori infection may cause a monoclonal proliferation of B lymphocytes, leading to MALT lymphoma as well as polyclonal proliferation of T lymphocytes which subsequently infiltrated into the surface epithelium as a host immune reaction, resulting in lymphocytic gastritis.
Gastric Mucosa/*pathology ; Gastritis/*complications/microbiology/pathology ; Helicobacter Infections/*complications ; *Helicobacter pylori ; Humans ; Lymphocytes/*pathology ; Lymphoma, B-Cell, Marginal Zone/*complications/microbiology ; Male ; Middle Aged ; Stomach Neoplasms/*complications

No abstract availble.
Adult ; Gastric Mucosa/*pathology ; Gastritis, Hypertrophic/microbiology/*pathology ; Gastroscopy ; Helicobacter Infections/complications/*drug therapy ; *Helicobacter pylori ; Humans ; Male

OBJECTIVETo investigate the difference in Helicobacter pylori (Hp) infection rate between the patients with laryngeal squamous cell carcinoma and the patients with benign laryngeal lesions and to explore the role of Hp infection in the pathogenesis of laryngeal squamous carcinoma.

METHODSNested polymerase chain reaction (nPCR) and Hp culture were used to identify the Hp in laryngeal mucosa in 30 patients with laryngeal carcinoma and 15 patients with benign laryngeal lesions including polyps of vocal cords or epiglottic cysts.

RESULTSnPCR showed that Hp-positive rate (73.3%) of patients with laryngeal carcinoma was significantly higher than that (20.0%) of control patients with benign laryngeal lesions (χ(2) = 11.520, P = 0.010). Regarding the 22 positive neoplastic cases that have 44 tissues, out of the 22 tumor tissues, 10 were positive with Hp (45.4%), and among 22 tissues beside the tumor, 19 were positive (86.4%). This event also indicated a statistical significance (χ(2) = 4.697, P = 0.030). Hp culture showed that Hp was negative in all specimens.

CONCLUSIONSHp exist in the laryngeal mucosa, but with the higher rate of Hp infection in the patients with laryngeal squamous cell carcinoma than that in the patients with benign laryngeal lesions, which suggests Hp may be one of pathogenic factors of laryngeal squamous cell carcinoma.

Adult ; Aged ; Carcinoma, Squamous Cell ; complications ; microbiology ; pathology ; Female ; Helicobacter Infections ; complications ; Helicobacter pylori ; isolation & purification ; Humans ; Laryngeal Neoplasms ; complications ; microbiology ; pathology ; Male ; Middle Aged ; Polyps ; complications ; microbiology ; pathology ; Vocal Cords ; microbiology ; pathology

BACKGROUND/AIMS: Helicobacter pylori (H. pylori) infection can lead to gastric adenoma and carcinoma through atrophic gastritis and intestinal metaplasia. Imbalance between apoptosis and proliferation may play a role in gastric carcinogenesis. We tried to investigate H. pylori infection rate, grade of gastritis, environmental risk factors, expression rate of apoptosis and cell proliferation in mucosa adjacent to tumor, and we also tried to find significant factors associated with gastric carcinogenesis. METHODS: Endoscopically diagnosed twenty cases of intestinal type gastric carcinoma, 20 cases of gastric adenoma, and 40 cases of control (normal or gastritis) were enrolled. H. pylori infection rate, histologic grading, apoptosis and immunohistochemical stain (Ki-67 and p53) to check mucosal proliferation were done in endoscopically biopsied tissues at antrum and body at least 2 cm apart from adenoma or carcinoma. RESULTS: In three groups, H. pylori infection rates were not significantly different. In the multivariate analysis, only atrophy of gland was a significant risk factor for adenoma compared to control group (OR 3.7). Intestinal metaplasia in antrum and alcohol drinking were significant risk factors for carcinoma compared to control group (OR 4.4 and 4.9 respectively). Expressions of apoptosis, Ki-67 and p53 were not significantly different in three groups. CONCLUSIONS: Intestinal metaplasia in antrum and alcohol drinking are significant risk factors for gastric carcinoma. Degree of mucosal proliferation and apoptosis in gastric mucosa adjacent to tumor are not significantly different in three groups.
Adenocarcinoma/microbiology/*pathology ; Adenoma/microbiology/*pathology ; Adult ; Aged ; Aged, 80 and over ; *Apoptosis ; *Cell Proliferation ; English Abstract ; Female ; Gastric Mucosa/*pathology ; Gastritis/microbiology/pathology ; Helicobacter Infections/complications/pathology ; Helicobacter pylori ; Humans ; Male ; Middle Aged ; Risk Factors ; Stomach Neoplasms/microbiology/*pathology

Intestinal metaplasia (IM) has been regarded as a premalignant condition. However, the pathogenesis of IM is not fully understood. The aim of this study was to evaluate the role of CDX1 and CDX2 in the formation of IM and the progression to dysplasia and gastric cancer (GC). A total of 270 subjects included 90 with GC, dysplasia and age- and sex-matched controls. Real-time PCR (RT-PCR) was performed with body specimens for CDX1 and CDX2. The expression of CDX2 was significantly higher in H. pylori positive group than H. pylori negative group (P = 0.045). CDX1 and CDX2 expression increased proportional to the IM grade of the body (P < 0.001). CDX2 expression was significantly higher in incomplete type of IM than in complete type (P = 0.045). The expression of CDX1 in dysplasia group was significantly higher than in the control group (P = 0.001); in addition, CDX1 and CDX2 in cancer group was significantly higher than control group (P < 0.001, and P < 0.001, respectively). Aberrant expression of CDX1 and CDX2 correlated with H. pylori infection and grade of IM in the body. Furthermore, the results suggest that CDX1 and CDX2 play a role in the progression to GC and dysplasia.
Aged ; Female ; Helicobacter Infections/complications/microbiology ; Helicobacter pylori/isolation & purification ; Homeodomain Proteins/*genetics/metabolism ; Humans ; Intestinal Diseases/*genetics/microbiology/pathology ; Male ; Metaplasia/pathology ; Middle Aged ; Polymerase Chain Reaction ; Precancerous Conditions/metabolism/pathology ; Stomach Neoplasms/etiology/*genetics/microbiology

OBJECTIVEA systematic meta-analysis was performed to explore the role of cytotoxin-associated gene-A (CagA) seropositive strains of Helicobacter pylori (H. pylori) in the pathogenesis of atherosclerotic diseases. Data sources Data from Medline, EMBASE, CBMdisc, CNKI and the Cochrane Collaboration database were searched. Similar search strategies were applied to each of these databases. Study selection The review was restricted to the case-control studies on infective, chronic virulent CagA strains of H. pylori, involving the risk of ischemic stroke and coronary heart disease, ineligible studies were excluded. Two reviewers independently extracted the data and assessed study quality.

RESULTSTotally 26 case-control studies (11 studies on ischemic stroke and 15 studies on coronary heart disease) were retrieved and considered. The combined data revealed that the chronic seropositive virulent strains of H. pylori infection had a trend of increasing the risk of ischemic strokes and coronary heart diseases, yielding pooled ORs of 2.68 (95% CI: 2.20, 3.27) and 2.11 (95% CI: 1.70, 2.62), respectively. We also performed subgroup analyses, dividing the total population into Caucasian and Chinese subgroups. Through the subgroup analysis, no significant difference was found between the subgroups.

CONCLUSIONSOur results support the hypothesis that CagA-seropositive strains infection is significantly associated with susceptibility to ischemic strokes and coronary heart diseases. The magnitude of the association with atherosclerotic diseases needs to be confirmed by prospective studies and the studies on CagA-seropositive strains eradication are more important.

Antibodies, Bacterial ; blood ; Antigens, Bacterial ; immunology ; Atherosclerosis ; etiology ; pathology ; Bacterial Proteins ; immunology ; Helicobacter Infections ; blood ; complications ; microbiology ; Helicobacter pylori ; immunology ; pathogenicity ; Virulence

BACKGROUND: The role of Helicobacter pylori (H. pylori) in the pathogenesis of coronary artery disease (CAD) is still controversial, and the relation between current H. pylori infection and CAD has not been fully examined. This study evaluated the relation between H. pylori infection as confirmed by gastroduodenoscopic biopsy and CAD. METHODS: We determined the presence of H. pylori infections, via gastroduodenoscopy, in 88 patients of the normal coronary angiographic group and also in 175 patients of the CAD group, and the latter patients had more than 50% coronary stenosis angiographically demonstrated. We excluded those patients with a history of previous H. pylori eradication and/or malignancy. A small piece of tissue from the antrum, which was obtained by gastroduodenoscopic biopsy, was stained by Warthin-starry silver stain. We defined a negative staining result that there was no stained tissue in the sample and the stained tissue was also positive for H. pylori infection. RESULTS: There was no significant difference, except for gender, age, smoking and high density lipoprotein cholesterol (HDL-c), of the demographic and laboratory characteristics between the groups. Twenty seven (30.7%) patients of the normal control group and 71 (40.6%) patients of the CAD group were positive of H. pylori infection, yet there was no statistical difference. We angiographically followed up the 80 patients of the CAD group who were treated by percutaneous coronary intervention (PCI) at 6 to 9 months after their primary intervention. Twenty two (37.9%) of the 58 patients of the H. pylori negative group and 10 (45.5%) of the 22 patients of the H. pylori positive group were treated with reintervention, but reintervention was also not significantly different between the group with H. pylori infection and the group without the infection. CONCLUSIONS: These data indicated that H. pylori infection had a modest influence on CAD and progressive atheroma, but the showed a tendency to increase. Further studies are needed to evaluate the relationship between H. pylori infection and CAD.
Aged ; Angioplasty, Transluminal, Percutaneous Coronary ; Biopsy ; Case-Control Studies ; Coronary Angiography ; Coronary Artery Disease/*microbiology/radiography/therapy ; Duodenoscopy ; Female ; Gastroscopy ; Helicobacter Infections/complications/*microbiology/pathology ; Helicobacter pylori/*isolation & purification ; Humans ; Male ; Middle Aged ; Pyloric Antrum/pathology ; Time Factors

We describe a 58-year-old woman who was incidentally found to have gastric and colonic polyposis, hypoalbuminemia, cutaneous hyperpigmentation and onychodystrophy (Cronkhite-Canada syndrome). Histology of polyps from the stomach showed features of juvenile or retention type (hamartomatous) polyps with Helicobacter pylori (H. pylori) infection. The large pedunculated colonic polyps showed hamartomatous polyps with adenomatous component and polypectomy was performed. After the treatment with H. pylori eradication and omeprazole, the gastric polyposis, hypoalbuminemia and anemia regressed, and endoscopic polypectomy of gastric polyps were performed. After the continuous use of omeprazole for 14 months, the patient showed complete resolution of clinical features of Cronkhite-Canada syndome. The experience of this case suggests that eradication of H. pylori and proton pump inhibitor treatment might be considered in patients with gastric polyposis combined with Cronkhite-Canada syndome.
Anti-Ulcer Agents/*therapeutic use ; Colonic Polyps/complications/microbiology/pathology ; Female ; Helicobacter Infections/complications/*drug therapy ; *Helicobacter pylori ; Humans ; Hyperpigmentation/pathology ; Middle Aged ; Nails, Malformed/pathology ; Omeprazole/*therapeutic use ; Polyps/*complications/microbiology/pathology ; Proton Pumps/antagonists & inhibitors ; Stomach Neoplasms/*complications/microbiology/pathology ; Syndrome

OBJECTIVETo determine serum pepsinogen levels in patients with liver cirrhosis and investigate the functions of the gastric mucosa in these patients with concurrent portal hypertensive gastropathy (PHG).

METHODSFifty-one patients with liver cirrhosis and 22 healthy controls were studied by gastroscopy. The hepatic function of the patients with or without PHG were evaluated with Child-Pugh grade. Helicobacter pylori infection was detected using rapid urease test or exhalation of carbon 13. The serum pepsinogen I and II levels were tested by latex-enhanced immunoturbidimetry to calculate the PGI/PGII ratio (PGR).

RESULTSIn cirrhotic patients, the levels of serum PGI and PGR were lower than those in the healthy controls. The patients without PHG had a serum PGI level of 49.48+23.86 µg/L, significantly lower than that in PHG patients (74.85+30.27 µg/L, P=0.000). The levels of serum PG II in patients with H.pylori infection was significantly higher that in patients free of H.pylori infection (P=0.003).

CONCLUSIONThe serum level of PGI decreases obviously in patients with hepatic cirrhosis and PHG, who can have damages of the gastric mucosa lamina propria and reduced secretory function of the gastric mucosa. H.pylori infection may affect the level of PGII. There is no significant correlation between serum PG level and liver function, but to a certain extent, serum PG level especially PGI can reflect the function of gastric mucosa in patients of liver cirrhosis.

Adult ; Case-Control Studies ; Female ; Gastric Mucosa ; pathology ; Helicobacter Infections ; Humans ; Hypertension, Portal ; complications ; Liver Cirrhosis ; complications ; Male ; Middle Aged ; Pepsinogen A ; blood ; Stomach Diseases ; blood ; etiology ; microbiology