Helicobacter pylori infection is a major risk factor for gastric carcinoma in young patients

BACKGROUND: Helicobacter pylori has been established as a risk factor for gastric carcinoma (GCa). Since before the discovery of H. pylori, atrophic gastritis and intestinal metaplasia have been linked to GCa, especially the intestinal-type tumor. The prevalence of H. pylori infection and atrophic gastritis increase with age. Thus, analysis of H. pylori infection in young patients with GCa could help clarify the role of this bacterium in the development of GCa. Accordingly, we investigated the relationship between H. pylori infection, GCa, and histologic gastritis in patients less than 30 years old. METHODS: Fifty GCa patients less than 30 years (mean, 26.4 years) and 100 sex- and age-matched controls (mean, 26.8 years) were examined for the presence of H. pylori infection and histologic gastritis. RESULTS: The prevalence of H. pylori infection was significantly higher in GCa patients than in controls (94% versus 40%, P < 0.01). Its prevalence was not associated with tumor location, tumor stage, or histologic type. Gastritis, atrophy, and intestinal metaplasia significantly increased the risk of GCa. By means of multiple logistic regression analysis, the odds ratio for the risk of GCa in H. pylori-positive subjects was found to be 23.5 (95% confidence interval, 6.84-80.7). CONCLUSIONS: We confirmed a strong association between H. pylori infection and GCa in young patients. Along with H. pylori infection, histologic gastritis might play an important role in the pathogenesis of GCa in these patients.     

9 Helicobacter pylori as a risk factor for cancer

In 1985, gastric cancer was the second most common cause of cancer death in the world. The rapid decline in gastric cancer rates over the last few decades has been attributed to a decline in the prevalence of environmental risk factors for gastric cancer and/or an increase in the prevalence of protective factors. One such risk factor could be the bacterium Helicobacter pylori. Epidemiological studies have shown that areas with high gastric cancer rates often have a correspondingly high prevalence of H. pylori and prospective studies have shown that subjects with serological evidence of H. pylori infection were significantly more likely to go on to develop gastric cancer than those who did not.Helicobacter pylori itself does not appear to be either genotoxic or mutagenic. Infection is, however, associated with increased cell turnover, a chronic immune response accompanied by increased levels of reactive oxygen metabolites and a reduction in gastric levels of ascorbic acid, all conditions that could favour the development of cancer. Nonetheless, the majority of those who are infected with H. pylori do not go on to develop gastric cancer and other factors, such as the strain of the infecting organism or consumption of dietary antioxidants including vitamin C, could also affect the risk of cancer.Finally, it has been estimated that more than one third, and possibly as many as 90% of gastric cancers might be attributable to infection with H. pylori. Prevention and treatment of infection are, therefore, possible approaches to reducing gastric cancer rates. It is, however, unclear what, if any, effect eradication of the infection would have on an individual's risk of gastric cancer and, to date, anti-Helicobacter therapy has only been shown to be of potential benefit in the treatment of low grade gastric MALT lymphomas.     

幽门螺杆菌感染:特发性心房颤动的一个新的危险因素

1982年Barry Marshall和Robin Warren首先发现了幽门螺杆菌（Hp），并获2005年诺贝尔生理学和医学奖。2005年，Montenero等在Heart杂志上发表科学信件，首次提出慢性Hp感染可能是一种潜在的导致特发性心房颤动（房颤）的新的危险因素。本文旨在观察Hp感染与特发性房颤发病是否有关和房颤患者是否存在一种炎症状态。     

Helicobacter pylori infection and the risk of gastric malignancy

OBJECTIVE: This prospective cohort study investigated the impact of Helicobacter pylori infection on the development of various gastric malignancies. METHODS: We prospectively followed up 1,225 dyspeptic Taiwanese who had nonulcer dyspepsia, gastric ulcers, or duodenal ulcers at enrollment. Among them, 618 (50.4%) had H. pylori infection and 607 (49.6%) did not. Patients underwent endoscopy at enrollment and at 1- to 3-yr intervals thereafter. RESULTS: During a mean follow-up of 6.3 yr, gastric adenocarcinoma developed in 7 of the 618 H. pylori-infected patients, but in none of the 607 uninfected patients (1.1%vs 0.0%, P= 0.015). The incidence of gastric lymphoma was 0.2% (1/618) and 0% in H. pylori-infected and uninfected patients. Taken together, the development rate of gastric malignancy in H. pylori-infected patients was significantly higher than that in uninfected patients (1.3%vs 0%, P= 0.007). Among H. pylori-infected subjects, the incidence of gastric malignancy was similar between those receiving and not receiving eradication therapy (1.4%vs 1.2%). Multivariate analysis showed that intestinal metaplasia was the only independent factor predicting subsequent development of gastric malignancy in H. pylori-infected subjects with an odds ratio of 4.5 (95% CI 1.1-19.1). CONCLUSIONS: In this prospective cohort study, all gastric malignancies, including adenocarcinoma and lymphoma, developed in H. pylori-infected patients. The finding implies that H. pylori is a necessary cause of most gastric malignancies. Follow-up for H. pylori-infected patients who have intestinal metaplasia is indicated.     

Genital ulceration as a risk factor for human immunodeficiency virus infection

Among 115 heterosexual men who presented with genital ulcers to a sexually transmitted disease clinic in Nairobi, Kenya, the prevalence of serum antibody to HIV was 16.5%. A past history of genital ulcers was reported by 12 (63%) of 19 men with antibody to HIV versus 30 (31%) of 96 without antibody (P = 0.008). HIV infection was also positively associated with lack of circumcision, but was not associated with the etiology of the current genital ulcer. Logistic regression analysis (adjusted for age, number of recent sex partners, recent prostitute contact, circumcision, tribal ethnic identity, past history of urethritis, and current diagnoses) confirmed only the association between prior history of genital ulcer disease and HIV infection; (P = 0.04, odds ratio 2.35, 95% confidence limits, 1.01-5.47). The incidence of genital ulcers, particularly chancroid, is much higher in parts of Africa than in Europe or North America. This may contribute to the increased risk of heterosexual transmission of HIV in Africa. Aggressive control of chancroid and syphilis may offer one very feasible approach to reducing transmission of HIV in this region.     

Helicobacter pylori infection and low serum pepsinogen I level as risk factors for gastric carcinoma

AIM: To study whether examination of CagA antibodies could increase the odds ratio for gastric cancer in a casecontrol study, and how often other serum markers of gastric cancer risk could be found in Helicobacter pylori-negative patients. METHODS: H pylori CagA and parietal cell antibodies (PCAs), and serum pepsinogen I (SPGI) levels were compared between patients with gastric cancer and controls who received endoscopic examination due to reasons other than gastrointestinal malignancy. RESULTS: The odds ratio (OR) for gastric cancer was 2.9 (95% CI 1.4-5.8) in H pylori + patients, and 2.4 (95% CI 1.2-4.9) in CagA+ patients. When results of H pylori and CagA antibodies were combined, OR increased to 5.0 (95% CI 2.5-10.0). Furthermore, if cardia cancer patients were excluded, the OR increased to 6.8 (95% CI 3.1-14.8). Among patients with a low SPGI level, the OR was 12.0 (95% CI 4.1-35.3). However, the risk was significant only in the older age group. The number of patients with low SPGI was significantly higher in H pylori -/CagA+ patients as compared to other cancer patients. CONCLUSION: Examination of both H pylori and CagA antibodies increases the OR for gastric cancer in our casecontrol study. CagA antibodies are important in detecting previous H pylori infection in advanced atrophic gastritis or cancer when spontaneous decline of H pylori antibodies occurs. SPGI may be helpful in screening elderly gastric cancer patients.     

Helicobacter pylori and risk for gastric adenocarcinoma

Gastric cancer is the second most common cause of cancer death in the world. Helicobacter pylori infection is now a well-accepted cause of this malignancy; in some parts of the world, up to eighty percent of all gastric cancers are at least in part caused by H. pylori infection. H. pylori infection typically starts in childhood as an inflammatory process in the stomach. The changes in the gastric microenvironment facilitate gastric cancer over time. Among infected individuals, genotype of H. pylori, coincident environmental exposures, and genetic factors of host seem to play roles in determining who will get gastric cancer and who will not. Unfortunately, it remains unknown whether treatment of H. pylori prevents gastric cancer. Thus, screening for H. pylori to prevent cancer is not yet widely recommended. Some consensus groups, however, have recommended screening for and treating H. pylori infection in individuals with family histories of gastric malignancy. In high-risk countries, screening programs for early gastric cancer itself may improve therapeutic outcome for this highly lethal disease.     

Helicobacter pylori infection as a possible risk factor for respiratory system disease: a review of the literature

Helicobacter pylori (HP) infection may cause extradigestive manifestations directly or indirectly, by potential mechanisms. HP infection triggers a marked local inflammatory response and a chronic systemic immune response. Some of the mediators that are thought to be possibly involved in the pathogenesis of extradigestive diseases caused by HP infection include IL-1, TNF-alpha, interferon (IFN)-gamma, leukotriene C4 and platelet-activating factor. Previous epidemiological and serological case control studies have revealed that HP infection might have a role in the development of chronic bronchitis, bronchiectasis, lung cancer and tuberculosis. However HP infection does not appear to have a role in the development of bronchial asthma. Considering the importance and prevalence of respiratory system diseases, it may be time to conduct well-designed sets of studies to clarify whether there is an association with HP infection and respiratory system diseases, and to answer questions that have been posed regarding the patterns of histology, genotypes of HP, and the effects of eradication therapy. The aim of this review was to analyze the possible association between HP and respiratory disease and provide a critical review of the relevant literature.     

Helicobacter pylori infection and gastric cancer

According to several prospective controlled epidemiologic studies, the positive rate of H. pylori antibody was shown to be higher in the patients with gastric cancer than in the control group. Retrospective studies on the association between gastric cancer and H. pylori have been conducted in a large number of subjects and the results can be classified broadly into two categories, i.e., findings affirming an association and others denying it. Research concerning the association between gastric cancer and H. pylori has achieved great progress over time, leading to the recognition of this relationship by the WHO. One of the greatest concerns is to ascertain whether the final outcome of H. pylori-induced gastritis may lead to gastric cancer. The onset of gastric cancer can be explained as being caused not only by H. pylori infection, but also by a combination of various factors such as food and the environment. However, the possibility that the occurrence of gastric cancer, like the recurrence of peptic ulcer, can be prevented by eradication of H. pylori has also been suggested. Further progress in clinical research is needed to resolve this issue.     

Helicobacter pylori as a risk factor for central serous chorioretinopathy: Literature review

Helicobacter pylori(H. pylori), a Gram-negative bacterium, is one of the most frequent causes of gastrointestinal infections worldwide. It has been associated as a pathogen for the human body with many systemic diseases, including different eye diseases. We will focus on a specific eye disease called idiopathic central serous chorioretinopathy(ICSCR). This disease is characterized by a serous detachment of the neurosensory retina in the macular region, which affects the vision to different degrees. Currently, the pathophysiology of ICSCR is not clear and there is no effective treatment. However, several potential risk factors have been elucidated. One of the factors that has more frequently been associated with ICSCR is stress. As H. pylori was identified as a possible etiological factor for occlusive arterial diseases in young people who were particularly stressed, it was thought that H. pylori might also be present in ICSCR. Therefore, some physicians started to test its presence in patents with ICSCR. If H. pylori happened to be associated with ICSCR, the treatment of gastrointestinal infection could also improve visual symptoms and help to remediate this eye disease. Although H. pylori is highly prevalent in the general population, a true cor-relation seems to exist. We present a review on the relationship between ICSCR and H. pylori.     

Helicobacter pylori infection and gastric cancer

Gastric cancer remains a major health burden on many societies claiming hundreds of thousands of lives every year. The discovery of Helicobacter pylori has no doubt revolutionised our understanding of this malignancy, which is now regarded as a paradigm for infection-induced chronic inflammation-mediated cancer. In this paper, we discuss the evidence for the association between H. pylori and gastric adenocarcinoma and MALT lymphoma. We also discuss the pathogenesis of these two forms of cancer and the factors that determine their outcome. There is no doubt that the knowledge accumulated over the past two decades will be translated into eventual victory over this killer cancer, largely because we now appreciate that the best way to prevent the cancer is by preventing acquisition of the infection in the first place, or by eradicating the infection in infected subjects. Defining the optimal timing of intervention is going to be the challenge facing us over the next two decades.     

Significance ofHelicobacter pylori infection as a risk factor in gastric cancer: Serological and histological studies

We conducted a case-control study to examine the association ofHelicobacter pylori infection as a risk factor in gastric cancer in the Japanese population. Serum IgG antibodies forHelicobacter pylori were determined in 55 consecutive patients with gastric cancer and in 75 age- and sex-matched mass survey subjects and 57 age- and sex-matched cancer-free patients with conditions considered at a high risk for development of gastric cancer (precancerous condition). We examined the histology in all subjects and particular focus was placed on the extent ofHelicobacter pylori-associated gastritis. The seroprevalence ofHelicobacter pylori in gastric cancer patients (82%) and those with a precancerous condition (89%) was significantly higher (P<0.005) than that in the mass survey subjects (60%). Positive relative risk associations were found for patients with gastric cancer (odds ratio, 3, with 95% confidence intervals of 1.69–5.33) and those with a precancerous condition (odds ratio, 5.66, with 95% confidence intervals 2.66–12.03). Significant differences were found when comparisons were made among the case-control groups who wereH. pylori-positive and had inflammatory cell infiltration (P=0.0127). The characteristics ofHelicobacter pylori in histologically examined gastric mucosa showed differences betweenHelicobacter pylori-infected and uninfected persons in all groups. However, for none of these groups was there a significant difference between background mucosa forHelicobacter pylori-infected persons with or without gastric cancer.Helicobacter pylori seroprevalence is strongly associated with an increased risk of gastric cancer and with a precancerous condition; histological investigation did not define additional factors that might be associated with increased cancer risk.     

幽门螺杆菌感染与原发性胃淋巴瘤

目的探讨幽门螺杆菌（Ｈｐ）感染与原发性胃淋巴瘤、胃ＭＡＬＴ淋巴瘤的关系．方法经内镜、手术诊断的胃淋巴瘤患者２９例，其中男１９例，女１０例；年龄３０岁～７５岁，中位数年龄５２５岁．胃窦部１３例，胃体部９例，贲门部２例．凹陷溃疡型９例，蕈样隆起型８例，结节型１２例．胃粘膜标本切片，采用ＨＥ及ＷａｒｔｈｉｎＳｔａｒｙ染色后观察组织中有无Ｈｐ感染．结果原发性胃淋巴瘤患者２９例，胃粘膜组织中发现Ｈｐ感染２４例，阳性率８２８％．其中胃ＭＡＬＴ淋巴瘤８例，Ｈｐ感染７例，阳性率８７５％．明显高于同期胃良性病变Ｈｐ阳性率４６％（Ｐ＜００１）．２９例中１１例进行了术后随访，３例仍存在Ｈｐ感染，阳性率２７３％．结论Ｈｐ感染在原发性胃淋巴瘤的发病机制中起一定作用．     

Helicobacter pylori infection: Beyond gastric manifestations

Helicobacter pylori(H. pylori) is a bacterium that infects more than a half of world's population. Although it is mainly related to the development of gastroduodenal diseases, several studies have shown that such infection may also influence the development and severity of various extragastric diseases. According to the current evidence, whereas this bacterium is a risk factor for some of these manifestations, it might play a protective role in other pathological conditions. In that context, when considered the gastrointestinal tract, H. pylori positivity have been related to Inflammatory Bowel Disease, Gastroesophageal Reflux Disease, Non-Alcoholic Fatty Liver Disease, Hepatic Carcinoma, Cholelithiasis, and Cholecystitis. Moreover, lower serum levels of iron and vitamin B12 have been found in patients with H. pylori infection, leading to the emergence of anemias in a portion of them. With regards to neurological manifestations, a growing number of studies have associated that bacterium with multiple sclerosis, Alzheimer's disease, Parkinson's disease, and Guillain-Barré syndrome. Interestingly, the risk of developing cardiovascular disorders, such as atherosclerosis, is also influenced by the infection. Besides that, the H. pylori-associated inflammation may also lead to increased insulin resistance, leading to a higher risk of diabetes mellitus among infected individuals. Finally, the occurrence of dermatological and ophthalmic disorders have also been related to that microorganism. In this sense, this minireview aims to gather the main studies associating H. pylori infection with extragastric conditions, and also to explore the main mechanisms that mayexplain the role of H. pylori in those diseases.     

Helicobacter pylori infection and early gastric cancer

BACKGROUND: Helicobacter pylori has recently been associated with an increased risk of gastric cancer. This study aimed to examine the association between H. pylori, histologic chronic gastritis, and intestinal metaplasia in early gastric cancers of different histologic types. STUDY: Seventy-four patients who were surgically diagnosed as having early gastric cancer were included in this study. All tissue specimens were obtained from patients by endoscopic biopsy and were classified histopathologically as intestinal-type early gastric cancer in 55 patients and diffuse-type early gastric cancer in 19 patients. RESULTS: H. pylori infection was found in 67 patients (90.5%) but not found in seven (9.5%). And the prevalence of H. pylori infection with nongastric cancer patients was also high (68.5%). There was no significant difference between the intestinal-type and the diffuse-type early gastric cancer in chronic active gastritis and atrophic chronic gastritis. Intestinal metaplasia was observed more frequently in patients with the intestinal-type than with the diffuse-type early gastric cancer (P = 0.0102). CONCLUSIONS: Infection with H. pylori has an important relationship to both histopathologic types of early gastric cancer.     

Natural course of Helicobacter pylori gastric infection

Helicobacter pylori acquisition induces chronic gastritis that affects antrum, corpus or both. In approximately half of the cases, Helicobacter pylori gastritis slowly (years, decades) develops to atrophic gastritis, thereby resulting in severe abnormalities in the function of the stomach. In humans, the appearance of intestinal metaplasia associates with atrophic gastritis (loss of normal antral and/or oxyntic glands), and intestinal metaplasia linearly increases in grade and extent with increasing age and progression of atrophy. Several mechanisms may play in role in the development of atrophic gastritis and intestinal metaplasia; i.e., including genetic liability of the host to destruction of cells and glands, specific cytotoxic strains of Helicobacter pylori, environmental factors other than the bacterial ones, and some functional properties of the stomach, such as output of acid and intragastric acidity. Atrophic and metaplastic alterations may also result from genotoxic and mutagenic injuries which are triggered by the inflammation, or are exogenous.