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Oral administration of hyperoxygenatedsolution for the prophylaxis of gastric ulcerationinduced by stress or Helicobacter pylori

MA Hong-Wei,WU Ya-Qiong,ZHANG Hai-Feng
- , 2015,
Abstract: Oxygen was first discovered by Sweden chemist Scheele in 1773 and convinced as an essential factor forliving by French scientists in 1777. To tackle with different hypoxic emergencies, corresponding medical approaches,e.g. mask or nasal catheter oxygen inhalation, breathing machine, hyperbaric oxygen therapy etc., have been contrived insuccession. However, one mortal trouble exists in all these conventional ways, i.e. they must rely on the ventilation and gasexchange via lungs, thus not being able to promptly render oxygen to specific hypoxia tissues. Hyperoxygenated solution(HOS), a new kind of medical liquid which can be orally taken or intravenously administrated, has been widely applied asan auxiliary method of offering oxygen in China. A large number of experiments have proved its validity in the treatmentof myocardial and cerebral ischemia/reperfusion injury, nerve lesions, shock, respiratory diseases, neonatal hypoxia andso forth. These findings suggest that HOS might not only play a role of increasing oxygen pressure in local region, butalso conspicuously contribute to improving the pathologic process of hypoxia, which coincidently is the vital link instress-induced lesions in the gastrointestinal tract. Additionally, Helicobacter pylori (H. pylori), a kind of microaerophilic(anaerobic) bacterium which can hardly survive in an aerobic atmosphere, has also been identified as an independent riskfactor for the occurrence and development of ulceration. Considering the etiology of peptic ulceration and the features ofHOS, we hypothesize that drinking HOS might prevent gastric ulceration caused by stress or anaerobic H. pylori.
Seroepidemiology of Helicobacter pylori Infection in Tepehuanos Aged 15 Years and Older in Durango, Mexico  [PDF]
Cosme Alvarado-Esquivel
Journal of Pathogens , 2013, DOI: 10.1155/2013/243246
Abstract: This study aimed to determine the seroepidemiology of Helicobacter pylori infection in Tepehuanos (an indigenous ethnic group living in rural Mexico). The prevalence of anti-Helicobacter pylori IgG antibodies was examined in 156 Tepehuanos in Durango State, Mexico, using an enzyme-linked immunoassay. In addition, sociodemographic, clinical, and behavioral characteristics of Tepehuanos associated with seropositivity were investigated. In total, 103 (66%) of the 156 participants (mean age years) had Helicobacter pylori IgG antibodies. Fifty-four (52.4%) of the 103 seropositive individuals had Helicobacter pylori IgG antibody levels higher than 100?U/mL. Males and females had comparable seroprevalence of Helicobacter pylori infection and Helicobacter pylori IgG antibody levels. The seroprevalence was significantly higher in women with pregnancies than those without this obstetric characteristic. Logistic regression showed that Helicobacter pylori infection was positively associated with low education (OR?=?3.37; 95% CI:?1.13–10.00; ) and laborer occupation (OR?=?2.71; 95% CI:?1.14–6.42; ). This is the first report of seroprevalence and contributing factors for Helicobacter pylori infection in Tepehuanos and of the association of Helicobacter pylori infection with laborer occupation. Results warrants further research. 1. Introduction The spiral-shaped and flagellated bacillus Helicobacter pylori causes infections in humans worldwide [1]. Estimates indicate that H. pylori is currently infecting approximately one half of the world’s population [1, 2]. Although most infections with H. pylori are asymptomatic, a severe gastric disease including chronic gastritis, peptic ulcer, gastric mucosa-associated lymphoid tissue lymphoma, and gastric cancer may occur in some individuals [1–4]. According to the current knowledge, dissemination of H. pylori might occur from person to person [5] and by oral-oral or oral-fecal routes [6]. Infections with H, pylori might also occur by drinking contaminated water [6, 7]. The seroprevalence of H. pylori varies substantially among countries being significantly higher in developing countries than in developed countries [8]. The prevalence of infection also varies among geographical regions and ethnic groups [6]. Very little knowledge about the epidemiology of H. pylori infection in Mexico exists. There is a lack of information about H. pylori infection in Tepehuanos (an ethnic group in northern Mexico). Tepehuanos consist of indigenous people living mostly in little remote rural communities. A cross-sectional study was performed
Presence of Helicobacter pylori in betel chewers and non betel chewers with and without oral cancers
Neluka Fernando, Gnanapragasam Jayakumar, Naomal Perera, Indranee Amarasingha, Fahra Meedin, John Holton
BMC Oral Health , 2009, DOI: 10.1186/1472-6831-9-23
Abstract: One hundred and seventy three subjects, of whom fifty three were patients presenting with oral cancer to the Cancer Institute Maharagama, sixty healthy betel chewers and sixty healthy non-betel chewers from the Religious and Welfare Service Centre Maharagama were tested for H. pylori by serology. Thirty oral biopsies from oral cancer patients were cultured under microaerophilic condition to isolate H. pylori. The statistic used was Chi-square test.Of the fifty-three oral cancer patients, forty-four were betel chewers. Among the 53 oral cancer patients examined, ten of forty-four (10/44 = 22.7%) patients who are betel chewers and four of nine (4/9 = 44.4%) patients who are non-betel chewers were detected positive for IgG antibody against H. pylori. In the healthy group (betel chewers and non betel chewers) ten (16.7%) of the healthy betel chewers tested positive for H. pylori by serology. None of the healthy non-betel chewers tested positive for H. pyloriFourteen [26.4%] of oral cancer patients tested positive for H. pylori by serology, of which two were also culture positive (Only thirty samples were cultured). The presence of H. pylori in betel chewers (with or without cancer) compared to non-betel chewers was statistically significant. (Chi-square test p < 0.05) The use of tobacco and areca nut in betel chewers was significant with the presence of H. pylori (p < 0.05).There is a significant higher proportion of H. pylori in betel chewers compared to non-betel chewers but not between oral cancer patients compared to patients without oral cancer. Hence Betel chewing may predispose to colonisation with H. pylori in the digestive tract through swallowing the quid or during betel chewing.Helicobacter pylori is a micro-aerophilic bacterium found principally in the stomach [1]. Infection with this organism is widespread, including Sri Lanka [2-4] and epidemiological studies have clearly demonstrated a major etiological role of H. pylori for peptic ulcer disease, gastric
Comparación de Helicobacter pylori en cavidad oral y mucosa gástrica de acuerdo a genotipo de virulencia (cagA y vacAm 1) Comparison of Helicobacter pylori in oral cavity and gastric mucosa according to virulence genotype (cagA and vacA m 1)  [cached]
Ester Sepúlveda,Jessica Moreno,María L Spencer,Sandra Quilodrán
Revista chilena de infectología , 2012,
Abstract: Objetivo: Comparar el genotipo de virulencia (genes cagA y vacA m1) de Helicobacter pylori, obtenido simultáneamente de mucosa gástrica y cavidad oral. Material y Métodos: Para esto se incluyeron muestras de biopsias gástricas de 18 pacientes. Las muestras orales de estos pacientes fueron obtenidas de placa bacteriana y saliva del piso de boca y base de la lengua. Las muestras fueron estudiadas con RPC convencional y RPC en tiempo real (RPC-TR). Los genes de virulencia cagA y vacA m1 fueron estudiados con RPC-TR. Resultados: De acuerdo a la presencia o ausencia de los genes de virulencia cagA y vacA m1 detectados en las muestras gástricas y orales, se pudieron diferenciar siete combinaciones diferentes. Conclusión: Estos resultados sugieren que existe una variedad de genotipos de virulencia en Helicobacter pylori en el estómago y la cavidad oral, predominando en los pacientes incluidos en este estudio las cepas con genotipos asociados a menor virulencia (cagA-, vacA m1-). Objective: To compare the virulence genotype (cagA and vacA ml genes) of Helicobacter pylori obtained simultaneously from gastric mucosa and oral cavity. Material and Methods: Gastric samples of 18 patients were obtained by endoscopic biopsies. Oral samples of these patients were obtained from dental plaque and saliva swabs from the floor of the mouth and the base of the tongue. All samples were studied by conventional PCR and real-time PCR (RT-PCR). Virulence genes cagA and vacA ml were studied by RT- PCR. Results: According to presence and/or absence of cagA and vacAm1 genes, seven different combinations were observed. Conclusion: These results suggest that there is a variety of genetic profiles of Helicobacter pylori in the stomach and oral cavity, with a predominance of less virulent genotypes in the patients included in this study (cagA-, vacA m1-).
Age-Dependent Association among Helicobacter pylori Infection, Serum Pepsinogen Levels and Immune Response of Children to Live Oral Cholera Vaccine CVD 103-HgR  [PDF]
Khitam Muhsen, Rosanna Lagos, Mardi K. Reymann, David Y. Graham, Marcela F. Pasetti, Myron M. Levine
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0083999
Abstract: Background Through its effects on gastric secretion, we hypothesized that Helicobacter pylori infection may influence oral immunization. Accordingly, we examined the association between H. pylori infection, serum pepsinogen (PG) (measures for H. pylori gastritis) and vibriocidal antibody (a correlate of protection) seroconversion following oral immunization with CVD 103-HgR live cholera vaccine among children of different ages. Methods Sera from 422 Chilean children who were vaccinated with a single dose of CVD 103-HgR were tested by ELISA for serum IgG antibodies to H. pylori, PG I and PG II levels and antibodies to Shigella flexneri 2a lipopolysaccharide and hepatitis A virus (as markers of low socioeconomic status and exposure to enteric pathogens). Results The likelihood of vibriocidal antibody seroconversion following vaccination with CVD 103-HgR was significantly decreased in H. pylori-seropositive children age 6 months to 4 years with PG II>8 μg/L (adjusted OR 0.14 (95% CI 0.03–0.61; P = 0.009), and also in H. pylori seropositives with lower PG II level (adjusted OR 0.34, 95% CI 0.14–0.83; P = 0.017), compared to H. pylori-seronegatives. H. pylori-seropositive children aged 5–9 years with serum PG I>30 μg/L (indicating more severe gastritis) had higher odds of vibriocidal seroconversion than those with lower PG I levels (adjusted OR 4.41, 95%CI 1.26–15.38; P = 0.02). There was no significant association between exposures to S. flexneri 2a or hepatitis A virus and vibriocidal seroconversion. Conclusions As H. pylori gastritis progresses with increasing pediatric age in developing country venues, changes in gastric secretion ensue that we believe explain the observed differences in age-related immune responses to immunization with live oral cholera vaccine. The effect of H. pylori and changes of gastric acid secretion on the immunogenicity of various oral vaccines should be studied in different developing, transitional and industrialized country settings.
Helicobacter pylori infection and oral cavity
Anna Paradowska,Agnieszka Sieja,Marcin Braksator
Polish Gastroenterology , 2010,
Abstract: In the last century, the thought that ulcerative disease is connected to secretion of acids only was very common. The bacteriology of ulcerative disease was established in the XIX century and described for the first time by a Polish scientist Professor Walery Jaworski, but was not taken seriously until the 1970's when it was re-discovered by Marshall and Warren. The discovery was awarded Nobel Prize in Medicine in 2005. The bacteria, called Helicobacter pylori, plays a key role in epidemiology of gastritis, gastric and duodenal ulcerations and cancers. The transmission of the disease can be oral-oral, faecal-oral or gastro-oral. A very important factor in pathogenesis is improper hygiene. Oral cavity may be a habitat for Helicobacter pylori. Bacteria may be present in subgingival biofilm, saliva and dental plaque. Even though many studies have been performed, the true correlation of the presence of the bacterium in the oral cavity and co-existence of ulcerative disease or periodontitis remains unclear and requires further studies.
Oral Cavity as an Extragastric Reservoir of Helicobacter pylori  [PDF]
Arwa Al Sayed,Pradeep S. Anand,Kavitha P. Kamath,Shankargouda Patil,R. S. Preethanath,Sukumaran Anil
ISRN Gastroenterology , 2014, DOI: 10.1155/2014/261369
Abstract: Background. Several studies were reported on the prevalence, and relationship between the existence of Helicobacter pylori (H. pylori) in oral cavity and in stomach of patients. The purpose of this study was to systematically review the existing literature on the presence of H. pylori in the oral cavity and its link to gastric infection, the existence of coinfection, and the impact of anti-H. pylori therapy on the dental plaque and vice versa. Method. Two authors independently searched the Medline, EMBASE, Cochrane Library, Web of Science, Google Scholar, and Scopus databases for relevant studies. The articles were analyzed critically and all qualified studies were included. The search was carried out by using a combined text and the MeSH search strategies: using the key words Helicobacter, Helicobacter pylori, and H. pylori in combination with dental plaque, periodontitis, and oral hygiene. Results. The data was presented in 8 tables and each topic separately discussed. Conclusion. Based on the systematic review of the available literature on H. pylori infection and its presence in the oral cavity, it can be concluded that dental plaque can act as a reservoir, and proper oral hygiene maintenance is essential to prevent reinfection. Due to the diversified methods and population groups involved in the available literature, no concrete evidence can be laid down. Further studies are necessary to establish the role of H. pylori in the oral cavity and its eradication on preventing the gastroduodenal infection. 1. Introduction Helicobacter pylori (H. pylori) is one of the most common bacterial infections in humans [1]. The presence of the organism H. pylori (initially termed Campylobacter pyloridis) in the antral mucosa of humans was first reported in 1983 [2]. H. pylori has been closely linked to chronic gastritis, peptic ulcer, gastric cancer, and mucosa-associated lymphoid tissue (MALT) lymphoma [3, 4]. The International Agency for Research on Cancer of the World Health Organization (WHO) has designated H. pylori as a Group 1 carcinogen [5]. Besides gastrointestinal diseases, recent data seems to suggest a possible association of this microorganism with other conditions such as anemia [6], altered serum levels of lipoproteins [7], and coronary atherosclerosis [8]. Although H. pylori is present in the stomach of about half of the world’s population, we do not yet clearly understand its transmission. Available data suggests that oral-oral and fecal-oral routes are the most likely routes of transmission of this organism [9, 10]. However, no extragastric
Correlation of Helicobacter pylori and gastric carcinoma.  [cached]
Khanna A,Seth P,Nath G,Dixit V
Journal of Postgraduate Medicine , 2002,
Abstract: BACKGROUND: Difference of opinion about the prevalence of H. pylori association with gastric cancer exists in the literature. AIMS: To study the correlation of Helicobacter pylori (H. pylori) to gastric carcinoma. METHODS: 50 proved cases of gastric cancer were studied by rapid urease test, culture, histopathology and ELISA test for H. pylori IgG. RESULTS: 68% of cases of gastric cancer were found to be positive for H. pylori infection as compared to 74% of healthy controls. CONCLUSIONS: The prevalence rate of H. pylori infection in our patients of gastric cancer was lower than in the control population though statistically not significant, suggesting that H. pylori may not be responsible for gastric carcinogenesis in this population.
Helicobacter pylori and gastric cancer
Ota?evi? Marica M.,Nagorni Aleksandar V.,Stankovi?-?or?evi? Dobrila M.,Dini? Marina
Archive of Oncology , 2003, DOI: 10.2298/aoo0304233o
Abstract: BACKGROUND: Helicobacter pylori (H. pylori) is classified as a Group 1 carcinogen, because H. pylori infection considerably increases the risk of gastric cancer development. METHODS: The study involved a total of 191 patients divided into two groups. The first group comprised 117 patients who underwent endoscopy. A total of 203 biopsy specimens of the gastric mucosa were taken and analyzed using microbiological and histopathological methods. The second group comprised 74 patients with gastric cancer, who were examined for the gastric cancer type, the presence of H. pylori infection and the cancer localization. The presence of H. pylori infection in the tissue was con-firmed by staining pathohistological sections according to the method of Warthin-Starry. The microbilogical diagnosis involved the staining of direct tissue smears according to the method of Gram, as well as the cultivation of the specimens. To test the hypothesis for possible differences in H. pylori positive findings between the treatment groups, x2 test with Yates correction or Fisher exact test were used. RESULTS: The first treatment group comprised 117 patients with various clinical diagnoses. Gastric cancer was diagnosed in 8 patients, and of these 87.50% were found to have H. pylori. No statistically significant difference in H. pylori positive tests was detected between the patients with gastric ulcer and the patients with gastric cancer (Fisher exact test: p=1.00; p>0.05) nor was it established between the patients with duodenal ulcer and those with gastric cancer (Fisher exact test: p= 1.00; p>0.05). The second treatment group comprised 74 patients, of whom 52 (70.27%) had intestinal-type gastric cancer and 22 (29.72%) had diffuse-type gastric cancer. No statistically significant difference in the positive tests for H. pylori was registered between the patients with intestinal-type and those with diffuse-type gastric cancer (x2=0.07; p=0.798; p>0.05). The most frequent localization of the cancer was the antrum. CONCLUSION: The results are supportive of the hypothesis on a correlation between H. pylori infection and gastric adenocarcinoma development, but no differences between the intestinal and diffuse type of adenocarcinoma have been revealed with respect to the malignant process.
Concomitant Colonization of Helicobacter pylori in Dental Plaque and Gastric Biopsy  [PDF]
Amin Talebi Bezmin Abadi,Ashraf Mohabati Mobarez,Omid Teymournejad,Mona Karbalaei
Journal of Pathogens , 2014, DOI: 10.1155/2014/871601
Abstract: Frequently reported H. pylori antimicrobial therapy failures suggest that there might be a different niche where the bacteria can stay safe. Current study aims to examine potential role of oral colonization of H. pylori to feed reinfection after primary therapy. However, patients who were admitted to the gastroscopy section were chosen and gastric biopsy and dental plaque specimens were collected. Molecular and biochemical tests were applied to confirm H. pylori identity in different colonization niches. Results showed that 88.8% of dyspeptic patients had epigastric pains with nocturnal awakening when they were hungry ( ). All patients who received therapy already were again H. pylori positive while they are still carrying H. pylori in dental plaque ( ). Moreover, H. pylori infection was sought in 100% of gastric biopsy’s dyspeptic patients who had ulcerated esophagitis and erosive duodenitis and who were H. pylori positive, and 75% of dyspeptic patients with duodenum deformity had this bacterium in gastric biopsies ( ). Present study showed that only successful eradication of gastric H. pylori cannot guarantee prevention of reinfection. Conclusively, a new strategy which indicates concomitant eradication in oral and gastric colonization can result in clearance of H. pylori infection. 1. Introduction Helicobacter pylori (H. pylori) is a Gram-negative, spiral, and motile bacterium that is present in the human stomach of approximately half of the world’s population [1]. H. pylori is an important gastrointestinal pathogen that is strongly associated with gastritis as well as peptic ulcer disease. There is strong evidence that H. pylori has an undeniable role in occurrence of gastric abnormality, atrophic inflammation, and gastric cancer [2]. Colonization begins in childhood; however, little is known about its timing and actual route of bacterial transmission [3, 4]. Recent findings are indicating a narrow link between oral and gastric colonization of H. pylori [5]. Frequently failed antibiotic therapy to cure H. pylori infection suggests that there might be certain different sites where the organism can survive [1, 6]. To date, the exact mechanism of transmission of H. pylori is not fully understood, a crucial fact which implies on unknown routes and reservoir locations that are still undiscovered. Indeed, defeated therapeutic approaches to cure gastric H. pylori infection triggered a thought that different locality might be involved in reinfection of this persistent bacterium [6]. Nonetheless, alarm symptoms and endoscopic finding are such approach to
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