The best treatment for H. pylori eradication regimens should have cure rates of at least 80%, be without major side effects, and induce minimal bacterial resistance. Antibiotics alone have not achieved this. Luminal acidity influences both the effectiveness of some antimicrobial agents and the survival of the bacteri; thus antibiotics have been combined with acid suppression such as proton pump inhibitors (PPIs), bismuth, or H2 antagonists. The “classic” regimen is treatment twice daily for 7 days with a PPI and clarithromycin plus either amoxicillin or metronidazole Bismuth has been used in the treatmentof peptic ulcer disease and 1 part o quadruple therapy for H.Pylori but compliance ofchildren for it is low.
The purpose of this study was the evaluation ofHelicobacterpylori infections inchildren and adults from two indigenous communities of Delta Amacuro State, Venezuela, that differ in hygienic conditions of the housing. The evaluation was performed in 98 children (mean age 7 ± 3.37 years) and their mothers (33.96 ± 13.77 years) from two communities of Warao lineage. Anti-H. pylori serum IgG and secretory anti-H. pylori IgA antibodies were de- termined, as well as total secretory IgA and H. pylori antigens in feces. Serological prevalence of H. pylori infection was 38% inchildren and 84% their in mothers. Children from the community that had the most deficient sanitary and hygienic conditions had significantly lower titers of specific IgG antibodies and total secretory IgA (P < 0.0001) and a high percentage of them had H. pylori antigens in their feces (P < 0.0001). The levels of specific IgA were similar in both groups. The results indicate that in these populations there is a high prevalence of H. pylori infection and that poor hygienic conditions can increase the risk of infection and damage to the gastrointestinal tract.
Change in the profile of patients who attend the service may be reflected in the found result. The “Hospital São Paulo” linked to UNIFESP/EPM attends patient of the Public Health System and of private health insurance companies. However, the studied data base included only patients from the Public Health System, since the data bank does not encompass patients of the private health insurance companies. During the period there was no alteration in the reference system and the patients were usually referred by the Pediatric Gastroenterology outpatient clinic of the institution. Thus, we think that alterations in the attended socioeconomic profile would only reflect alterations in the socioeconomic profile of the
An experimental murine model was used to verify the viability and pathogenicity of coccoid Helicobacterpylori. For this purpose, 27 BALB/c mice were inoculated intragastrically with 1 ml broth culture (10 8 organisms/ml) of a coccoid H. pylori clinical isolate. The animals were divided into two groups. Nine were infected on a one-time basis (GA1) and 18 were infected on two consecutive days (GA2). Other 27 mice were inoculated with Brucella broth and divided in the same way; they composed the control group. Mice were killed at 2, 3, 7, 14 and 21 days post inoculation (pi). Fragments of stomach and duodenum were collected, fixed with 12% formalin and stained by hematoxilin-eosin and Giemsa for histopathological examination. Until the 14th day, only reinfected mice had mild- to-moderate inflammatory infiltrate in the stomach. The infiltration was predominantly lymphomonocytic, although plasma cells and eosinophils could be seen. However, at 21st day, severe eosinophilic infiltration was present in the lamina propria and submucosa of gastric corpus. In subgroup GA1, animals presented lymphomonocytic infiltration in the stomach from 14th day pi. Our results showed that coccoid H. pylori was able to induce an acute inflammatory response in stomach of reinfected mice since the initial periods of infection.
METHODS: Thirty patients with peptic ulcer diagnosed by upper endoscopy and for Helicobacterpylori infection by rapid urease test and histologic examination received omeprazole 40 mg, secnidazole 1000 mg, and azithromycin 500 mg, administered once daily for 3 days. A follow-up exam was performed 12 weeks after the end of the treatment. Patients who were negative for Helicobacterpylori infection by rapid urease test and histologic examination were considered cured.
most important agent of gastritis and as a risk factor for peptic ulcer disease and gastric adenocarcinoma. Currently many diagnostic methods exist for detecting H. pylori, however they all have limitations, thus it is recommend a combination of at least two methods. The aim of this study was to evaluate diagnostic methods, such as in-house urease test, culture and Polymerase Chain Reaction (PCR), for the detection of the H. pyloriin gastric biopsy specimens of 144 dyspeptic patients, using as gold standard the association between histology and rapid urease test. According to the gold standard used in this study, 48 (33.3%) patients were infected with H. pylori, while 96 (66.7%) were classified as not infected. The in-house urease test and the PCR were the most sensitive methods (100%), followed by culture (85.4%). However, the in- house urease test and the culture were the most specific (100%), followed by PCR (75%). In conclusion, this
The current treatment regimen for H. pylori infection consists of a proton pump inhibitor (PPI) and two commonly used antibiotics, such as metronidazole and amoxicillin or clarithromycin. As well, various other antibiotics have been suggested for use in combination with PPIs, including furazolidone, erythromycin, and tetracycline 2,3 .
All adenotonsillar specimens included in this study were negative when PNA–FISH or PCR–DEIA were used. The PNA–FISH method has been previously tested in different types of samples and with different microorganisms, and has shown a high speciﬁcity for H. pylori . PCR is recognized as having high speciﬁcity if the target gene and the primers are carefully chosen. In this study, we have used as ampliﬁcation target H. pylori vacA gene that, besides having no homology to other bacterial species, is present in all H. pylori strains. The primers used are well established and their high sensitivity and speciﬁcity has been previously demonstrated [10,11]. PCR sensitivity was increased by hybridization of ampliﬁed products with a speciﬁc vacA probe . Considering that PNA–FISH and PCR–DEIA are the most speciﬁc and sensitive methods and that all tissue samples analyzed were negative, results obtained by rapid urease test and immunohis- tochemistry are false positives. Several studies have reported the presence of H. pyloriin adenoid and/or tonsillar tissues based on the solely use of rapid urease test [6,7]. However, we and others showed that, in cases positive for the rapid urease test, the use of additional detection methods reveals that those are likely false- positive results [14,15]. One very important aspect concerns the speciﬁcity of the rapid urease test and of immunohistochemistry. These are related with the probability of the presence in the sample of microorganisms, other than H. pylori, that could origin cross reactivity leading to false-positive results. So, although these techniques have a high speciﬁcity when used in gastric samples, the speciﬁcity may be lower in samples from polymicrobial environments such as the adenotonsillar tissues . The rapid urease test is not in fact a speciﬁc test for H. pylori, but for urease- producing microorganisms. Therefore, the positive results that we have obtained probably reﬂect the presence in adenotonsillar tissues of other urease-producing bacteria. Likewise, and although immunohistochemistry allows higher reproducibility of H. pylori detection in gastric samples when compared with conventional
Helicobacterpylori is a spiral-shaped Gram-negative bacterium. It colonizes the gastric mucosa of humans and persists for decades if not treated . Helicobacterpylori infection affects more than half of the world’s population and invariably results in chronic gastritis. The clinical results of this infection range from asymptomatic gastritis to peptic ulcers and gastric cancer . The infection is mostly asymptomatic, and most of the infected population never manifests clinically significant conditions. However, some individuals develop diseases, such as peptic ulcers and mucosa-associated lymphoid tissue lymphoma [1,3,4]. Several studies suggest progressive gastric mucosal damage induced by this pathogen , since clinical symptoms of gastric disorders appear most frequently in adults, while H. pylori acquisition occurs in childhood .
he present study did not evaluate an adequate sample of the pop- ulation, and it was restricted to a convenience sample ofchildren at- tending a public hospital. his is an important limitation of the study. However, this law does not diminish the importance of the present study, because it provides data that are necessary for studying the epi- demiology of H. pylori infection in other epidemiological studies. he decision to restrict the eligibility to children with respiratory symptoms avoided the selection bias inherent in infected individuals with diges- tive symptoms. 26,27
The abstract form of this study was presented as poster in 1st International Organic Electronic Material Tec- hnologies Conference (OEMT 2015), March 25-28, 2015, Elazig, Turkey. The authors thank Dr. Vildan Caner, De- partment of Medical Biology, Faculty of Medicine, Pamuk- kale University, Denizli, Turkey, for kindly providing some clinical strains and the management of the Elazig Veterinary Control and Research Institute for securing lab- oratory facilities for this study. We are also grateful to Dr. Francis Megraud, INSERM U853, Laboratoire de Bacte- riologie - C.H.U. Pellegrin, France; Dr. Alfizah Hanafiah, Department of Medical Microbiology and Immunology, Faculty of Medicine, UKM Medical Centre, Kuala Lum- pur, Malaysia and Dr. Emma Sproston, Bureau of Micro- bial Hazards, Health Canada, Ottawa, Canada for critical review of the manuscript.
Journal of Evolution of Medical and Dental Sciences/Volume1/ Issue4/October-2012 Page 342 Rapid urease test is one of the invasive tests based on the principle that abundant urease enzyme is being produced by H. Pylori that hydrolyses urea to ammonia ; phenol red indicator shows the alkalinity produced thereby and the medium turns deep pink in colour.An earlier study 4 done in the same institution reported a prevalence of 10.93%.The present prevalence is
There are also conflicting reports as to whether the extent of GM decreases after eradication of H. pylori. Some studies have shown no decrease in the extent of GM after eradication of H. pylori (5-7,9-11), whereas a significant reduction in the extent of GM was demonstrated in others (4,8). In agree- ment with the latter reports, the results of the present study showed that the extent of GM significantly decreased and complete regres- sion occurred in more than half (15/28) the patients 6 months after eradication of H. pylori. In addition, the patients with success- ful eradication of H. pylori show a signifi- cantly higher prevalence of GM regression than those with no eradication. These find- ings further confirm the important contribu- tory role of H. pylori infection in the devel- opment and persistence of GM.
To our knowledge, this is the first study in the literature that treated HP in chronic cases of CSC and reported improvement following an evaluation of BCVA and an OCT examination. A similar study was performed in 2002 (10); however, in that study, HP was not eradicated, the sample size (16 eyes) was smaller than the current study (18 eyes), and improvements in BCVA and OCT were not evaluated. A French study found HP to be significantly more prevalent in patients diagnosed with CSC than in the normal population (11). In our study, a higher incidence ofHelicobacterpylori infection (82.35% - 15 patients and 18 eyes) was found than the previously reported prevalence in southern Brazil (63%) (18,19). Interestingly, 13 of 14 patients showed improvement of CCSC following treatment for HP. However, one of these cases recurred, and laser photo- coagulation was required after a negative gastric biopsy. In three patients, CCSC recurrence was associated with the recurrence of HP infection, and serous detachment resolved upon anti-HP retreatment in two of the cases; in the third case, the patient asked for both photodynamic therapy and anti-HP medication. In most of the responding cases, serous detachment resolved within one month after antibiotic treatment. One previously reported case of CCSC improved clinically when the gastric infection was eradicated, and recurrences of CCSC in this patient were associated with the return of the bacterial infection (9). The recurrence rate of 27% (5 of 18 eyes) indicates that it is a frequent problem associated with CSC, and this has been previously reported (3,5).
Helicobacterpylori (H. pylori)-infection causes persistent inflammation with different clinical outcomes in humans, including chronic gastritis, peptic ulcer, and gastric cancer. The key determinants of these outcomes are the severity and distribution of the H. pylori-induced inflammation. Recent evidence has demonstrated that H. pylori strains possess genotypic diversity whose products trigger inflammatory process and the main mediators and cytokines, which may engender differential host inflammatory responses with distintict clinical outcomes. H. pylori strains that possess the cag pathogenecity island induce more severe inflammation via activation of gene transcription, thus enhancing the risk for peptic ulcer and distal gastric cancer. The oxidative and nitrosative stress induced by inflammation plays an important role in gastric carcinogenesis as a mediator of carcinogen formation, DNA damage, and imbalances between cell proliferation and apoptosis.
The exact prevalence of H. pylori infection in MALT lymphoma is unknown and varies depending on the study from 50% to almost 100%. This variability could be explained by the number of tests used for detection of H. pylori and their kind. If you use only one test more likely are false negative results. As for the types of tests, the prevalen- ce of H. pylori infection is higher when using serological and urea based test compared to biopsy. This is explained by extensive mucosal lesions in MALT lymphoma that may le- ad to the reduction in H. pylori colonization, to undetectable levels. Also, the prevalence of H. pylori infection depends on the depth of invasion of lymphoma, so the lymphoma limited to the mucosa and submucosa prevalence of infection is hig- her than in lymphomas with a deeper propagation. These re- sults support the hypothesis that H. pylori is present in the early stage of MALT lymphoma, but later, with the progres- sion of lymphoma may result in the loss of H. pylori 15–17 . In all of our patients with MALT lymphoma H. pylori infection was proven. Such a high percentage of H. pylori infection in our patients could be explained by the fact of a large number of biopsy samples, and the two tests used for the detection of H. pylori (biopsy urease test and Giemsa stain) and that MALT lymphomas were at an early stage, limited to the mu- cosa and/or submucosa.
The ATBC Study, a randomized, double-blind, placebo- controlled, primary prevention trial, was designed to test the hypothesis that daily supplementation with alpha-tocopherol, beta- carotene, or both would reduce the incidence of lung or other cancers among male smokers. Details of this study have been published . In brief, Finnish males between 50 and 69 years of age were identified through the Central Population Register. Questionnaires were mailed to those with available addresses. Men who smoked $5 cigarettes per day and who agreed to participate were mailed an invitation to a local field station for further evaluation. After excluding men with proven malignancy (other than nonmelanoma skin cancer or carcinoma in situ), severe angina on exertion, chronic renal insufficiency, liver cirrhosis, chronic alcoholism, current anticoagulant therapy, other medical problems that could limit participation for 6 years, or current use of supplements with vitamin E (.20 mg/d) or vitamin A (.20,000 IU/d = 2000 retinol equivalents) or beta-carotene (.6 mg/d), 29,246 men were randomized. Later, 113 men were found to be ineligible, leaving 29,133 eligible Finnish male smokers enrolled in ATBC between 1985 and 1988. Both the US National Cancer Institute and the Finnish National Public Health Institute institutional review boards approved the ATBC Study, and all participants provided written informed consent. The men continue to be followed as a cohort since the trial ended in 1993.
ABSTRACT – Context - Helicobacterpylori has been associated with worsening of gastroesophageal relux disease (GERD). Objective - To evaluate the effect of H. pylori eradication in GERD patients. Methods - We conducted a prospective, randomized, controlled trial performing symptom evaluation, endoscopy, histology, manometry and esophageal pH testing on GERD patients. Patients infected with H. pylori were randomized to: 1) eradication treatment plus proton pump inhibitors treatment, or 2) proton pump inhibitors alone. Patients not infected constituted a negative control group. After 3 months, patients were re-evaluated by symptom assessment, endoscopy, histology and manometry. Results - GERD treatment resulted in signiicantly higher lower esophageal sphincter pressure, as measured by mean expiratory pressure, in H. pylori negative patients. There was signiicantly lower proportion of hypotensive waves and signiicantly higher proportion of normotensive waves in non-eradicated patients. All symptom scores were signiicantly reduced in the post-treatment period compared to baseline, to values that were similar among the three groups, in the post-treatment period. In the post-treatment period, erosive esophagitis was signiicantly less frequent on those not eradicated. Conclusion - Manometric, clinical and endoscopic data showed no beneit in eradicating H. pyloriin GERD. Our data supports the hypothesis that H. pylori eradication does not inluence GERD.
In the article: BRUSCKY, Dayanne Melo V.; ROCHA, Luiz Alexandre R. da; COSTA, Aldo José F.. Recurrence of chronic urticaria caused by reinfection by Helicobacterpylori. Rev. paul. pediatr. São Paulo, v. 31, n. 2, jun. 2013. Available from: <http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0103-05822013000200021&lng=pt&nrm=iso>. Cited 2014 Mar 20. http://dx.doi.org/10.1590/S0103-05822013000200021.
biomarker for Helicobacterpylori-associated gastroduodenal disorders. Another controversial issue in the ﬁeld of H. pylori biomarker and disease research is whether physicians can use this type of data in clinical trials. While characterizing accurate H. pylori biomarkers associated with certain diseases seems difﬁcult, new, full-genome sequencing studies may answer unsolved related issues in the near future.