Serum prolidase activity and oxidative status in Helicobacter pylori infection

OBJECTIVES: During the course of Helicobacter pylori infection, increased oxidative stress plays an important role in the pathogenesis of gastroduodenal mucosal inflammation, which can cause gastric mucosal atrophy that characterized by the replacement of the gastric mucosal glands by collagen fibers. In the present study, we aimed to determine serum prolidase activity and oxidative status, and to find out if there is any association between serum prolidase activity and oxidative status in H. pylori infection. DESIGN AND METHODS: Forty H. pylori-positive and 32 H. pylori-negative subjects were enrolled. Serum prolidase activity was measured spectrophotometrically. Oxidative status was determined using total antioxidant capacity and total oxidant status measurement and calculation of oxidative stress index. RESULTS: Total antioxidant capacity level was lower in H. pylori-positive group than H. pylori-negative group (p<0.001), whereas total oxidant status, oxidative stress index and prolidase activity were higher (all p<0.05). Significant correlation was observed between serum prolidase activity, and total antioxidant capacity, total oxidant status and oxidative stress index (p<0.01, r=-0.367; p<0.05, r=0.283; p<0.01, r=0.379; respectively) in H. pylori-positive subjects. CONCLUSION: H. pylori infection may be associated with increased oxidative stress and increased serum prolidase activity. Increased oxidative stress seems to be associated with increased serum prolidase activity and this association may help to provide a better understanding about the pathogenesis of H. pylori infection.     

Effect of Helicobacter pylori infection and eradication therapy on interleukin-6 levels in patients with Familial Mediterranean Fever

It is being questioned if Helicobacter pylori infection, which causes a chronic inflammatory response, can increase the frequency and severity of attacks in patients with Familial Mediterranean Fever (FMF) and if the impact of inflammatory response can be diminished by eradication of the infection. To evaluate if there is difference in interleukin (IL)-6 levels of H. pylori-positive and -negative patients both before and during FMF attacks; if there is a change in IL-6 levels following successful eradication treatment; and if MEFV gene mutations have an effect on IL-6 levels. IL-6 levels were evaluated in 47 FMF patients before and during FMF attacks. Genetic testing to determine M694V, M694I, E148Q, V726V, M680I mutations was also performed in all patients. IL-6 levels were also determined after successful eradication of the infection in H. pylori-positive patients. IL-6 levels were compared in H. pylori-positive and -negative patients, and before and after eradication treatment in patients who cleared the infection. Number of patients in tested mutation groups was not enough to compare IL-6 levels in these groups. Thirty-four patients (73.9%) were H. pylori-positive. Before FMF attack there was no statistically significant difference in IL-6 levels of H. pylori-positive and -negative groups. IL-6 levels were significantly higher in both groups during the attacks than before the attacks (p < 0.05). There was a statistically significant decline in IL-6 levels both before and during FMF attacks, following eradication therapy in patients who cleared the infection (p < 0.05). In patients with homozygous M694V mutation, IL-6 levels before and during the FMF attacks were not significantly different in H. pylori-positive and -negative groups, despite a much lower level found in H. pylori-negative group (p > 0.05). Comparisons were not performed in other mutation groups because of small number of patients in each group. C-reactive protein (CRP) and fibrinogen levels were not significantly different between the groups (p > 0.05). We believe that the observation of IL-6 levels are lower both before and during FMF attacks both in H. pylori-negative patients and in patients who cleared the infection after eradication therapy is very important in the determination of the role of eradication of H. pylori on decreasing the frequency and severity of FMF attacks. As for today, the correlation between H. pylori infection and FMF seems unlikely; however, studies evaluating the interaction of cytokines in both diseases and their relations and roles will be needed to reach better conclusions.     

Helicobacter pylori eradication shifts monocyte Fcgamma receptor balance toward inhibitory FcgammaRIIB in immune thrombocytopenic purpura patients

Immune thrombocytopenia purpura (ITP) is a bleeding disorder in which platelet-specific autoantibodies cause a loss of platelets. In a subset of patients with ITP and infected with Helicobacter pylori, the number of platelets recovers after eradication of H. pylori. To examine the role of H. pylori infection in the pathogenesis of ITP, the response of 34 ITP patients to treatment with a standard H. pylori eradication regimen, irrespective of whether they were infected with H. pylori, was evaluated. Eradication of H. pylori was achieved in all H. pylori-positive patients, and a significant increase in platelets was observed in 61% of these patients. By contrast, none of the H. pylori-negative patients showed increased platelets. At baseline, monocytes from the H. pylori-positive patients exhibited an enhanced phagocytic capacity and low levels of the inhibitory Fcgamma receptor IIB (FcgammaRIIB). One week after starting the H. pylori eradication regimen, this activated monocyte phenotype was suppressed and improvements in autoimmune and platelet kinetic parameters followed. Modulation of monocyte FcgammaR balance was also found in association with H. pylori infection in individuals who did not have ITP and in mice. Our findings strongly suggest that the recovery in platelet numbers observed in ITP patients after H. pylori eradication is mediated through a change in FcgammaR balance toward the inhibitory FcgammaRIIB.     

Non-invasive diagnosis of Helicobacter pylori infection: simplified 13C-urea breath test, stool antigen testing, or DNA PCR in human feces in a clinical laboratory setting?

OBJECTIVES: (1) To compare two stool antigen EIAs (HpSA, FemtoLab) and PCR of ureaseA and cagA in feces, with (13)C-urea breath test (UBT). (2) To ascertain whether a simplified UBT (breath collection time = 10 min) is as reliable as the standard assay (30 min). DESIGN AND METHODS: Helicobacter pylori status was recorded in Group 1 (n = 187) by UBT, H. pylori stool antigen, ureA and cagA PCR in feces. UBT with 10, 20 and 30 min sampling was performed in Group 2 patients (n = 283). RESULTS: The sensitivity and specificity of HpSA, FemtoLab, and ureA were 67% and 99%, 90% and 96%, 35% and 98%, respectively. cagA results were positive in 16/48 H. pylori-positive, and in 5/100 H. pylori-negative patients. The results of UBT with a 10- and 30-min sampling strictly overlapped. CONCLUSION: UBT with 10 min breath collection and FemtoLab stool antigen assay are the most reliable non-invasive tests to diagnose H. pylori infection.     

Normal serum pepsinogen I levels in adults: a population-based study with special reference to Helicobacter pylori infection and parietal cell antibodies

OBJECTIVE: Low serum pepsinogen I (PG I) values are common in subjects with advanced corpus atrophy with or without parietal cell antibodies (PCA). Elevated values are usual during Helicobacter pylori infection. MATERIAL AND METHODS: PG I levels were determined in two randomly selected cross-sectional adult population samples using the Gastroset PGI test kits. The sera (408 in 1973 and 504 in 1994), tested earlier for H. pylori infection and now for PCA, represented subjects living in Vammala, Finland. RESULTS: In the PCA-negative population, the mean (+/-SD) PG I level was significantly higher in men than in women among both H. pylori-negative (88.13+/-34.16 microg/l versus 72.43+/-29.31 microg/l; p<0.0001) and H. pylori-positive (110.50+/-50.59 microg/l, versus 97.74+/-44.82 microg/l, p<0.0001) subjects; the difference between all H. pylori-positive and -negative subjects was also significant (p<0.001). In the 10-year age groups, age had no impact on the mean PG I levels in H. pylori-negative subjects (p=0.860). In the PCA-positive population, the 10 H. pylori-positive subjects had higher mean PG I levels (112.96+/-53.62 microg/l) than the 13 H. pylori-negative subjects (32.57+/-27.59 microg/l; p=0.002); the latter mean was also significantly lower than that of the PCA- and H. pylori-negative subjects (80.08+/-32.69 microg/l; p<0.0001). CONCLUSIONS: Men had higher normal PG I values than women, but there was no significant variation by age. H. pylori infection was associated with elevated PG I levels and a small decrease with increasing age. Non-infected PCA-positive subjects showed the lowest mean PG I level.     

Long-term outcomes of gastric mucosa-associated lymphoid tissue lymphomas after Helicobacter pylori eradication therapy

Mucosa-associated lymphoid tissue (MALT) lymphomas are localized primarily in the gastrointestinal tract and are characterized by an indolent nature and favorable outcome with specific therapy. Gastric MALT lymphomas are closely linked to Helicobacter pylori (H. pylori) infection, for which eradication therapy is recognized as an effective primary treatment for the disease. However, there is little information about long-term outcomes after the therapy. In the present study, we elucidated the long-term outcomes of 74 patients (70 H. pylori-positive and 4 negative cases) followed up by endoscopy at least 12 months after exclusive eradication therapy alone. The median follow-up period was 46 months. When the remission status was estimated at the time point of 12 months post-eradication, the numbers of patients with complete remission (CR), histologically residual disease with macroscopic normalization (hRD), partial remission with more than 50% tumor reduction (PR) or no response (NR) were 56, 12, 2 and 4, respectively. During follow-ups of over 12 months post-eradication, 11 of the 12 hRD cases were belatedly induced to CR but one CR case histologically relapsed into hRD. One of the 2 PR cases eventually turned into hRD 20 months later. Therefore, 66 CR, 3 hRD, 1 PR, and 4 NR cases (including 3 H. pylori-negative) were identified at the last follow-up of the present study. All 74 patients were followed up without any second-line therapies, but none exhibited disease progression. Thus, the long-term outcome of localized gastric MALT lymphoma after H. pylori eradication therapy was favorable. A watch and wait strategy may be a reasonable approach for hRD since the majority might be in the process of turning into delayed CR.     

Chronic Helicobacter pylori infection and migraine: a case-control study

OBJECTIVE: To determine whether chronic Helicobacter pylori infection is a risk factor for migraine. BACKGROUND: Preliminary studies have shown a high prevalence of Helicobacter pylori infection in patients with primary headaches. METHODS: One hundred three consecutive patients with migraine were enrolled in the study and compared with a group of 103 matched controls. Helicobacter pylori infection was diagnosed by means of both (13)C-urea breath test and serology. RESULTS: Of patients with migraine, 30.1% were positive for Helicobacter pylori, compared with 31.1% of controls (P = NS). The odds ratio for migraine associated with chronic Helicobacter pylori infection was 0.96 (95% confidence interval, 0.51 to 1.80). Demographic, clinical, and psychological characteristics of Helicobacter pylori-positive migraineurs were compared with those of migrainous patients without infection. Helicobacter pylori-positive patients had a significantly (P<.05) lower incidence of food sensitivity than Helicobacter pylori-negative patients. No significant difference was found in any other feature examined. CONCLUSIONS: Our study suggests that chronic Helicobacter pylori infection is not more frequent in patients with migraine than in controls and that infection does not modify clinical features of the disease.     

Predictors of failure of Helicobacter pylori eradication and predictors of ulcer recurrence: a randomized controlled trial

OBJECTIVE: In light of evidence that Helicobacter pylori treatment fails 5% to 20% of the time, the objective of this study was to determine predictors of unsuccessful H. pylori eradication and of duodenal ulcer recurrence. DESIGN: Randomized, double-blind, placebo-controlled trial. SETTING: Gastroenterology services of 2 general hospitals in Montreal, Que. PATIENTS: All patients (aged 16 to 90) with an endoscopically proven duodenal ulcer within the previous year and H. pylori infection detected on antral biopsy were asked to participate; 85 were included. INTERVENTIONS: Patients were randomized in double-blind fashion to 1 of 2 eradication therapies, consisting of metronidazole, bismuth subcitrate and either amoxicillin or placebo. Endoscopy was performed at follow-up every 3 months for 12 months. OUTCOME MEASURES: Demographic data, characteristics of patients and disease, previous history and family history of ulcer disease, compliance at day 10 and day 28 of therapy; in vitro metronidazole resistance of H. pylori; eradication of H. pylori (determined by endoscopic biopsy 3 months after therapy); and ulcer recurrence within 12 months after therapy. RESULTS: Metronidazole resistance (odds ratio [OR] 0.11, 95% confidence interval [CI] 0.017 to 0.69) was the only independent predictor of eradication. Compliance (as defined in the study), density of organisms on culture, as well as several other factors examined, were not significant predictors. Treatment group, although a significant factor on univariate analysis, was not an independent predictor on multivariate analysis, as there were relatively good eradication rates (82% and 97% among compliant patients) in both groups. With regard to ulcer recurrence, 3 independent predictors were identified: failed H. pylori eradication (OR 86.5, 95% CI 4.2 to 1769), unemployment (OR 13.2, 95% CI 1.8 to 95) and a family history of ulcer disease (OR 12.2, 95% CI 1.2 to 128). CONCLUSIONS: The best predictor of ulcer recurrence is failure of H. pylori eradication, which, in turn, depends on metronidazole resistance. Hence, treatments containing metronidazole should be avoided in populations with high rates of metronidazole resistance. A family history of ulcer disease and unemployment were also predictors of ulcer recurrence, which suggests a potential role for treatment of contacts.     

Peptic ulcer pathophysiology

Despite extensive research, the etiology of peptic ulcer disease remains unclear. Given the multiple processes that control acid and pepsin secretion and defense and repair of the gastroduodenal mucosa, it is likely that the cause of ulceration differs between individuals. Acid and pepsin appear to be necessary but not sufficient ingredients in the ulcerative process. It is clear that the majority of gastric ulcers and a substantial number of duodenal ulcers do not have increased gastric acid secretion. Recent research has focused more on protection and repair of the stomach and duodenum. NSAIDs cause a significant number of gastric and duodenal ulcers; this is probably due to inhibition of prostaglandin production with loss of its protective effects. In the absence of NSAIDs and gastrinoma, it appears that most gastric ulcers and all duodenal ulcers occur in the setting of H. pylori infection. Evidence is mounting in support of H. pylori as a necessary ingredient in the ulcerative process, similar to acid and pepsin. It is not known whether the bacteria or the accompanying inflammation is the more important factor in the pathophysiology. Although the pathophysiology of gastric ulcer and duodenal ulcer is similar, there are clearly differences between the two groups. Duodenal ulcer is typified by H. pylori infection and duodenitis and in many cases impaired duodenal bicarbonate secretion in the face of moderate increases in acid and peptic activity. These facts suggest the following process: increased peptic activity coupled with decreased duodenal buffering capacity may lead to increased mucosal injury and result in gastric metaplasia. In the presence of antral H. pylori, the gastric metaplasia can become colonized and inflamed. The inflammation or the infection itself then disrupts the process of mucosal defense or regeneration resulting in ulceration. A cycle of further injury and increased inflammation with loss of the framework for regeneration may then cause a chronic ulcer. Gastric ulcer often occurs with decreased acid-peptic activity, suggesting that mucosal defensive impairments are more important. The combination of inflammation, protective deficiencies, and moderate amounts of acid and pepsin may be enough to induce ulceration. Many questions remain in understanding the pathophysiology of peptic ulcer disease. The physiology and pathophysiology of mucosal regeneration and the mechanisms by which H. pylori and inflammation disrupt normal gastroduodenal function will be fruitful areas of future investigation.     

Relation between reflux of bile acids into the stomach and gastric mucosal atrophy, intestinal metaplasia in biopsy specimens

During endoscopic examinations we collected fluid in the stomach that included reflux fluid from the duodenum, and assessed the effect of quantitatively determined bile acids on glandular atrophy and intestinal metaplasia using biopsy specimens. A total of 294 outpatients were enrolled in this study. Total bile acid concentration was measured by an enzyme immunoassay. Glandular atrophy and intestinal metaplasia scores were graded according to the Updated Sydney System. An effect of refluxed bile acids on atrophy and intestinal metaplasia was shown in the high-concentration reflux group in comparison with the control group. However, when the odds ratios (ORs) were calculated according to whether Helicobacter pylori (H. pylori) infection was present, no significant associations were shown between reflux bile acids and atrophy in either the H. pylori-positive cases or -negative cases. The same was true for intestinal metaplasia in the H. pylori-positive cases, whereas intestinal metaplasia was more pronounced in the high-concentration reflux group in the H. pylori-negative cases (OR 2.4, 95%CI 1.1-5.6). We could not clarify the effect of the reflux of bile acids into the stomach in the progression of atrophy. High-concentration bile acids had an effect on the progression of intestinal metaplasia in the H. pylori-negative cases.     

Comparison between magnifying endoscopy and histological, culture and urease test findings from the gastric mucosa of the corpus

BACKGROUND AND STUDY AIMS: The incidence of Helicobacter pylori infection in Japan is high. Unlike the case in Western countries, H. pylori-induced gastritis in Japanese patients has a tendency to spread to the corpus. H. pylori-induced gastritis is characterized by a number of specific endoscopic findings. In a previous study, the endoscopic features and a magnified view of the gastric mucosa of the corpus of H. pylori-negative normal stomach were described. This report describes the specific histological features and magnified views of the H. pylori-negative stomach and compares them with those seen during H. pylori-induced gastritis. PATIENTS AND METHODS: The anterior wall or greater curvature of the middle body of the stomachs of 297 patients were observed by magnifying endoscopy (x 80). Forceps biopsy was performed at the following locations: i) the magnified site, for histological examination; ii) the antral mucosa, for culture/urease test, and histology; and iii) greater curvature of the upper body for culture/urease test. RESULTS: 72 patients were diagnosed as having H. pylori-negative normal stomach and 225 as having H. pylori-positive gastritis. The magnified views were classified into four types: i) collecting venules, with true capillaries forming a network, and gastric pits resembling pinholes (type Z-0; n = 80); ii) irregular true capillaries but no collecting venules observed (type Z-1; n = 36); iii) white gastric pits and sulci, with neither collecting venules nor true capillaries being seen (Z-2; n = 110); and iv) dilated pits with surrounding redness (Z-3; n = 71). All cases of H. pylori-negative normal stomach were type Z-0, whereas H. pylori-induced gastritis was present in all cases where the classification was Z-1, Z-2, or Z-3. Type Z-0 differed significantly from types Z-1, Z-2, and Z-3 with regard to the grade of inflammation, activity, and presence of H. pylori. CONCLUSIONS: Collecting venules and true capillaries forming a network with gastric pits in the center (type Z-0) were observed in the H. pylori-negative normal mucosa. The magnified views of H. pylori-related gastritis clearly differed from type Z-0.     

Eradication of Helicobacter pylori increases platelet count in patients with idiopathic thrombocytopenic purpura in Japan

BACKGROUND: The effect of Helicobacter pylori eradication on the platelet count in patients with thrombocytopenic purpura is controversial. In this multicentre study, we prospectively assessed the effect of H. pylori eradication therapy in idiopathic thrombocytopenic purpura patients. MATERIALS AND METHODS: Thirty-five consecutive patients with chronic idiopathic thrombocytopenic purpura (11 males and 24 females, a median age of 57) were assessed for H. pylori infection by use of a urea breath test. All patients received 1-week triple therapy (amoxicillin, clarithromycin, and lansoprazole) to eradicate H. pylori. At 6 months, idiopathic thrombocytopenic purpura patients with a platelet count recovery of greater than 100 x 10(9) L(-1) were defined as idiopathic thrombocytopenic purpura responders. RESULTS: Helicobacter pylori infection was observed in 25 (71%) of the 35 patients. All infected patients were cured. Eleven patients were identified as idiopathic thrombocytopenic purpura responders; 24 were considered nonresponders. Platelet counts improved by more than 100 x 10(9) L(-1) in 11 (44%) of the 25 patients cured of H. pylori infection, while none of the 10 patients H. pylori-negative patients experienced the same improvement (P = 0.015). Univariate analysis showed that H. pylori infection and its eradication were significant factors associated with platelet recovery (P = 0.015). CONCLUSIONS: Helicobacter pylori infection played a role in the pathogenesis of idiopathic thrombocytopenic purpura in approximately 30% of all patients assessed and 45% of the patients with H. pylori infection. Eradication of H. pylori in idiopathic thrombocytopenic purpura patients led to improved disease activity.     

The effect of Helicobacter pylori eradication on duodenal gastric metaplasia

We investigated the incidence of duodenal gastric metaplasia and its response to Helicobacter pylori eradication in patients with duodenal ulcer or erosive duodenitis. Gastric and duodenal biopsies were taken from patients with endoscopically detected H. pylori positive duodenal ulcer or erosive duodenitis, and the presence and extent of duodenal gastric metaplasia was recorded. Patients were given omeprazole 20 mg twice daily for 2 weeks, and amoxicillin 1 g and clarithromycin 500 mg twice daily for 10 days, and then ranitidine for a further 8 weeks. Biopsies were repeated 6 months after the start of treatment. Duodenal gastric metaplasia was initially present in 22 patients (52%) and was more frequent in ulcer patients than in duodenitis patients, but not significantly so (69% versus 45%). After treatment, H. pylori was eradicated in 68% of duodenal gastric metaplasia patients and the duodenum was normal endoscopically in 85% of these patients. Duodenal gastric metaplasia was improved or eliminated in 12/15 H. pylori eradicators (80%) and in 5/7 H. pylori non-eradicators (71%), a non-significant difference. The improvement in duodenal gastric metaplasia appeared to be independent of H. pylori eradication.     

Gastropathy and diarrhea in diabetic patients: the presence of helicobacteriosis and PAS-positive vascular deposits in gastric and duodenal mucosa

AIM: To determine the presence of vascular periodic acid-Schiff's reagent (PAS) positive deposits in the gastric and duodenal mucosa of diabetic patients and controls. METHODS: Forty-six poorly controlled diabetic patients with digestive symptoms, aged 23 to 63 years (32 type I patients on insulin therapy with a mean diabetes duration of 14.2 +/- 3.1 years (mean +/- SE) and 13 type II patients with a mean diabetes duration of 7.2 +/- 2.3 years) were included. Of these, 17 had mainly gastropathic symptoms while 13 had diarrhea, and the remaining 16 patients had nonspecific symptoms. Forty control individuals of similar age and gender were included. Biopsy specimens were taken from areas of grossly normal gastric and duodenal mucosa. RESULTS: Gastric mucosa samples were pathological in 38 of 46 diabetic patients (18 cases of chronic active H. pylori antral gastritis, 13 cases of chronic active H. pylori pangastritis and 7 cases of nonspecific chronic gastritis). Duodenal mucosa samples were pathological in 32/46 diabetic patients. In the control group, 21 of 40 gastric samples (5 cases of chronic active H. pylori antral gastritis, 3 cases of chronic active H. pylori pangastritis and 13 cases of H. pylori-negative chronic gastritis) and 12/40 duodenal samples were pathological. Both helicobacteriosis and gastric and duodenal mucosa pathologies were significantly (p < 0.01) more common in diabetic patients than in controls. No significant associations were found between histological findings of gastric mucosa and of duodenal mucosa in diabetics and the control group. PAS-positive material in the vascular wall of gastric (16/46 vs. 2/40 in controls) and duodenal mucosa specimens (25/46 vs. 5/40 in controls) was significantly more common among diabetics (p = 0.001 for gastric and p < 0.001 for duodenal mucosa). No significant association was found between the presence of gastropathy or diarrhea compared to the presence of neuropathy, retinopathy, nephropathy or the type of diabetes. CONCLUSION: Endoscopic specimens from the gastroduodenum of diabetic patients revealed a large quantity of PAS positive vascular deposits, probably reflecting the condition of the mucosal vessels in our patients.     

Do conventional cleaning and disinfection techniques avoid the risk of endoscopic Helicobacter pylori transmission?

BACKGROUND AND STUDY AIMS: The aim of the present study was to determine whether endoscopes serve as a reservoir for Helicobacter pylori and whether the disinfection technique currently recommended for manual cleaning and disinfection of the instruments completely removes the risk of H. pylori transmission. PATIENTS AND METHODS: A prospective study was carried out in 400 patients who were undergoing upper gastrointestinal endoscopy for routine clinical indications. The patients' H. pylori status of the patients was identified using a urea detection system (HUT) and culture. H. pylori contamination was assayed by culturing rinsing samples from the endoscopes before and after manual cleaning and disinfection. Gastric biopsies were assayed using rapid urease testing (Helicobacter urease test, HUT) of two antral and gastric body biopsies and cultures. RESULTS: A total of 128 of the 400 patients examined were found to be H. pylori-positive using HUT testing. Endoscopes were contaminated in 54 of the 128 rinsing samples from endoscopes used in H. pylori-positive patients (42 %) before cleaning and disinfection. One of the 128 rinsing samples (0.8 %) was found to be contaminated with H. pylori even after routine manual cleaning and disinfection - indicating that these cleaning and disinfection procedures may be insufficient to eradicate H. pylori from endoscopes completely. No seroconversion was observed during serological follow-up in the patient who had previously been examined with an endoscope contaminated with H. pylori. The patient was still found to be seronegative 5 months after inoculation. CONCLUSIONS: Endoscopes are frequently contaminated with H. pylori immediately after gastroduodenal endoscopy in H. pylori-infected patients. Iatrogenic transmission is possible, as H. pylori can survive manual cleaning and disinfection with 2 % glutaraldehyde, particularly when there is ineffective cleaning before disinfection.     

Association of cagA+ Helicobacter pylori with adenotonsillar hypertrophy

Cytotoxin-associated gene A (cagA) of Helicobacter pylori (H. pylori) encodes a highly immunogenic and virulence-associated protein. The presence of cagA(+) H. pylori strains in tonsil and adenoid tissues may affect clinical outcome. The aim of the present study was to determine the presence of H. pylori cagA gene in tonsil and adenoid tissues and to establish the potential association of cagA(+) H. pylori in recurrent adenotonsillitis (RAT) and adenotonsillar hypertrophy (ATH). For this aim, a total of 118 tissue samples (71 tonsil and 47 adenoid tissues) were collected from a total of 71 children: 28 cases with RAT and 43 cases with ATH. The samples were analyzed for glmM gene to detect the infection with H. pylori by polymerase chain reaction (PCR). H. pylori-positive samples were further analyzed for the presence of the cagA gene. The PCR analysis showed that 29 samples (24.6%) were positive for H. pylori. Seventeen out of these 29 samples (58.6%) were found positive for cagA; the cagA gene was detected in 12 samples of ATH and 5 samples of RAT. The presence rate of cagA gene was significantly higher (p < 0.05) in ATH patients than that found in RAT patients. These results suggest that presence of cagA(+) H. pylori may be associated with development of ATH.     

Serum antibodies anti-H. pylori and anti-CagA: a comparison between four different assays.

The authors compare efficacy of two ELISA assays (one supplied by DIAMEDIX [Delta Biological s.r.l.], and the other by RADIM [RADIM I]) in detecting total anti-H. pylori antibodies, and of two further ELISA methods (one supplied by EUROSPITAL [Helori CTX IgG] and the other by RADIM [RADIM 2]) in identifying anti-CagA antibodies, using sera from 69 controls (20 adults and 49 children) and from 96 patients, obtained before endoscopy. Seventy-three of the patients had H. pylori infection, while the remaining 23 were H. pylori negative (histology and polymerase chain reaction [PCR]). Fifty-two of the H. pylori positive patients, had cagA-positive strain infection, identified by PCR. The DIAMEDIX assay was found to be more sensitive (92%) than RADIM 1 (79%) in identifying H. pylori positive patients, irrespective of the infecting strain. On the other hand, the DIAMEDIX assay was less specific than RADIM 1 for H. pylori-negative patients (43% vs. 83%). However, when patients already treated for H. pylori infection were excluded from the group of H. pylori-negative patients, the DIAMEDIX assay had a specificity of 89%. In identifying anti-CagA antibodies, the kit supplied by RADIM (RADIM 2) had a sensitivity of 90% and a specificity of 94%, whereas that supplied by EUROSPITAL had a sensitivity of 100% and a specificity of 76%. The performances of the two methods in the identification of anti-CagA antibodies were found to be similar. The authors conclude that, in view of its high sensitivity, the DIAMEDIX assay may be useful in screening for H. pylori infection.     

Relationship between the birth cohort pattern of Helicobacter pylori infection and the epidemiology of duodenal ulcer

BACKGROUND: Helicobacter-pylori-related duodenal ulcer (DU) is an important cause of dyspepsia. AIM: To determine the relationship between the pattern of H. pylori infection and the epidemiology of duodenal ulcer in a single population. DESIGN: Prospective two-part study of (i) patients with DU referred for endoscopy because of dyspepsia, and (ii) the incidence of H. pylori infection in the general population of the same area. METHODS: Details of 533 DU patients were recorded, and related to the pattern of H. pylori infection among 10 537 adults in the same community, determined by the (13)C-urea breath test. RESULTS: In patients with DU, birth year was more important than age in determining the rate of presentation for endoscopy (the 'birth cohort' effect). H. pylori infection showed a similar birth cohort effect, and the prevalence decreased steadily in those born in successive years, from 28.8% in the 1930s to 3.5% in the 1970s. The proportion of dyspeptic patients who had duodenal ulcers also fell progressively, from 22.2% in 1979 to 5.7% in 1998. H. pylori prevalence and duodenal ulcer incidence were closely correlated at all ages. DISCUSSION: Duodenal ulcer prevalence (as judged by the rate of referral of duodenal ulcer patients for endoscopy) is determined principally by the distribution of H. pylori infection in the local population. The birth cohort effect seen in adult duodenal ulcer patients reflects the acquisition of H. pylori in childhood. In Bristol, H. pylori prevalence and duodenal ulcer incidence are both declining to very low levels.     

The role of Helicobacter pylori in gastroduodenal disease.

Peptic ulcers are the result of a wide variety of factors, with H. pylori probably being one of the more significant. H. pylori has been most strongly associated with gastritis and duodenal ulcer disease. The relationship of H. pylori to gastric ulcers is less substantial. The eradication of H. pylori can be achieved in the majority of patients with triple antibiotic therapy. However, resistance to metronidazole occurs readily. Eradication of H. pylori can change the course of duodenal ulcer disease by decreasing recurrence rate from 80% to zero. Nonetheless, treatment for H. pylori should only be done in randomized trials at the current time because of the lack of completely effective therapy and the high risks of side effects. The mechanism by which H. pylori influences duodenal ulcer recurrence is unclear. Pathogenic mechanisms of the organism also need to be further elucidated.