BACKGROUND:In this clinical trial we compared the effects of broccoli sprouts powder, as an alternative and complementary treatment, to those of standard triple therapy, as a common medical treatment, on cardiovascular risk factors following the H.pylori eradication in patients with type 2 diabetes.

METHODS:Eighty-six type 2 diabetic patients with positive H.pylori stool antigen test (HpSAg) were randomized to receive one of the three following regimens: STT) Standard triple therapy (omeprazole 20 mg, clarithromycin 500 mg, amoxicillin 1000 mg, twice a day for 14 days), BSP) 6 g/d broccoli sprouts powder for 28 days, and combination of these as STT + BSP. After 4 weeks of treatment, H.pylori eradication rates were assessed by HpSAg. Anthropometric measures, blood pressure, serum lipids and lipoproteins as well as serum high sensitive- C reactive protein were also assessed at baseline and at the second examination.

RESULTS:Seventy-seven participants completed the study [STT (n = 28), BSP (n = 25), STT + BSP (n = 24)]. The H.pylori eradication rates were 89.3%, 56.0% and 91.7% in STT, BSP and STT + BSP groups, respectively. After the treatment, both systolic and diastolic blood pressure significantly decreased in STT + BSP group (P < 0.05). Serum triglycerides and TG/HDL-C ratio increased in STT patients group (<0.05). Serum hs-CRP levels significantly decreased in the patients who were treated with BSP per se (3.0 ± 2.5 at baseline vs. 2.3 ± 2.1 after the treatment, P < 0.05).

CONCLUSION:Compared to standard triple therapy, BSP regimen in addition to considerable effects on H.pylori eradication had also favorable properties on cardiovascular risk factors following the H.pylori eradication.

BACKGROUND/AIMS: To test the impact of vitamin C supplementation on triple therapy for H. pylori eradication. METHODOLOGY: A total of 171 H. pylori-infected patients were randomized to receive different one-week triple therapies, including 20 mg omeprazole, 1 g amoxicillin, plus the following twice daily: (1) 250 mg clarithromycin (C250 group, n=55); (2) 250 mg clarithromycin and 500 mg vitamin C (V-C250 group, n=61); (3) 500 mg clarithromycin (C500 group, n=55). Six weeks after treatment, the success of H. pylori eradication was assessed by a 13C-urea breath test. Each collected H. pylori strain was defined as either clarithromycin susceptible or resistant by E-test. RESULTS: The demographic background, clarithromycin susceptibility of H. pylori, and drug compliance were similar among the three groups (p=NS). For clarithromycin susceptible infection, the V-C250 group had a higher eradication rate than the C250 group (ITT: 85% vs. 68% and PP: 90% vs. 73%, p = 0.03), but had an equivalent rate to the C500 group (p=NS). For clarithromycin resistant infection, all three groups had a similarly poor eradication rate of less than 34%. CONCLUSIONS: Adding vitamin C to one-week triple therapy can reduce the dosage of clarithromycin, but preserve the high eradication efficacy for clarithromycin susceptible H. pylori infection.

ETHNOPHARMACOLOGICAL RELEVANCE:The fungus Hericium erinaceus (Bull.) Pers is used in Chinese traditional medicine to treat symptoms related to gastric ulcers. Different extracts from the fungus were assessed for anti-Helicobacter pylori activity to investigate the antibacterial activity of the ethanol extracts from H. erinaceus and verify the traditional indication of use.

MATERIALS AND METHODS:The fruiting bodies of H. erinaceus were concentrated with ethanol by HPD-100 macroporous resin and the whole extract was partitioned by petroleum ether and chloroform to afford fractions with using a silica gel column. Several pure compounds of petroleum ether extracts were obtained and analyzed using nuclear magnetic resonance (NMR). The activity of the extracts and fractions towards H. pylori was assessed by the microdilution assay and by the disk diffusion assay in vitro. From the most active fraction, two pure compounds were isolated and identified as the main components with anti-H. pylori activity from the fungus H. erinaceus. The cytotoxicity of these two compounds against the human erythroleu-kemia cell line K562 was also evaluated.

RESULTS:The crude ethanol extracts from the fungus H. erinaceus were inhibitory to H. pylori. The petroleum ether extracts (PE1s, PE2s) and the chloroform extracts (TEs) demonstrated strong inhibition to H. pylori. The inhibition of H. pylori was observed through an agar dilution test with minimal inhibition concentration (MIC) values from 400μg/mL to 12.5µg/mL. Two pure compounds, 1-(5-chloro-2-hydroxyphenyl)-3-methyl-1-butanone and 2,5-bis(methoxycarbonyl)terephthalic acid were isolated from the petroleum ether fractions and identified using (1)H NMR and (13)C NMR spectra analysis. The MIC value for 1-(5-chloro-2-hydroxyphenyl)-3-methyl-1-butanone was 12.5-50µg/mL and the MIC value for 2,5-bis(methoxycarbonyl)terephthalic acid was 6.25-25µg/mL. Both two compounds showed weak cytotoxicity against K562 with IC50<200mM.

CONCLUSIONS:This study revealed that the extracts from petroleum ether contribute to the anti-H. pylori activity. The compounds obtained from petroleum ether extracts, 1-(5-chloro-2-hydroxyphenyl)-3-methyl-1-butanone and 2,5-bis(methoxycarbonyl)terephthalic acid, inhibit the growth of H. pylori.

The antibacterial activity of an oil extract of Chamomilla recutita flowers against Helicobacter pylori (H. pylori) was evaluated by the agar dilution method using Colombia agar with 10% sheep blood, an inoculum of McFarland 0.5 and incubation in an anaerobic atmosphere at 37 degrees C for 3 days. The oil extract was prepared by olive oil extraction of Chamomilla recutita flowers using rotary pulsation. The MIC(90) (minimal inhibitory concentration) and MIC(50) were 125 mg/mL and 62.5 mg/mL, respectively. It was shown that the Chamomilla recutita oil extract inhibited the production of urease by H. pylori. In addition, it was found that the morphological and fermentative properties of H. pylori were affected by application of the Chamomilla recutita oil extract.

Helicobacter pylori infection in humans is associated with chronic type B gastritis, peptic ulcer disease, and gastric carcinoma. A high intake of carotenoids and vitamin C has been proposed to prevent development of gastric malignancies. The aim of this study was to explore if the microalga Haematococcus pluvialis rich in the carotenoid astaxanthin and vitamin C can inhibit experimental H. pylori infection in a BALB/cA mouse model. Six-week-old BALB/cA mice were infected with the mouse-passaged H. pylori strain 119/95. At 2 weeks postinoculation mice were treated orally once daily for 10 days (i) with different doses of algal meal rich in astaxanthin (0.4, 2, and 4 g/kg of body weight, with the astaxanthin content at 10, 50, and 100 mg/kg, respectively), (ii) with a control meal (algal meal without astaxanthin, 4 g/kg), or (iii) with vitamin C (400 mg/kg). Five mice from each group were sacrificed 1 day after the cessation of treatment, and the other five animals were sacrificed 10 days after the cessation of treatment. Culture of H. pylori and determination of the inflammation score of the gastric mucosae were used to determine the outcome of the treatment. Mice treated with astaxanthin-rich algal meal or vitamin C showed significantly lower colonization levels and lower inflammation scores than those of untreated or control-meal-treated animals at 1 day and 10 days after the cessation of treatment. Lipid peroxidation was significantly decreased in mice treated with the astaxanthin-rich algal meal and vitamin C compared with that of animals not treated or treated with the control meal. Both astaxanthin-rich algal meal and vitamin C showed an inhibitory effect on H. pylori growth in vitro. In conclusion, antioxidants may be a new strategy for treating H. pylori infection in humans.

Ethanol and methylene chloride extracts of cinnamon were compared for their effect on Helicobacter pylori growth and urease activity. Methylene chloride extract was found to inhibit growth of H. pylori, while ethanol extract counteracted its urease activity. Cinnamon extract (from methylene chloride) inhibited H. pylori at concentration range of common antibiotics. Complete inhibition in vitro was achieved by 50 microg/ml in solid medium (egg yolk emulsion agar) and by 15 microg/ml in liquid medium (supplemented brain heart infusion broth). The cinnamon extracts were more inhibitory on free urease than on whole cell urease.

BACKGROUND: Helicobacter pylori (HP) is a gramnegative bacterium and well recognized as being the primary etiological agent responsible for the development of gastritis, dyspepsia, peptic ulcer disease and gastric cancer. In developing countries, a high prevalence of HP infection is associated with an increased incidence of gastric cancer. Thailand, however, while having a high prevalence of HP infections, has a lower than expected gastric cancer rate than other developing countries. It has been suggested that the diet and life style in Thailand may explain this discrepancy. MATERIALS AND METHODS: The in vitro susceptibility of 18 strains of HP to 20 extracts of spice and food plants used in Thai traditional medicine for the treatment of GI disorders was assessed. RESULTS: Methanol extracts of Myristica fragrans (aril) inhibited the growth of all HP strains with minimum inhibitory concentration (MIC) of 12.5 micrograms/ml; extracts from Barringtonia acutangula (leaf) and Kaempferia galanga (rhizome) had an MIC of 25.0 micrograms/ml; Cassia grandis (leaf), Cleome viscosa (leaf), Myristica fragrans (leaf) and Syzygium aromaticum (leaf) had MICs of 50.0 micrograms/ml. Extracts with an MIC of 100.0 micrograms/ml included Pouzolzia pentandra (leaf), Cycas siamensis (leaf), Litsea elliptica (leaf) and Melaleuca quinquenervia (leaf). CONCLUSION: Plants used in Thai traditional medicine to treat gastrointestinal ailments inhibit the growth of HP. These data indicate that these plants may have chemopreventative activities and thus may partly explain the reduced incidence of gastric cancer in Thailand.

Several crude and purified polysaccharides from black currant seeds (Ribes nigrum L.) have been isolated, analysed and examined on their effects against Helicobacter pylori in in situ adhesion studies on sections of human gastric mucosa. After pre-treatment of Helicobacter pylori with 0.01 to 0.1 % solutions of the isolated raw polysaccharide (RPS), the epithelial binding of the bacteria was considerably reduced in a concentration-dependent manner, as compared with a non-treated control suspension. Preincubation of the mucosal sections with 0.1 % solutions did not result in a reduced binding of non-treated bacteria. An anion-exchange fraction of RPS eluted with 0.1 M phosphate buffer exhibited a comparable, concentration-dependent reduction of adhesion, whereas the water-eluted fraction was ineffective at the respective concentrations. Both subfractions consisted of similar 1,3-linked galactans, decorated with side chains possessing 1,4-galacturonic acid, galactose and arabinose residues. Molecular weight profiling by GPC revealed that the antiadhesive activity of the buffer eluate correlated with high molecular weight components ranging from about 1000 Da to 340 kDa, whereas the ones of the inactive water eluate had molecular weights of about 100 and 25 kDa, respectively. None of the active fractions revealed inhibitory effects on bacterial growth in vitro. We conclude that acidic, high molecular weight galactans are responsible for the antiadhesive qualities of black currant seed extracts and that these polymers are able to block Helicobacter surface receptors, thus inhibiting their interaction with specific binding factors located on human gastric epithelia.

AIM: This study aims to assess the antioxidant property of vitamins E and C in Helicobacter pylori infection, and to determine if adding them to standard triple therapy plus bismuth subcitrate increases the H. pylori eradication rate. METHODS: This study included 160 patients infected with H. pylori, who were randomized into one of two groups. Patients in group A (n = 80) received lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days, while patients in group B (n = 80) received vitamin C (500 mg, b.i.d.) and vitamin E (200 IU, b.i.d.) for 30 days, in addition to lansoprazole (30 mg, b.i.d.), amoxicillin (1000 mg, b.i.d.), clarithromycin (500 mg, b.i.d.), and bismuth subcitrate (300 mg, q.i.d.) for 14 days. Total antioxidant capacity (TAC) was evaluated with a Randox kit. Success rate was calculated using both intention-to-treat (ITT) and per-protocol (PP) analyses. RESULTS: One hundred and sixty patients were analyzed using ITT analysis. One hundred and fifty-three patients completed the study. In group A, H. pylori eradication was achieved in 48 (60%) of the 80 patients included in the ITT analysis, and in 48 (64%) of the 75 patients included in the PP analysis. In group B, H. pylori eradication was achieved in 73 (91.25%) of the 80 included in the ITT analysis and in 73 (93.5%) of the 78 patients included in the PP analysis. The eradication rate was significantly higher in group B than in group A (p<.005). TAC was at the lower limit of normal in both groups and the difference between them was not statistically significant (p>.05). CONCLUSION: In group B, H. pylori eradication rate was 91.25%, which is higher than the ideal 80% eradication rate. The results of the present study show that adding the prescribed doses of vitamins E and C to antimicrobial therapy is effective in eradicating H. pylori infection.

The primary objective in the study is determination of efficacy of probiotic preparation as a supportive therapy in eradication of Helicobacter pylori.The study was multicenter, prospective, randomized, placebo controlled, and double-blind. The subjects first filled out a specially designed questionnaire to assess the severity of the 10 symptoms, which can be related to eradication therapy to be monitored during the trial. Each subject then received 28 capsules of probiotic preparation or matching placebo capsules, which they were supposed to take over the following 14 days, twice a day, at least 2 hours prior to or after the antibiotic therapy administration.A total of 804 patients were enrolled in the trial, of which 650 (80.85%) were included in the analysis. The results show a significantly larger share of cured subjects in the probiotic arm versus the placebo arm (87.38% vs 72.55%; P < 0.001). Additionally, presence and intensity of epigastric pain, bloating, flatulence, taste disturbance, loss of appetite, nausea, vomiting, heartburn, rash, and diarrhea were monitored over the study period. At 15 days postinclusion, probiotic treatment was found superior to placebo in 7 of 10mentioned symptoms. Average intensity for symptoms potentially related to antibiotic therapy was significantly higher in the placebo group, 0.76 vs 0.55 (P < 0.001).Adding probiotics to the standard triple therapy for H pylori eradication significantly contributes to treatment efficacy and distinctly decreases the adverse effects of therapy and the symptoms of the underlying disease.

Pelargonium sidoides is a medical herb and respective extracts are used very frequently for the treatment of respiratory tract infections. However, the effects of Pelargonium sidoides and a special extract prepared from its roots (EPs 7630) on human immune cells are not fully understood. Here we demonstrate that EPs 7630 induced a rapid and dose-dependent production of TNF-α, IL-6, and IL-10 by human blood immune cells. This EPs 7630-induced cytokine profile was more pro-inflammatory in comparison with the profile induced by viral or bacterial infection-mimicking agents. The search for EPs 7630 target cells revealed that T-cells did not respond to EPs 7630 stimulation by production of TNF-α, IL-6, or IL-10. Furthermore, pretreatment of T-cells with EPs 7630 did not modulate their TNF-α, IL-6, and IL-10 secretion during subsequent activation. In contrast to lymphocytes, monocytes showed clear intracellular TNF-α staining after EPs 7630 treatment. Accordingly,EPs 7630 predominantly provoked activation of MAP kinases and inhibition of p38 strongly reduced the monocyte TNF-α production. The pretreatment of blood immune cells with EPs 7630 lowered their secretion of TNF-α and IL-10 and caused an IL-6 dominant response during second stimulation with viralor bacterial infection-mimicking agents. In summary, we demonstrate that EPs 7630 activates human monocytes, induces MAP kinase-dependent pro-inflammatory cytokines in these cells, and specifically modulates their production capacity of mediators known to lead to an increase of acute phase proteinproduction in the liver, neutrophil generation in the bone marrow, and the generation of adaptive Th17 and Th22 cells.

Pelargonium sidoides is a medical herb and respective extracts are used very frequently for the treatment of respiratory tract infections. However, the effects of Pelargonium sidoides and a special extract prepared from its roots (EPs 7630) on human immune cells are not fully understood. Here we demonstrate that EPs 7630 induced a rapid and dose-dependent production of TNF-α, IL-6, and IL-10 by human blood immune cells. This EPs 7630-induced cytokine profile was more pro-inflammatory in comparison with the profile induced by viral or bacterial infection-mimicking agents. The search for EPs 7630 target cells revealed that T-cells did not respond to EPs 7630 stimulation by production of TNF-α, IL-6, or IL-10. Furthermore, pretreatment of T-cells with EPs 7630 did not modulate their TNF-α, IL-6, and IL-10 secretion during subsequent activation. In contrast to lymphocytes, monocytes showed clear intracellular TNF-α staining after EPs 7630 treatment. Accordingly,EPs 7630 predominantly provoked activation of MAP kinases and inhibition of p38 strongly reduced the monocyte TNF-α production. The pretreatment of blood immune cells with EPs 7630 lowered their secretion of TNF-α and IL-10 and caused an IL-6 dominant response during second stimulation with viralor bacterial infection-mimicking agents. In summary, we demonstrate that EPs 7630 activates human monocytes, induces MAP kinase-dependent pro-inflammatory cytokines in these cells, and specifically modulates their production capacity of mediators known to lead to an increase of acute phase proteinproduction in the liver, neutrophil generation in the bone marrow, and the generation of adaptive Th17 and Th22 cells.

BACKGROUND: The benefits of breast-feeding for the prevention of infection in infants and young children have been widely recognized, but epidemiologic studies regarding the role of breast-feeding in protecting against Helicobacter pylori infection have produced conflicting results.

METHODS: We performed a systematic review of relevant epidemiologic studies conducted during the period 1984-2007 after abstracting data from articles that met our inclusion criteria. Study quality was assessed using the Newcastle-Ottawa scale. With use of the random effects model, we calculated the summary odds ratios (ORs) and 95% confidence intervals (CIs) for H. pylori infection according to history of breast-feeding.

RESULTS: For the 14 studies that met inclusion criteria, the summary OR for H. pylori infection was 0.78 (95% CI, 0.61-0.99; 1-sided P = .002). Nine of the 14 studies reported ORs of<1.0, and 6 of these studies reported statistically significant protective effects. Only 1 study reported a statistically significant OR of>1.0. In studies in which the subjects resided in middle- or low-income nations, the summary OR was 0.55 (95% CI, 0.33-0.93; P = .01), compared with 0.93 (95% CI, 0.73-1.19; P = .28) in studies in which subjects resided in high-income nations. The summary OR for studies that use the (13)C-urea breath test was 0.67 (95% CI, 0.32-1.39), compared with 0.91 (95% CI, 0.74-1.11) for studies that used the H. pylori IgG serologic test. We found no statistically significant dose-dependent protective effect against H. pylori associated with increasing duration of breast-feeding.

CONCLUSIONS: Breast-feeding is protective against H. pylori infection, especially in middle- and low-income nations.