Traditional Chinese medicine in the treatment of Helicobacter pylorirelated gastritis:The mechanisms of signalling pathway regulations

Helicobacter pylori-associated gastritis(HPAG)is a common condition of the gastrointestinal tract.However,extensive and long-term antibiotic use has resulted in numerous adverse effects,including increased resistance,gastrointestinal dysfunction,and increased recurrence rates.When these concerns develop,traditional Chinese medicine(TCM)may have advantages.TCM is based on the concept of completeness and aims to eliminate pathogens and strengthen the body.It has the potential to prevent this condition while also boosting the rate of Helicobacter pylori eradication.This review elaborates on the mechanism of TCM treatment for HPAG based on cellular signalling pathways,which reflects the flexibility of TCM in treating diseases and the advantages of multi-level,multipathway,and multi-target treatments for HPAG.

Estimate the Prevalence of Helicobacter pylori Infection among Diabetes & Non-Diabetes Mellitus Patients and Its Correlation with Malignant Gastritis Patients Attending in Lower Shabelle Region (Somalia)

Background: Several conducted studies have reported a higher and more frequent Helicobacter pylori infection rate in type 2 diabetes mellitus (T2DM). The aim of this study was to estimation the prevalence of H. pylori and its association between H. pylori infection and T2DM. Materials and Methods: A sectional-cross study was conducted based on 200 patients studded with socioeconomic characteristics through a questionnaire & H. pylori was diagnosed by serum anti-H. pylori immunoglobulin G (IgG) and IgA. Furthermore, patients were investigated for fasting blood glucose (FBG) levels, glycosylated hemoglobin (HbA1c), serum cholesterol, and other biochemistry parameters. Results: The findings showed The prevalence of Hp positive infection was significantly higher in the total sample was 134 with (67%). While 66 out of 200 patients with (33%) was H. pylori negative infection. of H. pylori. Further, the mean values were statistically significant for diabetes with H. pylori infection for IgG > 300 titer and IgA > 250 titer, regarding, HbA1C (7.52 ± 0.41) (P Conclusions: The current study revealed that H. pylori prevalence infections were significantly higher in diabetic patients studied compared to non-diabetic patients. Furthermore, T2DM patients infected with H. pylori positive reported a higher prevalence rate of symptoms than H. pylori negative.

Helicobacter Pylori-induced Gastritis Model in BALB/c Mice Infected With Fresh Isolates from a Human Complex Ulcer Patient

A useful helicobacter pylori-induced gastritis model using BALB/c mice was established for mimicking of human gastritis induced by Helicobacter pylori (H. pylori). The H. pylori isolates were obtained freshly from a human complex ulcer patient. BALB/c mice were fasted for 24 h and then 0.25 mL of 0.2 mol·L -1 NaHCO 3 was administered after by gavage to each mouse and 0.5 mL of 10 9 colonies formation unit per milliliter (CFU/mL) of H. pylori was administered 15 min. On the 3 rd day and 5 th day, the H. pylori inoculations were repeated. The inoculated mice were sacrificed in batch on the 5 th day, in the 2 nd week, 3 rd week and 4 th week. The gastric mucous membrane near pyloric portion was removed, treated and then cultured under microaerobic condition for detection of H.pylori. The remainders of the gastric membrane were fixed by 10% formaldehyde solution for pathological detection. The results showed that the H. pylori could be separated from the gastric membranes of inoculated mice. Obvious invasion of inflammatory cells in the gastric membranes of inoculated mice could be observed from pathological sections. It can be concluded that the inoculating fresh human H. pylori isolates can produce mouse gastritis. This model of BALB/c mice can be used for evaluating the therapeutic agents for the treatment of gastritis induced by H. pylori.

Association between central serous chorioretinopathy and Helicobacter pylori infection: a systematic review and Meta-analysis

AIM:To investigate the association between central serous chorioretinopathy(CSC)and Helicobacter pylori(Hp)by summarizing all available evidence.METHODS:The Scopus,Embase,EBSCO,PubMed,Web of Science,and Cochrane Library databases for all relevant studies published from inception to October 2022 were searched,and manually searched for relevant reference lists as a supplement.Studies investigating the association between CSC and Hp infection were included.Finally,8 case-control studies were included in the Meta-analysis after study selection.RESULTS:The results showed no significant correlation between Hp infection and CSC[odds ratio(OR)1.89,95%confidential interval(CI)0.58–6.15,I2=96%,P=0.29].After subgroup analysis based on the degree of development of the study(developing/developed countries),it was found that the results of the two subgroups were the same as the whole,and no significant difference between the two subgroups existed.Meta-regression showed that the effect of sample size on heterogeneity among studies was more prominent(P<0.01,adjusted R^(2)=89.72%),which can explain 89.72%of the sources of heterogeneity.CONCLUSION:This Meta-analysis reveals no significant correlation between Hp infection and CSC,which still warrants further well-designed extensive sample studies to reach a more reliable conclusion and promote a better understanding of the treatment of CSC.

Urinary metabolic profiles during Helicobacter pylori eradication in chronic gastritis

BACKGROUND Helicobacter pylori(H.pylori)infection is a major risk factor for chronic gastritis,affecting approximately half of the global population.H.pylori eradication is a popular treatment method for H.pylori-positive chronic gastritis,but its mecha-nism remains unclear.Urinary metabolomics has been used to elucidate the mechanisms of gastric disease treatment.However,no clinical study has been conducted on urinary metabolomics of chronic gastritis.AIM To elucidate the urinary metabolic profiles during H.pylori eradication in patients with chronic gastritis.METHODS We applied LC–MS-based metabolomics and network pharmacology to in-vestigate the relationships between urinary metabolites and H.pylori-positive chronic gastritis via a clinical follow-up study.RESULTS Our study revealed the different urinary metabolic profiles of H.pylori-positive chronic gastritis before and after H.pylori eradication.The metabolites regulated by H.pylori eradication therapy include cis-aconitic acid,isocitric acid,citric acid,L-tyrosine,L-phenylalanine,L-tryptophan,and hippuric acid,which were involved in four metabolic pathways:(1)Phenylalanine metabolism;(2)phenylalanine,tyrosine,and tryptophan biosynthesis;(3)citrate cycle;and(4)glyoxylate and dicarboxylate metabolism.Integrated metabolomics and network pharmacology revealed that MPO,COMT,TPO,TH,EPX,CMA1,DDC,TPH1,and LPO were the key proteins involved in the biological progress of H.pylori eradication in chronic gastritis.CONCLUSION Our research provides a new perspective for exploring the significance of urinary metabolites in evaluating the treatment and prognosis of H.pylori-positive chronic gastritis patients.

Metabolic dynamics in chronic gastritis:Examining urinary profiles post Helicobacter pylori eradication

Chronic gastritis is the persistent and insidious inflammation of the gastric lining.Helicobacter pylori(H.pylori)has been identified as the most common cause of chronic gastritis and consequently elimination of H.pylori can lead to its cure.This editorial explores the use of urinary metabolic profiles before and after eradication to identify biomarkers that can aid in prognosis and treatment.Despite providing promising insights,there are limitations such as a small sample size(17 patients),a narrow treatment period of 2 wk,and treatment heterogeneity,which raise concerns.Nevertheless,these findings have opened a gateway to enhancing the treatment and prognosis of chronic gastritis through urinary metabolomics.

Is Helicobacter pylori infection protective against esophageal cancer?

Helicobacter pylori(H.pylori)infection affects a substantial proportion of the global population and causes various gastric disorders,including gastric cancer.Recent studies have found an inverse relationship between H.pylori infection and eso-phageal cancer(EC),suggesting a protective role against EC.This editorial focuses on the possible mechanisms underlying the role of H.pylori infection in EC and explores the role of gut microbiota in esophageal carcinogenesis and the prac-ticality of H.pylori eradication.EC has two major subtypes:Esophageal squamous cell carcinoma(ESCC)and esophageal adenocarcinoma(EAC),which have different etiologies and risk factors.Gut microbiota can contribute to EC via inflammation-induced carcinogenesis,immunomodulation,lactagenesis,and genotoxin production.H.pylori infection is said to be inversely related to EAC,protecting against EAC by inducing atrophic gastritis,altering serum ghrelin levels,and triggering cancer cell apoptosis.Though H.pylori infection has no significant association with ESCC,COX-2-1195 polymorphisms and endogenous nitrosamine production can impact the risk of ESCC in H.pylori-infected in-dividuals.There are concerns regarding a plausible increase in EC after H.pylori eradication treatments.However,H.pylori eradication is not associated with an increased risk of EC,making it safe from an EC perspective.

Effect of acacetin on inhibition of apoptosis in Helicobacter pyloriinfected gastric epithelial cell line

BACKGROUND Helicobacter pylori(H.pylori)infection can cause extensive apoptosis of gastric epithelial cells,serving as a critical catalyst in the progression from chronic gastritis,gastrointestinal metaplasia,and atypical gastric hyperplasia to gastric carcinoma.Prompt eradication of H.pylori is paramount for ameliorating the pathophysiological conditions associated with chronic inflammation of the gastric mucosa and the primary prevention of gastric cancer.Acacetin,which has multifaceted pharmacological activities such as anti-cancer,anti-inflammatory,and antioxidative properties,has been extensively investigated across various domains.Nevertheless,the impact and underlying mechanisms of action of acacetin on H.pylori-infected gastric mucosal epithelial cells remain unclear.AIM To explore the defensive effects of acacetin on apoptosis in H.pylori-infected GES-1 cells and to investigate the underlying mechanisms.METHODS GES-1 cells were treated with H.pylori and acacetin in vitro.Cell viability was assessed using the CCK-8 assay,cell mortality rate via lactate dehydrogenase assay,alterations in cell migration and healing capacities through the wound healing assay,rates of apoptosis via flow cytometry and TUNEL staining,and expression levels of apoptosis-associated proteins through western blot analysis.RESULTS H.pylori infection led to decreased GES-1 cell viability,increased cell mortality,suppressed cell migration,increased rate of apoptosis,increased expressions of Bax and cle-caspase3,and decreased Bcl-2 expression.Conversely,acacetin treatment enhanced cell viability,mitigated apoptosis induced by H.pylori infection,and modulated the expression of apoptosis-regulatory proteins by upregulating Bcl-2 and downregulating Bax and cleaved caspase-3.CONCLUSION Acacetin significantly improved GES-1 cell viability and inhibited apoptosis in H.pylori-infected GES-1 cells,thereby exerting a protective effect on gastric mucosal epithelial cells.

Non-improvement of atrophic gastritis in cases of gastric cancer after successful Helicobacter pylori eradication therapy

BACKGROUND Helicobacter pylori(H.pylori)infection is closely related to the development of gastric cancer(GC).However,GC can develop even after H.pylori eradication.Therefore,it would be extremely useful if GC could be predicted after eradication.The Kyoto classification score for gastritis(GA)is closely related to cancer risk.However,how the score for GC changes after eradication before onset is not well understood.AIM To investigate the characteristics of the progression of Kyoto classification scores for GC after H.pylori eradication.METHODS Eradication of H.pylori was confirmed in all patients using either the urea breath test or the stool antigen test.The Kyoto classification score of GC patients was evaluated by endoscopy at the time of event onset and three years earlier.In ad-dition,the modified atrophy score was evaluated and compared between the GC group and the control GA group.RESULTS In total,30 cases of early GC and 30 cases of chronic GA were evaluated.The pathology of the cancer cases was differentiated adenocarcinoma,except for one case of undifferentiated adenocarcinoma.The total score of the Kyoto classifi-cation was significantly higher in the GC group both at the time of cancer onset and three years earlier(4.97 vs 3.73,P=0.0034;4.2 vs 3.1,P=0.0035,respectively).The modified atrophy score was significantly higher in the GC group both at the time of cancer onset and three years earlier and was significantly improved only in the GA group(5.3 vs 5.3,P=0.5;3.73 vs 3.1,P=0.0475,respectively).CONCLUSION The course of the modified atrophy score is useful for predicting the onset of GC after eradication.Patients with severe atrophy after H.pylori eradication require careful monitoring.

Treatment of Helicobacter pylori infection in atrophic gastritis

Helicobacter pylori(Hp) is a major human pathogen causing chronic, progressive gastric mucosal damage and is linked to gastric atrophy and cancer. Hp-positive individuals constitute the major reservoir for transmission of infection. There is no ideal treatment for Hp. Hp infection is not cured by a single antibiotic, and sometimes, a combined treatment with three or more antibiotics is ineffective. Atrophic gastritis(AG) is a chronic disease whose main features are atrophy and/or intestinal metaplasia of the gastric glands, which arise from long-standing Hp infection. AG is reportedly linked to an increased risk for gastric cancer, particularly when extensive intestinal metaplasia is present. Active or past Hp infection may be detected by conventional methods in about two-thirds of AG patients. By immunoblotting of sera against Hp whole-cell protein lysates, a previous exposure to Hp infection is detected in all AG patients. According to guidelines, AG patients with Hp positivity should receive eradication treatment. The goals of treatment are as follows:(1) Cure of infection, resolution of inflammation and normalization of gastric functions;(2) possible reversal of atrophic and metaplastic changes of the gastric mucosa; and(3) prevention of gastric cancer. An ideal antibiotic regimen for Hp should achieve eradication rates of approximately 90%, and complex multidrug regimens are required to reach this goal. Amongst the factors associated with treatment failure are high bacterial load, high gastric acidity, Hp strain, smoking, low compliance, overweight, and increasing antibiotic resistance. AG, when involving the corporal mucosa, is linked to reduced gastric acid secretion. At a non-acidic intra-gastric p H, the efficacy of the common treatment regimens combining proton pump inhibitors with one or more antibiotics may not be the same as that observed in patients with Hp gastritis in an acid-producing stomach. Although the efficacy of these therapeutic regimens has been thoroughly tested in subjects with Hp infection, there is a paucity of evidence in the subgroupof patients with AG. Bismuth-based therapy may be an attractive treatment in the specific setting of AG, and specific studies on the efficacy of bismuth-based therapies are needed in patients with AG.

Proteomic analysis reveals molecular biological details in varioliform gastritis without Helicobacter pylori infection

AIM:To investigate and elucidate the molecular mechanism underlying varioliform gastritis for early detection,prevention and intervention of gastric cancer.METHODS:A combination of two-dimensional gel electrophoresis and mass spectrometry was used to detect the differentially expressed proteins between varioliform gastritis and matched normal mucosa.The selected proteins were confirmed by Western blotting and reverse transcription polymerase chain reaction(RT-PCR) in additional samples and the function of some proteins in varioliform gastritis was analyzed by bio-method preliminarily.RESULTS:We identified 21 differentially expressed proteins in varioliform gastritis,and compared them with matched normal mucosa.Eleven proteins were upregulated and ten downregulated in varioliform gastritis when compared with the same proteins in individualmatched normal gastric mucosa.These proteins are related to metabolism,oxidation,cytoskeleton,apoptosis,signal transduction and other aspects of cells.Two novel proteins,thioredoxin domain-containing protein 5(TXNDC5) upregulated in varioliform gastritis,and neuropolypeptide h3 [phosphatidylethanolamine-binding protein 1(PEBP1)] downregulated in varioliform gastritis,were further investigated.Their expressions were validated by Western blotting and RT-PCR in 12 cases of varioliform gastritis which was matched with normal mucosa.The expression level of PEBP1 in varioliform gastritis was significantly lower(P<0.05) while that of TXNDC5 was significantly higher than that in matched normal gastric mucosa(P<0.05).CONCLUSION:There are some changes of protein expression in varioliform gastritis.Downregulation of PEBP1 and upregulation of TXNDC5 are involved in the development of varioliform gastritis.

Association of autoimmune type atrophic corpus gastritis with Helicobacter pylori infection

AIM:To study the association between Helicobacter pylori(H.pylori)infection and autoimmune type atrophic gastritis. METHODS:Twenty-three patients with different grades of atrophic gastritis were analysed using enzyme immunoassay-based serology,immunoblot-based serology,and histology to reveal a past or a present H.pylori infection.In addition,serum markers for gastric atrophy(pepsinogenⅠ,pepsinogenⅠ/Ⅱand gastrin)and autoimmunity[parietal cell antibodies(PCA), and intrinsic factor(IF),antibodies]were determined. RESULTS:Of the 14 patients with severe gastricatrophy,as demonstrated by histology and serum markers,and no evidence for an ongoing H.pylori infection,eight showed H.pylori antibodies by immunoblotting.All eight had elevated PCA and 4/8 also had IF antibodies.Of the six immunoblot-negative patients with severe corpus atrophy,PCA and IF antibodies were detected in four.Among the patients with low to moderate grade atrophic gastritis(all except one with an ongoing H.pylori infection),serum markers for gastric atrophy and autoimmunity were seldom detected.However,one H.pylori negative patient with mild atrophic gastritis had PCA and IF antibodies suggestive of a pre-atrophic autoimmune gastritis. CONCLUSION:Signs of H.pylori infection in autoimmune gastritis,and positive autoimmune serum markers in H.pylori gastritis suggest an etiological role for H.pylori in autoimmune gastritis.

Helicobacter pylori infection with atrophic gastritis: An independent risk factor for colorectal adenomas

BACKGROUND The significance of Helicobacter pylori(H.pylori)infection and atrophic gastritis(AG)in the prevalence of colorectal adenomas has been examined in a limited number of studies.However,these studies reported disputed conclusions.AIM To investigate whether H.pylori infection,AG,and H.pylori-related AG increase the risk of colorectal adenomas.METHODS This retrospective cross-sectional study included 6018 health-check individuals.The relevant data for physical examination,laboratory testing,13C-urea breath testing,gastroscopy,colonoscopy and histopathological examination of gastric and colorectal biopsies were recorded.Univariate and multivariate logistic regression analyses were performed to determine the association between H.pylori-related AG and colorectal adenomas.RESULTS Overall,1012 subjects(16.8%)were diagnosed with colorectal adenomas,of whom 143(2.4%)had advanced adenomas.Among the enrolled patients,the prevalence of H.pylori infection and AG was observed as 49.5%(2981/6018)and 10.0%(602/6018),respectively.Subjects with H.pylori infection had an elevated risk of colorectal adenomas(adjusted odds ratio[OR]of 1.220,95%confidence interval(CI):1.053-1.413,P=0.008)but no increased risk of advance adenomas(adjusted OR=1.303,95%CI:0.922-1.842,P=0.134).AG was significantly correlated to an increased risk of colorectal adenomas(unadjusted OR=1.668,95%CI:1.352-2.059,P<0.001;adjusted OR=1.237,95%CI:0.988-1.549,P=0.064).H.pylori infection accompanied by AG was significantly associated with an increased risk of adenomas(adjusted OR=1.491,95%CI:1.103-2.015,P=0.009)and advanced adenomas(adjusted OR=1.910,95%CI:1.022-3.572,P=0.043).CONCLUSION H.pylori-related AG was associated with a high risk of colorectal adenomas and advanced adenomas in Chinese individuals.

Two stomach-originated lactobacillus strains improve Helicobacter pylori infected murine gastritis

AIM:To investigate the potential anti-Helicobacter pylori(H.pylori ) and anti-inflammation in vivo effects of two lactobacillus strains from human stomach.METHODS:Forty H.pylori infected Balb/c mice were randomly divided into 4 groups:proton pump inhibitor and antibiotics triple treated group,Lactobacillus fermenti(L.fermenti ) treated group,Lactobacillus acidophilus treated group and normal saline control group.Ten uninfected mice were also included as blank control group.The infection of H.pylori was detected by rapid urease tests,Giemsa staining and bacterial culture.The colonization of H.pylori was assessed in bacterial density score and gastric inflammation was assessed in histological score.The colonization of L.fermenti was performed by fluorescent probe.RESULTS:Histopathologic evaluation showed significant release of mucosal inflammation in gastric antrum and gastric body in lactobacillus treated groups and triple treated group.H.pylori eradication rate in both lactobacillus treated groups and triple treated group were higher than normal saline control group.Lactobacillus treated groups and triple treated group showed significant decrease of H.pylori bacterial density.CONCLUSION:Both lactobacillus strains have a significant anti-H.pylori activity;L.fermenti displays more efficient antagonistic activity in vivo against H.pylori infection.

Correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori infection and symptoms in patients with chronic gastritis

AIM: To evaluate the correlation between CD4, CD8 cell infiltration in gastric mucosa, Helicobacter pylori(H pylori)infection and symptoms or the assemblage of symptoms in cases with chronic gastritis.METHODS: Biopsy samples at the gastric antrum were obtained from 62 patients with chronic gastritis. CD4 and CD8 cell infiltration was evaluated by immunohistochemical assays on frozen sections of the biopsy samples. Fifteen symptoms referring to digestion-related activity and nondigestion related activity were observed. The correlation between lymphocyte infiltration and each symptom or symptom assemblage was analyzed by logistic regression and K-mean cluster methods.RESULTS: CD4 cell infiltrations in gastric mucosa were much more in patients with H pylori infection, while CD8 cell infiltrations were similar in patients with or without H pylori infection. Logistic regression analysis showed that the symptoms including heavy feeling in head or body (t= 2.563), and thirst (t= 2.478) were significantly related with CD4 cell infiltration in gastric mucosa (P＜0.05), and cool limbs with aversion to cold were related with CD8cell infiltration (t = 2.872, P＜0.05). Further analysis showed that non-digestive related symptom assemblage could increase the predicted percentage of CD4 and CD8cell infiltration in gastric mucosa, including lower CD4infiltration by 12.5%, higher CD8 infiltration by 33.3%,and also non-H pylori infection by 23.6%.K-means cluster analysis of all symptoms and CD4 and CD8 cell infiltration in gastric mucosa showed a similar tendency to increase the predicted percentage of CD4, CD8 cell infiltration and H pylori infection.CONCLUSION: Based on correlation between the gastric mucosa lymphocyte infiltration, H pylori infection and clinical symptoms, symptoms or symptomatic assemblages play an important role in making further classification of chronic gastritis, which might help find a more specific therapy for chronic gastritis.

Expression of cytokeratins in Helicobacter pylori-associated chronic gastritis of adult patients infected with cagA+strains:An immunohistochemical study

AIM： To investigate the expression of different cytokeratins （CKs） in gastric epithelium of adult patients with chronic gastritis infected with Helicobacter pylori （H pylon） cagA ＋ strains. METHODS： The expression of CK 7, 8, 18, 19 and 20 was studied immunohistochemically in antral gastric biopsies of 84 patients. All the CKs were immunostained in cagA＋Hpylori gastritis （57 cases）, non-Hpylori gastritis （17 cases） and normal gastric mucosa （10 cases）. RESULTS： In cagA＋ H pylori gastritis, CK8 was expressed comparably to the normal antral mucosa from surface epithelium to deep glands. Distribution of CK18 and CK 19 was unchanged, i.e. transmucosal, but intensity of the expression was different in foveolar region in comparison to normal gastric mucosa. Cytokeratin 18 immunoreactivity was significantly higher in the foveolar epithelium of H pylori-positive gastritis compared to both Hpylori-negative gastritis and controls. On the contrary, decrease in CK19 immunoreactivity occurred in foveolar epithelium of H pylori-positive gastritis. In both normal and inflamed antral mucosa without Hpyloriinfection, CK20 was expressed stronglyl moderately and homogenously in surface epithelium and upper foveolar region, but in H pylod -induced gastritis significant decrease of expression in foveolar region was noted. Generally, in both normal antral mucosa and H pylori-negative gastritis, expression of CK7 was not observed, while in about half cagA＋ H pylori-infected patients, moderate focal CK7 immunoreactivity of the neck and coiled gland areas was registered, especially in areas with more severe inflammatory infiltrate. CONCLUSION： Alterations in expression of CK 7, 18, 19 and 20 together with normal expression of CK8 occur in antral mucosa of H pylori-associated chronic gastritis in adult patients infected with cagA＋ strains. Alterations in different cytokeratins expression might contribute to weakening of epithelial tight junctions observed in H pylori-infected gastric mucosa.

Innate immunity–the hallmark of Helicobacter pylori infection in pediatric chronic gastritis

BACKGROUND Innate immunity was found to be associated with both persistence of Helicobacter pylori(H.pylori)infection and increased risk of gastric cancer.AIM To identify the risk factors associated with H.pylori infection and to establish the role of TLR9 rs352140 in suppressing or promoting inflammation related to this infection in children.METHODS We performed a study of 155 children with digestive symptoms,who were divided into two groups according to the histopathological exam:Group 1–48 children with H.pylori-induced chronic gastritis,and Group 2–control group.RESULTS Rural area and poor living conditions were significantly associated with H.pylori chronic gastritis(P=0.0042/P<0.0001).Both positive immunoglobulin A anti H.pylori and the rapid urease test were significantly associated with H.pylori infection(P<0.0001).Significantly higher values of leukocytes and neutrophils within the peripheral blood were found in children with H.pylori chronic gastritis(P=0.111/P=0.284).We found a significant positive correlation between the variant TT genotype of TLR9 rs352140 polymorphism and both leucocytes and neutrophils(P=0.0225/P=0.0292).CONCLUSION Variant TT genotype carriers of the TLR9 rs352140 gene polymorphism might have a more severe degree of inflammation.

Assessing GastroPanel serum markers as a non-invasive method for the diagnosis of atrophic gastritis and <i>Helicobacter pylori</i>infection

Gastric colonization by Helicobacter pylori increases the risk of gastric disorders, including atrophic gastritis which can be diagnosed based on levels of serum biomarkers like Gastrin and Pepsinogen. We therefore examined the efficacy of a serological-based method namely GastroPanel Blood kit, in diagnosing and scoring gastritis associated to Helicobacter pylori infection. Patients with dyspeptic symptoms were prospectively recruited on voluntary basis at the Yaounde Central Hospital and University Teaching Hospital, from March to July 2011. The degree of atrophy was classified according to levels in patient serum of pepsinogens I and II (PGI and PGII) and Gastrin 17 (G17) and compared with histological profiles as reference method. A specific ELISA test was used for the detection of H. pylori IgG antibodies. In total, 86 volunteers from 21 to 83 years old (mean = 46.4 ± 3.3) were enrolled, including 74.4% of women and 25.6% of men. The prevalence of gastritis was statistically similar between Gastro Blood Panel test and histology used as reference method (89.5% versus 83.7%: p > 0.20). Diagnosis based on serum makers showed high sensitivity (93.1%) in comparison with the reference method. However, the serological based method has diagnosed more atrophic gastritis than the reference (17.4% versus 7.0%: p 0.05). Furthermore, the prevalence of H. pylori infection did not differ significantly between serological method (84.9%) and reference method (81.4%). These results suggest that diagnosis of atrophic gastritis and H. pylori infection obtained with an optional serological method (GastroPanel) is in a strong agreement with the biopsy findings, and thus can be a useful non endoscopic assessment of stomach mucosal atrophy in patients with dyspepsia.

Asymptomatic Helicobacter pylori infection and its relation to chronic gastritis

Ninety-two asymptomafic subjects were investigated to determine whether they were in-fected with Helicobacter pylori(HP)by means of fiber gastroscopy, urease test andWarthin-Starry silver stain.As a result of this work,49 subjects with HP infection were found.Under gastroscope,24 of 92 subjects had normal gastric mucosa 45 suffered frompiebaldism-like congestion of the gastric mucosa and 23 mucosal erosion,but the differencesamong the detectable rotes of them had no statistical significance(P】0.05).Forty-six of the subjects with HP infection were seen in the 67 patients with gastritis and only 3 in the subjectswith normal mucosa.The positive rates of HP infection in the patients with moderate and serfous gastritis were significant highly(P【0.01),as compared with that in mild gastritis.It could besuggested that HP infection and the gastritis associated with it may universally exist in“healthy persons”without symptom.

Reduced secretion of epidermal growth factor in duodenal ulcer patients with Helicobacter pylori infection

AIM To investigate the concentration changes of epidermal growth factor (EGF) in duodenal ulcer patients with H. pylori infection.