Gastroduodenal Inflammation Research Articles

Comparison of Haematological Variables in Helicobacter Pylori-Infected Patients with Ulcer and without Ulcer: A Cross-sectional Study

Introduction: Helicobacter pylori (H. pylori) is predominantly responsible for acute and chronic progressive gastroduodenal inflammation. Symptoms of gastric diseases vary from dyspepsia to altered bowel movements, leading to ulcers and potential gastrointestinal bleeding. Consequently, H. pylori can have a variable effect on the gastrointestinal tract and other organs. Ongoing research has shown associations between H. pylori and haematological manifestations. Recent studies have reported a 90% incidence of duodenal ulcers and an 80% incidence of gastric ulcers in patients with H. pylori infection. Aim: To investigate haematological manifestations in H. pyloriinfected patients with and without ulcers, and to compare the haematological variables. Materials and Methods: This cross-sectional study was conducted in the Department of Gastroenterology at King George’s Medical University in Lucknow, India, from October 2021 to October 2022. One hundred patients diagnosed with H. pylori-positive biopsy through endoscopy were enrolled in the study. Among these patients, 51% had ulcers with H. pylori infection (enrolled as cases), while 49% were H. pylori infected but without ulcers (enrolled as controls). Samples were analysed for Haemoglobin (Hb) levels, Red Blood Cell (RBC) count, Reticulocyte Count (RetC), serum iron, serum ferritin, Total Iron Binding Capacity (TIBC), serum vitamin B12, and Homocysteine (HCy) levels. Statistical analysis involved independent sample t-tests to compare continuous data and chi-square tests to compare categorical data. Results: The majority of patients included in the study, both with ulcers (70.6%) and without ulcers (59.2%), were males with mean±Standard Deviation (SD) ages of 32.39±7.25 years and 29.86±7.66 years, respectively. In the present study, low reticulocyte count, anaemia, deranged RBC count, low serum iron, high TIBC, and low ferritin were observed in 9%, 22%, 61%, 11%, 12%, and 8% of the patients, respectively. Vitamin B12 deficiency and hyperhomocysteinemia were observed in 6% and 1% of the cases, respectively. Among patients with ulcers, the strongest correlation was found between serum iron and serum ferritin (r-value=0.901), while the weakest correlation was found between vitamin B12 and RetC (r-value=0.206). Among patients without ulcers, the strongest correlation was found between serum iron and Hb (r-value=0.884), while the weakest correlation was found between TIBC and HCy (r-value=0.270). Conclusion: The present study demonstrates a significant association between H. pylori infection-induced ulcers and decreased mean reticulocyte count, serum iron, and serum ferritin levels. Recognising these haematological derangements and including them as indications for H. pylori eradication may lead to a remarkable improvement in the management regime.

Antibiotic Resistance of Helicobacter pylori in Children with Gastritis and Peptic Ulcers in Mekong Delta, Vietnam.

Background: Helicobacter pylori (H. pylori) infection causes gastritis, duodenal and gastric ulcers, and gastric cancer. H. pylori eradication efficacy is low worldwide, and antibiotic resistance is the leading cause of therapy failure; therefore, this study was performed to determine the characteristics of antibiotic resistance of H. pylori in children with gastritis, duodenal and gastric ulcer. Methods: A cross-sectional study was conducted on 237 pediatric patients diagnosed with gastroduodenal inflammation and ulcer at two hospitals in Vietnam from March 2019 to April 2022. Pediatric patients with positive H. pylori tests continued to do E-tests to measure the minimum inhibitory concentration of the antibiotic so that we could prescribe effective antibiotics based on the sensitivity. Results: In 237 pediatric patients (51.1% males) with a median age of 10.3 years (range 5–16 years), endoscopic images showed that inflammatory lesions and peptic ulcers accounted for 69.2% and 30.8%, respectively. Resistance rates of H. pylori were 80.6% to clarithromycin (CLR), 71.7% to amoxicillin (AMX), 49.4% to metronidazole (MTZ), 45.1% to levofloxacin (LEV), and 11.4% to tetracycline (TET); dual resistance to AMX + CLR was 64.2%, AMX + LEV 35%, AMX + MTZ 33.3%, CLR + MTZ 32.5%, and TET + MTZ 7.2%. The frequency of clarithromycin resistance was significantly increased, particularly in pediatric patients who had received prior H. pylori treatment. The percentage of amoxicillin resistance increased with age; amoxicillin resistance of H. pylori was more prevalent among pediatric patients with peptic ulcers than those with gastroduodenal inflammation and higher in males than females. Conclusions: The proportions of resistance to CLR, AMX, MTZ, and LEV were extremely high, in contrast to TET, which was lower in pediatric patients. Our study suggests that the standard triple therapy with CLR should be limited as the empiric therapy for pediatric patients, and we should consider using eradication regimens with TET for children over 8 years of age if the medical facility is not qualified to perform antibiotic susceptibility tests of H. pylori in the Mekong Delta.

Association of ATG16L1 genetic variant with Helicobacter pylori infection in Egyptian patients with chronic gastritis disease

BackgroundHelicobacter pylori infection remains a major risk for gastroduodenal inflammation and ulceration with capability to disrupt the defensive autophagy pathway in the gastric mucosal cell thus producing resilient infection. A single-nucleotide mutation in the autophagy gene ATG16L1 which controls the host immune responses to viruses and bacteria was identified as a risk factor for increasing survival and persistence of many microbial infections. AimTo assess the association of ATG16L1 T300A gene mutation with the susceptibility to H. pylori infection in patients with chronic gastritis disease. MethodsATG16L1 T300A mutation was determined by TaqMan genotyping allele specific discrimination real-time PCR assay applying specific primers, (rs2241880 A/G) and probes for A and G allele. ResultPatients with mutant homozygous GG genotype was associated with a 4.5 times increase in the risk of H. pylori infection relative to the wild homozygous AA and the heterozygous AG genotypes (p value = 0.009, OR = 4.472; 95% CI, 0.07–0.74). The carriage rate of the mutant G allele was significantly higher in H. pylori positive cases (64%) relative to (42%) in H. pylori negative cases (p value = 0.002, OR = 2.455, 95% CI, 0.3 (0.09–1.01), and this was associated with about a 2.5 times increase in the risk for H. pylori infection. ConclusionGenetic variant ATG16L1 T300A mutation increased the risk of H. pylori infection in Egyptian patients with chronic gastritis disease.

Bacterionomics and vironomics in carcinogenesis

Virus and bacteria are microbes which are very common cause human infection. Most of the bacterial infection can be eradicated by antibiotics and infection symptoms disappear. But for virus infection, once infected, the virus will persistently stay in the host, even undergo not only a lytic cycle but also integrated into host genome. Nowadays, at least 6 virus type are consistently related to human cancer, such as EBV,HPV,HTLV,HBV,HCV,HKSV, and the new one Merkel Virus (MCV). Although not every infected people will get cancer, but around 20% of the whole cancer in human are caused by viral oncogene. Class one oncogenic bacterial is Helicobacter pylori . Infection with this bacteria can cause persistent gastro duodenal inflammation which cause some alteration in gastric cell growth into transformation. Expression of Cag gene and Vac gene and some expression of OMP protein usually link to gastric cancer. Molecular mechanisms of carcinogenesis for every virus which cause infection is a very complex , which include several processes caused by cell transformation. Besides, other host and environmental factors are also play a significant role in cancer development. Some scientist put a Hallmark analysis as a model to quickly summarize what pathobiology process will happen and what gene or protein caused the process. The Hallmark analysis comprise of several process which may happen simultaneously because some of the Hallmark is caused by the same protein. The Hallmark consists of various virus strategies in oncogenesis such as promoting angiogenesis, avoiding immune destruction, genome instability and mutation, deregulating cellular energetic, resisting cell death, sustaining proliferative signaling, evading growth suppressors, enabling cellular immortality, promoting inflammation and activation metastasis. For example, infection by HPV, will cause low grade dysplasia which can continue to invasive cervical cancer. After host cell transformation, in the long control region genes, E6 and E7 protein will cause several strategies in oncogenesis including resisting cell death and evading growth suppressors. HBV infection will end without any serious liver damage, but after cell transformation, almost all Hallmark strategies of viral oncogenesis are happening step by step in line with the severity of liver cell damage. As the onset of cancer development after infection can last years, there are an opportunity to design either vaccine or genetic therapy to minimalize further risk of cancer in human

The Relationship between Oral Hygiene Index and Gastric Helicobacter Pylori Positivity

Objective: Helicobacter pylori (HP) is a bacterial pathogen that leads to gastroduodenal inflammation, gastric and duodenal ulcer and atrophic gastritis. Colonization of bacteria can be shown by using rapid-urease test during endoscopy. There are conflicting data about the route of transmission and reservoir. It’s thought to be transmitted primarily by oral route. Many studies showed results supporting that the presence of bacteria in dental plaques has effects on gastric colonization and eradication. There are data about the potential inhibitory effect of oral flora on HP. We aimed to analyze the association of simplified oral hygiene index -a possible representation of a healthy oral flora- with HP positivity. Methods: Patients undergoing upper gastrointestinal system endoscopy for symptoms of dyspepsia were assessed by a dentist for the simplified oral hygiene index (OHI). Patients were classified as good, poor and bad groups based on oral hygiene index scale. Pre-pyloric biopsy materials were assessed using rapid-urease test. Oral hygiene indexes were analyzed retrospectively, groups were compared for HP positivity. Results: 66 patients (30 females, 45.5%) were included. Mean age of patients was 34.17±14.7 years. 11 (16.7%), 29 (43.9%) and 26 (39.4%) patients were classified as in good, poor and bad hygiene index groups, respectively. In patients with good OHI gastric HP positivity was less frequent. Conclusion: Decreased frequency in gastric HP may be observed with maintaining an ideal oral hygiene. Key words: Endoscopy, helicobacter pylori, oral hygiene index

헬리코박터 파일로리(Helicobacter pylori) 감염 및 치료법 개요

Helicobacter pylori는 사람의 위점막에서 발견되는 전염성이 있는 중요한 병원균이다. 장기간 기생하면서 만성위염, 소화성궤양, 위 변연부 B세포 림프종, 그리고 위암을 일으키는 세균으로 알려져 있다. 국내에서는 프로톤펌프 억제제(proton pump inhibitor, PPI)와 두 가지 항생제(amoxicillin, clarithromycin)를 포함하는 표준 삼제 요법을 1차 치료로 사용하여 왔으나, 점점 증가하고 있는 항생제 내성으로 인해 제균율은 점차 감소하고 있다. 여기서는 H. pylori의 현재의 치료법들과 이들 치료법들의 문제점들을 검토하고, 표적치료의 필요성과 표적치료에 활용할 수 있는 약물전달체로서의 점토광물의 가능성에 대해 알아보고, 이들을 이용한 새로운 치료 방향에 대한 향후 연구계획 등에 대해서 논하고자 한다. Helicobacter pylori is an important transmissible human pathogen found on the luminal surface of the gastric epithelium. The organism can persist in the stomach indefinitely and causes gastroduodenal inflammation that may proceed to atrophic gastritis, peptic ulcer, gastric MALT lymphoma, and gastric cancer. Standard triple therapy which consists of proton pump inhibitor (PPI) plus two antibiotics (amoxicillin and clarithromycin) is now generally used in Korea, however, eradication rates of H. pylori has been decreasing due to increasing antibiotic resistance. In this review, current second-line treatment regimens, difficult problems on treatment, necessity of local target therapy, applicability of clay minerals as a drug delivery system (DDS), and a new therapeutic strategy and its study plans will be discussed.

Role of dietary polyphenols in the management of peptic ulcer.

Peptic ulcer disease is a multifactorial and complex disease involving gastric and duodenal ulcers. Despite medical advances, the management of peptic ulcer and its complications remains a challenge, with high morbidity and death rates for the disease. An accumulating body of evidence suggests that, among a broad reach of natural molecules, dietary polyphenols with multiple biological mechanisms of action play a pivotal part in the management of gastric and duodenal ulcers. The current review confirmed that dietary polyphenols possess protective and therapeutic potential in peptic ulcer mediated by: improving cytoprotection, re-epithelialization, neovascularization, and angiogenesis; up-regulating tissue growth factors and prostaglandins; down-regulating anti-angiogenic factors; enhancing endothelial nitric oxide synthase-derived NO; suppressing oxidative mucosal damage; amplifying antioxidant performance, antacid, and anti-secretory activity; increasing endogenous mucosal defensive agents; and blocking Helicobacter pylori colonization associated gastric morphological changes and gastroduodenal inflammation and ulceration. In addition, anti-inflammatory activity due to down-regulation of proinflammatory cytokines and cellular and intercellular adhesion agents, suppressing leukocyte-endothelium interaction, inhibiting nuclear signaling pathways of inflammatory process, and modulating intracellular transduction and transcription pathways have key roles in the anti-ulcer action of dietary polyphenols. In conclusion, administration of a significant amount of dietary polyphenols in the human diet or as part of dietary supplementation along with conventional treatment can result in perfect security and treatment of peptic ulcer. Further well-designed preclinical and clinical tests are recommended in order to recognize higher levels of evidence for the confirmation of bioefficacy and safety of dietary polyphenols in the management of peptic ulcer.

Immunomodulatory Effects of Vagus Nerve and Acetylcholine in Gastroduodenal Area

Objective: Neuroimmune interplay is one of the basic elements that determine mucosal health and disease. Continuing discussion of the vagus nerve in maintenance of homeostasis of gastroduodenal area, we aim to revise immunomodulating effects of acetylcholine. Results: Vagus nerve plays a major role in gut mucosa immunity due to cytoprotective properties and modulation of leukocytes activity. Stimulation of vagus nerve after mucosa damage is accompanied by cholinergic anti-inflammatory pathway that is realized directly through alfa7-nicotinergic cholinoreceptors on neutrophils, macrophages and lymphocytes, which activation causes decrease of NF-kB expression and TNF and IL-6 secretion. Indirect effect of acetylcholine through enteroendocrine cells regulation is quite important in determination of neuro-immune-endocrine interplay in gastroduodenal mucosa. In addition, the changes in vagus nerve activity and neurohumoral control of gastroduodenal area under antisecretory therapy of gastroduodenal diseases are deliberated in this review. Conclusion: Vagus nerve dysfunction is likely to be the main cause of gastroduodenal inflammation, dysregeneration and cancerogenesis.

Helicobacter pylori Antigen HP0986 (TieA) Interacts with Cultured Gastric Epithelial Cells and Induces IL8 Secretion via NF‐κB Mediated Pathway

The envisaged roles and partly understood functional properties of Helicobacter pylori protein HP0986 are significant in the context of proinflammatory and or proapoptotic activities, the two important facilitators of pathogen survival and persistence. In addition, sequence analysis of this gene predicts a restriction endonuclease function which remained unknown thus far. To evaluate the role of HP0986 in gastric inflammation, we studied its expression profile using a large number of clinical isolates but a limited number of biopsies and patient sera. Also, we studied antigenic role of HP0986 in altering cytokine responses of human gastric epithelial (AGS) cells including its interaction with and localization within the AGS cells. For in vitro expression study of HP0986, 110 H.pylori clinical isolates were cultured from patients with functional dyspepsia. For expression analysis by qRT PCR of HP0986, 10 gastric biopsy specimens were studied. HP0986 was also used to detect antibodies in patient sera. AGS cells were incubated with recombinant HP0986 to determine cytokine response and NF-κB activation. Transient transfection with HP0986 cloned in pEGFPN1 was used to study its subcellular localization or homing in AGS cells. Out of 110 cultured H.pylori strains, 34 (31%) were positive for HP0986 and this observation was correlated with in vitro expression profiles. HP0986 mRNA was detected in 7 of the 10 biopsy specimens. Further, HP0986 induced IL-8 secretion in gastric epithelial cells in a dose and time-dependent manner via NF-κB pathway. Serum antibodies against HP0986 were positively associated with H.pylori positive patients. Transient transfection of AGS cells revealed both cytoplasmic and nuclear localization of HP0986. HP0986 was moderately prevalent in clinical isolates and its expression profile in cultures and gastric biopsies points to its being naturally expressed. Collective observations including the induction of IL-8 via TNFR1 and NF-κB, subcellular localization, and seropositivity data point to a significant role of HP0986 in gastroduodenal inflammation. We propose to name the HP0986 gene/protein as 'TNFR1 interacting endonuclease A (TieA or tieA)'.

Urease from Helicobacter pylori is inactivated by sulforaphane and other isothiocyanates

Infections by Helicobacter pylori are very common, causing gastroduodenal inflammation including peptic ulcers, and increasing the risk of gastric neoplasia. The isothiocyanate (ITC) sulforaphane [SF; 1-isothiocyanato-4-(methylsulfinyl)butane] derived from edible crucifers such as broccoli is potently bactericidal against Helicobacter, including antibiotic-resistant strains, suggesting a possible dietary therapy. Gastric H. pylori infections express high urease activity which generates ammonia, neutralizes gastric acidity, and promotes inflammation. The finding that SF inhibits (inactivates) urease (jack bean and Helicobacter) raised the issue of whether these properties might be functionally related. The rates of inactivation of urease activity depend on enzyme and SF concentrations and show first order kinetics. Treatment with SF results in time-dependent increases in the ultraviolet absorption of partially purified Helicobacter urease in the 260–320 nm region. This provides direct spectroscopic evidence for the formation of dithiocarbamates between the ITC group of SF and cysteine thiols of urease. The potencies of inactivation of Helicobacter urease by isothiocyanates structurally related to SF were surprisingly variable. Natural isothiocyanates closely related to SF, previously shown to be bactericidal (berteroin, hirsutin, phenethyl isothiocyanate, alyssin, and erucin), did not inactivate urease activity. Furthermore, SF is bactericidal against both urease positive and negative H. pylori strains. In contrast, some isothiocyanates such as benzoyl-ITC, are very potent urease inactivators, but are not bactericidal. The bactericidal effects of SF and other ITC against Helicobacter are therefore not obligatorily linked to urease inactivation, but may reduce the inflammatory component of Helicobacter infections.

Cystic fibrosis, gastroduodenal inflammation, duodenal ulcer, and H. pylori infection: The “cystic fibrosis paradox” revisited

In cystic fibrosis (CF) patients a duodenal impaired bicarbonate secretion and unbuffered gastric acid are always described and the development of duodenal ulceration is uncommon (CF paradox). Helicobacter pylori (HP) infection is the main cause for duodenal ulceration and its prevalence in CF patients is controversial. The objective of this study is to evaluate HP prevalence, gastric histology, and duodenal ulceration in adult FC patients. 32 adult CF patients were submitted to (13)C-urea breath test and serum immunoblotting test for HP diagnosis. Among them, 20 patients were submitted to endoscopy. 19/32 (68%) patients showed positive serology. Endoscopy showed erosive duodenitis (15%), and duodenal ulcer scar in 10%. On duodenal histology, 94.5%, showed active inflammation and 66.7% gastric metaplasia. HP infection prevalence in adult CF patients was similar to that of general Brazilian population. CF patients have all the duodenal spectrum of alterations, including duodenal ulcer. CF paradox may not exist.

Development of monoclonal antibody-based immunoassays for detection of Helicobacter pylori neutrophil-activating protein

Neutrophil-activating protein (NAP) is a major virulence factor expressed by Helicobacter pylori isolates associated with severe chronic gastroduodenal inflammation and peptic ulcers. NAP is one of the main protective antigens and a target for vaccine development against Helicobacter infection. In addition, NAP is a potent immune stimulator with potential application as a general vaccine adjuvant and in treatment of allergic diseases and cancer immunotherapy. NAP-specific immunoassays are needed for both H. pylori diagnostics and characterization of NAP-based vaccines and immunomodulatory preparations. We generated a panel of NAP-specific monoclonal antibodies (MAbs) by immunization of BALB/c mice with synthetic NAP peptides. The antibody reactivity against recombinant or native NAP antigen was characterized by enzyme-linked immunosorbent assay (ELISA), immunoblotting and immunofluorescence. A sensitive capture ELISA was developed using MAbs 23C8 and 16F4 (directed against different NAP epitopes) for detection of native or measles virus (MV) vector-expressed recombinant NAP in a concentration range of 4ng/ml to 2000ng/ml. MAb 23C8 antigen-binding depends on Tyr101 in a variable amino acid sequence of the NAP molecule, indicating the existence of antigenic variants among H. pylori strains. MAb 16F4 reacted with NAP from different H. pylori strains and was a sensitive tool for detection of small amounts of isolated NAP antigen or whole bacteria by immunoblotting or immunofluorescence. In conclusion, MAb-based immunoassays are highly specific and sensitive for detection of native NAP antigen and recombinant NAP immunostimulatory transgenes expressed by replication competent virus vectors.

Facing resistance of H.pylori infection.

Helicobacter pylori is an important human pathogen and a gram-negative, spiral shaped and microaerophilic bacteria with persistence colonization in gastric mucosa, causes gastroduodenal inflammation and destruction, resulting in diseases such as duodenal ulcer disease, gastric ulcer disease. When H.pylori discovered by Warren and Marshall, effective therapy developed for this infection and resulted in remarkable change in management of PUD and dyspepsia. Nowadays, the increasing prevalence of drug resistance has complicated successful therapy, considering more attention for appropriate therapy. Ideally, therapy should be based on pretreatment drug susceptibility testing, and empiric use of eradication therapies should assume the presence of antimicrobial drug resistance and use increased doses for 14 days.

Lansoprazole as part of triple therapy in eradication of <i>H. pylori</i> in Sudanese patients with gastro-duodenal inflammation

Background: Eradication of H. pylori is important goal in the management of uncomplicated peptic ulcer disease and other conditions associated with H.pylori. The survival capabilities of H. pylori in the stomach makes it difficult to eradicate and effective treatment requires multidrug regimens. Objectives: To study the efficacy of lansoprazole, Amoxicillin and metronidazole in the eradication of H. pylori. Methods: A total of 35 patients (22 males and 13 females) with gastro-duodenal inflammation and positive for H. pylori were studied. Gastro-duodenoscopy was repeated four weeks after completion of treatment to assess the healing of inflammation. Biopsies were taken from the stomach and tested for H. pylori before and after treatment. Results: Twenty eight patients (93%) reported improvement in symptoms. Eradication of H. pylori was confirmed with negative rapid urease test in 20(67%) patients. Complete healing of the gastro-duodenal inflammation was achieved in 22 patients (73%), partial healing in 6 patients, while only 2(7%) patients showed no healing. Conclusion: The reduced eradication rate of this drug combination in this study (67%) compared to a previous one (96%) could be explained partly by the development of antibiotic resistance (possibly to metronidazole) during the last few years. Keywords: ulcer, urease, endoscopy, metronidazole.Sudan Journal of Medical Sciences Vol. 3 (1) 2008: pp. 41-44

San-Huang-Xie-Xin-Tang inhibits Helicobacter pylori-induced inflammation in human gastric epithelial AGS cells

Helicobacter pylori infection leads to gastroduodenal inflammation, peptic ulceration, gastric lymphoma and gastric cancer. Certain herbal remedies have been used to treat gastric disease. In this study, we examined the anti-inflammatory effect of San-Huang-Xie-Xin-Tang (SHXT) and its main component baicalin on Helicobacter pylori-infected human gastric epithelial AGS cell. AGS cells were treated with Helicobacter pylori at a bacterium/cell ratio of 300:1. mRNA expression and protein levels were determined by reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and western blot analysis, respectively. Interleukin-8 (IL-8) level and the translocation of nuclear factor kappa B (NF-κB) were measured by enzyme-linked immunosorbent assay (ELISA) and enzyme-linked DNA–protein interaction assay (ELDIA), respectively. Nitric oxide production was measured by Griess reagent. We found that SHXT and baicalin inhibited Helicobacter pylori-induced cyclooxygenase-2 (COX-2) enhancement and IκBα degradation in both mRNA and protein levels. SHXT and baicalin also inhibited Helicobacter pylori-induced inducible nitric oxide synthase (iNOS) and IL-8 mRNA expression, and decreased NO and IL-8 production. Furthermore, SHXT and baicalin inhibited nuclear translocation of p50 subunit of NF-κB in Helicobacter pylori-infected AGS cells. Based on the above findings, SHXT and baicalin might exert anti-inflammatory and gastroprotective effects in Helicobacter pylori-induced gastric inflammation.

Helicobacter pylori Infection and Severity of Reflux-Induced Esophageal Disease in a Cohort of Patients with Columnar-Lined Esophagus

The relationship between Helicobacter pylori infection and reflux-induced esophageal diseased is controversial. We examined esophageal disease severity in patients with columnar-lined esophagus and compared results between patients with and without Helicobacter pylori infection. Medical records of 1000 patients diagnosed with columnar-lined esophagus were examined. Endoscopic and histological findings of reflux-induced esophageal disease were compared between H. pylori-positive and H. pylori-negative patients. Four hundred twenty-nine patients (42.9%) showed evidence of H. pylori status, of whom 239 (55.7%) were positive and 190 (44.3%) negative. There were no significant differences in length of columnar-lined segment (P = 0.305), frequency of associated esophagitis (P = 0.583), or presence of gastroduodenal inflammation (P = 0.335, P = 0.131) between the two groups. Histological grade of esophageal disease severity was similar between them, with no statistically significant differences (P = 0.231). We conclude that in patients with established columnar-lined esophagus, there appears to be no difference in severity of reflux-induced esophageal disease between those with and those without H. pylori infection.

Ulcers and Gastritis

This article reviews recently published reports on ulcers and gastritis. Helicobacter pylori is known to be an important pathogen involved in gastroduodenal inflammation and peptic ulcers. Conventional endoscopy is of limited usefulness in the evaluation of gastritis, but magnifying endoscopy is evidently helpful in the diagnosis of chronic atrophic gastritis, intestinal metaplasia, and H. pylori infection. A significant reduction in the incidence of refractory ulcers and the prevalence of H. pylori infection in patients with peptic ulcer disease followed the introduction of H. pylori eradication treatment. Chronic H. pylori infection is associated with gastric cancer, and the effect of H. pylori eradication on the prevention of gastric cancer is an important issue that is still a matter of controversy. Endoscopic hemostasis and intravenous proton-pump inhibitor (PPI) infusion represent a widely accepted approach to the treatment of peptic ulcer bleeding. In clinical practice, it is important to prevent recurrent bleeding and to treat patients who do not respond to endoscopic therapy or PPI treatment. Laparoscopic repair for peptic ulcer perforations, with postoperative eradication treatment, has gradually met with acceptance in patients with H. pylori infection. H. pylori infection and its treatment continue to be interesting problems in this field.

Cellular stress-related protein expression in Helicobacter pylori-infected gastric epithelial AGS cells

Helicobacter pylori infection leads to gastroduodenal inflammation, peptic ulceration, and gastric carcinoma. Moreover, H. pylori may induce disease-specific protein expression in gastric epithelial cells. The present study was aimed at determining differentially expressed proteins in H. pylori-infected gastric epithelial AGS cells. AGS cells were treated with H. pylori at a bacterium/cell ratio of 300:1 for 12 h. Altered protein patterns as separated by two-dimensional electrophoresis using pH gradients of 4–7 were conclusively identified by matrix-assisted laser desorption/ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis of the peptide digests. Four differentially expressed proteins, whose expression levels were increased by more than two-fold in H. pylori-infected cells, were analyzed. These proteins (14-3-3 protein α/β, cullin homolog 3, α-enolase, ezrin) are known to be related to cell proliferation, cell adhesion, and carcinogenesis, and may be mediated by cellular stress, such as reactive oxygen species. In conclusion, the identification of these differentially expressed proteins provide valuable information for the understanding of the pathophysiologic mechanisms of H. pylori-induced gastric diseases, and may be useful as prognostic indices of H. pylori-related gastric disorders.

HELICOBACTER PYLORI SEROLOGY AND EVALUATION OF GASTRODUODENAL DISEASE IN NIGERIANS WITH DYSPEPSIA

Helicobacter pylori (H. pylori) has been strongly associated with various gastroduodenal diseases worldwide with only a few studies emanating from developing countries. The objectives of this study were to determine the prevalence of serum Immunoglobulin G (IgG) and underlying gastroduodenal pathology in Nigerian patients with dyspepsia and ascertain the usefulness of H. pylori IgG screening in decreasing endoscopic workload in dyspeptics in Nigeria. Fifty-five patients with dyspepsia and 55 age and sex-matched apparently normal control were screened for H. pylori IgG using ImmunocombRII kits. Each of the 55 patients was also examined endoscopically with biopsies taken appropriately. Serology was positive in 94.5% and 92.7% of dyspeptic patients and controls respectively. Gastroduodenal inflammation was the commonest endoscopic finding, 43 (78.18%). Other findings were malignant gastric tumour 6(10.9%), reflux oesophagitis 3 (5.45%), gastric ulcer 2 (3.64%), and duodenal ulcer in 1 (1.82%). Chronic gastritis was the main histopathologic finding in the dyspeptic patients. It is concluded that serum H. pylori IgG cannot be used as a screening procedure to reduce endoscopic workload in Nigerian patients with dyspepsia. Key Words: dyspepsia; Helicobacter pylori serology; gastroduodenal disease African Journal Of Clinical And Experimental Microbiology Jan 2004 Vol.5 No.1 131-138

Oxidative-stress-related proteome changes in Helicobacter pylori-infected human gastric mucosa.

Helicobacter pylori infection leads to gastroduodenal inflammation, peptic ulceration and gastric carcinoma. Proteomic analysis of the human gastric mucosa from the patients with erosive gastritis, peptic ulcer or gastric cancer, which were either infected or not with H. pylori, was used to determine the differentially expressed proteins by H. pylori in the human gastric mucosa in order to investigate the pathogenic mechanism of H. pylori -induced gastric diseases. Prior to the experiment, the expression of the main 18 proteins were identified in the gastric mucosa and used for a proteome map of the human gastric mucosa. Using two-dimensional electrophoresis of the protein isolated from the H. pylori -infected tissues, Coomassie Brilliant Blue staining and computerized analysis of the stained gel, the expression of eight proteins were altered in the H. pylori -infected tissues compared with the non-infected tissues. MS analysis (matrix-assisted laser desorption/ionization-time of flight MS) of the tryptic fragment and a data search allowed the the identification of the four increased proteins (78 kDa glucose-regulated protein precursor, endoplasmin precursor, aldehyde dehydrogenase 2 and L-lactate dehydrogenase B chain) and the four decreased proteins (intracellular chloride channel protein 1, glutathione S-transferase, heat-shock protein 60 and cytokeratin 8) caused by H. pylori infection in the gastric mucosa. These proteins are related to cell proliferation, carcinogenesis, cytoskeletal function and cellular defence mechanism. The common feature is that these proteins are related to oxidative-stress-mediated cell damage. In conclusion, the established gastric mucosal proteome map might be useful for detecting the disease-related protein changes. The H. pylori -induced alterations in protein expression demonstrate the involvement of oxidative stress in the pathogenesis of H. pylori -induced gastric diseases, including inflammation, ulceration and carcinogenesis.