Duodenal Ulcer Group Research Articles

Gastrointestinal bleeding in children with Henoch-Schönlein purpura combined with prognostic nutrition index may predict endoscopic duodenal ulcers during hospitalization: A single-center retrospective case-control study.

Duodenal ulcer (DU) is the most common gastroscopic manifestation of abdominal Henoch-Schönlein purpura (HSP), which may cause severe bleeding and often requires esophagogastroduodenoscopy (EGD) to confirm the diagnosis. However, the condition of children with HSP changes rapidly; not all children are able to undergo EGD on time, and some hospitals do not have a pediatric EGD unit. Therefore, assessing the risk factors for developing DU in HSP using simple and readily available indicators is essential. Children with HSP at Wuhan Children Hospital from June 2020 to June 2022 were included in the training set and completed EGD. The patients were divided into 2 groups: those with (DU group) and without DU (non-DU group). Data were collected from the 2 groups, and univariate and multivariate logistic regression analyses were used to compare the 2 groups. Children with HSP admitted between July 2022 and June 2023 were included in the validation set. Four indicators, prognostic nutrition index, albumin (ALB), gastrointestinal (GI) bleeding, and duration of onset before EGD, were found in the DU and non-DU groups. GI bleeding and prognostic nutritional index (PNI) ≤ 53.0 have strong predictability for patients with HSP and DU. GI bleeding and PNI ≤ 53.0 may provide new reference evidence for condition assessment and treatment.

Association of Polygenic Variants Involved in Immunity and Inflammation with Duodenal Ulcer Risk and Their Interaction with Irregular Eating Habits.

Genetic and environmental factors are associated with developing and progressing duodenal ulcer (DU) risk. However, the exact nature of the disease pathophysiology and the single nucleotide polymorphism (SNP)-lifestyle interaction has yet to be determined. The purpose of the present study was to examine the SNPs linked to DU risk and their interaction with lifestyles and diets in a large hospital-based cohort of Asians. Based on an earlier diagnosis, the participants were divided into the DU (case; n = 1088) and non-DU (control, n = 56,713) groups. The SNP associated with DU risk were obtained from a genome-wide association study (GWAS), and those promoted genetic impact with SNP-SNP interactions were identified with generalized multifactor dimensionality reduction analysis. The interaction between polygenic risk score (PRS) calculated from the selected genetic variants and nutrient were examined. They were related to actin modification, immune response, and cell migration by modulating leucine-rich repeats (LRR) domain binding, Shaffer interferon regulatory factor 4 (IRF4) targets in myeloma vs. mature B lymphocyte, and Reactome runt-related transcription factor 3 (RUNX3). Among the selected SNPs, rs11230563 (R225W) showed missense mutation and low binding affinity with different food components in the autodock analysis. Glycyrrhizin, physalin B, janthitrem F, and casuarinin lowered it in only wild CD6 protein but not in mutated CD6. Plastoquinone 8, solamargine, saponin D, and matesaponin 2 decreased energy binding affinity in mutated CD6 proteins. The PRS of the 5-SNP and 6-SNP models exhibited a positive association with DU risk (OR = 3.14). The PRS of the 5-SNP PRS model interacted with irregular eating habits and smoking status. In participants with irregular eating habits or smokers, DU incidence was much higher in the participants with high PRS than in those with low PRS. In conclusion, the genetic impact of DU risk was mainly in regulating immunity, inflammation, and actin modification. Adults who are genetically susceptible to DU need to eat regularly and to be non-smokers. The results could be applied to personalize nutrition.

Characteristics of gastric mucosa microbiota in children with chronic gastritis and duodenal ulcer

Objective: To investigate the differences of gastric mucosa microbiota between children with chronic gastritis and duodenal ulcer under the condition of Helicobacter pylori (Hp) infection. Methods: This prospective cohort study involved 57 children with Hp infection diagnosed by gastric endoscopy who were admitted to the Children's Hospital of Zhejiang University School of Medicine due to "abdominal pain, abdominal distension and vomiting" between January 2018 to August 2018. According to gastroscopy and pathological examination, the children were divided into chronic gastritis group and duodenal ulcer group. Gastric mucosa from Hp infected patients were sampled, and the flora DNA was analyzed by high-throughput sequencing. The statistical difference of α diversity, β diversity between two groups were analyzed. The relative abundance of the two groups in each taxonomic level was analyzed statistically. T test, Rank sum test or χ2 test was used for comparison between the two groups. Results: A total of 57 children diagnosed with Hp infection were enrolled in this study, including 42 cases of chronic gastritis (the age was (9.3±2.8) years, 22 males and 20 females) and 15 cases of duodenal ulcer (the age was (11.1±3.3) years, 9 males and 6 females). Alpha diversity index Chao and ACE in Hp infected chronic gastritis group were significantly higher than those in Hp infected duodenal ulcer group (217±50 vs. 183±64, t=2.088, P=0.009;218±47 vs. 192±76, t=1.566, P=0.016, respectively). The Beta-diversity index such as nonmetric multidimensional scaling (NMDS) analysis were significantly different in the two groups (analysis of similarity R=0.304, P=0.028). Among the main bacteria genera, there were 6 genera with significant differences between the two groups, which were Prevotella (0.190% (0.008%-1.983%) vs. 0.021% (0.005%-2.398%), Z=-2.537, P=0.011), Alloprevotella (0.097% (0.010%-0.813%) vs. 0.015% (0.003%-0.576%), Z=-2.492, P=0.013), Haemophilus (0.109% (0.004%-0.985%) vs. 0.014% (0.004%-0.356%), Z=-2.900, P=0.004), Neisseria (0.074% (0.004%-0.999%) vs. 0.024% (0.003%-0.255%), Z=-2.718, P=0.007), Streptococcus (0.166% (0.008%-1.869%) vs. 0.045% (0.006%-0.879%), Z=-2.537, P=0.010), and an unclassified-Microbacteriaceae (0.214% (0.060%-1.762%) vs. 0.117% (0.010%-0.954%), Z=-2.120, P=0.034). Linear discriminant analysis (LDA) effect sized analysis showed that at the genus level, only Prevotella was significantly enriched in the duodenal ulcer group (LDA=2.90, P=0.010), while Streptococcus, Neisseria and Haemophilus were significantly enriched in the chronic gastritis group (LDA=2.83, 2.82, 2.69, P=0.011, 0.007, 0.004, respectively). Conclusions: The gastric mucosal microbiota in duodenal ulcer associated with Hp is significantly different from that in chronic gastritis. Hp may promote the occurrence of peptic ulcer together with gastric microbiota.

MOLECULAR CHARACTERISTICS OF CAGA GENE EPIYA MOTIFS OF HELICOBACTER PYLORI AMONG PATIENTS WITH GASTRODUODENAL DISEASES

Background: cagA gene EPIYA motifs of H. pylori play an important role in the pathogenesis of gastroduodenal disease. This study is aimed at (1) Identify patterns of cagA gene EPIYA motifs ofH. pyloristrains from gastric biopsy specimens; (2) Investigate the association between cagA gene EPIYA motifs and gastroduodenal diseases. Patients and methods: Eighty-nine gastroduodenal disease patients infected with cagA-positive H. pylori were enrolled in this study. The patterns of cagA gene EPIYA motifs were determined by PCR. Result: cagA-positive H. pylori strains with East Asian-type EPIYA motif were predominant (89.9%), whereas strains with Western-type EPIYA motif accounted for only 10.1%. There were two strains with rare East Asian-type EPIYA, as -ABDBD and -AABD. In the duodenal ulcer group, the prevalence of East Asian-type and Western-type EPIYA motifs were 80% and 20%, respectively. Meanwhile, East Asian-type and Westerntype EPIYA motifs accounted for 95.8% and 4.2%, respectively in the gastric cancer group. Conclusion: cagA gene EPIYA motifs of cagA-positive H. pylori were quite diverse with the predominance of East Asian-type EPIYA motif. There were two rare motifs as -ABDBD and -AABD. The frequency of strains with East Asian-type EPIYA motif was highest in the gastric cancer group, whereas it was lowest in the duodenal ulcer group. Key words: Helicobacter pylori, cagA gene, EPIYA motif, gastroduodenal diseases

Long-term changes in the gut microbiota after 14-day bismuth quadruple therapy in penicillin-allergic children.

Penicillin-allergic children who are infected with Helicobacter pylori constitute a relatively common subgroup. We aimed to study the short-term and long-term effects of bismuth quadruple therapy on gut microbiota in penicillin-allergic children. We prospectively recruited treatment-naive children with Hpylori infection and Hpylori-negative asymptomatic children as healthy controls. Patients received 14-day bismuth quadruple therapy consisting of omeprazole, clarithromycin, metronidazole, and bismuth. Fecal samples were collected at weeks 0, 2, 6, and 52. Alterations in the gut microbiota were analyzed by 16S rRNA gene sequencing. Twenty-two subjects (14 gastritis patients, 8 duodenal ulcer patients) and 23 controls participated in this study. At week 2, alpha diversity was reduced in both gastritis (P<.05) and ulcer (except P=.16 with Chao 1 index) patients compared with baseline. Some changes persisted at week 6, and all were restored at week 52. Beta diversity was significantly altered 2weeks after treatment in the gastritis and duodenal ulcer groups (P=.001, P=.002, respectively) and restored at weeks 6 and 52. The mean relative abundance of Bacteroidetes (P<.001, P=.005, respectively) decreased and that of Proteobacteria increased (P<.001, P=.03, respectively). All alterations recovered at week 6 and 52. In both the gastritis and ulcer groups at week 2, some beneficial bacteria were decreased including Bacteroides (P<.001 and P=.003), Faecalibacterium (P<.001 and P=.02), Phascolarctobacterium (P=.002 and P=.004), Roseburia ( P<.001 and P=.13), Bifidobacterium (P=.08 and P=.04), and Blautia (P<.001 and P=.002). Some detrimental bacteria were increased including Escherichia-Shigella (P<.001 and P=.19), Klebsiella (P<.001, and P=.09), Enterococcus (P<.001 and P=.007), and Streptococcus (P=.002 and P=.004). The changes returned to almost the pre-eradication level 1year after therapy. Bismuth quadruple therapy causes short-term dysbiosis of the gut microbiota. Most changes recovered 1-year post-eradication, indicating the long-term safety of Hpylori therapy.

Carrying a 112 bp-segment in Helicobacter pylori dupA may associate with increased risk of duodenal ulcer

The discovery of Helicobacter pylori in 1983 challenged researchers around the world to identify this pathogen's major virulence factors. The main rationale for this kind of research was to identify a biomarker associated with specific diseases following H. pylori colonization. Among different investigated virulence factors, duodenal ulcer promoting gene A (dupA) has been found to be associated with duodenal ulcer (DU), but its effect was different in various geographical regions. To determine the prevalence of dupA, we applied both classic primer pairs and our newly developed primers producing a highly conserved segment in PCR method. In our survey, 143 (47%) H. pylori isolates were obtained from 304H. pylori-colonized individuals [age range of 19–92; 113 (37%) males with the mean age of 50 and 191 (63%) females with the mean age of 49]. The presence of the dupA gene was investigated by using the different specific primers. The prevalence of the 112 bp segment isolated from H. pylori strains recovered from DU, GU and atrophy groups were significantly higher (81%, p value = .002, 64%, p = .065, 68% and p = .047 38%, respectively) than our control group, where the prevalence of the 112 bp segment was only 38%. Interestingly, a significant relationship was observed between the occurrence of DU and the presence of the 112 bp segment [p = .002; OR: 6.98; (95% CI: 1.94–25.00)]. Taken as a whole, we believe the 112 bp region of H. pylori dupA may serve as the first detected biomarker for the early detection of DU in patients admitted to hospitals.

Duodenal Ulcer as a Postoperative Complication in the Donor in Living-Donor Liver Transplantation

IntroductionDonor safety is one of the most important factors in living-donor liver transplantation. Duodenal ulcer (DU) is a common postoperative complication. Here we aimed to reveal the risk factors associated with postoperative DU in the donors. MethodsBetween April 2007 and March 2017, 318 cases underwent donor hepatectomy for liver transplantation at Kumamoto University Hospital. We classified the donors into two groups: a DU group and a non-DU group. DU was defined as mucosal break with unequivocal depth requiring an endoscopic procedure. The characteristics and clinical factors of the donors were retrospectively analyzed. ResultsPostoperative DU occurred in 17 donors during the study period. The mean interval after donor hepatectomy to occurrence of DU was 124.8 ± 185.4 days. The two groups were comparable in terms of age at time of the donor hepatectomy (P = .45). The male-to-female ratio (P = .03) was significantly different between the two groups and left-side hepatectomy was performed more often in the DU group (P = .003). Multivariable logistic regression revealed that left-side hepatectomy was independently associated with postoperative DU in the donors. ConclusionsThese findings indicated that left-side hepatectomy is a risk factor for postoperative DU in the donors.

Can serum progranulin levels be a biomarker following gastric ulcer therapy?

IntroductionProgranulin is a novel growth factor that has several physiological and pathological roles such as cell growth, tumourigenesis, embryogenesis, wound healing, and inflammation.AimTo compare the pre-treatment and post-treatment serum levels of the angiogenic factor vascular endothelial growth factor (VEGF), pro-inflammatory cytokine tumor necrosis factor α (TNF-α), and progranulin in peptic ulcer (PU) patients with a healthy control group.Material and methodsSerum VEGF, TNF-α, and progranulin levels were studied with ELISA in 42 PU patients (antral ulcer (AU): 22, duodenal ulcer (DU): 20) and 15 healthy controls.ResultsThe serum progranulin levels before treatment were 4237.35 ±1091.30 pg/ml in the patients with AU, 4682.64 ±1501.46 pg/ml in the patients with DU, 3055.66 ±626.88 pg/ml in the control group, and 4460 ±1315 pg/ml in the ulcer (AU and DU) group. The serum progranulin levels were 3607.7 ±869.4 pg/ml in the AU group, 4286.5 ±1208.78 pg/ml in the DU group, and 3947.1 ±1094.64 pg/ml in the ulcer group after the treatment. When comparing pre-treatment serum progranulin levels of the AU group, DU group, and ulcer group with the control group there were statistically significant differences (p < 0.001, p < 0.0001, p < 0.0001, respectively).ConclusionsThe disappearance of the difference in terms of post-treatment serum levels of progranulin between the AU group and the control group suggests that serum levels of progranulin can be used as a biomarker of gastric ulcer healing.

Saussurea Lappa Modulates Gastrointestinal Motility, Motilin and Cholecystokinin Expression in Ulcer Rats

AIM : To investigate effects of Saussurea lappa (S.lappa) on rat chronic duodenal ulcer induced by ethylic acid and the underlying mechanisms. METHODS : Wistar rat chronic duodenal ulcer was patterned according to Okabe model while two pairs of bipolar stainless steel electrodes were implanted onto the serosal layer of gastrointestinal tract. Then, the rats were treated with water, Omeprazole, diverse-dose S.lappa for 10 days. Gastrointestinal motility, intestine propulsion and duodenal ulcer crater were detected. Expressions of cholecystokinin and motilin in duodenum were detected by immunohistochemistry (IHC). Motilin serum level was measured with enzyme-linked immunosorbent assay (ELISA). RESULT ：Duodenal ulcer group rats had obvious disorders of gastrointestinal motility and brain-gut peptide secretion, including gastrointestinal myoelectric activity inhibition, migrating myoelectric complex (MMC) interruption, intestinal propulsion slowdown, cholecystokinin and motilin secretion decrease. Similarity to Omeprazole, S.lappa accelerated the coalescence of ethylic acid–induced duodenal ulcer significantly (p<0.01, vs model group), but no obvious dose-dependent effect was found. S.lappa also improved gastrointestinal myoelectric activity and accelerated intestinal propulsion. Furthermore, S.lappa could increase the expression levels of cholecystokinin and motilin in duodenum and increase motilin level in serum. CONCLUSION ：S.lappa can accelerate the coalescence of chronic duodenal ulcer, and increase gastrointestinal myoelectric activity and the expression of cholecystokinin and motilin in duodenum.

Helicobacter pylori infection in Lhasa People's Hospital from 2009 to 2013

Objective To investigate the infection status of Helicobacter pylori (Hp) in a Lhasa hospital. Methods A retrospective survey of Hp infection from 2009 to 2013 was conducted in Lhasa People's Hospital. The data of 14C-urea breath test and gastroscopy were analyzed. Results A total of 2 908 patients were enrolled, 1 518 (52.20%) were Hp positive, including 1 061 males (1 061/1 939, 54.72%) and 457 females (457/969, 47.16%). The Hp infection rate in males was higher than that in females (χ2=14.788, P= 0.000). The Hp infection rate by years from 2009 to 2013 was 55.97%(267/477), 49.79%(239/480), 54.66%(375/686), 52.06%(291/559) and 49.15%(347/706), respectively. The infection rate in 2013 was significantly lower than that in 2009 and 2011 (P=0.021, 0.040). There were no significant differences in Hp infection rates among Tibetan, Han and Hui ethnic groups. In 2020 cases who underwent endoscopic examination, 1 098 had Hp positive (54.36%). The Hp infection rate in chronic superficial gastritis group(39.91%) was significantly lower than that in erosive gastritis (χ2=30.143, P=0.000), gastric ulcer (χ2=22.434, P=0.000), gastric polyps (χ2=9.627, P=0.002), gastric cancer (χ2=9.506, P=0.002), duodenal ulcer (χ2=54.158, P=0.000), duodenitis (χ2=14.966, P=0.000) and compound ulcer groups (χ2=8.582, P=0.003). The Hp infection rate in duodenal ulcer group(68.42%) was significantly higher than that in chronic superficial gastritis (χ2=54.158, P=0.000), erosive gastritis (χ2=6.733, P=0.009), atrophic gastritis (χ2=21.496, P=0.000) and gastric ulcer groups (χ2=8.940, P=0.003). Conclusion Hp infection rate appears a decreasing trend in Lhasa area in last 5 years; among various gastro-duodenal diseases patients with duodenal ulcer have a highest Hp infection rate. Key words: Helicobacter pylori; Gastrointestinal diseases; Retrospective studies

Vacuolating cytotoxin genotypes are strong markers of gastric cancer and duodenal ulcer-associated Helicobacter pylori strains: a matched case-control study.

The Helicobacter pylori virulence gene, cagA, and active forms of the vacuolating cytotoxin gene, vacA, are major determinants of pathogenesis. However, previous studies linking these factors to disease risk have often included patients using aspirin/nonsteroidal anti-inflammatory agents (NSAIDs) or acid-suppressing drugs, both of which may confound results. Also, particularly for gastric cancer (GC), controls have often been of quite different ages. Here, we performed a careful study in a "clean" Belgian population with gastric cancer cases age and sex matched to 4 controls and with a parallel duodenal ulcer (DU) group. As in other populations, there was a close association between the presence of cagA and the vacA s1 genotype. For GC, associations were found for vacA s1-positive (P = 0.01, odds ratio [OR], 9.37; 95% confidence interval [CI], 1.16 to 201.89), i1-positive (P = 0.003; OR, 12.08; 95% CI, 1.50 to 259.64), and cagA-positive status (P < 0.05; OR, infinity; 95% CI, 0.76 to infinity). For DU, associations were found with vacA s1 (P = 0.002; OR, 6.04; 95% CI, 1.52 to 27.87) and i1 (P = 0.004; OR, 4.35; 95% CI, 1.36 to 14.78) status but not with cagA status. Neither condition showed independent associations with the vacA m1 allele or with more biologically active forms of cagA with longer 3' variable regions. In this Belgian population, the best markers of gastric cancer- and duodenal ulcer-associated strains are the vacA s1 and i1 genotypes. This fits with experimental data showing that the s and i regions are the key determinants of vacuolating cytotoxin activity.

Prevalence, diversity and disease association of Helicobacter pylori in dyspeptic patients from Pakistan

The etiological association of Helicobacter pylori with gastric ulcer (GU), gastric cancer (GC), and duodenal ulcer (DU) is well-known. Understanding the epidemiology of H. pylori facilitates the estimation of disease burden in a certain population. This study presents the diversity of H. pylori genotypes and their association with different clinical outcomes among dyspeptic patients in Pakistan over a period of four years. Gastric biopsy samples from a total of 450 dyspeptic individualswere subjected to PCR, genotypingand histology. A total of 201 (45%) cases were found positive for H. pylori. The detection rate was high in GU (91%), DU (86%) and GC (83%) cases compared with those cases who had intact gastric mucosa (18%). Histology revealed the presence of infection in 68% of cases of mild/chronic nonspecific gastritis with others belonging to the GU sequel. cagA gene carriage was observed in 104 (51%) cases or mostly from DU, GU and GC groups, of which 97 were Western type strains while 3 were East-Asian type strains that are rarely observed in South Asia. vacA allelic variant s1am1 was most commonly observed, followed by s1am2, and s1bm1, with direct correlation in diseased cases (gastritis, GU, DU and GC). Prevalent genotypic combinations were s1am1/cagA- in gastritis and s1am1/cagA+ in DU, GU, and GC. Our study indicates the predominant circulation of Western type cagA and vacAs1am1 type H. pylori strains in Pakistan.

Circulating levels of interleukin (IL)-12 and IL-13 in Helicobacter pylori-infected patients, and their associations with bacterial CagA and VacA virulence factors

The aim of this study was to determine the association of the Helicobacter pylori virulence factors, cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) antibodies, with serum levels of interleukin (IL)-12 and IL-13 in H. pylori-infected duodenal ulcer (DU) patients and H. pylori-infected asymptomatic (AS) carriers in order to elucidate any correlation between them. A total of 67 DU patients, 48 AS individuals, and 26 healthy H. pylori-negative subjects were enrolled in this study. Serum concentrations of IL-12 and IL-13 were determined by enzyme-linked immunosorbent assay (ELISA) method. Patient sera were tested by Western blot method to determine the presence of serum antibodies to bacterial virulence antigens p120 (CagA) and p95 (VacA). Serum concentrations of IL-12 and IL-13 were compared in 9 groups, including 4 AS phenotypes (CagA⁺VacA⁺, CagA⁺VacA⁻, CagA⁻VacA⁺, CagA⁻VacA⁻), 4 DU phenotypes (CagA⁺VacA⁺, CagA⁺VacA⁻, CagA⁻VacA⁺, CagA⁻VacA⁻), and 1 control group. The results revealed that DU patients positive for CagA, independent of the anti-VacA antibody status, showed drastically elevated levels of IL-12 (251 ± 43 pg/ml) when compared with the other groups (p = 0.0001). No significant difference was found between groups regarding levels of IL-13 (p > 0.05). Our findings indicate that in the DU group, the serum concentrations of IL-12 but not of IL-13 were influenced by bacterial CagA, independent of the VacA status, suggesting that high IL-12 levels may contribute to susceptibility to DU in CagA-positive individuals. These findings could possibly be considered to improve the predictive or prognostic values of inflammatory cytokines for DU, and also to design possible novel therapeutic approaches.

Circulating interleukin-27 levels in Helicobacter pylori-infected patients with gastric or duodenal ulcers, independent of the bacterial cytotoxin-associated gene A virulence factor

The aim was to evaluate the interleukin (IL)-27 levels in Helicobacter pylori (H. pylori)-infected patients with gastric ulcer (GU) or duodenal ulcer (DU) and to determine its association with H. pylori virulence factor cytotoxin-associated gene A (CagA). In all, 127 H. pylori infected patients (including 96 DU patients, of whom 61 were anti-CagA(+) and 35 were anti-CagA(-)) and 31 GU patients (of whom 15 were anti-CagA(+) and 16 were anti-CagA(-)), 60 asymptomatic (AS) carriers (of whom 30 were anti-CagA(+) and 30 were anti-CagA(-)) and 30 healthy H. pylori-negative participants (as a control) were enrolled in the study. Serum concentrations of IL-27 were measured by the enzyme-linked immunosorbent assay method. The mean levels of IL-27 in the GU (44.26 ± 7.12 pg/mL) and DU patients (40.84 ± 3.90 pg/mL) was significantly higher than those observed in the AS carriers (22.06 ± 1.90 pg/mL, P < 0.001) and the control group (18.12 ± 1.68 pg/mL, P < 0.001 and P < 0.002, respectively). In the GU, DU and AS groups the levels of IL-27 in anti-CagA(+) participants were not significantly differ from that in the anti-CagA(-) participants. These results showed that the mean concentration of IL-27 in H. pylori-infected peptic ulcer (PU) patients was higher than in AS carriers and the healthy control group. The serum concentrations of IL-27 were not affected by the CagA factor.

Associations of the IL‐1 and TNF gene polymorphisms in the susceptibility to duodenal ulcer disease in Chinese Han population

Our aim was to investigate whether genetic polymorphism of IL-1Beta-511, IL-1RN, TNF-A-308 are involved in the susceptibility to duodenal ulcer (DU). 437 unrelated Chinese Han patients with DU and 148 healthy controls were genotyped by the polymerase chain reaction-restriction fragment length polymorphism method for the IL-1B-511, TNF-A-308 gene polymorphisms and the VNTR polymorphism in intron 2 of the IL-1RN gene polymorphisms. There was no difference in the genetic polymorphism of IL-1Beta-511, IL-1RN and TNF-A-308 in the patients with DU compared with control. After stratified by Helicobacter pylori infection, they also could not reach significant differences in this study. No statistically significant differences were observed in DU group compared with control according to combination of the IL-1Beta-511 and IL-1RN genotypes regardless of H. pylori positivity. These findings show that no evidence for the involvement of a proinflammatory polymorphism in the IL-1Beta-511, IL-1RN and TNF-A-308 in the susceptibility to DU in China.

5- EVALUATION OF ENDOSCOPY BASED METHODS (HISTOPATHOLOGY, CYTOLOGY AND UREASE TEST) FOR THE DETECTION OF HELICOBACTER PYLORI

This study aimed to assess the accuracy of histopathology, brush cytology, and urease test in the diagnosis of Helicobacter pylori and to evaluate the effect of test duration on the sensitivity and specificity of positive urease test for the detection of H. pylori. Fifty patients [25 patients with gastritis group A and 25 patients with duodenal ulcer group B] selected from those attending endoscopy unit for dyspeptic symptoms, were enrolled in the study. Four endoscopic biopsies were taken from each patient. One biopsy from each of antrum and body were obtained for urease test (Urease test was read at 30 min, 1, 4 and 24 hour after biopsy insertion into the reagent), and one biopsy from each of antrum and body were used for histopathological examination. Antral brush cytology was taken also from each patient. The patients were considered H. pylori positive when minimum concordances of 2 out of 3 tests (Histopathology, brush cytology, and urease test) were positive. Fourteen patients were positive for H. pylori in group A, in comparison to seventeen patients in group B. The sensitivities of the histopathological examination, brush cytology, and urease test at 24 hours in group (A) were 58%, 79%, and 93% respectively. Corresponding figures for the specificity were 100%, 91%, and 46% respectively. While in group (B) the sensitivities were 82%, 82%, and 100% and the specificities were 100%, 100%, and 88% respectively. It is concluded that among the invasive methods, the association of the urease test with brush cytology constituted the best choice for confirming the diagnosis of H. pylori, due to the high sensitivity of the urease test and high specificity of brush cytology.

Association of the CagA status of Helicobacter pylori and serum levels of interleukin (IL)‐17 and IL‐23 in duodenal ulcer patients

It has been reported that the cytotoxin-associated gene A (cagA+) H. pylori strains induce severe gastric mucosal inflammation. The aim of this study was to investigate the association of the virulence factor CagA with IL-17 and IL-23 serum levels in duodenal ulcer (DU) patients and H. pylori-infected asymptomatic (AS) carriers. In total, 45 H. pylori-infected DU patients were enrolled to study: 23 tested positive for the anti-CagA antibody (anti-CagA+) and 22 tested negative for the anti-CagA antibody (anti-CagA-), 30 were AS carriers (15 were anti-CagA+ and 15 were anti-CagA-) and 15 were healthy uninfected participants (as a control group). The IL-17 and IL-23 serum levels of participants were measured by enzyme-linked immunosorbent assay method. The mean IL-17 levels in DU patients were significantly higher than those in AS and control groups (P < 0.001 and P < 0.0001 respectively). In the DU group, the mean IL-17 levels in participants testing positive for anti-CagA (10.84 +/- 5.79 pg/mL) were significantly higher than those observed in participants testing negative for anti-CagA (7.65 +/- 4.74 pg/mL; P < 0.05). The mean IL-23 levels in the DU and AS groups were significantly higher than in the control group (P < 0.02 and P < 0.03 respectively) but were not significantly different in participants testing positive and negative for anti-CagA. These results showed higher IL-17 and IL-23 serum levels in H. pylori-infected participants than in the control group. In the DU group the expression of IL-17 was influenced by the CagA factor.

C314T polymorphism in histamine N-methyltransferase gene and susceptibility to duodenal ulcer in Chinese population

BackgroundHistamine is a regulator of gastric acid secretion, which is involved in the development of duodenal ulcer (DU). Histamine is metabolized by both histamine N-methyltransferase (HNMT) and diamine oxidase, and its local action is terminated primarily by methylation which is catalyzed by HNMT. MethodsPolymerase chain reaction-restriction fragment length polymorphism assay was used to identify the polymorphism of the point mutation C314T of HNMT gene of 498 Chinese patients with DU and 151 healthy individuals. ResultsIn normal controls, the allele frequency of HNMT T314 was 3.3%, which was significantly lower than American Caucasians. The HNMT T314 allele was detected in 3.5% of the DU patients. In cases and controls, the frequency of C/C genotypes were 93.0% and 93.4%, respectively. The HNMT T/T genotype was not found in this population. No significant differences were seen in both genotype frequencies and allele frequencies between DU groups and controls. After stratified by H. pylori infection, they also could not reach significant differences in our current study. ConclusionThe HNMT T314 allele frequency is lower in Chinese population than in American Caucasians. No association can be found in the involvement of HNMT C314T polymorphism in the susceptibility to duodenal ulcer.

Screening of atrophic gastritis and gastric cancer by serum pepsinogen, gastrin‐17 and Helicobacter pylori immunoglobulin G antibodies

Currently the screening and diagnosis of gastric cancer and atrophic gastritis are mainly made by endoscopy and biopsy. The aim of this study was to evaluate the use of serum tests: serum pepsinogen I (PGI pepsinogen I/II ratio (PGR), gastrin-17 (G-17) and H. pylori-immunoglobulin G (IgG) antibodies to screen atrophic gastritis and gastric cancer. A total of 458 patients were recruited, and each underwent endoscopy with biopsies before the serum tests were performed. These patients were divided into five groups based on the endoscopic and histological findings: 92 patients in the atrophic gastritis group, 58 in the gastric ulcer group, 90 in the duodenal ulcer group, 141 in the gastric cancer group (40 early gastric cancer and 101 advanced gastric cancer) and 77 (including mild non-atrophic gastritis) served as a control group. Serum samples for PGI and II, G-17, and H. pylori-IgG antibodies estimation were analyzed by ELISA. PGI and PGR values decreased significantly both in atrophic gastritis and gastric cancer groups (P<0.01). For the best discrimination of atrophic gastritis, the cut-off values of PGI and PGR were 82.3 microg/L and 6.05, respectively. The PGI, PGR and G-17 values were related significantly with the grades and/or sites of atrophic gastritis (P<0.01). Patients with atrophic corpus gastritis had low PGI and PGR values and high G-17 level, and patients with atrophic antral gastritis had low G-17 level. G-17 increased significantly in the gastric cancer group (P<0.01). PGI and PGR values were significantly lower in patients with advanced gastric cancer than in patients with early gastric cancer, while there was no difference in G-17 level between them. The positivity rate of H. pylori-IgG antibodies was 54.55% in the control group. The PGI level was higher in H. pylori positive patients than in H. pylori negative ones (P<0.001), while there was no difference in G-17 level between them. The positivity rates of H. pylori-IgG antibodies were over 85% in all other four groups. Low serum PGI, PGR and G-17 values are biomarkers of atrophic antral gastritis. Atrophic be screened by serum PGI and PGR values. Gastric cancer can be screened on the basis of increased serum G-17 and remarkedly low serum PGI and PGR values. The H. pylori infection is related to the change of PG level.

Superoxide dismutase phenotypes in duodenal ulcers: A genetic marker?

Background: Cu-Zn superoxide dismutases are antioxidative defensive enzymes that catalyze the reduction of superoxide anions to hydrogen peroxide. Aim: The study focuses on the association of electromorph of superoxide dismutase with duodenal ulcers, which result due to an imbalance between aggressive and defensive factors. Materials and Methods: Endoscopically confirmed 210 duodenal ulcer patients and 185 healthy individuals for comparative analysis were considered for the present study. Phenotyping of superoxide dismutase was carried out by subjecting the RBC membranes to polyacrylamide gel electrophoresis, using appropriate staining protocols. Results: Statistical analysis of SOD phenotypes revealed a significant increase of SOD A*2 allele and Superoxide dismutases (SOD) 2-2 phenotype in duodenal ulcer group. Among these individuals, a predominance of Helicobacter pylori infection was observed. The increased preponderance of homozygotes can be explained on the basis of reduced and altered enzyme activity, which may lead to disturbance in homeostasis of antioxidant/oxidant culminating in high lipid peroxidative gastric mucosal tissue damage and ulceration. No variation in the distribution of SOD phenotypes with respect to Helicobacter pylori indicates the role of Mn-SOD rather than Cu-Zn SOD in the Helicobacter pylori infected cases as reported earlier. Conclusions: Superoxide dismutase as a genetic marker / gene modifier, encoding for an antioxidant enzyme in maintaining tissue homeostasis of the gastric mucosa is discussed.