Helicobacter pylori Infection in Endoscopic Biopsy Specimens of Gastric Antrum: Laboratory Diagnosis and Comparative Efficacy of Three Diagnostic Tests

Aims and objectives The present study was undertaken to compare the diagnostic yield of three available test procedures for detecting Helicobacter pylori (H. pylori) infection in endoscopic biopsies.Methods H. pylori infection was sought in 150 patients referred for upper gastrointestinal (GI) endoscopy. Multiple (about six) biopsy specimens were taken from pyloric antrum in each patient. Two biopsy specimens were subjected to one minute endoscopy room test - OMERT (a modified form of urease test), two were sent for histopathological analysis, where multiple sections were subjected to Giemsa staining and two were sent for microbiological evaluation after Gram's staining of heat fixed biopsy material.Results H. pylori positivity using histology, microbiology and OMERT was observed to be 33%, 30% and 27% respectively. However, overall 40% patients were infected when the results from three test procedures were combined, as H. pylori positivity was repeated more than once by these procedures separately. Histology was found to be superior to other two tests in our study, especially when multiple sections were examined, for the distribution of the organism was patchy. Amongst the infected, H. pylori was seen in only 30% of all 3-8 sections cut from a biopsy, whereas in 70% it was noted in a single section only.Conclusion The study revealed that histology has the highest detection rate and can be chosen as the "gold standard" amongst the three low cost test procedures available at present in our setup.     

消化性溃疡幽门螺杆菌(Hp)清除前后血Hp抗体、PG、GAS 变化的研究

幽门螺杆菌(Helicobacter pylori,Hp)阳性消化性溃疡患者在Hp清除前后血清抗Hp-IgG,抗Hp-IgM,胃蛋白酶原(Pep-sinogen,PG)和胃泌素(Gastrin,GAS)水平如何?奥美拉唑,硫糖铝,罗红霉素治疗Hp感染的消化性溃疡的效果如何?本课题对上述问题进行了研究。1材料与方法1.1一般资料病例选     

Frequencies of serum antibodies to Helicobacter pylori CagA and VacA in a Turkish population with various gastroduodenal diseases

Infection with Helicobacter pylori (H. pylori) strains secreting cytotoxin-associated gene A (CagA) and vacuolating cytotoxin A (VacA) proteins is associated with more severe gastroduodenal pathologies. However, this association varies among geographical regions and ethnic groups. We investigated the frequencies of antibodies to CagA and VacA proteins in 131 H. pylori-infected dyspeptic patients [40 duodenal ulcer (DU), 19 gastric ulcer (GU), 28 gastric cancer (GC), and 44 non-ulcer dyspepsia (NUD)] across 30 H. pylori-infected and endoscopically normal asymptomatic subjects (AS). Anti-CagA and anti-VacA antibodies were detected by Western blotting. The positivity rates of anti-CagA and anti-VacA antibodies were higher in patients with DU (92.5 and 75%), GU (89.5 and 84.2%) and GC (96.4 and 85.7%) than patients with NUD (70.5 and 50%) and AS (50 and 23.3%) (p < 0.05). CagA+ VacA+ phenotype was more frequent in patients with DU, GU and GC than patients with NUD and AS (75, 84.2, 85.7 vs. 47.7 and 20%, respectively) (p < 0.01). Our results showed that there is a significantly positive association between the presence of anti-CagA and anti-VacA antibodies and DU, GU and GC in our region.     

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

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

Association between Helicobacter pylori genotypes and gastric disorders in relation to the cag pathogenicity island

Helicobacter pylori is a bacterium associated with upper gastrointestinal diseases in humans. However, only a small proportion of infected people become sick. Although several studies have tried to establish an association between known virulence markers and clinical outcomes, in many cases the results have been conflicting. The aim of this study was to investigate the importance of virulence markers to predict clinical outcome in Brazil. Mixed infections by genetically unrelated strains detected by vacA genotyping were found in 18% of the patients. The cagA and cagE genes and the vacAs1 genotype were associated with the development of peptic ulcer disease (PUD). The cagAvacAs1m1 genotype was associated with PUD and duodenal ulcer (DU). Conversely, jhp947 was not associated with DU or PUD, indicating that this gene is not a universal virulence marker. These results also show that a high proportion of the patients were simultaneously infected by cag-positive and cag-negative H. pylori types. This finding suggests the existence of a dynamic equilibrium between the loss and gain of the cag pathogenicity island, probably depending on the physiologic conditions of the patient's stomach. To the best of our knowledge, this is the first study that has documented this finding in Brazil.     

Long-term endoscopic follow-up for peptic ulcer patients after eradication of H. pylori; comparison with the maintainance therapy by H2-blocker

This study was aimed to clarify the endoscopic findings and the decline of serum IgG titer after successful eradication of H. pylori in long-term (from 2 to 7 years). Forty-six H. pylori-positive peptic ulcer (22 GU and 26 DU) cases were eradicated with antimicrobial therapy. Sixty-nine non-eradicated DU cases who received maintainance therapy with H2-blocker were control group. Biopsy urease test (BUT) and culturing was performed to diagnose the H. pylori infection. Anti-H. pylori IgG titer (EIA) were also measured in some cases, pre and 6, 12, 24 months after the eradication. In 3 cases, H. pylori were recrudescent and only in a case, DU recurred during 5 years after eradication. Meanwhile, in 55% of control cases, DU were recurred during same periods. In 62% of eradicated cases, serum IgG-antibody to H. pylori declined below the cut-off level during 2 years after eradication. It was certified that eradication therapy against H. pylori prevents ulcer recurrence for long time, and re-rise of serum IgG titer to H. pylori might predict a recrudescence of infection.     

Medical treatment of peptic ulcer disease.

Our understanding of PUD and its treatment has improved dramatically during the past 15 years. During this time, many new effective drugs have been approved by the FDA, and possibly even more potent and effective therapies are now being evaluated. The H2-blockers, sucralfate, and antacids heal over 90% of duodenal ulcers in 6 to 8 weeks, and H2-blockers heal about 80% of gastric ulcers by 8 weeks and over 90% by 12 weeks. The new, more potent pump blockers (omeprazole) promise to be even more effective drugs, even for the healing of patients who are taking NSAIDS. However, the potential hazards of marked, long-term acid suppression must still be evaluated. Maintenance therapy with H2-blockers or sucralfate, ideally used for patients who would otherwise have frequent symptomatic recurrences of duodenal ulcer disease or who have had complications, reduces the relapses, especially symptomatic relapses. Maintenance therapy with H2-blockers also seems to reduce the recurrences of GUD, but this use has not yet received FDA approval. Elimination of H. pylori infection with antibiotics may prove to reduce recurrent ulcer disease and negate the need for maintenance therapy. Colloidal bismuth subcitrate alone, which suppresses but does not eradicate H. pylori infection, seems to be an effective ulcer drug and may even reduce the rate of early recurrences. Effective ulcer therapy, especially if it prevents recurrent disease, may reduce the complications of PUD, but this expectation has yet to be established. The use of prophylactic cytoprotective prostaglandins (misoprostol) reduces the incidence of NSAID-induced GUD.     

Blood flow and morphofunctional status of gastroduodenal mucosa in different phases of peptic ulcer

AIM: To investigate gastric and duodenal mucosal blood flow (MBF) in different phases of gastric ulcer (GU) and duodenal ulcer (DU) and its relation both to Helicobacter pylori (HP) infection and mucosal disorders. MATERIAL AND METHODS: Upper endoscopy and histological examinations (score of inflammation, atrophy, metaplasy) were performed in 407 patients with DU and 103 with GU. Gastric and duodenal MBF were assessed by the hydrogen gas clearance technique in 102 DU and 95 GU patients. HP was detected by histology. Gastric secretion was measured in the interdigestive period and after stimulation by pentagastrin. RESULTS: Lowering of MBF in gastric antrum and duodenum was observed in DU and GU patients only with score 3 of HP infection. DU healing is accompanied with a decrease of HP value and improvement of mucosal histology. At the same time MBF exhibits a significant rise: in the duodenum (by 45%) at the stage of white scar; in gastric antrum (by 26%) and body (by 40%) at healing stage, but a decrease in white scar. During healing of GU gastric MBF reached maximum in active ulcer but in white scar MBF was significantly lower. MBF at ulcer margin and MBF in ulcer crater was the same (30 ml/min/100 g) with MBF in the region of white scar with enhanced inflammation (score 2.1) before GU relapse. CONCLUSION: Changes of MBF in different phases of ulcer are, in part, determined both by HP and by mucosal morphological disorders. The ratio MBF increase in ulcer healing/MBF reduction in ulcer relapse is the same (30% from optimal) and it is restitution entity. The MBF level of 30 ml/min/100 g was assessed as crucial in ulcerogenesis. Lowering MBF in mucosa with remaining inflammation in the scar region may predict GU relapse.     

Helicobacter pylori associated antral gastritis in peptic ulcer disease patients and normal healthy population of kashmir, India

Aim: To study the association of Helicobacter pylori infection with chronic antral gastritis in peptic ulcer disease patients and healthy population of Kashmir.Methods: 50 peptic ulcer patients (duodenal ulcer = 46, gastric ulcer = 2 and combined duodenal and gastric ulcer = 2) and 30 asymptomatic healthy volunteers were included in this study. Peptic ulcer was diagnosed on endoscopic examination. 4-6 punch biopsies were taken from gastric antrum in all the individuals and in case of gastric ulcer an additional biopsy was taken from the edge of the ulcer to exclude its malignant nature. Helicobacter pylori (H. pylori) organism was diagnosed using three different test methods, viz. Histology (using Giemsa Stain), Microbiology (Gram Stain) and Biochemistry (using one minute Endoscopy Room Test). Histological diagnosis of H. pylori was taken as the "gold standard" for the presence of H. pylori organism. Histological diagnosis of gastritis was made using Hematoxylin and Eosin Stain and the gastritis was classified as active chronic gastritis and superficial chronic gastritis.Results: Out of 30 peptic ulcer disease patients with associated antral gastritis, 27 (90%) were positive for H. pylori on histological examination (13 superficial chronic gastritis and 14 active chronic gastritis) whereas out of 8 healthy volunteers with histological evidence of chronic antral gastritis, H. pylori was observed in 7 individuals (87.50%) (4 active chronic gastritis and 3 superficial chronic gastritis).Conclusion: A highly significant association between H. pylori infection with chronic antral gastritis both in peptic ulcer disease patients and healthy volunteers of Kashmir was found in this study. Association between H. pylori infection and chronic gastritis was 90% in peptic ulcer group and 87.50% in healthy population (P<0.005).     

Phospholipase C activity of Helicobacter pylori is not associated with the presence of the cagA gene

BACKGROUND: Knowledge about the possible role of phospholipase C (PLC) activity of microbial pathogens in the development of disease is increasing. Recently attention has focused on investigating PLC activity elaborated by Helicobacter pylori, but the role of this enzyme in H. pylori pathogenesis is still unknown. The aim of this study was to correlate PLC-activity of H. pylori on the basis of the cagA status with the clinical diagnosis of the patients. MATERIALS AND METHODS: Helicobacter pylori was isolated from patients with gastritis (G; n = 38), duodenal ulcer (DU; n = 15), gastric ulcer (GU; n = 11) and gastric cancer (GC; n = 12). Polymerase chain reaction primers DZ3/R009 which amplified a 1350-bp fragment were used to detect the cagA gene. PLC activity was determined using p-nitrophenylphosphorylcholine as substrate. RESULTS: Of the strains, 60% were cagA(+) and 40% were cagA(-). All strains showed PLC activity (2.20 +/- 0.91 U mg(-1) protein). PLC activity showed no association with the cagA status: cagA(+) (2.21 +/- 1.03 U mg(-1) protein), cagA(-) (2.18 +/- 0.79 U mg(-1) protein). Patients with GU had the highest PLC activity (2.77 +/- 1.26 U mg(-1) protein) and patients with GC had the lowest activity (1.8 +/- 0.57 U mg(-1) protein). CONCLUSIONS: Although PLC activity was present in all strains tested, it may only have pathological importance in patients with GU. However, the extent of PLC activity was independent of the presence of the cagA gene.     

Helicobacter pylori Infection in Various ABO Blood Groups of Kashmiri Population

Aim: This study was carried out to assess the prevalence of Helicobacter pylori infection in various ABO blood groups of people of Kashmir.Method: The study comprised 80 individuals - 50 peptic ulcer patients (whose disease was diagnosed by endoscopy) and 30 asymptomatic volunteers. Every subject's blood group and Rhesus status was determined by standard serological tests. Helicobacter pylori infection was diagnosed by three different methods viz., one minute endoscopy room test (urease test), Gram staining and by histology. The detection of Helicobacter pylori by histological examination using Giemsa staining was taken as the 'gold standard' for the presence of Helicobacter pylori infection.Results: Out of 80 individuals, 67 were males and 13 females aged between 18-65 years. The majority of peptic ulcer patients had blood group 'O' (n = 28.56%). The prevalence of Helicobacter pylori infection amongst peptic ulcer patients was 76%. There was no difference in Helicobacter pylori positivity in various blood groups.Conclusion: Blood group 'O' though a risk factor for peptic ulcer (Duodenal ulcer) is not a risk factor for acquiring Helicobacter pylori infection.     

老年人消化性溃疡与慢性萎缩性胃炎的相关性研究

目的研究老年人消化性溃疡与慢性萎缩性胃炎的相关性。方法对十二指肠溃疡（DU）、胃溃疡（GU）和复合性溃疡（CU）的老年患者胃窦、胃窦胃体交界处和胃体黏膜以及慢性胃炎（CG）患者胃窦黏膜活检标本进行组织学检查,统计各自胃黏膜的萎缩、肠化生、慢性炎症、活动性和幽门螺杆菌（Hp）感染的发生率。结果 DU患者胃窦、胃窦胃体交界处和胃体黏膜的萎缩发生率分别为54.0%、8.0%和16.0%,肠化生发生率分别为19.0%、6.0%和4.0%。其胃窦黏膜肠化生的发生率明显低于相应的GU、CU或CG者。3种消化性溃疡和CG患者均存在胃窦部慢性炎症,且老年消化性溃疡患者胃体部炎症的发生率较高,其胃炎活动性以胃窦部为主,且均较CG者高。结论老年人消化性溃疡均可有胃窦部灶性萎缩和肠化生发生,但DU胃窦黏膜肠化发生率最低,这可能是老年DU患者罹患胃癌危险性较低的原因之一。     

老年人消化性溃疡166例胃镜分析

目的了解我院老年人消化性溃疡（Pu）发病特点。方法分析166例老年人消化性溃疡胃镜报告结果。结果老年人PU的检出率为10.78％,男女之比为4.35：1;胃溃疡（GU）占62.65％,十二指肠溃疡（DU）占30.72％,GU与Du之比为2.08：1,复合性溃疡占6.62％,多发性溃疡占24.1％。结论老年人PU的患者男性多于女性,Gu多于DU,GU的好发部位是胃窦和胃角,DU的好发部位是十二指肠球前壁;PU的幽门螺杆菌（Hp）感染率为81.93％。     

Factors affecting efficacy of proton pump inhibitors in NAID-induced gastric ulcers

AIM: To determine factors which may influence efficacy of therapy with proton pump inhibitors (PPI) in gastric ulcer (GU) induced by nonsteroid anti-inflammatory drugs (NAID). MATERIAL AND METHODS: Two groups of GU patients treated with PPI in 2001-2005 were identified: 41 cases when ulcer healing was not achieved for 3 weeks and more (study group) and 218 cases treated for this time successfully (controls). The groups did not differ significantly by gender (females 84.6 and 78.6%) and age (59.2 +/- 16.8 and 58.7 +/- 12.4 years). RESULTS: The patients of the study group had ulcers of 10 mm and more in size much more frequently than the controls (OR 12.5, CI 5.8-26). Also, rheumatoid arthritis (RA), ulcer history, intake of glucocorticosteroids, cytotoxic drugs, ineffective preventive treatment with PPI (OR 5.3, CI 3.4-8.4; OR 3.1, CI 1.5-6.0; OR 3.1, CI 1.6-6.0; OR 3.4, CI 1.7-6.7; OR 2.7, CI 1.3-5.6, respectively) were recorded in the study group more often. Helicobacter pylori was absent in 75.6% patients of the study group but these findings can not be compared with those in the controls as the majority of them had not been examined for gastric H. pylori. CONCLUSION: Large ulcer, RA, ulcer history, treatment with GCS, cytotoxic drugs, PPI and, probably, the absence of H. pylori decrease efficacy of PPI in gastric ulcer induced by NAID.     

Genotyping of Helicobacter pylori strains from gastric biopsies by multiplex polymerase chain reaction. How advantageous is it?

Recent application of multiplex polymerase chain reaction (PCR) for genotyping Helicobacter pylori direct from biopsies revealed variable results (detection of amplicons from DNA extracted by boiling biopsies, variable size amplicons and deletions, uniform intensity of amplicon bands). We aimed to look at how applicable the technique is for determining cagA and vacA genotypes and to correlate the results with the severity of the disease. H. pylori strains from 52 patients (35 duodenal ulcers [DUs], 7 gastric ulcers [GUs], 10 gastritis) were included. Three antral biopsies were obtained for Campylobacter-like organism (CLO) and PCR. Primers for cagA, vacA s1s2, and m1m2 alleles were used. No PCR amplicons were detected from boiling biopsies; thus, DNA was extracted by QIAamp kit. H. pylori was positive in 84.6% of the patients (85.7% DU, 100% GU, and 70% gastritis). The cagA gene was detected in 86.6% DU, 71.4% GU, and 57.0% gastritis patients. The vacA allelic distribution among cagA-positive strains was 80.7% s1m1 in DU and 60.0% in GU patients, whereas 75.0% of gastritis had s1m2. No variability in the amplicon sizes was found, and the intensity of the amplicon bands was not uniform. A deleted band of approximately 420 bp below the m1 band was detected in strains from 2 DU and 1 GU patients. Although the multiplex PCR is a rapid and an effective tool for detecting several genes in a single-step system, one has to adjust for optimization of the technique when genotyping H. pylori direct from biopsies. A significant association was found between the cagA-positive vacA-s1m1 genotype and peptic ulcers.     

Strategies for peptic ulcer healing after 1 week proton pump inhibitor-based triple Helicobacter pylori eradication therapy in Japanese patients: differences of gastric ulcers and duodenal ulcers

Helicobacter pylori (H. pylori) eradication therapy alone is insufficient to ensure healing of large ulcers with H. pylori-positive gastric ulcer (GU). The question of what is the optimum antiulcer treatment following H. pylori eradication therapy has not been fully elucidated. Furthermore, the ulcer healing effects of eradication therapy itself with H. pylori-positive duodenal ulcer (DU) have not been investigated. In GU study, the eradication therapy + proton pump inhibitor (PPI) group (group A) were administered eradication therapy followed by 7 weeks of a PPI, and the eradication therapy + gastroprotective drug (GP) group (group B) eradication therapy followed by 7 weeks of a GP. In DU study, the eradication therapy + PPI group (group C) were administered eradication therapy followed by 5 weeks of a PPI, and the eradication therapy only group (group D) was eradication therapy alone. In GU study, healing rates for ulcer of ≥15 mm in diameter were significant greater in the group A. In DU study, high healing rates were seen both the group C and D. In conclusion, a PPI could significantly heal GU than a GP after eradication therapy in GU. Meanwhile, the eradication alone is sufficient for DU.     

湖南地区幽门螺杆菌CagA基因3’端多态性与胃小二指肠疾病的关系

目的 探讨湖南地区幽门螺杆菌（Helifcobacter Hpylori）细胞毒素相关基因（CagA基因）3＇端可变区序列特征及其与胃十二指肠疾病的关系.方法 本地区有明显上消化道症状患者235例,其中慢性胃炎（CG）57例,胃溃疡（GU）62例,十二指肠溃疡（DU）70例,胃癌（GC）46例.于胃镜检查时用灭菌活检钳取胃窦组织1块,分离培养出H.pylori 89株,用PCR法对上述菌株的CagA基因扩增及测序,并通过生物信息学软件进行多重序列比对和相似性分析.结果 H.pylori培养阳性率为37.9%（89/235）,其中H.pylori CagA阳性者占91.7%（77/84）,GU组、DU组和GC组CagA阳性率高于CG组,其差异有统计学意义（P〈0.05）.77株H.pylori CagA基因3＇端均具有3个EPIYA重复序列,其中第2个EPIYA序列存在3种突变型,占18.2%（14/77）.H.pylori CagA基因3＇端序列特征以东亚型为主,占88.3%（68/77）,东亚型的CagA阳性菌株在GU组、DU组及GC组高于CG组（P〈0.05）.所有东亚型CagA阳性菌株CagA序列特征类似于Yamaoka报道的A型.结论 湖南地区H.pylori CagA阳性菌株以东亚型为主,均具有3个EPIYA重复序列,其中第2个序列存在3种突变型,其与消化性溃疡和胃癌发生有关.     

Serum IL-8 as a possible marker for determining the status of<Emphasis Type="Italic">Helicobacter pylori</Emphasis> infection in patients with untreated and treated peptic ulcer

Failure to eradicateHelicobacter pylori can lead to peptic ulcer recurrence and gastric malignancy. Therefore, the objective of this study was to develop a noninvasive method for determining whetherH pylori infection was eradicated with antibiotic-based triple therapy. A total of 17 patients with duodenal ulcer (DU) and 17 with gastric ulcer (GU) were evaluated both before and after treatment. Outcomes included serum levels of interleukin-8 (IL-8), pepsinogen I, and gastrin, and the Wilcoxon signed rank test was used to test significance. Changes in these parameters were also correlated with disease status. In those patients where both GU and DU healing occurred as a result of treatment, most showed an increase in serum IL-8 and a decrease in serum pepsinogen. Serum gastrin levels were not significantly changed in either group. Posttreatment increases in serum IL-8 were seen in 15 of 17 (88%) recovered DU patients and 14 of 17 (82%) recovered GU patients (P < .05 for each). Posttreatment decreases in pepsinogen I were found in 15 of 17 DU and 15 of 17 GU patients (P < .05 for each). These preliminary findings suggest that an increase in serum IL-8 and possibly a decrease in pepsinogen I may be useful in identifying the successful eradication ofH pylori infection in patients with peptic ulcer treated with antibiotics. A more systematic analysis of these putative diagnostic markers is now warranted.     

Is ranitidine therapy sufficient for healing peptic ulcers associated with non‐steroidal anti‐inflammatory drug use?

Long-term use of non-steroidal anti-inflammatory drugs (NSAIDs) increases the risk of serious gastroduodenal events. To minimise these risks, patients often require concomitant acid-suppressive therapy. We conducted a literature review of clinical trials examining use of ranitidine 150 mg twice daily to heal gastroduodenal ulcers (GU) in NSAID recipients. Seven studies were identified. After 8 weeks' treatment with ranitidine, GU healing rates ranged from 50% to 74% and rates of duodenal ulcer (DU) healing ranged from 81% to 84%. Ranitidine was more effective when NSAIDs were discontinued (healing rates reaching 95% and 100%, respectively). The ulcer healing rate with sucralfate was similar to that of ranitidine. However, proton pump inhibitor (PPI) therapy was associated with significantly greater rates of both GU and DU healing than ranitidine; 8-week GU rates were 92% and 88% with esomeprazole 40 mg and 20 mg, respectively (vs. 74% with ranitidine, p < 0.01). For omeprazole, 8-week healing rates were 87% with omeprazole 40 mg and 84% with omeprazole 20 mg (vs. 64% for ranitidine, p < 0.001), and for lansoprazole the corresponding values were 73-74% and 66-69% for the 30 mg and 15 mg doses, respectively (vs. 50-53% for ranitidine, p < 0.05). In the PPI study reporting DU healing the values were 92% for omeprazole 20 mg (vs. 81% for ranitidine, p < 0.05) and 88% for omeprazole 40 mg (p = 0.17 vs. ranitidine). NSAID-associated GU are more likely to heal when patients receive concomitant treatment with a PPI rather than ranitidine.     

Reactions of humoral and cellular immunity in peptic ulcer in relation to the condition of the gastric mucosa

A total of 160 persons including 50 patients with duodenal ulcer (DU) and 38 with gastric ulcer (GU) were examined for antibodies to the parietal cells of the stomach (PCA) and cell cellular immunity responses to autologous antigen from the gastric mucosa. It was shown that both PCA of the stomach and cell immunity responses in patients with GU and DU occurred in an insignificant number of cases. No differences were revealed in the humoral and cellular immunity in GU and DU persons with and without concomitant gastritis or in the stage of exacerbation and ulcer cicatrization.