Nodular duodenitis involving CD8+ cell infiltration in patients with ulcerative colitis

BACKGROUND/AIMS: Limited efforts have been made to determine changes in the upper gastrointestinal tract in ulcerative colitis. The aim of this study was to analyze gastroduodenal lesions in patients with ulcerative colitis. METHODOLOGY: The endoscopical appearance of lesions in the duodenum and stomach was first examined. Biopsy specimens taken from 25 patients with ulcerative colitis, as well as 21 with Crohn's disease and 16 with nonspecific gastroduodenitis who had no Helicobacter pylori infection, were then evaluated by histology and immunohistochemistry for CD8, CD68 and HLA-DR. In ulcerative colitis patients, the HLA-phenotype was also analyzed by the standard NIH complement-dependent microlymphocyte toxicity assay. RESULTS: Endoscopically evident alteration of nodularity in the descending part of duodenum was prominent in ulcerative colitis and Crohn's disease, but not gastroduodenitis. Histological inflammatory change of the duodenal bulb in ulcerative colitis and Crohn's disease was mild as compared to gastroduodenitis cases. Endoscopic and histological change (redness and deformity of villi) in the duodenum were more prominent in ulcerative colitis patients with pancolitis than those with left-sided/proctitis. CD8+ cells infiltrating both the duodenum and stomach were increased in ulcerative colitis and Crohn's disease as compared to gastroduodenitis whereas focal perifoveolar accumulation of CD68+ cells and enhanced epithelial expression of HLA-DR were characteristic of Crohn's disease. Histopathological alteration in the duodenum was particularly prevalent in ulcerative colitis patients with HLA-DR4 and Cw1. CONCLUSIONS: Nodular, histologically mild duodenitis involving CD8+ cell infiltration, the severity of which positively correlates with the extent of colitis, is characteristic of ulcerative colitis.     

Prevalence peptic lesion in asymptomatic, healthy volunteers

Aim. To investigate the presence of lesions of the upper gastrointestinal tract of asymptomatic, healthy volunteers undergoing clinical pharmacology studies.Material and Methods. A series of 53 volunteers (45 male, 23 Helicobacter pylori negative and 30 Helicobacter pylori positive) underwent upper gastrointestinal endoscopy. Helicobacter pylori status was assessed using two methods (rapid urease test and histology) from antral and corpus biopsies.Results. Peptic lesions were found in 24 (45%) subjects: erosive oesophagitis, gastric/duodenal ulcers and gastric/duodenal erosions were found in 23%, 9% and 36% of these volunteers, respectively. Helicobacter plyori-positive subjects had significantly (p<0.05) more gastroduodenal lesions than Helicobacter pylori negative individuals (12/30 vs 3/23). The presence of peptic ulcers and erosive oesophagitis was similar in Helicobacter pylori-positive and -negative individuals.Conclusions. The possibility that peptic lesions might exist in otherwise asymptomatic, asymptomatic, healthy individuals cannot be ruled out. Helicobacter pylori-positive individuals have a significantly higher incidence of gastric and duodenal lesions than Helicobacter pylori negative subjects.     

Prevalence of Helicobacter pylori infection and correlation between severity of upper gastrointestinal lesions and H. pylori infection in Japanese patients with Crohn's disease

Background. The prevalence of Helicobacter pylori infection in Crohn's disease (CD) patients was investigated to determine whether the presence and severity of gastroduodenal lesions were related to H. pylori infection. Methods. Infection rates were compared between CD group (n = 90) and the control group (n = 525). Correlations between endoscopically detected lesions and H. pylori positive rates were investigated. The relationship between drug therapy and the prevalence of H. pylori infection was also analyzed. Results. H. pylori-positive rate of the 90 CD patients attending our clinic was 16.7%, significantly lower than the rate in healthy controls (40.2%) (P = 0.0001). The involvement of H. pylori infection in the gastroduodenal lesions of CD patients was also examined. The prevalence of gastroduodenal lesions in all CD patients was high, 92.2%. The lesions observed included ulcers, erosion, and "bamboo joint-like lesions" of the stomach, and ulcers, erosion, stenosis, and elevated lesions of the duodenum. None of these lesions were found to be related to H. pylori infection. However, H. pylori infection was found to exacerbate gastric ulcers (P = 0.036). The analysis of a possible relationship between a history of drug therapy and the low prevalence of H. pylori infection in CD patients showed that the prevalence of H. pylori infection was significantly lower in patients who had received antibiotics for 2 weeks or more (P = 0.002). Conclusions. The results suggest that H. pylori infection is essentially unrelated to the gastroduodenal lesions observed in CD. It seems likely, however, that H. pylori infection may exacerbate gastric ulcers and that H. pylori can be eradicated by prolonged use of antibiotics. Received: June 19, 2000 / Accepted: April 13, 2001     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients

Background. Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either, whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients.Aims. To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status.Patients and methods. A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination.Results. There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum.Conclusion. Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

Effects of Omeprazole and Eradication of Helicobacter pylori on Gastric and Duodenal Mucosal Enzyme Activities and DNA in Duodenal Ulcer Patients

Vetvik K, Schrumpf E, Mowinckel P, Aase S, Andersen K-J. Effects of omeprazole and eradication of Helicobacter pylori on gastric and duodenal mucosal enzyme activities and DNA in duodenal ulcer patients. Scand J Gastroenterol 1994;29:995-1000.

Background: Duodenal and gastric content of mucosal enzymes in duodenal ulcer (DU) patients differs from that of controls. The purpose of this study has been to examine the effect of omeprazole and eradication of Helicobacter pylori on mucosal enzymes in DU patients

Methods: The enzyme activities of seven gastric and duodenal mucosal marker enzymes from the brush border, lysosomes, and mitochondria have been studied. In study I the measurements were made in 29 patients with an active DU before and after 14 days of omeprazole treatment. In study II 22 duodenal ulcer patients were given bismuth subnitrate, oxytetracycline, and metronidazole (triple therapy) for 2 weeks to eradicate H. pylori. Biopsy specimens were taken from the duodenum and the stomach for enzyme measurements and histologic assessment. In study II additional specimens were obtained from the prepyloric region for urease tests and culture of H. pylori.

Results: The ulcer healing rates were more than 90% after both omeprazole and triple therapy. H. pylori was eradicated in 86% after triple therapy. The activities of the brush-border enzymes lactase, neutral-α-glucosidase, alkaline phosphatase, leucyl-β-naphthylami-dase, and γ-glutamyltransferase (γ-GT) increased significantly in the duodenal bulb and the descending duodenum during treatment with omeprazole. No changes in duodenal enzyme activity were detected after triple therapy, whereas a significant fall in γ-GT and acid phosphatase activities was seen in the stomach. The mucosal DNA in the gastric antrum decreased both after treatment with omeprazole and after triple therapy.

Conclusions: A similar decrease in mucosal DNA of the gastric antrum was demonstrated after both omeprazole and triple therapy with bismuth subnitrate, oxytetracycline, and metronidazole. Omeprazole also affects the content of duodenal mucosal enzymes, whereas triple therapy particularly affects the gastric mucosal enzyme activity.     

Regression of Gastroduodenal Mucosa-Associated Lymphoid Tissue Lymphoma after Eradication of Helicobacter pylori: A Case Report

Increasing evidence suggests that eradication therapy of Helicobacter pylori (H. pylori) may be an effective treatment for gastric lymphoma of mucosa-associated lymphoid tissue (MALToma), but it remains unclear whether a similar therapeutic effect may be obtained for MALToma at other sites. We describe here a case of regression of gastroduodenal MALToma after eradication therapy for H. pylori. A 39-year-old man underwent gastroscopy at a routine check-up, which demonstrated protruding lesions like a raised erosion in the antrum and multiple whitish granular lesions in the fornix. Simultaneously, multiple coarse nodular lesions were also found in the duodenal bulb. Forceps biopsy specimens obtained from both the stomach and bulb showed infiltration of small- to medium-sized lymphocytes with cleaved nuclei, centrocyte-like cells, together with atypical large lymphoid cells into the glandular lesion, and the rearrangement of immunoglobulin was positive, thereby allowing diagnosis of low grade MALToma with large cell transformation. H. pylori was positive in the stomach, while the presence of H, pylori was not detected microscopically in the bulb, although ectopic gastric mucosa was identified in the bulb. Regression of multiple coarse or granular lesions in both the stomach and bulb were observed three months after eradication of H. pylori. Thereafter the disappearance of MALToma was verified histologically a further six months later. There was no recurrence of MALToma detected over a two-year follow-up period. These findings suggest that eradication of H. pylori could be a treatment of first choice for MALToma occurring in the gastrointestinal tract outside the stomach.     

Endoscopic markers in adult coeliac disease

BACKGROUND: Various endoscopic markers have been described in coeliac disease, particularly in the second part of the duodenum, with minor attention generally being paid to the duodenal bulb. AIMS: To evaluate, prospectively, the presence of all endoscopic markers in the bulb and the second part of the duodenum on a large series of patients submitted to endoscopy for duodenal biopsy. PATIENTS AND METHODS. A total of 367 consecutive patients, submitted to endoscopy with duodenal biopsy for various indications, were considered. Biopsies were graded as normal, with partial villous atrophy (mild, moderate, severe) or with subtotal villous atrophy. Endoscopic markers and corresponding locations evaluated were: micronodular pattern [bulb and descending duodenum], mosaic appearance (bulb and descending duodenum), scalloped folds (descending duodenum), reduced or absent folds (descending duodenum). RESULTS: In 78 patients, a diagnosis of untreated coeliac disease was made. Endoscopic markers were seen in 73/78 patients, with only a single sign present (bulb or descending duodenum) in 12 patients. In the remaining 289 patients, normal histology and normal endoscopic findings were observed, except in two patients with reduced folds. Sensitivity, specificity, positive and negative predictive values and diagnostic accuracy regarding all endoscopic markers were 93.6%, 99.3%, 97.3%, 98.3% and 98.1%, respectively CONCLUSIONS: This study confirms the usefulness of endoscopic markers in detecting coeliac disease, underlining the importance of evaluating also abnormalities in the bulb and endoscopic single signs; although endoscopy may not detect all cases of coeliac disease, the recognition of endoscopic markers allows the selection for biopsy of unsuspected patients submitted to endoscopy for non-specific symptoms.     

CLINICAL EVALUATION OF NODULAR GASTRITIS IN ADULTS

Background: Nodular gastritis (NG) was considered a physiological change with little pathological significance, mostly in young women. In recent years, however, it has been often reported in patients with Helicobacter pylori (H. pylori) infection, or in patients with gastroduodenal ulcer/gastric cancer, suggesting possible clinical significance. Methods: From July 2003 to July 2006, 59 patients were diagnosed with NG among 32 404 patients examined endoscopically. The incidence of NG was evaluated in relation to age, sex, H. pylori infection status, symptoms leading to endoscopy, associated lesions in the upper digestive tract at the time of NG diagnosis, and existence of other systemic conditions. Results: The NG patients consisted of 13 out of 18 152 (0.07%) male patients and 46 out of 14 252 (0.32%) female patients, with a mean age of 45.3 ± 17.7 years. All 28 patients who were examined for H. pylori infection were positive. Endoscopic examination was performed for precordial pain and upper abdominal pain in 24 (40.7%) patients, symptoms of gastroesophageal reflux disease in eight (13.6%) patients, and symptoms of functional dyspepsia in six (10.2%) patients. NG was associated with duodenal ulcer in eight (13.6%) patients, hyperplastic gastric polyps in five (8.5%), gastric ulcer in one (1.7%), and gastric cancer in one (1.7%) patient. Conclusion: NG is a specific gastritis resulting from H. pylori infection that may be strongly associated with H. pylori‐related lesions.     

Diffuse gastroduodenitis and pouchitis associated with ulcerative colitis

INTRODUCTIONPouchitis after total colectomy with ileal pouch anal anastomosis can sometimes occur in patients with ulcerative colitis (UC). Despite intensive studies the cause of pouchitis remains unknown, but many contributing factors, such as faecal sta…     

Changes in Helicobacter pylori status in patients with rheumatoid arthritis under non‐steroidal anti‐inflammatory drugs

Background: The role of Helicobacter pylori infection in rheumatoid arthritis (RA) patients during treatment with non‐steroidal anti‐inflammatory drugs (NSAID) is still unclear. Methods: By means of endoscopy and biopsy, gastroduodenal lesions and H. pylori status were repeatedly examined in 88 RA patients at intervals ranging from 26 to 49 months. Histology and culture were applied to determine H. pylori status. Serial changes in gastroduodenal lesions and histologic score for mucosal atrophy were compared among groups classified by initial and second H. pylori status. Results: There were 28 patients with continuously positive H. pylori infection (CP group), 33 patients with continuously negative H. pylori infection (CN group), 7 patients in whom H. pylori status became negative (PN group), and 20 patients in whom H. pylori status could not be determined (UD group). Age, duration and species of NSAID, disease activity of RA, gastroprotective drugs applied and the prevalence of gastroduodenal mucosal lesions were not different among the groups at either the initial or the second examination. In the PN group, the score for mucosal atrophy at the second examination was significantly lower than at the initial examination, whereas no difference was found for the CP, CN and UD groups. Overall, histologic score for mucosal atrophy was higher in H. pylori‐positive patients than in H. pylori‐negative patients at both initial and second examination. Conclusions: In RA patients using NSAIDs, H. pylori infection may not affect the course of gastroduodenal lesions and activity of RA, but the infection contributes to mucosal atrophy.     

Influence ofHelicobacter pylori on tryptase and cathepsin D in peptic ulcer

We here ascertain whether tryptase (a serine endoprotease released by mast cells) and cathepsin D (CD, a lysosomal hydrolase that seems able to derange the extracellular matrix) play a part in peptic ulcer disease and whether they are linked toHelicobacter pylori (Hp) infection. We studied 13 controls, 25 patients with gastric ulcer, 47 with duodenal ulcer, and 11 with duodenitis. Tryptase and CD were measured in mucosal biopsies (body and antrum of the stomach and duodenum) using IRMA methods. Hp infection was histologically evaluated (Giemsa). Tryptase and CD levels were higher (25%) in patients with active peptic ulcer, whether gastric or duodenal. In Hp-positive patients the CD mucosal content was higher while tryptase mucosal levels were lower than in Hp-negative patients. Tryptase was correlated with gastrin content. CD seems to be mainly related to the phlogistic reaction of the mucosa to Hp infection; tryptase may reflect an indirect link between Hp infection, gastrin release, and the function of mast cells.     

Helicobacter pylori stimulates inducible nitric oxide synthase in diverse topographical patterns in various gastroduodenal disorders

Overproduction of nitric oxide by inducible nitric oxide synthase (iNOS) acts cytotoxically and contributes to inflammation. We explored the roles of iNOS in the pathogenesis of Helicobacter pylori-associated diseases. Using reverse-transcribed PCR, we examined topographical patterns of iNOS mRNA expression in the gastroduodenal mucosa in H. pylori-negative controls and H. pylori-positive patients with duodenal ulcer (DU), gastric ulcer (GU), and ulcer-free gastritis. iNOS expression showed topographical variations among the tested disorders. As compared to controls, DU had a significantly higher expression of iNOS mRNA in the duodenum, GU in the antrum and duodenum, and gastritis in the antrum and corpus. H. pylori eradication yielded a significant reduction of iNOS mRNA in the duodenum of DU and in the antrum of GU. Diverse topographical patterns of H. pylori-induced iNOS expression may contribute to mechanisms by which H. pylori elicits different clinical disorders.     

Adrenocorticosteroid therapy and gastroduodenal lesions

Gastroduodenoscopy was performed in 25 patients with various disorders, such as liver cirrhosis, nephrotic syndrome, and ulcerative colitis, to assess the effects of corticosteroids on the stomach and duodenum. The main criterion for entry into the trial was the absence of open ulcer, healed ulcer, erosion, or bleeding from the stomach or duodenum on pretreatment endoscopy performed within 48 hours before administration of corticosteroids. Endoscopy repeated at 2 to 4 weeks disclosed gastroduodenal lesions in 11 cases (44%)and no lesion in 14 cases (56%). The gastroduodenal lesions observed in 11 cases are as follows: one gastric ulcer (4.0%), six gastric erosions (24.0%), two gastroduodenal erosions (8.0%), and two duodenal erosions (8.0%). A lack of correlation between the patients' subjective complaints and endoscopic findings indicates the unreliability of patients' complaints and the importance of endoscopy in assessing gastroduodenal lesions. There were no differences in the total and average daily doses of corticosteroid between a group with gastric and/ or duodenal lesions and a group without such lesions. Corticosteroids may produce gastroduodenal lesions, regardless of the dose.     

Regression of MALT lymphomas coexisting in the duodenal bulb and the stomach by eradication of Helicobacter pylori

Helicobacter pylori eradication. During an endoscopic examination, multiple polyps in the duodenal bulb were observed in a 62-year-old woman. The pathology of the duodenal polyps was low-grade B-cell MALT lymphoma. Gastric MALT lymphoma was also detected in biopsies of rough mucosa from the gastric corpus. Southern blot analysis showed rearranged bands of DNA immunoglobulin heavy chain J portion (IgH-J) in both lesions, but the positions of these bands were different in the two lesions. H. pylori was recognized in the gastric mucosa by positive serum H. pylori antibody and urease tests, while bacterial bodies were not found in the duodenal bulb. With 1 year after the successful eradication of H. pylori, both the lesions, that in the duodenal bulb and that in the gastric corpus, had disappeared. Furthermore, positive rearrangement of IgH-J was not found at either of the lesion sites. In May 2000, 3 years after the treatment, endoscopic surveillance failed to find any recurrence of these malignant lymphomas. Received: October 6, 2000 / Accepted: March 2, 2001     

Gastroduodenal Lesions Associated with Two Different Piroxicam Formulations: An Endoscopic Comparison

This endoscopic study was performed to compare the gastroduodenal endoscopic findings after short-term treatment with plain and enteric-coated piroxicam tablets. Sixteen healthy male volunteers (mean age, 22 years; range, 19–27 years) were included in a double-blind, randomized study in which 20 mg piroxicam was given once daily for 2 weeks as plain tablets or enteric-coated tablets in a crossover fashion. The washout period was 5 weeks, and endoscopy was performed before each treatment period to ensure base-line conditions. Endoscopic evaluation of the stomach and duodenum was performed, with separate registration of the duodenum distally to the duodenal bulb. Visual analogue scales of 150 mm were used for grading the mucosal lesions, with separate registration of mucosal injection and erosive and haemorrhagic lesions. A 5-point scale (Lanza scale) was also used, to compare the two scoring systems. A significantly lower lesion score was found with the enteric-coated formulation for all endoscopic variables in both scoring regions. The sum of visual analogue scale scores in the stomach/ duodenal bulb after treatment was 121 mm and 74 mm, respectively (p < 0.01), and in the middle and distal duodenum the corresponding figures were 54 mm and 23 mm (p < 0.01). The fixed-point scoring gave identical conclusions, as did the separate scoring by a different investigator evaluating the same endoscopies. Subjective symptoms were similar for the two formulations, and no carryover effects were detected. We conclude that enteric coating of piroxicam tablets may offer a means of protecting the gastroduodenal mucosa in short-term treatment of healthy subjects.     

Pathogenesis of duodenal ulcer disease: the rest of the story

Although several duodenal ulcer disease-specific abnormalities in gastric function have been described (e.g. exaggerated gastrin releasing peptide-stimulated acid secretion and an abnormal sensitivity of the parietal cells to gastrin), none has withstood careful examination. We describe here the critical nature of the duodenal acid load in precipitating and washing out bile salts, which inhibit the growth of Helicobacter pylori(H. pylori) in the development of duodenal ulcer disease. The risk of duodenal ulcer is enhanced by infection with pro-inflammatory H. pylori(e.g. with an intact cag pathogenicity island). Progressive damage to the duodenum promotes gastric metaplasia, resulting in sites for H. pylori growth and more inflammation. This cycle results in an increasing inability of the duodenal bulb to neutralize acid entering from the stomach until changes in duodenal bulb structure and function are sufficient for an ulcer to develop. Cure of the H. pylori infection results in a sustained fall in duodenal acid load as well as a marked (and continuing) reduction in inflammation, which results in the cure of chronic ulcer disease.     

Prevalence of gastric metaplasia in the duodenal bulb is low in Helicobacter pylori positive non-ulcer dyspepsia patients.

BACKGROUND: Gastric metaplasia in duodenum is a common phenomena in duodenal ulcer patients. However, the role of gastric metaplasia in patients with non-ulcer dyspepsia is not clear. It is not known either whether Helicobacter pylori infected non-ulcer patients who are CagA-seropositive have gastric metaplasia in duodenum more often than CagA-negative patients. AIMS: To compare prevalence of gastric metaplasia in duodenum in non-ulcer dyspepsia patients according to Helicobacter pylori status. PATIENTS AND METHODS: A series of 400 unselected dyspeptic patients in primary care were investigated. Patients with no endoscopic evidence of organic disease (n=236) were enrolled in the study. Duodenal bulb and gastric biopsies were collected, as well as blood samples for Helicobacter pylori determination. RESULTS: There were no differences between CagA-seropositive and -seronegative Helicobacter pylori infected patients as far as concerns gastric metaplasia in duodenal bulb (20% vs 25%). Helicobacter pylori negative non-ulcer patients more often had gastric metaplastic changes (46%, p<0.0001) in duodenum. CONCLUSION: Helicobacter pylori infection has no major role in development of gastric metaplasia in duodenal bulb in non-ulcer dyspeptic patients. Furthermore, it does not result in positive CagA-serology, an increased risk for gastric metaplasia compared with CagA-seronegative cases.     

DIAGNOSIS AND CLINICAL COURSE OF ULCERATIVE GASTRODUODENAL LESION ASSOCIATED WITH ULCERATIVE COLITIS: POSSIBLE RELATIONSHIP WITH POUCHITIS

Background and Aim: Ulcerative colitis (UC) is not only characterized by pathological lesions localized to colonic mucosa, but also to various complications involving other organs, including postoperative pouchitis. Among these complications, diffuse gastroduodenitis with lesions resembling colonic lesions has been reported, albeit rarely. The aim of the present study was to attempt to characterize the lesions of the upper gastrointestinal tract occurring as a complication of UC, and to assess the frequency and clinical course of these lesions. Methods: A total of 322 UC patients who had undergone upper gastrointestinal endoscopy were retrospectively analyzed. We assessed the frequency of endoscopic findings, including diffuse gastroduodenal lesions resembling colonic lesions. Ulcerative gastroduodenal lesion (UGDL) associated with UC was diagnosed if lesions satisfied the following criteria: (i) improvement of the lesions with treatment of UC; and/or (ii) resemblance to UC in pathological findings. Results: UGDL satisfying the aforementioned criteria was found in 15 (4.7%) of 322 patients. All the 15 patients had UGDL accompanied by pancolitis or after proctocolectomy. Frequency in 146 patients with pancolitis was 6.2% (nine patients) and that in 81 patients who had undergone proctocolectomy was 7.4% (six patients). Four patients with diffuse ulcerative upper‐gastrointestinal mucosal inflammation (DUMI) had pouchitis. In all patients except one, the lesions resolved easily with medical treatment. Conclusions: In more than half of the post‐proctocolectomy patients, UGDL was related to the occurrence of pouchitis. The existence of characteristic UGDL must be taken into account in the diagnosis and treatment of UC, and UGDL is possibly related to the occurrence of pouchitis.     

Detection of serum anti-Helicobacter pylori immunoglobulin G in patients with different digestive malignant tumors

AIM: To investigate the seroprevalence of Helicobacter pylori infection in patients with different digestive malignant tumors. METHODS: Enzyme linked immunosorbent assay (ELISA) was used to detect serum anti-Helicobacter pylori IgG antibody in 374 patients with different digestive malignant tumors and 310 healthy subjects (normal control group). RESULTS: The seroprevalence of Helicobacter pylori infection was 61.50% (230/374) and 46.77% (145/310), respectively, in patients with digestive tumors and normal controls (P<0.05). The seroprevalence was 52.38% (33/63), 86.60% (84/97), 83.14% (84/101), 45.24 (19/42), 51.13% (18/35) and 44.44% (16/36), respectively in patients with carcinomas of esophagus, stomach, duodenum, rectum, colon and liver (P<0.01). In patients with intestinal and diffuse type gastric cancers, the seroprevalence was 93.75% (60/64) and 72.73% (24/33), respectively (P<0.05). In patients with gastric antral and cardiac cancers, the seroprevalence was 96.43% (54/56) and 73.17% (30/41), respectively (P<0.05). In patients with ulcerous and proliferous type duodenal cancers, the seroprevalence of H pylori infection was 91.04% (61/67) and 52.27% (23/44), respectively (P<0.05). In patients with duodenal bulb and descending cancers, the seroprevalence was 94.20% (65/69) and 45.20% (19/42), respectively (P<0.05). CONCLUSION: H pylori infection is associated with occurrence and development of gastric and duodenal carcinomas. Furthermore, it is also associated with histological type and locations of gastric and duodenal carcinomas.     

Link betweenHelicobacter pylori-associated gastritis and duodenal ulcer

We examined the interrelationships among the degree of fundic mucosal atrophy, the prevalence ofHelicobacter pylori in the gastric antrum, the gastric juice, and the duodenum with and without gastric metaplasia, in 20 duodenal ulcer patients and 20 non-duodenal ulcer patients. The detection rates ofH. pylori in the antrum, the gastric juice, and the duodenum were significantly higher in duodenal ulcer patients (80%, 65%, and 60%) than in non-duodenal ulcer subjects (50%, 20%, and 5%). The frequency ofH. pylori was significantly lower in the gastric juice (30%) and the duodenum (10%) in non-duodenal ulcer patients with antralH. pylori, compared with those in duodenal ulcer patients with antralH. pylori. All of seven patients with both gastric metaplasia andH. pylori infection in the duodenum had duodenal ulcer, whereas only 1 of 14 patients without either gastric metaplasia orH. pylori infection in the duodenum had duodenal ulcer. There was normal or mild atrophic mucosa in the fundus of duodenal ulcer patients withH. pylori in the antrum, whereas moderate or severe atrophic mucosa in non-duodenal ulcer patients withH. pylori gastritis. These results suggest that the preserved fundic mucosa, gastric metaplasia in the duodenum, and a greater load ofH. pylori to the duodenum through the gastric juice may be prerequisites for the formation of duodenal ulcers.