Histological Examination Of Gastric Biopsies Research Articles

Autoimmune Atrophic Gastritis: A Clinical Review.

Autoimmune atrophic gastritis (AAG) is a chronic condition characterized by the presence of atrophy in the oxyntic mucosa due to anti-parietal cell antibodies. This review provides a comprehensive and up-to-date overview of autoimmune atrophic gastritis, reporting recent evidence on epidemiology, pathogenesis, diagnosis, clinical presentation, risk of malignancies, and management. The prevalence of AAG has been estimated at between 0.3% and 2.7% in the general population. The diagnosis of AAG is based on a combination of the serologic profile and the histological examination of gastric biopsies. Patients with AAG are often asymptomatic but can also have dyspeptic or reflux symptoms. The atrophy of the oxyntic mucosa leads to iron and vitamin B12 malabsorption, which may result in anemia and neurological affections. Autoimmune atrophic gastritis is associated with an increased risk of type I neuroendocrine tumors (NETs) and gastric cancer, with an incidence rate of 2.8% and 0.5% per person/year, respectively. Management is directed to reinstate vitamins and iron and to prevent malignancies with endoscopic surveillance. In conclusion, atrophic autoimmune gastritis is an infrequent condition, often asymptomatic and misdiagnosed, that requires an early diagnosis for appropriate vitamin supplementation and endoscopic follow-up for the early diagnosis of NETs and gastric cancer.

Clinical Management of Patients with Gastric MALT Lymphoma: A Gastroenterologist's Point of View.

Gastric mucosa-associated lymphoid tissue (MALT) lymphomas (GML) are non-Hodgkin lymphomas arising from the marginal zone of the lymphoid tissue of the stomach. They are usually induced by chronic infection with Helicobacter pylori (H. pylori); however, H. pylori-negative GML is of increasing incidence. The diagnosis of GML is based on histological examination of gastric biopsies, but the role of upper endoscopy is crucial since it is the first step in the diagnostic process and, with currently available novel endoscopic techniques, may even allow an in vivo diagnosis of GML per se. The treatment of GML, which is usually localized, always includes the eradication of H. pylori, which should be performed even in H. pylori-negative GML. In the case of GML persistence after eradication of the bacteria, low-dose radiotherapy may be proposed, while systemic treatments (immunochemotherapy) should be reserved for very rare disseminated cases. In GML patients, at diagnosis but even after complete remission, special attention must be paid to an increased risk of gastric adenocarcinoma, especially in the presence of associated gastric precancerous lesions (gastric atrophy and gastric intestinal metaplasia), which requires adequate endoscopic surveillance of these patients.

Pullulation bactérienne gastrique : une observation histologique inhabituelle, à ne pas méconnaître

Gastric bacterial overgrowth is a rare situation, which may be associated with short- and long-term complications. It must be known from pathologists, since it might be detected incidentally at histological examination of gastric biopsies. We report here the case of a 74-year old woman, obese, without significant medical history, apart from a gastro-esophageal reflux treated by the long-term administration of proton pump inhibitors (PPI). In this patient, gastric bacterial overgrowth was detected at histological examination of gastric biopsies performed after colectomy for left colon adenocarcinoma. Large clusters of small, round, "coccoid" bacteria were present in the gastric mucus. Their characteristics were suggestive of enterobacteria. Bacterial proliferation was associated with severe and diffuse lesions of active gastritis. The course was rapidly unfavorable, and the patient rapidly deceased with multiple infections and multi-organ failure. In our observation, the pathogenesis of gastric bacterial overgrowth was probably multifactorial. It might have been facilitated by long-term PPI treatment and obesity, which are known risk factors, and promoted, in the post-operative setting, by multiple infections and immune failure. Our observation underlines that gastric bacterial overgrowth might be associated with severe gastritis, which might justify antibiotherapy. Other consequences of prolonged gastric dysbiosis cannot be excluded, such as the promotion of neoplastic lesions.

Analysis of the Influence of Interleukin-1β Gene Polymorphism on Gastric Inflammatory Response and Precancerous Lesions Development in Patients with Functional Dyspepsia

ABSTRACT The present study aimed to evaluate the influence of the IL1B -31C/T polymorphism on gastric inflammatory response and precancerous lesions development – atrophic gastritis (AG) and intestinal metaplasia (IM) – in patients positive for Helicobacter pylori infection with functional dyspepsia (FD). The diagnosis of FD followed the Rome III criteria, and the H. pylori infection was evaluated by urease test and histological examination of gastric biopsies (corpus, antrum, and incisura). The severity of chronic inflammation and inflammatory activity, as well as the presence of precancerous lesions were evaluated accordingly to the updated Sydney System. Genotyping of the IL1B -31C/T polymorphism (rs1143627) was performed by polymerase chain reaction-restriction fragment length polymorphism. A total of 303 patients positive for H. pylori infection with FD were analyzed (81.8% women; mean age of 46.3 ± 12.3 years). No differences were observed in overall genotype frequencies among outcomes evaluated. However, in the dominant -31C allele model (CC+CT vs. TT), the frequency of the TT genotype was significantly higher among patients with moderate/severe chronic inflammation of the antrum than the frequency of the CC+CT genotypes (80.8% vs. 65.2%; OR = 2.25; 95% CI = 1.23-4.24; P = .005). The presence of AG and IM in the gastric mucosa of patients was of 19.5% and 19.1%, respectively. No significant association was observed concerning the frequencies of the genotypes of IL1B -31C/T polymorphism with development of precancerous lesions. In conclusion, our data suggest that genetic variants of the IL1B -31C/T polymorphism play a role in chronic inflammation of the gastric mucosa in H. pylori-infected FD patients.

Suppurative gastritis in a HIV-positive patient: A case report

Introduction. Suppurative gastritis (SG) is a rare disease characterized by a bacterial infection of the stomach wall. This condition has high mortality rate, especially in patients with predisposing factors such as alcoholism, immunodeficiency and previous endoscopic gastric procedures. Case report. A 41 year old male was hospitalized with epigastric pain, fever and vomiting. The symptoms started a few days after esophagogastroduodenoscopy (EGD). His personal medical history included periodical excessive alcohol consumption. Based on initial blood tests the patient was diagnosed with sepsis and was promptly started a treatment with antibiotics. In the first few days of hospitalization there was an improvement in inflammation marker levels, but the patient was still febrile and with the referred epigastric pain. A computed tomography scan showed marked thickening of the gastric wall and EGD revealed deep ulcers in the stomach with fibrinopurulent exudate. Histological examination of gastric biopsies showed necrosis and abscesses. Blood cultures were positive for Stenotrophomonas maltophilia and Pseudomonas aeruginosa with subsequent change in antibiotics. The repeated blood tests showed leucopenia and the patient tested positive for human immunodeficiency virus (HIV). A second EGD showed pus in the stomach, with a gastric aspirate culture positive for Enterococcus spp. The treatment was modified and a third EGD showed healed gastric mucosa confirmed by histopathological evaluation. Conclusion. Taking in consideration the high mortality rate of SG, it is necessary to make an early diagnosis and start the treatment against specific pathogens, since it can be crucial for a better outcome of this clinical condition.

Association of Helicobacter pylori infection with somatostatin deficiency and its relation to post-endoscopic retrograde cholangiopancreatography pancreatitis

Background Post-endoscopic retrograde cholangiopancreatography pancreatitis (PEP) is the most common complication of endoscopic retrograde cholangiopancreatography (ERCP). It can be diagnosed clinically in patients complaining of severe abdominal pain with rising of serum amylase and lipase more than three-folds of high normal levels within 24 h of the procedure. Aim The aim of this work was to determine if there is an association between Helicobacter pylori infection and low somatostatin level and its relation to PEP. Patients and methods A total of 80 patients with obstructive jaundice requiring ERCP were enrolled in this study and were, divided according to H. pylori infection into the following: 37 H. pylori positive patients (group A) and 43 H. pylori negative patients (group B). All patients were subjected to full history taking; clinical examination, serum bilirubin, serum amylase and serum lipase just before and 24 h after ERCP; histological examination of gastric biopsies to detect H. pylori and serum somatostatin level with follow-up for 24 h for any symptom or signs suggestive of PEP. Results The percentage of PEP was 10.8% in group A and 9.3% in group B, with an overall percentage of 10%. Patients who experienced PEP had a statistically significant lower somatostatin level than patients who did not experience PEP. Significant increase in somatostatin level was registered in H. pylori-infected patients. Certain ERCP-related maneuvers, such as difficult ampullary cannulation, repeated pancreatic duct cannulation and precut sphincterotomy, carry the risk of PEP. Conclusion No association between H. pylori infection and PEP was seen. Low somatostatin level can be useful in prediction of PEP.

Evolving patterns in the diagnosis of reactive gastropathy: Data from a prospective Central European multicenter study with proposal of a new histologic scoring system

Histologic examination of gastric biopsies is crucial for determining the cause of gastritis. This prospective multicenter study was undertaken to investigate different histologic parameters arguing in favor or against the diagnosis of reactive gastropathy and to correlate findings with patient's symptoms and endoscopic findings. A total of 1123 individuals aged 15–93 years participated in a prospective multicenter study (histoGERD trial). Diagnosis of Helicobacter gastritis was made following the Updated Sydney System. Diagnosis of reactive gastropathy was based upon Dixon's parameters of foveolar hyperplasia, smooth muscle fibers in the lamina propria and vasodilatation and congestion of mucosal capillaries. Including paucity of acute and chronic inflammatory cells in analysis, a new score with visual analog scales for the diagnosis of reactive gastropathy was developed. All three histologic parameters in favor of the diagnosis of reactive gastropathy were positively associated with the endoscopic diagnosis of gastritis (p<0.001), yet negatively with Helicobacter infection (p<0.001). In contrast, presence of acute and chronic inflammatory cells in lamina propria was positively associated with Helicobacter infection (p<0.001), yet not with the endoscopic diagnosis of gastritis. Our score demonstrated strong association between histologic and endoscopic diagnoses (p<0.001), yet not with patient's symptoms. In conclusion, our data prove foveolar hyperplasia, smooth muscle fibers and vasodilatation and congestion as key histologic parameters for the diagnosis of reactive gastropathy. The proposed score may enhance the diagnostic accuracy. It should be validated in future studies.

684 Glycogenic Acanthosis of the Esophagus: Is it Associated with Helicobacter Pylori Infection in Children?

Background and AimGlycogenic acanthosis (GA) is usually reported as a histologic finding. The pathogenesis and aetiology of GA has not been explained definitively yet.There are many studies about the relationship...

Diffuse duodenal nodular lymphoid hyperplasia: a large cohort of patients etiologically related to Helicobacter pyloriinfection

BackgroundNodular lymphoid hyperplasia of gastrointestinal tract is a rare disorder, often associated with immunodeficiency syndromes. There are no published reports of its association with Helicobacter pylori infection.MethodsFrom March 2005 till February 2010, we prospectively followed all patients with diffuse duodenal nodular lymphoid hyperplasia (DDNLH). Patients underwent esophagogastroduodenoscopy with targeted biopsies, colonoscopy, and small bowel video capsule endoscopy. Duodenal nodular lesions were graded from 0 to 4 based on their size and density. Patients were screened for celiac sprue (IgA endomysial antibody), immunoglobulin abnormalities (immunoglobulin levels & serum protein electrophoresis), small intestine bacterial overgrowth (lactulose hydrogen breath test), and Helicobacter pylori infection (rapid urease test, and histological examination of gastric biopsies). Patients infected with Helicobacter pylori received sequential antibiotic therapy and eradication of infection was evaluated by 14C urea breath test. Follow up duodenoscopies with biopsies were performed to ascertain resolution of nodular lesions.ResultsForty patients (Males 23, females 17; mean age ± 1SD 35.6 ± 14.6 years) with DDNLH were studied. Patients presented with epigastric pain, vomiting, and weight loss. Esophagogastroduodenoscopy showed diffuse nodular lesions (size varying from 2 to 5 mm or more) of varying grades (mean score ± 1SD 2.70 ± 0.84) involving postbulbar duodenum. Video capsule endoscopies revealed nodular disease exclusively limited to duodenum. None of the patients had immunoglobulin deficiency or small intestine bacterial overgrowth or positive IgA endomysial antibodies. All patients were infected with Helicobacter pylori infection. Sequential antibiotic therapy eradicated Helicobacter pylori infection in 26 patients. Follow up duodenoscopies in these patients showed significant reduction of duodenal nodular lesions score (2.69 ± 0.79 to 1.50 ± 1.10; p < 0.001). Nodular lesions showed complete resolution in 5 patients and significant resolution in remaining 21 patients. Patients with resistant Helicobacter pylori infection showed no significant reduction of nodular lesions score (2.71 ± 0.96 to 2.64 ± 1.15; p = 0.58). Nodules partially regressed in score in 2 patients, showed no interval change in 10 patients and progressed in 2 patients.ConclusionsWe report on a large cohort of patients with DDNLH, etiologically related to Helicobacter pylori infection.

Assessment of systemic matrix metalloproteinase and their regulator response in children with Helicobacter pylori gastritis

Background. Helicobacter pylori causes gastritis and is the most important risk factor of peptic ulcer disease and gastric cancer. In chronic adulthood H. pylori infection some matrix metalloproteinases (MMPs), which are proteolytic metalloendopeptidases regulated by tissue inhibitors of metalloproteinases (TIMPs), are upregulated. Our aim was to determine circulating levels of MMPs and their regulators TIMP-1, human neutrophil elastase (HNE) and myeloperoxidase (MPO) in childhood H. pylori infection. Design and methods. Twenty-six H. pylori positive and 34 H. pylori negative children whose H. pylori status was verified by histological examination of gastric biopsies were included. Serum samples were analysed by enzyme-linked immunosorbent assay. Results. Significantly decreased serum levels of TIMP-1 were detected in H. pylori-infected children (median, 97.50 ng/mL) as compared to H. pylori-negative children (median, 118.5 ng/mL, p = 0.003). However, there were no significant differences in serum levels of MMP−2, −7, −8, −9, and their regulators HNE and MPO between H. pylori-positive and -negative children. Conclusions. Differing from the recent findings in adulthood H. pylori infection, only circulating TIMP-1 levels were significantly different between H. pylori-positive and -negative children. Whether this reflects the first sign of a proteolytic cascade later leading to increased levels of MMPs remains to be shown.

Treatment of type I gastric neuroendocrine tumors with somatostatin analogs

There are limited data on response and long-term follow-up of octreotide therapy in type-I gastric neuroendocrine tumors. The objective of the present study was to assess the response of type-I gastric neuroendocrine tumors to octreotide-long acting, repeatable (LAR) therapy and evaluate long-term follow up of such patients after therapy. Three patients with documented type-I gastric neuroendocrine tumors from a tertiary gastroenterology centre were studied. Octreotide-LAR therapy 20 mg intramuscularly every 28 days was administered for one year. Serum gastrin and chromogranin levels, gastroscopies and biopsies from tumor nodules at 6 months and one year on therapy and every 6 months after completion of drug therapy were taken. Follow-up after completion of therapy extended for 3 years in two and 2.5 years in one patient. During octreotide therapy there was normalization of serum gastrin levels and serum chromogranin levels. Tumors in all three patients had regressed at 6 months of treatment. Following cessation of therapy, there was progressive rise of serum gastrin to pre-treatment levels. Serum chromogranin levels remained within normal limits. Gastroscopic and histologic examination of gastric biopsies did not reveal recurrence of tumors in any patients. All patients tolerated therapy well and became asymptomatic soon after drug therapy. Octreotide-LAR therapy causes regression of type-I gastric neuroendocrine tumors. After completion of drug therapy there was no recurrence of tumors even with continued hypergastrinemia. Octreotide therapy should be considered as one of the treatment options in such patients.

Epstein-Barr Virus Gastritis

We describe an exceedingly rare case of severe gastritis that was temporally associated with primary Epstein-Barr virus (EBV) infection. The patient was a 59-year-old immunocompetent man who presented with intermittent fever of unknown origin and epigastric pain for 18 days. A computed tomographic scan of the abdomen showed diffuse thickening of the gastric wall and esophagogastroduodenoscopy revealed numerous ulcers in the stomach. Histologic examination of gastric biopsies showed a dense and diffuse atypical lymphoid infiltrate in the lamina propria with erosions and focal lymphoepithelial lesions. No lymphoid follicles or Helicobacter microorganisms were identified. Immunohistochemical studies demonstrated the lymphoid infiltrate to consist of mixed T and B cells. Immunoglobulin heavy chain gene arrangement analysis showed a polyclonal pattern. The plasma cells present in the biopsies exhibited no light chain restriction as determined by in situ hybridization. Concurrent clinical work-up revealed peripheral lymphocytosis with atypical lymphocytes and positive serum IgM antibody to EBV capsid antigen in the absence of IgG antibody. These findings indicated that the gastric abnormalities were related to primary EBV infection as the predominant manifestation of infectious mononucleosis. This was further confirmed by subsequent in situ hybridization showing numerous EBV-positive lymphocytes in the gastric mucosa. The patient's symptoms were spontaneously resolved with only supportive treatment. A follow-up endoscopy 2 months later showed completely normal gastric mucosa and he remained well with no gastrointestinal complaints for 2 and a half years. This case illustrates the importance of a high index of suspicion to avoid misdiagnosis of gastric lymphoma that requires more aggressive therapies.

Cut-off point, timing and pitfalls of the 13C-urea breath test as measured by infrared spectrometry

Background. The best timing and the best cut-off level of the 13C-urea breath test have not yet been well established.Aims. To evaluate the cut-off value and the influence of medication on the 13C-urea breath test as measured by infrared spectrometry.Methods. A series of 223 patients, sent for endoscopy performed13C-urea breath test in fasting conditions with 75 mg of 13C-urea and 20 ml of citric acid. Breath samples were collected before and then 10, 20, 25 and 30 minutes after ingestion. As gold standard, histological examination of gastric biopsies was used. A questionnaire was completed concerning the intake of medication, likely to influence the test, in the 2 months preceding the test. Sensitivity, specificity, positive predictive value and negative predictive value at 10, 20, 25 and 30 minutes at different cut-off values (3, 3.5, 4, 4.5, 5.0 0/00 DOB) were calculated.Results. A total of 182 patients did not take medication. There was no significant difference between the different cut-off levels at different times. Compared with the group of 41 patients who did take medication, likely to influence the test, the differences were significant (Fisher exact test)Conclusion. There was no significant difference between the different cut-off values. A 10-minute test with a cut-off level between 4 and 5%0 delta over baseline (sensitivity: 100%, specificity: 95%) is, therefore, proposed. To avoid false negative results due to unknown intake of medication, every patient submitted to the 13C-urea breath test should fill out a questionnaire.

Noninvasive tests as a substitute for histology in the diagnosis of Helicobacter pylori infection

Background: Rapid urease tests for Helicobacter pylori have a sensitivity of 80% to 90%. Therefore histologic examination of gastric biopsies is recommended as a “backup” diagnostic test in rapid urease test–negative patients. However, noninvasive tests (urea breath test, serology, whole blood antibody tests) may provide a more rapid diagnosis and be less expensive but offer similar accuracy. Methods: Sixty-seven patients (no prior treatment for H pylori, no proton pump inhibitors, antibiotics, or bismuth within 4 weeks) undergoing endoscopy for evaluation of dyspepsia symptoms and testing rapid urease test–negative by antral biopsy were enrolled. All had the following tests: gastric biopsies (2 antral, 1 fundus; H&E and Alcian Yellow stain) examined for gastritis and H pylori ; 13C-UBT; capillary blood for whole blood rapid antibody tests: FlexSure HP, QuickVue, AccuStat, and Stat-Simple Pylori; serum for FlexSure HP; HM-CAP enzyme-linked immunoassay. H pylori infection was diagnosed (reference standard) if chronic gastritis was present on histology and at least 2 of the 3 following tests were positive: urea breath test, H pylori organisms unequivocally demonstrated in biopsies on special stain, and/or enzyme-linked immunoassay. The test and treatment costs per patient were calculated. Results: Of 67 patients with a negative rapid urease test, 4 were positive for H pylori. None had active peptic ulcer disease. Histology only identified 1 patient with organisms visible on special stain. Using chronic active gastritis (neutrophilic and mononuclear infiltrate) as a diagnostic criterion for H pylori, 6 patients would have been judged positive. However, only 2 of these were truly positive by the reference standard (positive predictive value 33%). Negative predictive value for presence of organisms and chronic active gastritis was 95% and 97%, respectively. All of the noninvasive tests identified all 4 truly positive patients correctly. Urea breath test and FlexSure whole blood assay yielded a substantial number of false-positive results (positive predictive value 31% and 36%, respectively); positive predictive value for the other tests ranged from 50% to 80%. All tests except histology had a negative predictive value of 100%. Histology was the most costly test (p < 0.001 compared with all other tests), followed by urea breath test and HM-CAP serology (p < 0.001 compared with all rapid antibody tests). Conclusions: Whole blood or serum antibody testing is a rapid, accurate, and cost-effective means for establishing H pylori status in rapid urease test–negative patients. Whole blood or serology rapid antibody testing should substitute for histology when the patient has not been previously treated for H pylori. (Gastrointest Endosc 2000;52:20-6.)

Severe acute gastritis associated with Helicobacter pylori infection

We describe the case of a young female referred to our unit because of acute upper abdominal symptoms. Upper gastrointestinal endoscopy showed a gastric picture resembling lymphoma or acute non-steroidal anti-inflammatory drug gastropathy (deep, large and irregular ulcers), but the clinical history and the histological examination of gastric biopsies were consistent only with acute gastritis Helicobacter pylori-correlated. The patient was treated with omeprazole and antibiotics with complete recovery. As the patient's cat had suffered from an acute gastrointestinal distress two weeks earlier, a case of zoonosis was hypothesized and an upper gastrointestinal endoscopy was performed also on the cat. Unfortunately, we were not able to detect Helicobacter pylori in the cat gastric mucosa, but only urease-producing spiral microorganisms. Possible sources of infection and pathogenetic mechanisms of the severe gastritis are discussed.

H. pylori infection in HIV-positive patients. A serohistological study.

Sixty-seven consecutive patients infected with the human immunodeficiency virus (HIV-1), 72% of which with overt AIDS, were examinated by upper endoscopy due to various indications and evaluated for the prevalence of H. pylori infection. The infection was studied by performing both histological examination of gastric biopsies and serological testing for anti-H. pylori IgG antibodies. The H. pylori prevalence rate was 55% in histology; no significant differences were observed in HIV-infected subjects and those with overt AIDS (52% vs 63%, respectively; P = NS). Positive histological testing appeared to be directly related to the peripheral CD4+ lymphocyte count (minimum rates of 43% were detected in patients with CD4+ < 100 x 10(6)/liter and maximum rates of 78% in patients with CD4+ > 200 x 10(6)/liter, respectively; P < 0.05) and inversely related to the frequency of antibiotic treatments performed over the six months prior to endoscopy. Low CD4+ counts were also apparently associated with low-grade H. pylori infection. Serological testing was positive for anti-H. pylori IgG antibodies in 39% of patients; compared to histology, serology displayed a sensitivity of 57% and a specificity of 81%. The discrepancy between histological and serological positive results for H. pylori was noted to be higher in the more advanced phases of HIV infection. Based upon our results, the serological testing for anti-H. pylori IgG antibodies seems to require cautious interpretation in HIV-positive patients.

Helicobacter pyloriin Japan

Recent international consensus statements have concluded that Helicobacter pylori is a causal factor in peptic ulcer disease and a Group 1 carcinogen in humans, and that all patients with peptic ulcer associated with H. pylori infection should receive eradication therapy. There are marked differences in the presentation of peptic ulcer disease between Japanese patients and those from other countries, however, and thus a committee of the Japanese Society of Gastroenterology has been set up to develop guidelines for clinical trials in patients with gastric or duodenal ulcers associated with H. pylori. According to these guidelines, eradication therapy should normally consist of dual therapy with a proton pump inhibitor, such as omeprazole, and an antibiotic; a nitroimidazole can be added, however, if necessary. The diagnosis of H. pylori should be made on the basis of a positive culture of the organism or histological examination of gastric biopsies, together with a positive urease test or 13C-urea breath test. Eradication should be confirmed by the same means 4-6 weeks after treatment. Other research is investigating the relationship between H. pylori and gastric cancer, an important issue in view of the high incidence of this condition in Japan. There is evidence that the Mongolian gerbil may be a useful animal model to investigate this question.

Endoscopic Features of Helicobacter pylori-Related Gastritis

It is still controversial whether certain endoscopic features can be used to diagnose Helicobacter pylori (Hp)-related gastritis. To clarify this issue, we performed two consecutive prospective studies. In the first study, we tried to identify endoscopic criteria associated with Hp-related gastritis from a total of 66 predefined gastric features on endoscopy. These features were selected by a stepwise logistic regression analysis in 101 patients. The validity of these features gained from this first study was then evaluated in a second study in 86 patients (40 with Hp gastritis, 8 with Hp-unrelated gastritis and 38 with normal gastric mucosa). Three features, namely an abnormal antral surface texture, a mammillated corpus surface, and white antral erosions, were identified in the first study as independent predictors of Hp-related gastritis. However, the sensitivity and specificity of these three criteria, as assessed in the second study, were only 75% and 63% respectively. We conclude that it is not possible to diagnose Hp-related gastritis on the basis of the endoscopic appearance alone. The diagnosis should be based on other criteria, such as a rapid urease test, or a histological examination of gastric biopsies, or both.

Gastric histology and plasma gastrin response to a meal in patients with duodenal ulcer disease after five years treatment with ranitidine

Fifty asymptomatic patients with duodenal ulcer disease, aged 31-82 years, who had received ranitidine maintenance therapy continuously for five or more years without a symptomatic recurrence, were studied. Fasting plasma gastrin concentrations were normal (mean 24 pmol/L, S.D. +/- 22) while the post-prandial gastrin response was variable with maximum plasma concentrations ranging from 16 to 309 pmol/L. Endoscopy revealed six asymptomatic peptic ulcers. Histological examination of gastric biopsies showed mild, superficial inflammatory cell infiltration of the fundic mucosa, but more extensive inflammatory cell infiltration with some atrophy of the mucosal glands in the antral mucosa. Patchy intestinal metaplasia was evident in the antral mucosa of 18 patients. No fundic ECL cell hyperplasia was seen. Helicobacter pylori were detected in the corpus and antrum of most patients. These results suggest that maintenance treatment with ranitidine for 5 years is not associated with either significant hypergastrinaemia or with changes in the fundic mucosa which could be interpreted as pre-malignant.