Cyanide toxicity and thiosulfate protection during chronic administration of sodium nitroprusside in the dog: correlation with a human case

Three adult spayed female hunting dogs had an unusual form of chronic active gastritis. The disease lasted for months to several years. Vomiting was the most consistent clinical sign. One dog had leukocytosis with 30 percent eosinophils. The stomach of each dog was enlarged and greatly thickened. Collagen deposits, granulation tissue and eosinophils replaced most of the gastric wall. Disease of the gastric arteries ranged from fibrinoid necrosis to panarteritis. Granulation tissue obstructed the omental arteries of one dog. There also was splenic reticuloendothelial hyperplasia with fibrosis, hemorrhage and congestion, and chronic eosinophilic lymphadenitis. Although the cause of this disease was not determined, its basis probably was immunologic.     

Gastritis duodenitis, and circulating levels of gastrin in duodenal ulcer before and after vagotomy

Biopsy specimens have been taken from five standard sites in the stomach and from the duodenal bulb in order to investigate the association of gastritis and duodenitis with duodenal ulcer. Twenty patients with chronic duodenal ulcer were investigated in this manner and in addition had gastric secretion tests and a radio-immune assay of serum gastrin under differing conditions. The patients were then treated either by a truncal vagotomy and pyloroplasty (TVP) or by a highly selective vagotomy without a drainage procedure (HSV). All the investigations were repeated three months postoperatively. Duodenal ulcer was usually associated with gastriitis, although this varied in extent and severity from patient to patient. In nearly all the patients, gastritis was present at the pyloric end of the stomach and along the lesser curve. In more than half of the patients, gastritis was also present in the body of the stomach but the fundus was usually spared. Chronic duodenitis was found in the duodenal bulb in all these patients. After vagotomy there was a marked increase in both the extent and severity of the proximal gastritis in both treatment groups but the distal gastritis remain almost unchanged. There was little change in the incidence of duodenitis after vagotomy but its severity was lessened. No correlation was found between the peak acid output (PAO) in response to Histalog and the severity of the gastritis or the duodenitis either before or after operation, with one exception. The postoperative PAO was significantly less in those patients who developed a severe proximal gastritis after vagotomy. No relationship was found between the severity of the distal gastritis and the levels of serum gastrin. No correlation was found between either the basal or peak acid output and the corresponding serum gastrin levels before or after vagotomy.     

Radiologic evaluation of the liver and gastrointestinal tract in rats infected with Taenia taeniaeformis

In rats infected with the cestode Taenia taeniaeformis, hepatomegaly results from development of parasitic cysts in the liver. Diffuse nodular mucosal hyperplasia in the glandular region (corpus and antrum) of the stomach, and gross thickening of the intestinal mucosa also result. Between postinfection days (PID) 21 and 84, radiologic observations were made after oral administration of a barium sulfate suspension in T taeniaeformis-infected rats and in age/sex-matched controls. There was radiographic evidence of hepatic enlargement at PID 21. Enlargement of the gastric folds was first observed along the greater curvature of the stomach at PID 35. Fimbriation of small intestinal mucosal surfaces resulted from thickening of the intestinal villi and was observed in the duodenum at PID 21. Intestinal motility was assessed, and contractions were counted, using image intensification fluoroscopy, then were recorded on videotape. There were no significant differences between control and infected rats for gastric emptying time, intestinal transit time, and number of intestinal contractions per minute. Barium contrast radiography clearly indicated large gastric folds, thickening of the small intestinal villi, and hepatic enlargement, and was useful for assessing gastrointestinal motility.     

Prevalence and pattern of Helicobacter pylori gastritis in the gastric cardia

OBJECTIVES: Helicobacter pylori has a predilection for antral colonization. Local acid production is the major determinant of colonization. Because production is low in the antrum and cardia, H. pylori should also colonize the cardia. We therefore investigated the histologic pattern of gastritis and the prevalence of H. pylori in the cardia compared with the antrum and corpus. METHODS: From 135 H. pylori-infected patients with gastritis, ulcer disease, or reflux esophagitis, biopsies were obtained from the antrum, corpus, and cardia. The prevalence, topography, and histologic parameters of gastritis were examined. RESULTS: All 135 patients had active antral H. pylori gastritis: in the cardia, 132 of these patients (97.7%) showed active gastritis, and 124 patients (91.9%) had H. pylori visible on staining. Gastritis of the cardia in most patients resembled antral gastritis, but the density of bacteria and the inflammatory responses were less marked. The most striking finding in the cardia of patients with gastroesophageal reflux was a lower density of bacteria compared with antrum and corpus. Intestinal metaplasia was found in 32 patients in antral mucosa (23.7%) versus 28 patients in the cardia (20.7%), versus 11 patients in the corpus (8.1%), and was multifocal in 17 patients (12.6%). CONCLUSIONS: H. pylori gastritis commonly involves the cardia. The histologic density of the bacteria and inflammatory responses are lower than in the antrum. Intestinal metaplasia in the cardia is a common finding in H. pylori gastritis. The cause of the lower bacterial density in the cardia of patients with reflux esophagitis needs further investigation.     

Free and total bupivacaine plasma concentrations after continuous epidural anaesthesia in infants and children

OBJECTIVES: The aim of this study was to elucidate the prevalence of Helicobacter pylori and its distribution in order to clarify the frequency of H. pylori infection and the most appropriate site of endoscopic biopsy for studies of H. pylori infection associated with different gastric diseases. DESIGNS AND METHODS: Swiss role mucosal strips from 275 resected stomachs, which included the greater curvature, anterior wall and lesser curvature of the antrum, incisura and corpus, were stained with haematoxylin-eosin and H. pylori antibody. RESULTS: The prevalence of H. pylori infection was 97% in duodenal ulcers, 98% in gastric ulcers, 98% in intestinal-type carcinomas and 99% in diffuse-type carcinomas. H. pylori was present at a rate of 100% in any site in cases of duodenal ulcer, but was diffusely distributed in the antrum and patchily distributed in the corpus. The detection rate of H. pylori was 50-100% in gastric ulcers, 30-100% in intestinal-type adenocarcinomas and 63-100% in diffuse-type adenocarcinomas depending on the site of the stomach examined. CONCLUSIONS: The prevalence of H. pylori infection was very high in peptic ulcers of the duodenum and stomach and gastric carcinomas of Japanese patients. Biopsy specimens for evaluation of H. pylori infection should be taken routinely from both the greater curvature of the antrum and corpus. Immunohistochemical staining should be used to assay for H. pylori when few organisms are present or eradication therapy has been used.     

"Cre"-ating mouse mutants-a meeting review on conditional mouse genetics

BACKGROUND: The antireflux capacity of various gastric fundoplications combines the creation of a valve (flapper or nipple) with recreation of a sharp cardioesophageal angle. Experimental comparison of valve competency and appropriate valve geometry is incomplete despite wide application of these techniques. Our primary aim was to compare the competency of several antireflux valves in explanted cadaver stomachs. Our secondary aim was to understand better the geometry of the gastric fundus in empty and full stomachs. METHODS: Stomachs with 6-8 cm of distal esophagus were harvested from 18 fresh cadavers. With the stomach empty, the greater and lesser curvature length and the transverse dimensions of the anterior and posterior surface of the stomach in the fundus, body, and antrum were measured. The pylorus was tied off over a catheter; the stomachs were inflated with water; and reflux occurred. Intragastric pressure was measured during inflation with a needle inserted in the side of the stomach. A clamp was then placed on the esophagus, and the stomach was inflated to a pressure of 10 mmHg. Gastric measurements were recalculated in the distended stomach. The stomachs were deflated, the clamp removed, and a 2-cm Nissen fundoplication as well as 270 degrees and 180 degrees posterior fundoplications were performed over a 60 Fr dilator. The stomachs were reinflated while the pressure was transduced. The inflation was stopped when reflux occurred or when the fundoplication disrupted. RESULTS: The stomachs expanded symmetrically when filled with water except for the fundus in which the anterior gastric wall lengthened by more than 100% and the posterior gastric wall lengthened by about 50%. In the untreated stomachs, reflux occurred at a pressure of 3.0 +/- 1.0 mmHg. After fundoplication, reflux never occurred, but the sutures pulled out of the stomach or esophagus at 28.6 +/- 16.8 mmHg. Posterior fundoplications refluxed water in several stomachs. CONCLUSIONS: When filled, the anterior fundus expands to a greater degree than the posterior fundus, offering more tissue for creation of floppy fundoplication. The "floppy" Nissen fundoplication is completely competent, suffering a degradation before allowing reflux. The posterior partial fundoplication is unpredictable in its competency.     

Review article: the development of atrophic gastritis--Helicobacter pylori and the effects of acid suppressive therapy

Helicobacter pylori is uniquely adapted to survival in the strongly acidic gastric lumen. In vitro, both acid and certain acid suppressors affect bacterial growth. In vivo, there is little evidence that acid suppressors have any effect on bacterial survival. In contrast, decrease of acid secretion quickly leads to a spreading of the bacterial infection throughout the body and fundus of the stomach, which is accompanied by an increase of the associated gastritis. Helicobacter pylori gastritis may, in a substantial number of infected subjects, ultimately lead to atrophy and intestinal metaplasia, conditions with an increased risk for gastric cancer. This review summarizes the data on the interrelation between Helicobacter pylori, gastric acid secretion and development of atrophic gastritis.     

Socioeconomic correlates of infant mortality in Hong Kong, 1979-93

Contractions change the configuration of the lesser curvature of the stomach while they indent the greater curvature. We studied these lesser curvature changes by measuring the position and angle of the gastric incisura on still frames captured from videotapes of isolated cat stomachs suspended in physiologic solution. In response to filling with 100 mL Krebs' solution stomachs generated a tonic contraction of the fundus/body segment and gave rise to a peristaltic contraction that spread from the body and through the antrum to the pylorus. In preparations where we left the duodenal cannula open we found that the incisura moves toward the gastro-oesophageal (GO) junction and the angle of the incisura widens as the contraction passes through the stomach and empties its contents. Furthermore, the angle of the incisura is most acute when the full stomach starts contracting in its fundic segment and again when the contraction involves the gastric sinus (the wedge-shaped segment adjacent to the incisura which forms the transition between the body and the antrum of the stomach). In preparations where the duodenal cannula was kept closed, the angle of the incisura becomes most acute when the contraction involves the gastric body and when the luminal pressure peaks. We conclude that changes in the position and angulation of the incisura are part of the mechanical response of the stomach to filling and emptying; unlike the peristaltic contraction along the greater curvature the net movement of the incisura goes in the orad direction. Movements of the incisura profoundly affect the configuration of the stomach and hence the distribution of luminal contents between various gastric segments. The gastric sling muscles are responsible for the formation of the gastric incisura but their role in any movements of the incisura remains to be defined.     

A long-term follow-up study with endoscope in chronic gastritis

A 10 to 17 years endoscope follow-up was performed to 138 cases of chronic gastritis. The result showed that 118 cases still proved to be chronic gastritis, and the increase of chronic atrophic gastritis (CAG) in numbers. 15 cases developed into peptic ulcer. 5 cases to carcinoma (4 cases were early carcinoma). The time of cancerization differed from 2 to 12 years. The rate of cancerization of CAG reached 7.46%. The rate of cancerization of intestinal metaplasia (IM) were 8.20%. 13 cases of IM were mucus histo-chemical stained, and five of them contained sulfuric acid mucus, one of the 5 cases cancerized. 3 of 14 cases with atypical hyperplasia (ATP) turned into stomach cancer. We believe that chronic gastritis, especially CAG with ATP and IM, or with sulfuric acid mucus of IM had a high possibility of cancerization with the increase of age, and should be followed up for a long time.     

Expression of differential nitric oxide synthase isoforms in human normal gastric mucosa and gastric cancer tissue

The present study investigated the expression and distribution of three isoforms of nitric oxide synthase (NOS) in different anatomical regions of the human stomach and in gastric neoplastic tissues by immunohistochemistry using specific antibodies. Intracellular localization of individual isoenzymes of NOS was detected in normal gastric mucosa. Gastric cancer tissues had a marked reduction of all three NOS isoforms expression. The expression of the endothelial NOS, neuronal NOS and inducible NOS in the tumor tissue was significantly lower than in normal gastric mucosa (P = 0.01, P = 0.02, P < 0.01, respectively). In the tumor tissue the expression of inducible NOS was significantly lower than the expression of both constitutive forms of NOS (P < 0.01). There was a tendency to higher expression of both constitutive forms of NOS in earlier stages T2 of the tumor compared to advanced T4 tumor. In contrast, the expression of inducible NOS was higher than in the advanced T4 tumor than in the earlier stages T2 of the tumor. The mapping of the expression of endothelial NOS, neuronal NOS and inducible NOS in human stomach showed higher expression of NOS isoforms in the distal third than in the proximal third of the stomach (P = 0.03, P = 0.04, P = 0.01, respectively). We conclude that there is greater expression of NOS in the stomach corpus and in antrum than in the proximal third of the normal human stomach mirroring the anatomical predilection of common pathological changes in this part of the human stomach. Furthermore, there was loss of the expression of individual isoenzymes in gastric neoplasms.     

Surgical treatment of gastroesophageal reflux disease

Antireflux surgery is successful in 85-90% of eligible patients, with relief of symptoms, cure of oesophagitis and possibly prevention of progression of the dysplasia in a Barrett's oesophagus. The mortality in the latest publications is given as 0.05%. The morbidity, apart from recurrences, is not yet sufficiently known. Some 250 antireflux operations are performed annually in the Netherlands, fewer than 20% of the estimated requirement of 10 operations per 100,000 of the population per year, and also fewer than in Scandinavia. Nissen fundoplication (folding the fundus of the stomach around the entire circumference (360 degrees) of the oesophagus) is generally accepted as the standard primary operation. Nissen fundoplication during laparoscopy seems to be just as good. Results of randomized clinical trials will have to be awaited to prove this assumption. Belsey's operation (folding the fundus around 270 degrees of the circumference of the oesophagus via thoracotomy) is nowadays performed almost exclusively in recurrent reflux disease and in persistent dysphagia after a primary operation.     

Diagnosis of otitis media with effusion by acoustic reflectometry

Colonization of human gastric mucosa with Helicobacter pylori leads to chronic active gastritis and induces the occurrence of an acquired mucosa-associated lymphoid tissue (MALT) in the stomach. This remodelling of the gastric mucosa together with chronic antigen persistence may induce autoimmune reactions. The aim of this study was to investigate humoral autoimmune reactions to human gastric mucosa in H. pylori gastritis and their clinical relevance. Sera from patients with dyspeptic symptoms were tested for presence of IgG immunoglobulins against H. pylori. Gastric infection with H. pylori and alterations of gastric mucosa were demonstrated by histological examination of gastric biopsy specimens. All sera were tested for reactivity against human gastric mucosa by immunohistochemistry. Two different in-situ binding sites of antigastric autoantibodies were observed. Binding to canalicular structures within parietal cells was significantly correlated with antibodies to H. pylori, elevated basal gastrin levels and atrophy of gastric corpus glands. Our data indicate that autoimmune reactions to antigens in the human gastric mucosa occur in H. pylori gastritis and that they may play a role in the pathogenesis of the disease.     

Gastroesophageal reflux disease versus Helicobacter pylori infection as the cause of gastric carditis

To explore the potential contributions of gastroesophageal reflux disease, as opposed to Helicobacter pylori infection, to the development of gastric carditis, we evaluated gastric carditis (using the criteria of the updated Sydney system for the classification of gastritis), clinical and morphologic features of esophagitis, and H. pylori infection (evaluation of Steiner stains) in biopsy specimens from the gastroesophageal squamocolumnar junction. We correlated clinical, endoscopic, and histologic features in an unselected group of 116 patients. Some degree of carditis was found in 107 (92%) of the patients. The mean age of the patients increased with increasing severity of carditis (P < .05). The various groups of patients with different degrees of carditis did not differ significantly in sex ratio, ethnic background, presence of obesity, percentage having symptoms of gastroesophageal reflux disease (such as heartburn, regurgitation, dysphagia, or odynophagia), endoscopic evidence of esophagitis and columnar epithelium in the distal esophagus, or histologic evidence of active esophagitis. The presence, however, of active gastritis and H. pylori infection in the distal stomach and/or in the cardia was significantly associated with carditis. In patients without carditis, H. pylori was not detected in any cardiac or distal gastric biopsy specimen. In contrast, H. pylori was demonstrated in gastric tissue samples (either from the cardia or distally) of patients with carditis, with the prevalence rate increasing with greater degrees of cardiac inflammation. The H. pylori prevalence rate was 12% in the group with mild carditis, 40% in those with moderate carditis, and 57% in patients with marked carditis (P = .0001). In summary, carditis is commonly found in patients with symptoms related to upper gastrointestinal diseases. From analysis of our study cohort, we concluded that carditis was significantly associated with H. pylori infection and active gastritis but not with symptoms or signs of gastroesophageal reflux disease. These findings suggest that carditis with histologic features similar to those of gastritis in the distal stomach was a sequel of H. pylori infection and represented a part of an H. pylori--associated gastric inflammation.     

Dopamine receptor D2 Ser/Cys311 variant associated with disorganized symptomatology of schizophrenia

AIMS: To investigate the prevalence of lymphocytic gastritis in patients with coeliac disease. METHODS: Gastric biopsies from 70 patients with coeliac disease were examined by light microscopy for the presence of lymphocytic gastritis, defined as 25 or more intraepithelial lymphocytes/100 gastric columnar epithelial cells. RESULTS: Lymphocytic gastritis was found in seven cases. Positive cases had a mean of 32.1 intraepithelial lymphocytes/100 columnar cells, compared with a mean of 13.9 in negative cases, and 5.15 in noncoeliac controls. No differences were found for age, sex, gastric corpus or antrum, or degree of inflammation in the gastric lamina propria. All intraepithelial lymphocytes were of T cell lineage. Cases not showing lymphocytic gastritis did however show significantly increased gastric intraepithelial lymphocytes compared with non-coeliac controls. Eighteen of 70 cases were positive for Helicobacter pylori, and four of seven cases of lymphocytic gastritis were H pylori positive; no significant difference was observed between H pylori positive and negative patients. Three cases had concomitant ulcerative enteritis, of which none showed lymphocytic gastritis, while five cases had concomitant enteropathy associated T cell lymphoma, of which one showed lymphocytic gastritis. CONCLUSIONS: Lymphocytic gastritis occurred in 10% of patients with coeliac disease. Cases without lymphocytic gastritis nevertheless showed increased gastric intraepithelial lymphocytes. Coeliac disease may on occasion be a diffuse lymphocytic enteropathy occurring in response to gluten. Lymphocytic gastritis outside coeliac disease may involve an immune response to luminal antigens, such as H pylori, not unlike the response to gluten in patients with coeliac disease.     

Gastritis. Cause and significance]

Despite the high incidence and the increasing frequency gastritis is a true pathological process of the gastric mucosa. The importance of gastritis is not due to the symptoms but due to the altered reagibility of the stomach mucosa against exogenous and endogenous noxes. Two different forms fo chronic atrophic gastritis are to be distinguish concerning localization and etiology. Type A possibly is caused by an immunological process and is localized in the corpus mucosa. The more frequent typ B is localized in the antral mucosa and may be caused by exogen factors. None of these different forms of gastritis is a true precancerosis. However, dysplasia and enterocolic metaplasia which can appear in the course of chronic atrophic gastritis should be payed special attention because of a possible increased frequency of malignancy.     

Gastric emptying time with 99mTc-resin solid experiment meal

Half gastric emptying time (GET1/2) was measured by using radionuclide gamma-photography with 99mTc-resin solid experiment meal. The results were as follows: 1. GET1/2 in the normal controls (10 cases) was 51.62 +/- 3.69 minutes. 2. GET1/2 in mild chronic atrophic gastritis (CAG) patients was 51.68 +/- 9.20 Min, not significantly different with the normal controls (P > 0.05). GET1/2 in 15 cases with moderate and severe CAG was 70.39 +/- 14.86 Min, which was apparently longer than that in normal controls (P < 0.01). 3. There was no significant difference in GET1/2 between carcinoma of the gastric corpus, fundus and cardia (50.77 +/- 2.73 Min) as well as the normal controls (P > 0.05). GET1/2 of the cancer of gastric antrum was 89.06 +/- 19.55 Min, being longer than that in normal controls (P < 0.01). 4. No obvious difference was observed between the GET1/2 of patients with corpus and fundus peptic ulcer (55.36 +/- 6.80 Min.) and the normal controls (P > 0.05). It was apparently longer in patients with antral peptic ulcer (76.62 +/- 16.96 Min.) than in patients with ulcers of corpus, fundus and normal controls (P < 0.01). 5. GET1/2 in patients with duodenal ulcer (42.49 +/- 6.26 Min.) was apparently shorter than those with gastric ulcer and normal controls. 6. GET1/2 in diabetic patients was 70.01 +/- 29, 46 Min, it was obviously longer in those patients with autonomic nervous dysfunction (84.03 +/- 22.31 Min.) than that those without (34.14 +/- 7.90 Min.).(ABSTRACT TRUNCATED AT 250 WORDS)     

Orally effective iron chelators for the treatment of iron overload disease: the case for a further look at pyridoxal isonicotinoyl hydrazone and its analogs

Taeniasis is very common all over the world and invades the upper small bowel in humans. It is very unusual to see this parasite in the stomach. We report a case of gastric taeniasis that led to granulomatous gastritis. The elimination of the parasite resulted in complete disappearance of the granulomas in the corpus and antrum and in complete recovery of the patient.     

Adjuvant therapy with a glycoprotein IIb-IIa inhibitor (abciximab) in coronary angioplasties with a high thrombotic risk

OBJECTIVES/DESIGN: Chronic inflammation is increasingly being linked to ischaemia, but the mechanism is poorly understood, and little is known about its effect on local gastric endothelial microvessels. We aimed at studying the number and surface area of gastric mucosal endothelial microstructures in the presence or absence of chronic gastritis. METHODS: Immunohistochemical assessments were carried out on gastric antral and body biopsies taken from patients with chronic gastritis and others with normal histology. The primary antibody (QB-END/10) was raised against CD34 antigen within the endothelial cell membranes. A computer attached to a microscope was used to count the number and measure the surface area of mucosal endothelial entities. RESULTS: In patients with Helicobacter pylori gastritis (n = 19), the median number of endothelial microstructures per section was 43 in the antrum and 86 in the gastric body, compared with 205 (P = 0.00004) and 165 (P = 0.002), respectively, in subjects with normal gastric histology (n = 11). The median surface area of the endothelial microstructures was also reduced in patients with gastritis. The normal gastric antrum had more endothelial entities than the normal body (median of 205 vs 165; P = 0.007). CONCLUSIONS: Within the normal stomach, the antrum is more richly vascularized than the gastric body. However, active chronic gastritis is associated with reduction in both the number and surface area of mucosal endothelial microstructures, with the reduction being more marked in the antrum. This is different from acute inflammation, and is relevant to our understanding of the natural history of mucosal defence, particularly the greater susceptibility of the gastric antrum to ulceration, compared with the gastric body.     

Chronic gastric ulcer in the rat produced by wounding at the fundo-antral junction

Standardized 8-mm mucosal wounds were made in the rat stomach at the rumeno-fundic junction, fundus, fundo-antral junction, and antrum, and examined at intervals up to 8 months. All wounds at the rumeno-fundic junction and fundus were healed within 4 weeks and at the antrum within 12 weeks. The majority of wounds at the fundo-antral junction remained chronic and at 8 months 41 of 50 rats still had ulcers 2 mm or greater in diameter. These findings suggest that the fundo-antral junction is an area which is susceptible to the development of chronic ulcers. This is a simple and reliable method of producing chronic gastric ulcers and does not alter the continuity or disturb the function of the gastrointestinal tract.     

Receiver operator characteristic analysis of endoscopy as a test for gastritis

Endoscopic evaluation of the presence or absence of gastritis is often performed in lieu of biopsy and histologic diagnosis. The purpose of our study was to assess the value of endoscopic examination as a diagnostic test for gastritis. Two endoscopists prospectively assessed the antrum of 73 patients undergoing upper gastrointestinal endoscopy and graded, on a scale of 0-4 (0 = completely absent, 4 = definitely present), the likelihood of gastritis. The following features were also assessed at the time of endoscopy: erythema, nodularity, erosion, edema, and friability. Two concomitant antral biopsies (3 cm from the pylorus on the greater curvature of the stomach) were performed regardless of the endoscopic impression. The histologic findings were graded independently on a scale of 0-3 by two pathologists who were not aware of the endoscopic findings. The following histologic features were graded: acute inflammation, chronic inflammation, lymphoid aggregates, intestinal metaplasia, and quantity of Helicobacter pylori organisms. Receiver operator characteristic analysis, a method derived from signal detection theory, assesses the trade-off of sensitivity and specificity over all cutoff points of a test and is considered the best method by which to compare tests and determine the diagnostic utility of a given test. Receiver operator characteristic analysis gave an area of 0.65 +/- 0.01 SE for endoscopy as a test for gastritis (0.5 = chance, 1 = perfect) as defined by the histologic presence of inflammation. Additionally, endoscopy as a test for the presence of histologically proven Helicobacter pylori gave an area of 0.55 +/- 0.01 SE. All endoscopically graded features treated as separate tests for gastritis and/or H. pylori gave areas of approximately 0.44-0.61, indicative of a poor test. While H. pylori was always associated with at least some degree of inflammation, linear regression analysis revealed no correlation among any of the histologic features or of any histologic feature with any endoscopic feature. We conclude that a tissue diagnosis is essential for the proper diagnosis of gastritis.