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Gastric biopsies represent one of the most frequent specimens that the pathologist faces in routine activity. In the last decade or so, the landscape of gastric pathology has been changing with a significant and constant decline of H. pylori -related pathologies in Western countries coupled with the expansion of iatrogenic lesions due to the use of next-generation drugs in the oncological setting. This overview will focus on the description of the elementary lesions observed in gastric biopsies and on the most recent published recommendations, guidelines and expert opinions., (Copyright © 2020 Società Italiana di Anatomia Patologica e Citopatologia Diagnostica, Divisione Italiana della International Academy of Pathology.)

Eosinophils participate in the immune response against Helicobacter pylori, but little is known about their role in the gastritis associated to the infection. We recently demonstrated that the Hp(2-20) peptide derived from H. pylori accelerates wound healing of gastric mucosa by interacting with N-formyl peptide receptors (FPRs) expressed on gastric epithelial cells. The aim of the present study was to investigate whether eosinophils play a role in the repair of gastric mucosa tissue during H. pylori infection. Immuno-histochemistry and transmission electron microscopy were used to detect eosinophils in gastric mucosal biopsies. Eosinophil re-distribution occurred in the gastric mucosa of H. pylori-infected patients: their density did not change in the deep mucosal layer, whereas it increased in the superficial lamina propria just below the foveolar epithelium; eosinophils entered the epithelium itself as well as the lumen of foveolae located close to the area harboring bacteria, which in turn were also engulfed by eosinophils. The H. pylori-derived peptide Hp(2-20) stimulated eosinophil migration through the engagement of FPR2 and FPR3, and also induced production of VEGF-A and TGF-beta, two key mediators of tissue remodelling. We also demonstrate that Hp(2-20) in vivo induced eosinophil infiltration in rat gastric mucosa after injury brought about by indomethacin. This study suggests that eosinophil infiltrate could modulate the capacity of gastric mucosa to maintain or recover its integrity thereby shedding light on the role of eosinophils in H. pylori infection.

Atrophic gastritis (resulting mainly from long-standing Helicobacter pylori infection) is a major risk factor for (intestinal-type) gastric cancer development and the extent/topography of the atrophic changes significantly correlates with the degree of cancer risk. The current format for histology reporting in cases of gastritis fails to establish an immediate link between gastritis phenotype and risk of malignancy. The histology report consequently does not give clinical practitioners and gastroenterologists an explicit message of use in orienting an individual patient's clinical management. Building on current knowledge of the biology of gastritis and incorporating experience gained worldwide by applying the Sydney System for more than 15 years, an international group of pathologists (Operative Link for Gastritis Assessment) has proposed a system for reporting gastritis in terms of stage (the OLGA staging system). Gastritis staging arranges the histological phenotypes of gastritis along a scale of progressively increasing gastric cancer risk, from the lowest (stage 0) to the highest (stage IV). This tutorial aims to provide unequivocal information on how to consistently apply the OLGA staging system in routine diagnostic histology practice.

Background: Prolonged gastric acid suppression leads to hypergastrinaemia, which promotes hyperplasia of the enterochromaffin-like (ECL) cells of the oxyntic mucosa. The objective was to determine the effects of 5 years of treatment with rabeprazole or omeprazole on the gastric mucosa., Methods: Two hundred and forty-three patients received rabeprazole (20 mg or 10 mg) or omeprazole (20 mg) once daily for up to 5 years, for gastro-oesophageal reflux disease and 51% completed the whole 5 year period. Gastric biopsy specimens were taken and examined for gastritis, Helicobacter pylori infection, and ECL cell status., Findings: H. pylori infection in the gastric corpus was more common than in the antrum, and remained constant, whereas antral H. pylori infection became less common as the study progressed. H. pylori infection was a highly significant predictor of higher gastritis scores, which were similar among the three treatment groups. ECL cell hyperplasia occurred in a minority of patients, and was associated with serum gastrin concentrations. No ECL cell dysplasia or tumours were observed. There were no significant differences among the treatment groups in gastritis or ECL cell hyperplasia grades., Interpretation: This study has confirmed the link between ECL cell hyperplasia and elevated serum gastrin concentrations, but has found no evidence that this progresses to high grades of hyperplasia during 5 years of treatment with rabeprazole or omeprazole.

Background: There are conflicting reports on the role of gastro-oesophageal reflux disease (GERD) and Helicobacter pylori infection in the aetiology of carditis., Aim: The role of reflux and H. pylori infection in causing carditis was assessed in 113 consecutive patients with GERD and in 25 controls., Methods: All subjects underwent endoscopy and pH test and carditis was diagnosed on biopsies taken across the squamocolumnar junction. Helicobacter pylori was assessed by histology and rapid urease test. GERD was diagnosed by endoscopic oesophagitis or abnormal pH test., Results: Carditis was detected in 53 of 71 GERD patients and in 15 of 20 controls. Among patients, 18 showed absent, 39 mild and 14 marked cardia inflammation and their H. pylori infection rates were 17, 23 and 57%, respectively (P < 0.025). Most patients with carditis (68%) lacked H. pylori infection. pH-metry was abnormal in 15 of 18 patients with normal cardia, 33 of 39 with mild carditis and 12 of 14 with marked inflammation., Conclusions: Carditis is a frequent finding in GERD and controls. Mild, non-active carditis is frequent in GERD patients. Marked inflammation is associated with both H. pylori and abnormal pH testing. Thus, both GERD and H. pylori infection may play a role in inducing carditis.

Background: Numerous therapeutic trials aimed at eradicating Helicobacter pylori (HP) from the gastric mucosa and preventing ulcer recurrence have been carried out; however, an optimal treatment has not yet been established with carefully controlled randomized studies., Objective: The aim of our study was to evaluate the efficacy of an association of omeprazole (OM) coupled with two antibiotics in the eradication of HP and prevention of duodenal ulcer (DU) recurrence., Methods: One hundred and eighty three patients with active DU were randomized under double-blind conditions to receive either OM 20 mg for 4 wk plus amoxycillin 3 g daily and metronidazole 1 g daily during the 2nd and 3rd wk (91 patients, group A) or OM 20 mg for 4 wk plus matching placebo (92 patients, group B). Endoscopy was performed before and at the end of the 4-wk treatment as well as 2, 6, and 12 months later. Biopsies were taken from the duodenum, antrum, and gastric body at each endoscopic examination for HP histological detection and for evaluation of inflammatory changes according to the Sydney system., Results: After 4 wk, 84/86 patients (98%) of group A and 80/86 (93%) of group B were healed of their ulcers. The percentage of eradication was 90% in group A and 1% in group B. During a 12-month follow-up, DU relapsed in 4/63 (6%, including two of three reinfected cases) HP-eradicated group A patients, 4/8 (50%) HP-noneradicated group A patients, and 52/65 (80%) persistently HP-positive group B patients. Rapid, complete, and persistent suppression of gastroduodenitis activity and gastric surface epithelium lesions was observed in most HP-eradicated group A patients, whereas a transient decrease of bacterial colonization and inflammatory scores in the antrum and a transient worsening of corpus gastritis were found in group B patients., Conclusions: The combined therapy with amoxycillin, metronidazole, and omeprazole is highly effective in both HP eradication and prevention of duodenal ulcer recurrence.

Investigation of extensively sampled nontumor gastric mucosa from 205 early gastric cancers showed Helicobacter pylori colonization in 85% of cases, including 100% of diffuse and 78% (83% in 97 cases with Swiss rolls) of glandular or mixed cancers. Intestinal metaplasia, including its type III variant, was prominent in the mucosa associated with glandular and mixed (but not diffuse) early cancers. Both glandular (usually called "intestinal") and diffuse-type cancers showed admixtures of intestinal and gastric tumor cell phenotypes. Both p53 gene mutations and p53 protein immunostaining were essentially restricted to glandular or mixed cancers and associated dysplastic lesions. Their appearance in the advanced stage of diffuse cancer was partly due to a change of the histologic pattern from glandular to diffuse during progression of some tumors. Loss of laminin, beta I integrin, or zonula adherens junctions was a common finding in both early and advanced diffuse cancer. It is concluded that two main pathways operate in gastric carcinogenesis, both starting from H. pylori gastritis and both leading to phenotypically variable, often mixed gastric/intestinal tumor growth. However, only one of the two pathways involves intestinal metaplasia, its type III variant, p53 gene alteration, and dysplasia to end in glandular cancer. In the other pathway, diffuse cancer apparently arises directly from hyperplastic, sometimes atypical necks of mostly nonmetaplastic gastric glands, through primary involvement of genes affecting cell-cell and cell-matrix junctional proteins.

Changes in Helicobacter pylori-associated gastritis of the antrum and corpus were investigated in a large number of patients treated with omeprazole, with or without the addition of amoxycillin. To investigate the role of H. pylori-associated gastritis in ulcerogenesis and its interplay with omeprazole, biopsies were taken and evaluated according to the Sydney system. Successful eradication of H. pylori (assessed histologically 4 weeks after the end of therapy) led to prompt and persistent suppression of gastritis activity, slow, partial regression of mononuclear inflammation and an ulcer recurrence rate of only 14% during the 6 months' follow-up. In patients treated with omeprazole and placebo, or where eradication treatment with omeprazole and amoxycillin had failed, transient clearance of H. pylori from the antral (but not oxyntic) mucosa was seen. In both of these groups of patients transient regression in the antrum, and worsening in the corpus, of gastritis activity and mononuclear inflammation were evident, coupled with ulcer recurrence rates of 72 and 46%, respectively. It was concluded that H. pylori colonization and gastritis activity play a crucial role in ulcerogenesis, that acid inhibition treatment improves antral H. pylori gastritis and worsens the oxyntic mucosal gastritis, and that this can be prevented by eradication of the H. pylori infection.

Background: A contribution of Helicobacter pylori gastritis to the pathogenesis of non-ulcer dyspepsia (NUD) remains uncertain., Methods: Administration of an appropriate clinical questionnaire followed by endoscopy allowed us to select, among 139 outpatients with dyspepsia, 87 non-ulcer dyspepsia patients with more severe and group-distinctive symptoms, 35 of whom were classified as having ulcer-like (ULD). 38 as dysmotility-like (DLD), and 14 as reflux-like dyspepsia (RLD). Biopsy specimens were evaluated for H. pylori gastritis in accordance with the Sydney system. The 70 H. pylori-positive cases were treated with omeprazole, 20 mg twice daily, and amoxycillin, 1 g three times daily for 2 weeks., Results: Higher rates of H. pylori colonization were found histologically in the gastric mucosa of ULD (91%) and RLD (86%) than in that of DLD (68%) or asymptomatic (42%) patients. ULD differed from RLD patients in their higher score of antritis activity. Three and 6 months after H. pylori eradication ULD (but not DLD) showed significant regression of dypspetic symptoms scores., Conclusions: It seems likely that H. pylori gastritis, with special reference to active antritis, is among causative factors of ULD. Its role in the pathogenesis of RLD and DLD needs further investigation.

To clarify the mechanisms of the gastric mucosal immune--inflammatory response to Helicobacter pylori infection, surgical and biopsy specimens from asymptomatic uninfected, gastritis-free individuals and from H. pylori-positive ulcer patients with chronic gastritis were investigated using light and electron microscopy. Activation of the antigen-transporting endocytic--endosomal system, enhanced expression of the antigen-processing enzyme cathepsin E and de novo expression of antigen-presenting human leukocyte antigen (HLA)-DR molecules have been detected in H. pylori-colonized gastric epithelium. These findings may be crucial in the production of a mucosal immune-inflammatory response to H. pylori infection. Cytoplasmic swelling and vacuolation, micropapillary change, mucin loss, erosion of the juxtaluminal cytoplasm and cell desquamation were the main effects of bacterial cytotoxicity on gastric surface-foveolar epithelium. Activated macrophages and granulocytes (partly linked to the mucosal IgG immune response) concentrate in the foveolar-neck region of the mucosa, where they may enhance damage and impair regeneration of the epithelium. Both direct bacterial cytotoxicity and inflammatory cell aggression against gastric epithelium may predispose the patient to peptic ulcer disease.

The incidence and mean score of Helicobacter pylori-related, active antroduodenitis, lesions of superficial antral epithelium and duodenal gastric-type metaplasia were higher in endoscopic biopsies from a large series of patients with duodenal ulcer, when compared with asymptomatic patients or patients with non-ulcer dyspepsia. In 65 out of 73 patients with duodenal ulcer who could be followed up, H. pylori was eradicated using a combination of amoxycillin, 3 g daily, metronidazole, 1 g daily, and omeprazole, 20 mg daily. Rapid and permanent (6-month follow-up) abolition of both gastroduodenitis activity and lesions of the gastric surface epithelium was observed in these 65 patients. There was also a progressive decrease in total immune-inflammatory cells but without a substantial change in duodenal gastric-type metaplasia. Similar, but transient and quantitatively less prominent, improvements were observed in the antroduodenal mucosa, which had been temporarily cleared of H. pylori by treatment with omeprazole alone. Conversely, increased gastritis activity, epithelial lesions and immune-inflammatory cell scores were found in the short term in the corpus mucosa, which was not cleared of H. pylori after omeprazole treatment. It is concluded that, of the various H. pylori-related mucosal changes, antroduodenitis activity and antral epithelial lesions most closely reflect the severity of mucosal damage and are probably the most important factors in duodenal ulcerogenesis. Their complete and rapid suppression after bacterial eradication may be a key factor in preventing ulcer relapse.

Lymphocytic gastritis is characterized by lymphocytic infiltration of the surface and pit epithelium. Its cause has not been established, but an association with Helicobacter pylori infection or celiac disease has been suggested. We evaluated the histologic features of both gastric and duodenal biopsy specimens from 245 consecutive children and adolescents, and found chronic gastritis in 60 children and celiac disease in 25. Chronic gastritis was associated with H. pylori infection in 36 children and with celiac disease in 15. Lymphocytic gastritis was found in nine children with celiac disease. Children with lymphocytic gastritis had a mean of 40.64 lymphocytes per 100 epithelial cells, compared with a mean of 3.92 lymphocytes per 100 epithelial cells in children with H. pylori-associated gastritis and 5.15 lymphocytes in normal control subjects. Immunohistochemical studies showed that the intraepithelial lymphocytes in lymphocytic gastritis were T cells. No child with lymphocytic gastritis had serologic evidence of past H. pylori infection. We conclude that lymphocytic gastritis in children is associated with celiac disease. Dyspeptic symptoms are frequent; the endoscopic appearance is not characteristic.

In both rodents and humans the development of gastrin-promoted gastric argyrophil enterochromaffin-like cell carcinoids requires the involvement of a genetic factor inherent to multiple endocrine neoplasia syndrome or of type A autoimmune chronic atrophic gastritis. Prolonged severe hypergastrinaemia acting on non-gastritic mucosa, as in Zollinger-Ellison syndrome patients, results in diffuse argyrophil enterochromaffin-like cell hyperplasia but, as a rule, does not produce tumours. Combination of chronic atrophic gastritis (mostly related to Helicobacter pylori infection) with hypergastrinaemia frequently causes linear and micronodular hyperplasia of argyrophil cells, whereas carcinoids are exceptional. No tumours or pre-neoplastic lesions have been observed in patients treated long-term with proton pump inhibitors, apart from rare cases in patients with combined Zollinger-Ellison and multiple endocrine neoplasia syndromes. A moderate increase in the incidence of argyrophil cell clustering, with or without hyperplasia, probably results from the parallel evolution of ulcer-associated Helicobacter gastritis into chronic atrophic gastritis. Eradication of H. pylori with a combination of proton pump inhibitors and antibiotics suppresses gastritis and prevents ulcer recurrence.

A series of 60 gastric endocrine tumors comprised 44 body-fundus argyrophil carcinoids, of which 23 arose in a background of hypergastrinemia and type A chronic atrophic gastritis (A-CAG), mainly with histologic patterns suggestive of an autoimmune process. Only 22 percent (compared with 19 percent of 58 tumor-free A-CAG cases) of 36 carcinoids and 21 percent of 19 A-CAG carcinoids investigated had Helicobacter pylori (HP) colonization, against 50 percent of 14 CAG-associated neuroendocrine carcinomas or mixed endocrine-exocrine tumors, 84 percent of 150 cases with early gastric cancer (p < 0.001 versus carcinoids), mostly with B- or AB-type CAG, 76 percent of 97 tumor-free AB-CAG, and 95 percent of 151 tumor-free B-CAG cases. Secondary hypergastrinemia and local mechanisms activated by chronic autoimmune gastritis are among factors involved in the pathogenesis of relatively indolent CAG-associated carcinoids, whereas active HP gastritis in cooperation with environmental carcinogens may likely cause more severe epithelial transformation, leading to ordinary cancer and, possibly, to neuroendocrine carcinomas or mixed endocrine-exocrine tumors.

A systematic investigation of the histologic pattern of antral and corpus gastritis has been carried out in 1177 patients with various clinical conditions. An increased rate and severity of antral mucosa gastritis activity as well as surface epithelium cytotoxic lesions and Helicobacter pylori colonization, coupled with low rates and severity of the same parameters in corpus mucosa gastritis (usually of superficial nature so as to spare the integrity of acidopeptic glands) were the main features associated with active gastroduodenal peptic ulcer or antroduodenal mucosal erosions. Simultaneous antisecretory (omeprazole) and antibiotic treatment of duodenal ulcer patients led to the eradication of Helicobacter in 54 to 82% of patients when amoxycillin alone was used as antibiotic, and up to 94% of patients, when metronidazole was added to amoxycillin, as against none of patients treated with omeprazole alone, despite effective healing of their ulcer lesion. Very low (usually less than 5% per year) recurrency rates are reported in the literature for patients undergoing bacterial eradication, as against 50 to 80% in non-eradicated patients whose ulcer was healed by short term antisecretory drug treatment.

Helicobacter pylori colonization and the incidence, severity, activity and topography of gastritis were investigated systematically in antrum and corpus mucosal biopsies of 1177 subjects undergoing endoscopy in the absence of gastric complaints (asymptomatic, 49) or for non-ulcer dyspepsia (NUD; 631 patients, 72 of whom had gastric and/or duodenal erosions), active gastric ulcer (GU, 76 patients), active duodenal ulcer (DU, 138 patients), and healed gastric (HGU, 39 cases) or duodenal ulcer (HDU, 230 cases). In the antrum, H. pylori colonization and the incidence, severity and activity of gastritis increased progressively in the sequence asymptomatic, erosion-free NUD, erosive NUD, healed ulcer and active ulcer. The same trend was observed in the corpus as regards H. pylori and gastritis incidence, whereas the severity and activity of gastritis were lower in active DU and erosive NUD and higher in active, proximal GU than in the remaining patients. Active DU and erosive NUD showed the highest incidence of non-atrophic gastritis and lowest type-A or AB atrophic gastritis, while active GU had lowest normal mucosa or type-A gastritis and highest type-B atrophic gastritis. In conclusion, H. pylori colonization and gastritis incidence, severity and, especially, activity of the antrum might all contribute to mucosal erosion and ulceration, whereas the same factors, at least in part and with the exception of proximal GU, seem to have a preventive role when affecting corpus mucosa.

Helicobacter Pylori (HP) were found in 878 (73%) of 1205 patients undergoing upper G-I endoscopy with multiple biopsies for gastroduodenal diseases. HP were present in similar percentages among patients with active (89%) or healed (81%) peptic ulcer as well as in non ulcerous dyspeptics affected with gastritis (85%). 96% of active chronic gastritis were infected by HP as compared with 55% of quiescent gastritis. Antral gastritis was more frequently active in patients with ulcer diseases (76%) than in dyspeptic and asyntomatic patients (50%). Healed gastric and duodenal ulcers showed decreased incidence of active antral gastritis (69) as compared with active ulcers. Conversely body gastritis was more frequently active in healed (37%) than in overt (18%) duodenal ulcers. 95 histologically normal stomachs as well as 9 cases exhibiting type A gastritis were devoid of HP. High rates of infection were found in 610 cases of chronic gastritis without atrophy as well as in 151 atrophic antral (type B) gastritis. Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in HP-infected mucosa. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated HP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions.

Twenty-three children with Helicobacter (Campylobacter) pylori-associated chronic gastritis are reported. Family history of peptic disease, previous digestive procedures, and nonspecific epigastric pain were the most frequently encountered clinical features. Antral nodularity at endoscopy and histologic evidence of follicular gastritis were characteristic morphological aspects. Rapid urease tests suggested the diagnosis in 90% of patients. Significant increases of serum IgG and IgA against Helicobacter pylori allowed the identification of infected children with 95% cumulative sensitivity. Treatment with amoxicillin and bismuth subcitrate eradicated the infection and improved gastritis in 13 of 19 children. These findings provide further evidence for the etiologic role of Helicobacter pylori in chronic antral gastritis in children.

Campylobacter-like organisms (CLOs) were histologically detected in 230 (74.5%) of 310 patients undergoing endoscopy with multiple gastric biopsies for symptoms suggestive of upper digestive disease. CLOs were found in 78.6% of nonulcerous dyspeptic patients, 82.2% of healed ulcers, 88.2% of duodenal or pyloric ulcers and 90.0% of gastric ulcers but only in 46.9% of gastric stumps and 47.6% of nonulcerous patients without dyspepsia. Among 274 subjects with gastritis, CLOs were found in 83.9%, while none of the 36 gastritis-free stomachs harbored CLOs. Severe atrophic gastritis was less frequently infected with CLO (55.5%) as compared with superficial, interstitial or preatrophic gastritis (84.4%). CLOs were only slightly more frequent in the presence of intraepithelial granulocytes and were never found in areas of complete intestinal metaplasia. Foveolar and superficial epithelia heavily infected with CLOs showed peculiar ultrastructural changes (micropapillary hyperplasia with luminal bulging of mucous cells, cytoplasmic vacuolization and edema, etc.) suggesting a direct link between CLO infection and epithelial damage, which in turn may have a role in the genesis of mucosal inflammation.

Campylobacter pylori (CP) were found in 84% of 384 patients with chronic gastritis and in none of 49 subjects without inflammation. CP were present in similar percentages among patients with active (90%) or healed peptic ulcer (84%), as well as in non-ulcerous dyspepsia complicated by gastritis (91%). Cytoplasmic vacuolization and swelling of foveolar-superficial cells with adhering bacteria, micropapillae and microerosions were commonly found in CP-infected mucosa. In 100 cases with gastritis both intraepithelial granulocytes and epithelial lesions were prominent features of heavily CP-infected antral mucosa. The occurrence of some cases with abundant, adhering CP but lacking epithelial lesions is in keeping with the different ability of various CP-strains to produce cytotoxins. In 16 of 19 children with type B chronic gastritis antibacterial therapy eradicated CP. This was followed by resolution or striking improvement of gastritis and disappearance of epithelial lesions. These data provide further morphological evidence of direct cytotoxic activity of CP toward gastric mucosal cells.

Summary Background : The majority of reflux patients have non-erosive reflux disease. Aim : To evaluate the influence of Helicobacter pylori on oesophageal acid exposure in patients with both non-erosive and erosive reflux disease and in a group of controls. The pattern and distribution of chronic gastritis were also assessed. Methods : One hundred and twelve consecutive patients with symptoms of gastro-oesophageal reflux disease agreed to undergo both upper gastrointestinal endoscopy and 24-h oesophageal pH-metry. Patients were grouped as H. pylori -positive or H. pylori -negative on the basis of both CLO-test and histology, and as cases with or without oesophagitis on the basis of endoscopy. The controls consisted of 19 subjects without reflux symptoms and with normal endoscopy and oesophageal pH-metry. Results : H. pylori was positive in 35 patients (31%) and in six controls (31%); oesophagitis was found in 44 patients (39%) and non-erosive reflux disease in 68 (61%). The prevalence of chronic gastritis in the antrum and corpus was higher in H. pylori -positive than in H. pylori -negative patients (P < 0.001), but was more frequently mild (P < 0.001) than moderate or severe. The percentage total time the oesophageal pH < 4.0 was higher in patients than in controls (P < 0.008–0.001), but there was no difference between H. pylori -positive and H. pylori -negative patients (12.3% vs. 12%, P = 0.43) or H. pylori -positive and H. pylori -negative controls (1.07% vs. 1.47%, P = 0.19). Conclusions : H. pylori infection had the same prevalence in reflux patients and in controls. It did not affect oesophageal acid exposure, as there was no difference between H. pylori -positive and H. pylori -negative individuals. The high prevalence of mild body gastritis in H. pylori -positive patients suggests that H. pylori eradication is unlikely to lead to gastric functional recovery, which might precipitate or worsen symptoms and lesions in patients with... [ABSTRACT FROM AUTHOR]

Morphometric assessment of gastric antral atrophy: comparison with visual evaluation Aims: As part of a multinational effort to reach a consensus in the definition and evaluation of atrophic gastritis, we applied morphometric techniques to 22 antral biopsy specimens examined visually by 12 experienced gastrointestinal pathologists. Methods and results: Atrophy was defined as loss of glands. Each pathologist graded atrophy with both non-standardized and standardized approaches. Discriminant function analyses of morphometric measurements were conducted to validate and grade atrophy. Kappa statistics were used to compare the performance of each pathologist against the group mode and against the discriminant functions’ grading of atrophy. Three morphometric indexes showed significant differences among categories of atrophy utilizing non-standardized as well as standardized visual atrophy grades: (i) the ratio of glandular length to total mucosal thickness; (ii) the proportion of the secretory compartment area occupied by glands; and (iii) the number of glandular cross sections per 40× microscopic field. The discriminant function analyses verified all cases classified visually as either non-atrophic, or moderately/severely atrophic; it verified as mildly atrophic 40% of the cases classified visually as mildly atrophic; and classified the remaining 60% as moderately or severely atrophic. The κ statistics were good or excellent for the majority of pathologists. Conclusions: The evaluation of antral atrophy, simply defined as loss of glands, can be reliable and reproducible. The visual grading of atrophy as absent, moderate and severe is entirely consistent with objective morphometric observations. [ABSTRACT FROM AUTHOR]

Background/Aims: The pathogenesis of dyspeptic/reflux symptoms and the clinico-pathologic profile of affected patients are still poorly understood. To improve our knowledge in this field we carried out a systematic, comparative analysis of symptom profiles and histopathologic patterns of oesophagogastroduodenal mucosa in a series of 221 subjects, 140 with and 81 without endoscopic evidence of hiatal hernia. Of these, 190 showed reflux and/or dyspeptic symptoms. Methods: Before endoscopy, all the subjects were questioned about the presence and severity of 12 individual symptoms. Biopsies were taken from the distal oesophagus, cardia, corpus, angulus, antrum and duodenal bulb, and were scored in accordance with the Sydney system. Results: Patient groups with a distinct clinico-pathologic profile were better identified when symptoms of adequate severity were compared with histopathologic parameters. A correlation between gastroesophageal reflux disease (GORD) symptoms and histologic signs of oesophagitis was mostly restricted to patients endoscopically positive for oesophagitis. Retroxiphoid pyrosis correlated with cardial gastritis but not with oesophagitis, either endoscopic or histologic, while ulcer-like epigastric pain correlated with active duodenitis and distal gastritis. No definite histopathologic background was detected in patients with putative dysmotility-like symptoms, endoscopy-negative GORD and low score or mixed symptoms. Conclusion: A contribution of Helicobacter pylori gastroduodenitis to the pathogenesis of some dyspeptic symptoms seems likely. However, the identification of specific histologic changes causing individual symptoms remains rather elusive, with the exception of active antroduodenitis in patients with ulcer-like pain and of active proximal gastritis in patients with severe retroxiphoid pyrosis. [ABSTRACT FROM AUTHOR]

Background and Aims: Upper gastrointestinal endoscopy (UGIE) and biopsies are needed for diagnosis of atrophic gastritis. Serum levels of Pepsinogen I (PGI) are used as a non-endoscopic test for atrophic corpus gastritis but non-endoscopic diagnosis of atrophic antrum gastritis has not been possible. The aim was to study whether the test panel composed of Elisa assays of Gastrin17 (sG17), PGI after a prandial protein stimulus and Hp antibodies (IgG) can be used as a tool for diagnosis of atrophic gastritis. Material and Methods: 104 subjects(M/F 56/48, mean age 55 yrs) was enrolled. A blood sample was collected for measurement of basal-G17, PGI and Hp IgG serum level; a second blood sample was collected 20 minutes after a prandial peptic stimulus evaluating sG17 serum level. Subjects were grouped according to five histological features, 1) Normal mucosa Hp- (N), 2) Non atrophic antrum gastritis Hp+ (S), 3) Atrophic gastritis of antrum Hp+ (A), 4) Atrophic gastritis of corpus Hp+/- (C), 5) Atrophic gastritis of antrum and corpus Hp+/- (AC). Results: sG17 serum level was higher in subjects with S (12,0 pmol/l) respect to subjects with A (1 pmol/l) (p<0,001) and with N (2,5 pmol/l)(p<0,001).PGI serum level was higher in subjects S and A (117,2µg/l and 119,7 µg/l) compared to subjects with atrophic corpus gastritis C (43,9µg/l)(p<0,001)and normal mucosa N (89,9 µg/l) (p<0,009).Combination of these three serological tests showed a sensitivity of 91% (32/35) and a specificity of 88%(61/69) in evaluating atrophic gastritis, overall accuracy of 87,5% (91/104) in identifying specific histological pattern using the test panel. Conclusions: Serum levels of sG17 and PGI combined with evaluation of Hp status by Hp IgG antibody represent a good non-invasive method to evaluate gastric atrophy and may use in a population screening program for gastric cancer to identify subjects at risk to be referred for upper-GI-endoscopy. [ABSTRACT FROM AUTHOR]