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M Rugge

Publications and source records attributed to M Rugge.

At least 37 records · Page 2Linked to original sources
PubMed2002

Histology predicts cirrhotic evolution of post transplant hepatitis C.

BACKGROUND: Hepatitis C recurring after orthotopic liver transplantation varies in severity and some patients rapidly develop fully established liver cirrhosis. Neither clinical nor biological markers of such rapid cirrhotic evolution are available. AIM: To assess the value of histology in identifying patients who will develop cirrhosis shortly after liver transplantation. PATIENTS AND METHODS: Only cases of recurrent hepatitis C diagnosed by both hepatitis C virus-RNA positive serum and liver changes consistent with hepatitis, with no other causes of allograft injury, were considered. A total of 128 liver biopsies were scored from 29 consecutive patients with a mean follow up of 48 (13.97) months. The histological activity index was evaluated according to Ishak et al. The time of the first histological diagnosis of recurrent hepatitis C in the absence of rejection was defined as time of histological recurrence (RHC-T). RESULTS: First histological diagnosis of recurrent hepatitis with no features of rejection was obtained at the six month biopsy in 23 of 29 cases. By the end of follow up, nine patients had developed cirrhosis (mean follow up 38 (14.39) months (range 18-60)). The remainder (mean follow up 46 (13.40) months (24-72)) showed a spectrum of fibrosis but no cirrhosis. Severe necroinflammatory lesions at RHC-T significantly correlated with rapid development of cirrhosis. At the RHC-T biopsy, only cases evolving into cirrhosis showed confluent necrosis. The median value of the histological activity index was 11 (mean 11.11 (1.76) (range 9-14)) in patients who developed cirrhosis and four (mean 4 (1.78) (range 1-8)) in the others (p<0.0001). A histological activity index > or =9 was associated with rapid development of cirrhosis in 100% of cases. CONCLUSIONS: After liver transplantation, the histological activity of recurrent hepatitis C predicts the risk of development of cirrhosis. By adopting Ishak's scoring system, a histological activity index > or =9 was 100% sensitive/specific in identifying subjects who rapidly developed cirrhosis.

Acute Disease↗
PubMed2001

Prevalence of intestinal metaplasia in the distal oesophagus, oesophagogastric junction and gastric cardia in symptomatic patients in north-east Italy: a prospective, descriptive survey. The Italian Ulcer Study Group "GISU".

BACKGROUND: Incidence of adenocarcinoma of distal oesophagus and gastric cardia, probably arising from areas of intestinal metaplasia, has been increasing rapidly. AIMS: To define prevalence of intestinal metaplasia of distal oesophagus, oesophagogastric junction and gastric cardia and to evaluate potential associated factors, by means of a prospective multicentre study including University and teaching hospitals, and primary and tertiary care centres. PATIENTS: Each of 24 institutions involved in study enrolled 10 consecutive patients undergoing first-time routine endoscopy for dyspeptic symptoms. METHODS: Patients answered symptom questionnaires and underwent gastroscopy Three biopsies were taken from distal oesophagus, oesophago-gastric junction and gastric cardia, and were stained with haematoxylin and eosin. Specimens were also evaluated for Helicobacter pylori infection. RESULTS: A total of 240 patients (124 male, 116 female; median age 56 years, range 20-90) were enrolled in study. Intestinal metaplasia affected distal oesophagus in 5, oesophago-gastric junction in 19 and gastric cardia in 10 patients. Low-grade dysplasia was found at distal oesophagus and/or oesophago-gastric junction of 3/24 patients with intestinal metaplasia vs 2/216 without intestinal metaplasia (p<0.05). A significant association was found between symptoms and presence of intestinal metaplasia, regardless of location, and between Helicobacter pylori infection and intestinal metaplasia at oesophago-gastric junction. CONCLUSIONS: Intestinal metaplasia of distal oesophagus, oesophagogastric-junction and gastric cardia is found in a significant proportion of symptomatic patients undergoing gastroscopy and is associated with dysplasia in many cases. Although prevalence of dysplasia seems to decrease when specialized columnar epithelium is found in short segment, or even focally in oesophago-gastric junction, these small foci of intestinal metaplastic cells may represent source of most adenocarcinomas of cardia.

Barrett Esophagus↗
PubMed2001

Review article: pre-neoplastic states of the gastric mucosa--a practical approach for the perplexed clinician.

The sequence leading to gastric cancer can be schematically reduced to Helicobacter pylori infection-chronic gastritis-atrophy-intestinal metaplasia-dysplasia-neoplasia. Although clinicians have not yet developed a uniform approach to the treatment of gastritis (when should H. pylori infection be treated?), the entity itself is not the subject of controversy. All other lesions are still the focus of debate. There are no guidelines for the management of patients with intestinal metaplasia; pathologists are still searching for universal diagnostic criteria for atrophic gastritis; dysplasia and early neoplasia have elicited scientific diatribes between Japanese and Western pathologists. Amidst such controversies and in the absence of guidelines to regulate the management of gastric lesions, the responsibility to provide sensible clinical advice is often bestowed upon pathologists. This review discusses whether pathologists have access to sufficient evidence to provide the requested advice, and whether a consensus on the management of gastric "pre-neoplastic" states is within reach. We conclude that, although many sensible and useful definitions, criteria and classifications are being generated, the final decision on how to manage the individual patient with gastric lesions will continue to be based on the communication between pathologist and clinician.

Adenocarcinoma↗
PubMed2001

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 40x 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 kappa 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.

Atrophy↗
PubMed2001

The phenotype of gastric mucosa coexisting with Barrett's oesophagus.

BACKGROUND/AIMS: Barrett's oesophagus complicates the gastro-oesophageal acid reflux. Helicobacter pylori infection, particularly with cagA positive strains, induces inflammatory/atrophic lesions of the gastric mucosa, which may impair acid output. No systematic study has investigated the phenotype of the gastric mucosa coexisting with Barrett's oesophagus. This study was designed to identify the phenotype of gastric mucosa associated with Barrett's oesophagus. METHODS: In this retrospective case control study, the phenotype of the gastric mucosa was histologically characterised in 53 consecutive patients with Barrett's oesophagus and in 53 (sex and age matched) non-ulcer dyspeptic controls. Both patients and controls underwent extensive sampling of the gastric mucosa (two antral, one incisural, and two oxyntic biopsies). Intestinal metaplasia (IM) was categorised (type I, complete IM; types II and III, incomplete IM) by the high iron diamine stain; cagA status was ascertained by genotyping. RESULTS: Helicobacter pylori was present in 19 of the 53 patients with Barrett's oesophagus and in 30 of the 53 controls (p < 0.02); eight of the 19 patients with Barrett's oesophagus and 28 of the 35 controls harboured cagA positive H pylori (p < 0.03). The histological severity of non-atrophic gastritis detected in the controls was significantly higher than that detected in the patients with Barrett's oesophagus (p < 0.0001). Multifocal atrophic gastritis was present in 4% of the patients with Barrett's oesophagus and in 23% of controls (p < 0.01). The odds ratio for the association between multifocal atrophic gastritis and Barrett's oesophagus was 0.20 (95% confidence interval, 0.006 to 0.60). Gastric IM was detected in 13.2% of the patients with Barrett's oesophagus and in 30.1% of the controls (p < 0.03). Type III IM at the gastric mucosa was only detected among controls. CONCLUSIONS: Barrett's oesophagus is associated with a low prevalence of H pylori cagA positive infection and multifocal atrophic gastritis. This pathobiological pattern is considered to be associated with a low risk of distal gastric cancer.

Adult↗
PubMed2001

Colonic metaplasia in the long-term follow-up of the ileal neobladder.

OBJECTIVE: To look for the presence of colonic metaplasia (CM), the shifting from sialomucins (SIs) to sulfomucins (SUs), considered as a probably premalignant lesion in the stomach in the mucosa of the ileal neobladder (IN). METHODS: 19 patients with IN were subjected to endoscopic biopsy; the samples were analyzed by means of histochemistry with high iron diamine, a test indicated to identify SIs and SUs. RESULTS: CM was never observed earlier than 1 year after the operation, was absent in 9/19 patients (mean follow-up 14 months) and present in 10/19 (mean follow-up 59 months). CONCLUSION: Time-dependent phenotypic changes, already described in the stomach as being premalignant, take place after constant contact with urine in the mucosa of the IN. It is at present unclear whether they may be defíned as only metaplastic or frankly preneoplastic; anyway, a careful follow-up remains indicated in all patients with íntestinal urinary diversions.

Aged↗
PubMed2001

Different effects of H. pylori water extracts on cytokines, pepsinogen C and gastrin mucosal release in patients with or without duodenal ulcer.

In the present study we ascertained whether cagA positive and negative H. pylori strains release water soluble products that can influence the production of gastric mucosal cytokines and endocrine (gastrin) or exocrine (pepsinogen C) secretion in 23 H. pylori positive and 19 H. pylori negative patients. Antral biopsies were obtained to classify inflammation, activity, atrophy, intestinal metaplasia and H. pylori density grade. The cagA gene was identified by means of the polymerase chain reaction (PCR) in H. pylori positive colonies after culture of mucosal samples. Three antral biopsies from each patient were incubated with (1.) Water extracts from cagA positive, (2.) Water extracts from cagA negative strains or (3.) H2O (control) at 37 degrees C in a CO2 incubator for 24 hrs. Gastrin, pepsinogen C, IL-1 beta, IL-8, GMCSF, and TNF alpha were measured in the supernatants and mucosal homogenates. H. pylori infection was significantly associated with an increased antral inflammation and activity (chi 2 = 21.7, p < 0.001 and chi 2 = 42.0, p < 0.001), and increased mucosal levels of IL-1 beta, IL-8 and TNF alpha. Water extracts from cagA positive strains enhanced the release of PGC in mucosal biopsy supernatants (p < 0.05) when patients were considered overall and the release of TNF alpha (p < 0.05) when only patients with duodenal ulcer were considered. Water extracts from cagA negative strains stimulated gastrin secretion (p < 0.05). None of the remaining cytokines were influenced by H. pylori water extracts. In conclusion, pepsinogen C and TNF alpha can be induced by cagA positive water extracts and may contribute to damage the gastric and duodenal mucosa. Our findings indicate that in patients with H. pylori infection the increase of the mucosal levels of IL-1 beta and IL-8 does not depend on H. pylori water soluble products, but probably depends on the entire bacterium.

Adult↗
PubMed2001

Fez1/lzts1 alterations in gastric carcinoma.

PURPOSE: Loss of heterozygosity (LOH) involving the short arm of chromosome 8 (8p) is a common feature of the malignant progression of human tumors, including gastric cancer. We have cloned and mapped a candidate tumor suppressor gene, FEZ1/LZTS1, to 8p22. Here we have analyzed whether FEZ1/LZTS1 alterations play a role in the development and progression of gastric carcinoma. EXPERIMENTAL DESIGN: We examined Fez1/Lzts1 expression in 8 gastric carcinoma cell lines by Western blot, and in 88 primary gastric carcinomas by immunohistochemistry. Twenty-six of these 88 primary gastric carcinomas were also microdissected and tested for LOH at the FEZ1/LZTS1 locus and for mutation of the FEZ1/LZTS1 gene. Furthermore, we studied the FEZ1/LZTS1 gene regulation and transcriptional control and the methylation status of the 5' region of the gene in all 8 gastric carcinoma cell lines. RESULTS: Fez1/Lzts1 protein was barely detectable in all of the gastric cancer cell lines tested and was absent or significantly reduced in 39 of the 88 (44.3%) gastric carcinomas analyzed by immunohistochemistry, with a significant correlation (P < 0.001) to diffuse histotype. DNA allelotyping analysis showed allelic loss in 3 of 17 (18%) and microsatellite instability in 4 of 17 (23.5%) cases informative for D8S261 at the FEZ1/LZTS1 locus. When we compared the presence of LOH with Fez1/Lzts1 expression, we found loss of protein expression in all three of the tumors with allelic imbalance at D8S261. A missense mutation was detected in one case that did not express Fez1/Lzts1. Hypermethylation of the CpG island flanking the Fez1/Lzts1 promoter was evident in six of the eight cell lines examined as well as in the normal control. CONCLUSIONS: Our findings support FEZ1/LZTS1 as a candidate tumor suppressor gene at 8p in a subtype of gastric cancer and suggest that its inactivation is attributable to several factors including genomic deletion and methylation.

Adaptor Proteins, Signal Transducing↗
PubMed2001

[Diagnosis of Helicobacter pylori infection: comparison of techniques].

UNLABELLED: Several diagnostic assays are available for evaluating Helicobacter pylori infection: histological examination, culture of gastric biopsies, urea breath test and serology. Recently a new enzyme immunoassay has been introduced for the detection of H. pylori antigens in stool samples (HpSA). The aim of our study was to evaluate and compare diagnostic efficacy of HpSA with histological examination, culture, urea breath test and serology in a group of 95 patients. Patients were classified H. pylori positive (43) or negative (52) on the basis of histology, culture and urea breath test. HpSA optical densities were significantly higher in infected patients compared to those obtained in H. pylori-negative patients (t = 5.47, p < 0.001). Overall, with a fixed cut-off of 0.1 unit of optical density, the sensitivity was 79% and the specificity 100%. In the H. pylori positive patients, HpSA optical density correlated with bacterial load histologically evaluated in the gastric antrum (r = 0.405, p < 0.05) and was inverse correlated with levels of serum IgG elicited against H. pylori (r = -0.315, p < 0.05). Considering patients with a positive HpSA finding and/or levels of anti-H. pylori antibodies upper than 30 U/mL, sensitivity in detecting infected patients was 98%. IN CONCLUSION: (1) immunodetection of H. pylori antigens in stools is a good alternative of breath test; (2) a reduction in H. pylori density grade might be accompanied by low HpSA optical density, leading to a false negative result and (3) combining the HpSA determination with the serum detection of anti-H. pylori antibodies a better clinical sensitivity is obtained.

Adult↗
PubMed2000

Antigastric autoantibodies in Helicobacter pylori infection: role in gastric mucosal inflammation.

UNLABELLED: The aim of the study was to ascertain whether there is an association between the presence of serum parietal cell autoantibodies (PCA) and: (1) Helicobacter pylori infection; (2) the presence and degree of gastritis and intestinal metaplasia; and (3) the H. pylori infecting strain. Gastric mucosal biopsies were obtained from 49 consecutive patients in order to assess and grade gastritis, make a histological diagnosis, and culture and genotype H. pylori. H. pylori infection was present in 26 patients (group 1), had been present in 17 patients (group 2), and the remaining 6 (group 3) had never had the infection. The infecting strain was cagA positive in 21 of 26 group 1 patients. Positive PCA results were found in 84%, 76%, and 14% of patients in groups 1, 2, and 3, respectively. PCA results were correlated with anti-H. pylori antibody titers (P<0.05). In group 2 patients, PCA were associated with the degree of antral gastritis (Fisher's exact test P<0.05). cagA status was not associated with the presence of PCA (chi2=0.68, NS). The frequency of positive findings for PCA in group 2 was higher in patients with (90%) than in those without (50%) intestinal metaplasia. IN CONCLUSION: (1) H. pylori infection is associated with the production of PCA, which, after eradication of the infection, persist and might contribute to the persistent antral chronic gastritis and intestinal metaplasia; (2) the gastric lesions associated with infections sustained by the more-virulent H. pylori strains do not appear to be due to the induction of antigastric autoantibodies.

Adolescent↗
PubMed2000

Gastric dysplasia: the Padova international classification.

A worldwide-accepted histologic, classification of the gastric carcinomatous and precancerous lesions is a prerequisite for a consistent recording of epidemiologic data and for both developing and evaluating primary and secondary preventive efforts. Different nomenclatures have been proposed for gastric precancerous lesions in eastern countries and in Japan. This article presents a classification of gastric precancerous lesions resulting from an international consensus conference involving pathologists of different countries. Five main diagnostic categories are identified. To allow comparisons with the nomenclature proposed by the Japanese Research Society for Gastric Cancer, each category was also assigned a numeric identification: 1 = normal, 2 = indefinite for dysplasia, 3 = noninvasive neoplasia, 4 = suspicious for invasive cancer, and 5 = cancer. The interobserver reproducibility of the histologic classification was tested in a series of 46 cases. By collapsing benign alterations (categories 1+2) versus noninvasive neoplasia (category 3) versus suspicious for invasive cancer and fully appearing carcinomatous lesions (categories 4+5), the general agreement value was 77.7%, whereas kappa coefficient was 0.63. By examining gastric precancerous lesions from diverse populations, the authors agreed that the gastric precancerous process is universal and the differences in nomenclatures are merely semantics. The international Padova classification of the gastric precancerous lesions is submitted to the attention of the international scientific community, which is invited to test and to improve on it.

Adenocarcinoma↗
PubMed2000

Topographic patterns of intestinal metaplasia and gastric cancer.

OBJECTIVE: The role of intestinal metaplasia in gastric oncogenesis has been demonstrated by both cross-sectional and longitudinal studies. This study was designed to determine whether, in a population at high risk for gastric cancer, different topographical patterns and phenotypes of intestinal metaplasia were associated with different degrees of cancer risk. METHODS: A total of 68 Colombian patients with gastric cancer and 67 controls with nonulcer dyspepsia were studied by an extensive biopsy protocol. Intestinal metaplasia was assessed semiquantitatively by histology and was characterized histochemically. In both patients and controls, the Spearman's correlation test was applied to the test if the gastric distribution of metaplastic lesions resulted in specific topographical patterns associated with different risks for cancer. RESULTS: Four topographical patterns of intestinalization emerged: 1) "Focal," in 14 cancer patients and 16 controls; 2) "Antrum-predominant," in seven cancer patients and six controls; 3) "Magenstrasse" (involving the lesser curvature from cardia to pylorus) in 25 cancer patients and four controls. This pattern was associated with higher cancer risk (OR = 5.7; 95% CI: 1.3-26) than were the two less extensive patterns; and 4) "Diffuse," involving essentially the entire gastric mucosa with the exception of the fundus, was unique to 13 cancer patients. The OR for cancer was 12.2; 95% CI: 2.0-72.9. Incomplete-type metaplasia significantly correlated with the extent of total metaplasia and was also associated with greater cancer risk. CONCLUSIONS: In a population with high risk for gastric cancer, the extension of intestinal metaplasia correlates with the extent of its "incomplete" phenotype and is significantly associated with increased cancer risk. Both the extent and location of intestinal metaplasia along the lesser curvature (from the cardia to the prepyloric zones) identify patients with the highest cancer risk.

Adenocarcinoma↗
PubMed2000

The p53 gene in patients under the age of 40 with gastric cancer: mutation rates are low but are associated with a cardiac location.

BACKGROUND: Determining both the frequency and the spectrum of p53 gene mutation in young patients with gastric cancer might provide clues to the host related genetic mechanism(s) in gastric carcinogenesis. PATIENTS AND METHODS: p53 mutations were assessed (by means of polymerase chain reaction-single strand conformation polymorphism (PCR-SSCP), followed by DNA sequencing) in a cohort of 105 consecutive Italian patients in whom gastric cancer was ascertained before the age of 41. RESULTS: A low prevalence of p53 mutations (eight of 105) was observed, with no significant difference between intestinal (three of 31; 10%) and diffuse (five of 74; 7%) phenotypes. A significantly higher prevalence of p53 mutations was associated with the cardiac location (odds ratio, 7.09; confidence interval, 1.56 to 32.11). In all but one case, p53 mutations were associated with a stage higher than I. All eight mutations were located at CpG sites, where G : C to A : T transitions have been associated with frequent methylation at the C5 position of cytosine. CONCLUSIONS: These findings show that, unlike what has been consistently demonstrated in the general population, p53 mutations are uncommon in gastric cancer occurring in young patients, and in such patients, p53 alterations are significantly associated with the cardiac location.

Adolescent↗
PubMed1999

Microsatellite instability and/or loss of heterozygosity in young gastric cancer patients in Italy.

Gastric cancers are rarely diagnosed before the age of 40 years and the incidence reaches a peak during the 7th decade in the general population. A molecular mechanism of early tumor onset may be determined by comparing microsatellite instability (MSI), indicative of error-prone mismatch repair, and loss of heterozygosity (LOH) between gastric cancers in patients < or = 40 years of age and those of older ages. Three to 5 chromosomal loci, where MSI and/or LOH are commonly found in gastric cancers in the general population, were examined in formalin-fixed, paraffin-embedded samples from 102 patients < or = 40 years of age using a polymerase chain reaction-based non-radioactive screening method. MSI and/or LOH at a minimum of 1 locus were detected in 11/102 patients. The frequency of MSI and/or LOH at the D11S904 locus was significantly higher than that at the D2S119, D2S123, D5S409 and IFNA regions. No preferential genetic changes at the D11S904 locus were observed in elderly patients. Among several clinicopathological variables, a statistically significant association with MSI and/or LOH was observed only for tumors located at the cardia, compared with tumors at the antrum and the corpus. Our findings suggest that a unique mechanism may be involved in increasing the susceptibility of the D11S904 locus for either MSI or LOH, especially for cardia tumors in young patients. Early onset of gastric cancers in patients < or = 40 years of age is associated with genetic changes at preferential chromosomal loci, including D11S904.

Adolescent↗
PubMed1999

Patients younger than 40 years with gastric carcinoma: Helicobacter pylori genotype and associated gastritis phenotype.

BACKGROUND: In the general population, Helicobacter pylori (H. pylori), particularly the cagA positive strain, has been associated with intestinal-type gastric carcinoma. Gastric carcinomas are rarely observed in patients age < or = 40 years. Host-related factors have been thought to be more important than environmental agents in these early-onset cancers. The aim of this study was to ascertain the possible role of H. pylori infection and that of cagA positive strains in the development of gastric carcinoma in these young patients. METHODS: In this case-control study, 105 gastric carcinoma patients (male-to-female ratio = 1.1; mean age, 34.4 years; range, 16-40 years) and an equal number of controls (matched for gender and age) were retrospectively selected from the same geographic area. The phenotypes of gastritis and H. pylori were histologically assessed, and the presence of the ureC gene, which is indicative of H. pylori infection, and the cagA genotype were determined by polymerase chain reaction. Gastric carcinoma risk was calculated by both univariate and multivariate statistical methods, taking into account the cancer phenotype, the gastritis phenotype detected in both patients and controls, and the H. pylori genotype. RESULTS: For 74 diffuse and 31 intestinal gastric carcinomas, multivariate logistic regression analysis produced results consistent with those of univariate statistical tests, showing a significant association between gastric carcinoma and both H. pylori infection (odds ratio [OR] = 2.79; 95% confidence interval [CI] = 1.52-5.11) and cagA positive status (OR = 2.94; 95% CI = 1.56-5.52). CONCLUSIONS: In young Italian patients with gastric carcinoma, the significant association with cagA positive H. pylori infection suggests that the bacterium has an etiologic role in both diffuse-type and intestinal-type gastric carcinoma.

Adenocarcinoma↗
PubMed1999

The dark side of the gastric biopsy.

Based on the assumption that both sides of a gastric biopsy sample have a similar appearance, the choice of which side of a specimen is to be sectioned is usually random. We tested the hypothesis that the diagnosis reached by examining the two sides of a gastric biopsy may differ. Eighty-one antral biopsy specimens from patients with neither focal lesions nor previous gastric surgery were evaluated. After preparing 8-10 sections from each of the two opposite faces of each biopsy, sections were scored for Helicobacter pylori, activity, atrophy, intestinal metaplasia, lymphoid follicles. The presence of other lesions was also noted. Intrabiopsy agreement (the consistency in the identification of histological lesions on the opposite sides of the same sample) was calculated by using kappa statistics. A kappa value lower than 0.5 was considered "poor"; between 0.51 and 1.00 "moderate to excellent." The intrabiopsy agreement kappa values were: activity = 0.83, atrophy = 0.54, intestinal metaplasia = 0.51 and lymphoid follicles = 0.19. A mean of 42 serial sections (ranging from a mean of 22 for lymphoid follicles to a mean of 81 for xanthogranulomata) was needed to achieve an excellent (ie, kappa > or = 0.75) intrabiopsy agreement between the features showed at the opposite sides of a biopsy specimen. Intrabiopsy variability may represent a hitherto unrecognized source of error, and it should be minimized or avoided. In a research context information about the number of sections examined from a biopsy would provide a crucial element necessary to evaluate the accuracy of the histological data.

Atrophy↗