Histological findings in gastric mucosa in patients treated with non-steroidal anti-inflammatory drugs.

AIMS--To identify distinguishing and general histological features related to the use of non-steroidal anti-inflammatory drugs (NSAID). METHODS--Slides from gastric antral biopsies of 50 patients with osteoarthritis taking NSAID were compared with slides from antral biopsies of 50 control cases matched for age, sex, and race. Semithin sections stained with toluidine blue were used. RESULTS--Chronic gastritis was seen in 76% of the patients taking NSAID and in 58% of the control cases; active inflammation was detected in 10% of the NSAID treated patients and in 24% of the control cases, and it appeared closely related with Helicobacter pylori infection. Some histological features common to all slides of patients taking NSAID were recognised. These consisted of focal erosions of the gastric epithelium and macroerosions, and they seemed to represent successive steps of a process of "desquamation". CONCLUSIONS--Some distinguishing morphological aspects appeared prominent; it is suggested that these may be related to the pathogenesis of NSAID linked peptic ulceration. On the other hand, epithelial damage due to NSAID appears very different from that due to Helicobacter pylori, another important factor involved in the aetiopathogenesis of peptic disease.     

Helicobacter pylori genotypes, host factors, and gastric mucosal histopathology in peptic ulcer disease

From 183 patients undergoing upper gastrointestinal endoscopy, we used antral and corpus gastric biopsies for bacterial culture and histopathologic examination, blood samples to detect immunoglobulin G antibodies against Helicobacter pylori, and H pylori genomic DNA to analyze cytotoxin-associated gene A (cagA) and vacuolating cytotoxin (vacA) genotypes. As expected, among H pylori biopsy-positive patients, those with duodenal ulcer (DU) (n = 34) had significantly more severe chronic and acute inflammation (P <.001) and epithelial degeneration (P =.004) in the gastric antrum than in the gastric corpus. Each of those 3 parameters and H pylori density were significantly higher in the antrum of patients with DU than in patients with gastric ulcer (GU) or no ulcer. Colonization with vacA s1/cagA-positive strains of H pylori was associated with inflammation and epithelial degeneration in gastric mucosa and increased risk for peptic ulcer disease (PUD), whereas colonization with vacA s2m2/cagA-negative strains was associated with mild gastric histopathology and was not associated with any significant risk for PUD. The predominant H pylori strains in African Americans were vacA s1bm1/cagA-positive, whereas all genotypes were well represented in non-Hispanic-Caucasians. By multivariate analysis, H pylori colonization was significantly associated with DU (Adjusted odds ratio [AdjOR] = 3.2 [1.4-7.2]) and nonsteroidal anti-inflammatory drugs (NSAID) use was inversely associated (AdjOR = 0.3 [0.2-0.7]). NSAID use (AdjOR = 4.3 [1.02-18.5]) and African-American ethnicity (AdjOR = 10.9 [2.6-50]) were significantly associated with GU. Smoking and age were not significantly associated with either DU or GU. These data indicate that DU is associated with an antral-dominant gastritis, and H pylori genotype and NSAID use independently contribute to the pathogenesis of PUD. HUM PATHOL 32:264-273. This is a US Government work. There are no restrictions on its use.     

Ten year follow up study of lymphocytic gastritis: further evidence on Helicobacter pylori as a cause of lymphocytic gastritis and corpus gastritis.

AIMS--To examine the course of lymphocytic gastritis and its relation to Helicobacter pylori (H pylori) infection in a 10 year follow up. METHODS--Ninety six patients were originally examined for dyspepsia in 1981. Gastroscopies with stepwise biopsies were performed on all the patients initially and after an interval of 10 years. RESULTS--Nine per cent of the patients (9/96) had features of lymphocytic gastritis in gastric biopsy at the first examination, and 12.5% (12/96) at the second examination; 7/9 patients (78%) had persistent lymphocytic gastritis during the follow up; in two the diagnostic features of lymphocytic gastritis had disappeared, and five had a new diagnosis of lymphocytic gastritis at the second examination. At the second examination 9/12 lymphocytic gastritis patients (75%) were H pylori positive histologically, while all had specific antibodies to H pylori. The lymphocytic gastritis patients had higher grades of gastritis (p = 0.009), neutrophilic and eosinophilic granulocytes, mononuclear inflammatory cells, and foveolar hyperplasia in the corpus mucosa, but smaller numbers of H pylori, than the H pylori positive patients without lymphocytic gastritis. The appearance of lymphocytic gastritis during the 10 year interval was associated with increases in the grades of corpus gastritis and neutrophilic granulocytes (p = 0.043 for both). During the follow up, the patients with lymphocytic gastritis, but not the H pylori positive patients without lymphocytic gastritis, appeared to have a significant increase in the grade of intestinal metaplasia in the corpus mucosa (p = 0.043). CONCLUSIONS--In some patients H pylori may cause a gastritis that predominates in the corpus and is associated with an increase in the intraepithelial lymphocyte count. This form of gastritis may cause progression of intestinal metaplasia.     

Histological study of chronic gastritis from the United Arab Emirates using the Sydney system of classification.

AIMS--To determine the prevalence of Helicobacter pylori in five main nationality groups with gastric ulcer, duodenal ulcer, and non-ulcer dyspepsia; and to determine the histopathological types of gastritis and assess the graded variables of Helicobacter associated gastritis. METHODS--Gastric antral and corpus biopsy specimens from 437 patients were examined for the prevalence of H pylori, 337 of which were classified and graded histologically according to the Sydney system. RESULTS--The overall colonisation rate of H pylori was 90%, and there was no significant difference between groups of different ethnic origins. The colonisation rates were 99%, 89%, and 78% in patients with duodenal ulcer, non-ulcer dyspepsia, and gastric ulcer, respectively. Helicobacter associated gastritis was the most common form of chronic gastritis (87%). H pylori density was greater in the antrum than the body. Gastric atrophy in helicobacter associated gastritis was seen in 54% of the cases (43% grade I, 10% grade II, 1% grade III) and increased the older the patients. Atrophy of the corpus alone was very rare (1%). Atrophy and intestinal metaplasia were more prevalent in patients with gastric ulcer than duodenal ulcer. CONCLUSION--The colonisation rate of H pylori was similar in the five groups studied and was almost invariably present in gastric biopsy specimens in patients with duodenal ulcer. H pylori associated gastritis was the most common form of gastritis. Atrophy was mainly of low grade and increased the older the patient.     

Gastrin (G) cells and somatostatin (D) cells in patients with dyspeptic symptoms: Helicobacter pylori associated and non-associated gastritis

BACKGROUND: Gastrin G cells and somatostatin D cells are important regulators of gastric acid secretion and alterations in their relative numbers may play a key role in gastroduodenal disease. AIM: To investigate the effect of Helicobacter pylori infection on the density of immunoreactive G and D cells in gastric antral and corpus biopsies from patients with dyspeptic complaints. METHODS: One hundred and twenty two patients with dyspeptic complaints had two antrum and two corpus biopsies taken during upper endoscopy. The severity of inflammation and the density of H pylori were evaluated semiquantitatively. In addition, the density and distribution of neuroendocrine cells, especially G and D cells, were examined using immunohistochemistry. Patients were divided into three groups, those with H pylori positive gastritis, H pylori negative gastritis, and histologically normal gastric mucosa. RESULTS: The number of immunoreactive G cells was significantly higher and the number of immunoreactive D cells lower in patients with H pylori positive gastritis compared with H pylori negative gastritis or histological normal gastric mucosa. The percentage of G cells as a percentage of mucosal endocrine cells was also raised and that of D cells was decreased. CONCLUSIONS: Helicobacter pylori infection produces alterations in the number of endocrine cells responsible for regulating acid secretion in relation to intragastric pH and feeding. The alterations correlate best with the severity of inflammation and not with H pylori density.     

Helicobacter pylori infection and erosive gastritis

One hundred and eleven patients were included in the study. Thirty seven had erosive gastritis, thirty four chronic gastritis and forty were controls without any gastrointestinal diseases confirmed by symptoms and upper gastrointestinal endoscopy. Patients with erosive gastritis were divided into non-steroidal anti-inflammatory drug (NSAID) users and non-users. H pylori status was determined by urease test, serology and/or histology. The prevalence of H pylori was compared between the various groups. The prevalence of H pylori infection in erosive gastritis, chronic gastritis and controls was 68%, 76% and 65%, respectively, the difference was not significant (P > 0.05), 8 out of 11 patients with erosive gastritis and NSAID use (73%) were positive for H pylori. Likewise 17/26 patients with erosive gastritis without NSAID use (65%) were positive for H pylori (P > 0.05). Body of the stomach (65%) was the commonest site for erosions compared to antrum (43%) or fundus (27%) (P < 0.02). H pylori infection does not predispose to erosive gastritis. NSAID use does not affect H pylori prevalence. Routine H pylori eradication is, therefore, not indicated in patients with erosive gastritis infection. Body of the stomach is the most predominant site for erosions.     

Can NSAID/ASA-induced erosions of the gastric mucosa be identified at histology?

Studies in animals have shown that NSAID/ASA-induced erosions have an ischaemic pathogenesis. We therefore studied the question of whether such erosions in human gastric biopsy material can be identified on the basis of the ischaemic necrosis. Histological sections prepared from forceps biopsy material obtained from 122 patients with erosions (at least three biopsy specimens from the erosion and two from antrum and corpus each) were classified by a pathologist blinded to the endoscopic findings and the medication used by the patients. NSAID/ASA erosions were diagnosed when a homogeneous eosinophilic ischaemic necrosis blending into the adjoining lamina propria presented. Helicobacter pylori (Hp)-induced erosions were diagnosed when, in the presence of Hp gastritis, erosive defects were covered with a non-homogeneous fibrinoid necrosis containing granulocytes and cell debris. Finally, the histological classification was compared with data on medication usage. The histological diagnosis was Hp-induced erosions in 59 patients, NSAID/ASA-induced erosions with no Hp gastritis in 23, and NSAID/ASA-induced erosions with concomitant Hp gastritis in 40. A comparison of this histological classification with the data provided by the referring physicians on patient medication revealed that 70% of the patients with histological diagnosis of NSAID/ASA-induced erosions in the absence of Hp gastritis, and 65% of those diagnosed to have NSAID/ASA-induced erosions and concomitant Hp gastritis, had been taking such drugs. Among the erosions diagnosed as H. pylori-induced, 81% of the patients were reported not to take such medication. The sensitivity of the diagnosis of NSAID/ASA-induced erosions was 72.9%, and specificity 79.6%. The results of the present study show that a high percentage of the NSAID/ASA-induced erosions of the gastric mucosa can indeed be correctly diagnosed at histology.     

Association of Helicobacter pylori with gastritis and peptic ulcer diseases

The occurrence of Helicobacter pylori(H.pylori) and its relationship with gastric mucosa were studied by light and electron microscopy and culture of biopsy specimens from gastric mucosa of 160 patients with upper gastrointestinal symptoms. H. pylori were present in 96.6% of patients with active chronic gastritis, 100% of patients with duodenal ulcer and 76.9% of patients with gastric ulcer, while present in only 6.3% of individuals with histologically normal gastric mucosa. The bacteria colonized the antral mucosa more frequently than the body or than the duodenal cap mucosa. The bacteria were rarely seen in the intestinalized epithelium per se, but there was no significant difference in prevalence of H. pylori between gastritis with intestinal metaplasia and gastritis without intestinal metaplasia. H. pylori could be seen in close association with the surface of gastric epithelial cells below the mucus layer without evidence of intracellular parasitism, All of the strains tested were susceptible to penicillin, erythromycin, and most of them susceptible to tinidazole and bismuth salts. It is concluded that H. pylori are highly associated with gastritis and peptic ulcer diseases and its prevalence rates in patients with those diseases is higher than in developed countries. This strong association of H. pylori infection with gastritis and peptic ulcer diseases suggest a possible etiologic role for the bacterium in those diseases.     

Helicobacter heilmannii gastritis: association with acid peptic diseases and comparison with Helicobacter pylori gastritis.

We analyzed 2 antral and 1 corpus full-thickness random endoscopic gastric mucosal samples obtained from 946 patients with duodenal ulcers (6077 biopsies) and from 281 patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (1794 biopsies). We stained tissue sections with hematoxylin and eosin and Warthin-Starry silver stain and immunostained them with polyclonal antibodies against Helicobacter pylori. Hematoxylin- and eosin-stained sections from 6 patients with Helicobacter heilmannii (18 biopsies) and 23 randomly selected patients with H. pylori (68 biopsies) were evaluated and semiquantitated for the presence of acute inflammation, chronic inflammation, glandular atrophy, intestinal metaplasia, H. pylori, H. heilmannii, lymphoid follicles, or vasodilatation. Additional specimens were obtained for H. pylori culture, a CLO test, and serologic examination. H. heilmannii was detected in 6 (0.49%) of 1227 patients (14 [0.18%] of 7871 biopsies). Of these, 4 (0.42%) of 946 were patients with duodenal ulcers (9 [0.15%] of 6077 biopsies), and 2 (0.71%) of 281 were patients with nonsteroidal anti-inflammatory drug-associated gastric ulcers (5 [0.28%] of 1794 biopsies). We found H. heilmannii with hematoxylin and eosin stain, Warthin-Starry stain, and immunoperoxidase stain for H. pylori. Culture for H. pylori was negative in the four patients with duodenal ulcers. The CLO and serologic tests were positive in three of five and five of five patients, respectively. Our results indicate that H. heilmannii, like H. pylori, is associated with peptic ulcer disease (both active and inactive gastritis) and that it preferentially colonizes the gastric antrum. The severity of the H. heilmannii-associated gastritis is less intense and lymphoid aggregates are less common than in H. pylori-associated gastritis. Morphologic detection seems to be the method of choice for detecting H. heilmanni. Immunoperoxidase stain specific for H. pylori also stains H. heilmannii, indicating cross-reacting antigenic epitopes between H. heilmannii and H. pylori.     

Helicobacter pylori infection and chronic gastritis in gastric cancer.

AIMS: To investigate the prevalence of Helicobacter pylori associated chronic gastritis in patients with gastric cancer. METHODS: Serum IgG antibodies for H pylori were determined in 54 consecutive patients with gastric carcinoma. The prevalence of H pylori in gastric mucosa was also examined histologically (modified Giemsa) in 32 patients from whom adequate biopsy specimens of the antrum and corpus were available. Thirty five patients with gastrointestinal tumours outside the stomach and 48 with non-gastrointestinal malignancies served as controls. RESULTS: Of the 54 patients, 38 (70%) had H pylori antibodies (IgG) in their serum (three additional patients had H pylori antibodies IgA, class specific but not IgG specific). This prevalence was significantly higher (p less than 0.05) than that (49%) in the 35 controls. No differences in prevalence of H pylori antibodies were found between gastric cancer cases of intestinal (IGCA) or diffuse (DGCA) type, both these types showing H pylori antibodies (IgG) in 71% of the patients. In the subgroup of 32 subjects, five patients had normal gastric mucosa and four showed corpus limited atrophy ("pernicious anaemia type" atrophy of type A). All of these nine patients had no evidence of current or previous H pylori infection in serum (no IgG antibodies) or in tissue sections (negative Giemsa staining). The remaining 23 patients had antral or pangastritis, and all had evidence of current or previous H pylori infection. CONCLUSIONS: H pylori associated chronic gastritis was the associated disease in 75% of the patients with gastric cancer occurring equally often in both IGCA and DGCA groups. About 25% of cases seem to have a normal stomach or severe corpus limited atrophy, neither of which showed evidence of concomitant H pylori infection.     

Relationship of TT virus and Helicobacter pylori infections in gastric tissues of patients with gastritis

Blood and gastric tissue biopsies of 34 patients with gastritis were tested for the presence of TT virus (TTV), a ubiquitous virus found in the blood of most humans. Thirty-one of these patients were TTV positive, and 27 patients had virus in both tissues. In addition, 13 of the patients who had TTV in gastric tissue were Helicobacter pylori positive. There was an association of higher TTV titers in gastric tissues of patients who were H. pylori positive than in those in whom the bacterium could not be detected. Furthermore, this association was stronger in H. pylori-positive patients with the presence of the cagA protein. Of 10 specimens in which genogroup determination was carried out in the gastric corpus, 5/5 that were H. pylori positive showed the presence of TTV genogroup 3, while for those that were H. pylori negative, 5/5 showed the presence of genogroup 1t. By contrast, genogroup 1 was found in the corpus of only one H. pylori-positive patient, and genogroup 3 in only one H. pylori-negative patient. The histological severity of gastritis did correlate significantly with loads in the gastric tissues. There was no significant difference in TTV titer in blood of patients regardless of H. pylori infection status. These findings pique interest in clarifying the role of TTV, alone or in association with H. pylori infection, in the pathogenesis of gastritis.     

Topographic expression of MUC5AC and MUC6 in the gastric mucosa infected by Helicobacter pylori and in associated diseases

We investigated the topographic expression of MUC5AC and MUC6 in relationship with gastric diseases. The immunoexpression of MUC5AC and MUC6 was evaluated in 75 adults presenting Helicobacter pylori gastritis (n = 22; 11 cagA positive), duodenal ulcer (DU, n = 11), gastric ulcer (GU, n = 9), gastric carcinoma (GC, n = 20), and normal mucosa (H. pylori negative, n = 13). Five gastric areas (antral and corporeal lesser and greater curvatures and incisura) were studied. H. pylori was detected by carbolfuchsin, urease, and culture; cagA was determined by PCR. All patients with DU (eight with GU and 13 with GC) were H. pylori-positive. In H. pylori gastritis, MUC5AC expression was higher in the antrum than in the corpus; no difference was observed with respect to cagA status. MUC5AC expression was higher in the antrum of gastritis than in DU, and it was lower in the incisura among GU patients compared to DU. MUC6 expression was higher in the antrum of H. pylori gastritis compared to DU and to uninfected patients. No difference was observed in the topographic pattern of expression of MUC5AC and MUC6 among GC cases. The topographic over- and under-expression of mucins in H. pylori-associated gastritis and peptic disease suggest a role for these mucins in the pathogenesis of H. pylori infection and associated diseases.     

Features of gastritis predisposing to gastric adenoma and early gastric cancer

BACKGROUND/AIMS: Helicobacter pylori gastritis is a risk factor for the development of gastric cancer. The results of several studies indicate that gastric adenomas, which are considered premalignant lesions, may also be associated with H pylori gastritis. However, it is not clear whether there are different patterns of gastritis in these patients compared with patients with gastric cancer or patients with H pylori gastritis alone. Therefore, this study was designed to investigate the patterns of gastritis in these three groups of patients. METHODS: The histological features of gastric mucosa at a distance from the tumour were analysed prospectively in 118 patients with gastric adenoma (mean age, 71.8; female to male ratio, 6 : 4). In addition, for every patient with H pylori associated gastric adenoma an age and sex matched control patient with either H pylori associated early gastric cancer of the intestinal type or H pylori gastritis only was investigated. RESULTS: Only 60 patients (50.9%) with gastric adenoma were infected with H pylori. In the remaining patients, complete atrophic gastritis predominated. In those patients with adenoma and H pylori infection, the gastritis was similar to that seen in patients with early gastric cancer (median score, 2 for activity and degree of gastritis in the antrum and corpus); intestinal metaplasia was common to both groups. These two groups differed significantly from patients with H pylori gastritis only (median grade and activity of gastritis, 1 in antrum and corpus), in whom intestinal metaplasia was rare. CONCLUSIONS: It appears that gastric adenomas and gastric intestinal cancer arise by analogous mechanisms. However, owing to severe atrophic gastritis and a lower incidence of H pylori, adenomas do not appear to be definite precursor lesions for gastric cancer.     

Histopathological changes in gastric mucosa colonized by H. pylori

Helicobacter pylori (H. pylori), infection has been linked to acute and chronic gastritis, non-ulcer-dyspepsia, peptic ulcer, gastric adenocarcinoma and gastric non-Hodgkin's lymphoma of mucosa-associated lymphoid tissue (MALT). The epithelial changes in H. pylori colonized gastric mucosa are easy to recognize in routine Haematoxylin & Eosin stained sections and are so distinctive that they can serve as a helpful histological indicator for the presence of H. pylori in gastric biopsies. The histopathology of seventy-five gastric biopsies showing colonization by H. pylori was studied. Histologically, the H. pylori colonized gastric epithelium showed characteristic changes that were topographically related to the bacteria. These changes included irregular surface, epithelial pits, individual cell dropout and microerosion, which were specific for H. pylori colonization. These were absent in areas not colonized by H. pylori and in 20 consecutive H. pylori negative gastric biopsies seen during the same study period. As specific treatment for H. pylori infection is available, identification of H. pylori colonization in gastric biopsies should be attempted in all cases of gastritis, peptic ulcers and non-ulcer-dyspepsia.     

The histopathology of non-steroidal anti-inflammatory drug induced gastroduodenal damage: correlation with Helicobacter pylori, ulcers, and haemorrhagic events

AIMS: The spectrum of microscopic lesions resulting from the chronic use of non-steroidal anti-inflammatory drugs (NSAIDs), known as chemical gastritis, remains unclear, and the variable prevalence reported in different studies makes this issue a matter of lively debate. The aim of this study was to evaluate the prevalence and importance of chemical gastritis in patients regularly taking NSAIDs. Owing to the high prevalence of Helicobacter pylori infection, particularly in subjects over 60 years of age, and in view of a possible association with damage, the presence of H pylori infection in the same tissue sample was also determined in all patients. METHODS: One hundred and ninety seven subjects were enrolled, 118 of whom were receiving chronic treatment with NSAIDs and 79 of whom were controls, pair matched for age, sex, and clinical symptoms (ulcer-like dyspepsia or upper digestive tract haemorrhage). Antral biopsies taken during upper gastroduodenal endoscopy were assessed for chemical gastritis according to a modified version of Dixon's score, and for Helicobacter correlated chronic active gastritis, according to the updated Sydney system. RESULTS: Chemical gastritis was identified in 11 patients taking NSAIDs (9%) and in four controls (5%) (p < 0.05). Helicobacter pylori was detected in 53 patients taking NSAIDs (45%) and in 34 controls (43%). Patients taking NSAIDs had a significantly higher number of erosions and ulcers and worse endoscores than controls. The presence of H pylori did not appear to increase histological damage, ulcer prevalence, or haemorrhagic events. CONCLUSIONS: Chemical gastritis is present in a limited number of patients regularly taking NSAIDs, and is not strongly correlated with NSAID induced damage. In many cases of peptic ulcer or upper gastrointestinal bleeding in patients taking NSAIDs, the presence of chemical gastritis or H pylori infection cannot solely account for the development of mucosal damage.     

Helicobacter (Campylobacter) pylori in gastric brushing cytology.

Helicobacter (formerly Campylobacter) pylori is frequently associated with chronic gastritis and peptic ulcer and has been implicated as an etiologic agent. Identification of H. pylori is important for specific treatment with antibiotics and bismuth compounds. We studied 27 patients who presented with symptoms of gastritis or peptic ulcer on whom paired gastric biopsies and gastric brushings for cytology had been performed. Biopsies were stained with H & E and Warthin-Starry or Giemsa for H. pylori. Previously, Papanicolaou-stained brushings were restained with Giemsa and reviewed blindly by two cytologists. Cytologic examination revealed the characteristic 1-3 mu curved or spiral gram-negative bacilli embedded in mucus in 12 of 27 (44%) of cases. Biopsies showed H. pylori in 13 of 27 (48%) of cases. Cytology and histology were concordant in 22 of 27 (81%) of cases. Three cases were positive on biopsy, negative on cytology; two of these were unsatisfactory cytology specimens. Two cases were positive on cytology, negative on biopsy, apparently sampling artifacts. Papanicolaou-stained slides were scored for several morphologic parameters; numbers of acute and chronic inflammatory cells and degree of cytologic atypia. None of these were predictive of the presence of H. pylori. We conclude that Giemsa-stained gastric brushings are a useful complement to gastric biopsies in establishing the diagnosis of H. pylori.     

Endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure

To evaluate the endoscopic and histological changes in upper gastrointestinal tract of patients with chronic renal failure 50 patients and 50 controls were studied. Upper gastrointestinal endoscopy was done and 2 biopsies each were taken from oesophagus, corpus and antrum of the stomach and duodenum. Sections were stained with haematoxylin & eosin, Alcian blue--Periodic acid Schiff's (pH 2.5), and Loeffler's methylene blue stains. Oesophagus was endoscopically normal in most of the patients. Predominant histological finding was chronic oesophagitis which was significantly higher in patients than controls (47.1% Vs 26%; p<0.05). Significantly higher (p<0.001) number of patients had gastritis, oedema and pale mucosa on endoscopic examination of stomach. Predominant histological changes were mucosal oedema (82.35%), gastritis (23.5%) and increase in number of bi- and multinucleated parietal cells with vacuolation and fragmentation of the cytoplasm (29%). Prevalence of H. pylori was less in patients as controls (35.2% Vs 54%; p< 0.01). Endoscopic examination of duodenum mainly showed duodenitis, pale mucosa, oedema and nodularity. Brunner's gland hyperplasia (82.4%), duodenitis (70.6%) and gastric metaplasia (29.4%) were the main histological features. H. pylori was seen in 5.9% cases of gastric metaplasia in duodenum. Patients with CRF have significant upper gastrointestinal tract abnormalities which mainly occur due to metabolic changes in response to high urea concentration in gastric juice and are not related to H. pylori infection.     

Cytoskeletal and kinetic epithelial differences between NSAID gastropathy and Helicobacter pylori gastritis: an immunohistochemical determination

AIMS: Distinguishing histological features between non-steroidal anti-inflammatory drug (NSAID) gastropathy and Helicobacter pylori gastritis have been accepted. However, the molecular basis explaining these dissimilar histologies has not been elucidated. In an attempt to clarify this question we investigated the differences in the structural cytoskeleton and proliferative activity of these two gastropathies. METHODS AND RESULTS: We assessed the distribution of five cytokeratins (CK) (CK7, 8, 18, 19 and 20) and Ki67 for the ability to distinguish NSAID from H. pylori gastropathies. In H. pylori gastritis, CK7, 8, 18 and 19 were expressed comparably to normal mucosa from the deep foveolae up to the tips of the glands. The detection of CK20, normally expressed in the upper foveolar region and surface, was decreased with only an epithelial surface reaction. In NSAID gastropathy, CK expression was increased in intensity, with normal distribution for CK8, 18 and 19. Modification of localization was noted for CK7 and 20, with labelling extending toward the deep foveolar region. Unlike H. pylori gastritis, no surface epithelial labelling with Ki67 was noted with NSAID gastropathy but downward elongation of the proliferative zone occurred instead. CONCLUSIONS: Contrasting cytostructural alterations and distinct proliferative patterns distinguish NSAID gastropathy from H. pylori gastritis, possibly reflecting different injury pathways.