Histology of the mucosa of gastric antrum and body before and after eradication of Helicobacter pylori.

1. Helicobacter pylori status and the histology of the antral and oxyntic mucosa were evaluated in 25 patients with duodenal ulcer treated with a triple schedule of furazolidone, metronidazole and amoxicillin, and in 16 patients treated only with cimetidine. 2. Before treatment, H. pylori was detected in all patients. One month after treatment with the antimicrobial agents, H. pylori was not found in 18 (72.0%) of 25 patients treated with the triple schedule. In the patients treated with cimetidine (N = 16) the H. pylori tests continued to be positive after treatment. 3. Inflammatory activity and intensity of gastritis were significantly reduced in patients treated with the antimicrobial agents but not in cimetidine-treated patients. Three patients who had negative cultures and improvement of gastritis 1 month after treatment became H. pylori positive again within 2 months, with concomitant reappearance of gastritis. 4. This study provides additional evidence that histological gastritis observed in H. pylori-positive patients with duodenal ulcer is due to the presence of the microorganism.

Histology of the mucosa of gastric antrum and body before and after eradication of Helicobacter pylori

1. Helicobacter pylori status and the histology of the antral and oxyntic mucosa were evaluated in 25 patients with duodenal ulcer treated with a triple schedule of furazolidone, metronidazole and amoxicillin, and in 16 patients treated only with cimetidine. 2. Before treatment, H. pylori was detected in all patients. One month after treatment with the antimicrobial agents, H. pylori was not found in 18 (72.0 per cent ) of 25 patients treated with the triple schedule. In the patients treated with cimetidine (N = 16) the H. pylori tests continued to be positive after treatment. 3. Inflammatory activity and intensity of gastritis were significantly reduced in patients treated with the antimicrobial agents but not in cimetidine-treated patients. Three patients who had negative cultures and improvement of gastritis 1 month after treatment became H. pylori positive again within 2 months, with concomitant reappearance of gastritis. 4. This study provides additional evidence that histological gastritis observed in H. pylori-positive patients with duodenal ulcer is due to the presence of the microorganism

Histamine content of the oxyntic mucosa from duodenal ulcer patients: effect of Helicobacter pylori eradication.

The histamine concentration of the oxyntic mucosa was determined in Helicobacter pylori-positive patients with duodenal ulcer before and after antimicrobial therapy and in H. pylori-negative subjects. Determination of serum gastrin was also performed in duodenal ulcer patients before and after H. pylori eradication. The histamine content of the oxyntic mucosa was lower in patients with duodenal ulcer than in H. pylori-negative subjects, but it increased after H. pylori eradication. Conversely, in patients in whom therapy failed to eradicate the microorganism, the histamine content remained unchanged. Serum gastrin levels fell after microorganism eradication, and the percentage of this fall was correlated with the percentage of increase in gastric histamine. In conclusion, our findings suggest that abnormalities of histamine store present in duodenal ulcer patients might be a feature of H. pylori infection.

Comparison of the urease test and of direct smear examination in the control of treatment of Helicobacter pylori-induced infection.

The sensitivity and specificity of the preformed urease test and of carbolfuchsin-stained smears for the diagnosis of the presence of Helicobacter pylori in gastric mucosa were evaluated before and after antimicrobial treatment. The results obtained by culture were used as the reference point. We studied 41 patients with endoscopically diagnosed duodenal ulcer. Twenty-five of these were treated with furazolidone (100 mg t.i.d.), amoxicillin (500 mg t.i.d.) and metronidazole (250 mg t.i.d.) for 5 days and then with only furazolidone (100 mg t.i.d.) for an additional 25 days. The 16 control patients were treated with cimetidine (800 mg, 4 times a day). The sensitivity of the urease test and of direct smear examination was 100% before treatment and 84.6% and 92.3%, respectively, after treatment. We conclude that the urease test and carbolfuchsin-stained smears, which are highly sensitive for H. pylori diagnosis, present reduced sensitivity when they are employed for the follow-up of patients treated with antimicrobials.

Comparison of the urease test and of direct smear examination in the control of treatment of Helicobacter pylori-induced infection

The sensitivity and specificity of the preformed urease test and of carbolfuchsin-stained smears for the diagnosis of the presence of Helicobacter pylori in gastric mucosa were evaluated before and after antimicrobial treatment. The results obtained by culture were used as the reference point. We studied 41 patients with endoscopically diagnosed duodenal ulcer. Twenty-five of these were treated with furazolidone (100 mg t.i.d.), amoxicillin (500 mg t.i.d.) and metronidazole (250 mg t.i.d.) for 5 days and then with only furazolidone (100 mg t.i.d.) for an additional 25 days. The 16 control patients were treated with cimetidine (800 mg, 4 times a day). The sensitivity of the urease test and of direct smear examination was 100 per cent before treatment and 84.6 per cent and 92.3 per cent , respectively, after treatment. We conclude that the urease test and carbolfuchsin-stained smears, which are highly sensitive for H. pylori diagnosis, present reduced sensitivity when they are employed for the follow-up of patients treated with antimicrobials

Indirect immunofluorescence determination of the frequency of anti-H. pylori antibodies in Brazilian blood donors.

1. The accuracy of an indirect immunofluorescence (IIF) test for the serodiagnosis of Helicobacter pylori infection was evaluated in adult patients and compared with culture, preformed urease test and smears stained with carbolfuchsin. 2. We studied 80 consecutive patients submitted to gastroduodenoscopy (17 of whom were found to have duodenal ulcer) plus 57 patients with duodenal ulcer. 3. H. pylori was identified by microbiological methods in 65 of the 80 consecutive patients and in all 57 patients with duodenal ulcer. 4. Among the 74 patients with duodenal ulcer, 71 presented antibody titers > or = 1:20 and 46 of the 48 H. pylori-positive patients without duodenal ulcer presented antibody titers > or = 1:20. 5. Thirteen of the 15 H. pylori-negative patients presented antibody titers < or = 1:10. 6. The sensitivity, specificity and positive predictive value of the IIF test were 95.9%, 88.8% and 98.4%, respectively. 7. The seroprevalence of H. pylori in 380 asymptomatic Brazilian blood donors was also studied by the IIF test. The presence of IgG antibodies against H. pylori was observed in 62.1% of the individuals. The prevalence of H. pylori infection increased with age and no difference was observed between males (60.3%) and females (66.6%).

Helicobacter pylori acute gastritis: histological, endoscopical, clinical, and therapeutic features.

We describe seven patients with Helicobacter pylori acute gastritis who presented endoscopical picture simulating gastric carcinoma or lymphoma. H. pylori was detected on the antral and on the oxyntic mucosa of all patients. At histological examination, no evidence of malignancy was observed in any of the patients. In the antral mucosa there were edema, hyperemia, and intense polymorphonuclear leukocyte infiltration (neutrophils and some eosinophils) in the lamina propria, mucus layer, and inside the glands. The patients were treated with amoxycillin (2 g/day for 2 months) associated with metronidazole (750 mg/day for 15 days), which reduced the symptoms dramatically. Endoscopy and biopsy, repeated 4 wk after treatment was stopped, showed that the patients had been cleared of H. pylori, and indicated a marked improvement of endoscopical and histological gastritis. These findings indicated that H. pylori acute gastritis can mimic gastric carcinoma or lymphoma. Therefore, histology and detection of H. pylori are essential for an accurate diagnosis.

[Furazolidone and cimetidine in patients with active duodenal ulcer and Helicobacter pylori in the gastric antrum]. / Furazolidona x cimetidina em pacientes portadores de úlcera duodenal ativa e Helicobacter pylori no antro gástrico.

In order to assess the effect of furazolidone on duodenal ulcer disease and Helicobacter pylori (Hp), a double-blind, double-dummy, randomized, prospective pilot study comparing furazolidone and cimetidine was carried out in 31 antral Hp positive patients with endoscopically proven active duodenal ulcer. Clinical, endoscopical, bacteriological and histological studies were done before and at four weeks of the study in all patients. If the ulcer was not healed, the treatment was extended for a further four weeks and all the procedures repeated. The healed ulcer patients were followed-up and re-endoscoped, regardless the presence of symptomatology, at least at 3 and 6mo after the end of treatment. It was observed that furazolidone cleared Hp (18% x 0%), healed the ulcer (91% x 87%) and reduced the relapse rate (30% x 92%; p < 0.025).

Parietal cell carcinoma of the stomach and Ménétrier's disease.

A case of gastric parietal cell carcinoma, a newly recognized entity, associated with Ménétrier's disease, is presented. The tumor presented a excavated ulcer 6 x 6 cm in diameter surrounding the cardiac region. Metastasis in the greater curvature and epiploon++ lymph nodes were identified. The mucosa of gastric body and fundus showed large thickened tortuous folds and the histological pattern of Ménétrier's disease.

Campylobacter pyloridis in the upper gastrointestinal tract: a Brazilian study.

The successful isolation of C. pyloridis from human gastric mucosa has renewed interest in these bacteria and their role as a causative agent for gastritis, and possible causal relationship between chronic gastritis and peptic ulceration. To determine the incidence of C. pyloridis in gastric biopsies we studied 51 consecutive Brazilian patients with a wide range of alimentary disorders presenting for endoscopy. At least three biopsies were taken from each site: antrum, any ulcer or cancer. Microbiological and histological studies were performed to identify the bacteria. The organism was found in 40/51 (78%) of patients. These was a close correlation between culture (100%), Gram (90%) and Gimenez staining (80%) in identifying the bacteria. All C. pyloridis positive patients had histological evidence of antral chronic gastritis (active or quiescent) even if the endoscopic appearance looked normal. All peptic ulcer patients (n = 17) showed C. pyloridis in the antrum. In the duodenum the bacteria were mainly seen in gastric type of mucosa. Our findings support the hypothesis that C. pyloridis is etiologically related to gastritis and possibly peptic ulceration.

Endoscopic findings after antacid, cimetidine and placebo for peptic ulcer--importance of staging the lesions.

Ninety four adult outpatients entered a randomized trial in which 30 patients were treated openly with antacid hourly and 64 patients with a double-blind regimen of either cimetidine (1 g/day) or placebo. After 4 weeks, 66.3% of the antacid-treated patients, 56.2% of the cimetidine-treated patients and 9.4% of the placebo patients showed ulcer healing. The difference between cimetidine and antacid was not statistically significant. The low percentage in the placebo group as compared to other trials may be attributed to the avoidance of supplementary antacid in this group and or to the criterion of staging the lesions both for entry into study and for evaluating the results.