Reflux esophagitis and Helicobacter pylori infection in patients with scleroderma.

OBJECTIVE: This study aimed to evaluate the possible effects of Helicobacter pylori (H. pylori) infection in reflux esophagitis with scleroderma. PATIENTS AND METHODS: There were a total of 138 patients with scleroderma in our hospital between October 1998 and June 2005. Among these patients, 64 consecutive patients of scleroderma, who did not receive medication for gastrointestinal diseases, underwent endoscopy after informed consent. H. pylori was examined using an H. pylori IgG ELISA. The endoscopists graded esophageal mucosal breaks according to the Los Angeles Classification of Esophagitis. RESULTS: Among the 64 patients, 37 patients (57.8%) were positive for H. pylori infection. Reflux esophagitis was observed in 10 of 37 H. pylori-positive patients and in 19 of 27 H. pylori-negative patients. Significantly fewer H. pylori-infected patients had reflux esophagitis than H. pylori-negative patients (p<0.01). The odds ratio for H. pylori infection and reflux esophagitis was 0.16 (95%CI; 0.052-0.47). CONCLUSION: These findings suggest an important role for H. pylori infection in reflux esophagitis with scleroderma.

Helicobacter pylori and gastro-oesophageal reflux disease: a cross-sectional epidemiological study.

BACKGROUND: H. pylori infection is accompanied by a lower prevalence of reflux disease. There is still an ongoing debate as to whether H. pylori actually protects against the development of reflux oesophagitis or is merely an epiphenomenon. A cross-sectional study was performed to study the relation of H. pylori with reflux oesophagitis, hiatus hernia and Barrett's oesophagus. MATERIAL AND METHODS: Consecutive patients undergoing upper gastrointestinal endoscopy in a period of ten years were studied. Included were patients with active reflux oesophagitis and/or hiatus hernia and/or Barrett's oesophagus. As a reference group, patients without macroscopic abnormalities were included. H. pylori was detected applying routine diagnostic modalities. RESULTS: In the ten years 11,691 consecutive patients were studied. Reflux oesophagitis was seen in 1535 patients, 307 patients had Barrett's oesophagus and a hiatus hernia was present in 2116 patients. The reference group consisted of 5341 patients. H. pylori was significantly less often detected in patients with reflux oesophagitis or Barrett's oesophagus compared with the reference group, 20 vs 29% (p<0.001). Also presence of H. pylori was significantly lower in patients with hiatus hernia 20 vs 29% (p<0.0001). CONCLUSION: The present study confirms, in a very large group of patients studied in one single centre, the findings of earlier papers. Patients without H. pylori gastritis suffer more often from reflux disease. There is a relation between H. pylori and reflux disease. However, the consequence of this relation will not be the same in every patient.

Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

In a prospective study of consecutive patients with reflux esophagitis and/or hiatal hernia and Barrett's esophagus, the prevalence of Helicobacter pylori was assessed. Antral biopsy specimens were studied and a serum sample for detection of IgG antibodies against Helicobacter pylori was taken. As a reference group patients presenting with a normal esophagus, stomach, and duodenum were taken. Reflux esophagitis was diagnosed in 118 patients, hiatal hernia without esophageal inflammation in 109, and Barrett's esophagus in 13. Helicobacter pylori was present in 74 (30%) of these patients and in 204 (51%) of the reference group. Prevalence of Helicobacter pylori was significantly lower in all groups compared with the reference group (P < 0.001). There was no difference when patients with esophagitis, Barrett's esophagus, or hiatal hernia were compared. Patients with esophagitis and Helicobacter pylori in their antrum are significantly older than esophagitis patients without concomitant Helicobacter infection, 61.5 (SD, 17) versus 53 (SD, 17) years (P < 0.001). It is concluded that the prevalence of Helicobacter pylori infection in patients with gastroesophageal reflux disease is significantly lower than in the reference group, irrespective of the severity of esophagitis. Helicobacter pylori infection has no role in the pathogenesis of reflux esophagitis.

Comparison of one or two weeks of lansoprazole, amoxicillin, and clarithromycin in the treatment of Helicobacter pylori.

BACKGROUND: The simplest, most effective, and least expensive Helicobacter pylori therapy remains to be determined. Two weeks of 30 mg lansoprazole bid, 1 gm amoxicillin bid, and 500 mg clarithromycin bid (LAC2) had been shown to be an effective therapy for H. pylori. The aim of this study was to assess whether 1 week of this regimen (LAC1) would have a similar efficacy. MATERIALS AND METHODS: H. pylori-positive patients assessed histologically, by rapid urease test, microbiologically, and by a 13C-urea breath test (13C-UBT) were randomized to receive either LAC1 or LAC2 in a single-center open study. Patients were interviewed 1 to 3 days after completion of therapy to evaluate adverse events and compliance. Efficacy was determined by 13C-UBT at least 4 weeks after antibiotic therapy. RESULTS: Seventy evaluable patients were randomized to receive LAC1 (n = 33) LAC2 (n = 37). Of the 33 LAC1 patients, 30 (91%) were treated successfully (95% confidence interval (CI) = 76-98%), compared with 32 of 37 (86%) in the LAC2 group (95% CI = 71-96%). There was no difference in efficacy between the two groups (Fisher's exact test p = 1.0; 95% CI = -10.3%-19.2%). Patients taking LAC1 experienced significantly fewer severe adverse events than those taking LAC2 (Mann-Whitney U test). One of 64 patients had primary resistance to clarithromycin, and treatment was unsuccessful in this case. Six of the 7 remaining treatment failures developed secondary resistance to clarithromycin. CONCLUSIONS: LAC1 is as effective as LAC2 and is associated with less toxicity. Posttreatment clarithromycin resistance is common in patients who do not experience success with therapy.

[Antral biopsy in the prevention of gastric disease]. / Biopsia antral como prevención de la patología gástrica.

Approximately 1% of the gastric neoplasies are nowadays associated with the infection of the gastric mucus by Helicobacter pylori. In view of the fact that its prevalency is very high and that it does not exist any objective and universal estimator in its diagnosis but the digestive endoscopy and biopsy, it is proposed, in candidate patients for a digestive endoscopy, although the explorer observes an endoscopic normality, to carry out, systematically, and antral biopsy for its subsequent diagnosis, treatment and prevention both of the gastric pathology and the infection by Helicobacter pylori.

Large hiatal hernias, anemia, and linear gastric erosion: studies of etiology and medical therapy.

Patients with large diaphragmatic hiatal hernias occasionally manifest severe iron deficiency anemia. The etiology is believed to be that of small erosions at the waist of the hernia which bleed slowly. Our study attempts to determine the incidence of this condition in clinical practice, and whether acid plays a role in the pathophysiology. Sixteen such patients were identified prospectively in a series of 5219 consecutive patients (0.31%) accrued over a 5-yr interval. Anemia was the presenting feature, rather than symptoms of gastroesophageal reflux disease. The erosions were endoscopically identified and biopsied. Anemia was treated and recurrence was prevented for a mean of 24.6 months with long-term iron replacement. Of eight patients treated with iron alone, four were willing to undergo follow-up endoscopy. Of these four, none demonstrated healing. Three of these nonhealers and eight additional patients were treated with both iron and H2 antagonists. Thus, 11 patients were treated with H2 antagonists and iron, whereas four patients were treated with iron alone. At 6 wk, reendoscopy showed healing of the erosions in seven of 11 patients on H2 antagonists, but in none of those treated with iron alone (p less than 0.05). The anemia was corrected in all patients with iron therapy. We conclude that 1) gastric acid appears to have some role in the pathogenesis of this lesion; 2) short-term therapy with H2-receptor antagonists promote healing of the erosions; and 3) long-term iron therapy alone is adequate for initial and maintenance therapy of the anemia.