Kari Seppälä

Eradication of Helicobacter pylori improves the healing rate and reduces the relapse rate of nonbleeding ulcers in patients with bleeding peptic ulcer

OBJECTIVE:A causal relationship between Helicobacter pylori (H. pylori) and peptic ulcer complications remains obscure. The aim of this study was to determine the importance of H. pylori and other risk factors for healing rate, ulcer recurrence, and rebleeding in patients with bleeding peptic ulcer.METHODS:A total of 223 patients with H. pylori positive bleeding peptic ulcer were randomly allocated to three treatment groups: 1) quadruple therapy (QT) (88 patients); 2) dual therapy (DT) (88 patients); and 3) omeprazole and placebo therapy (OPl) (47 patients). Endoscopic assessment was performed initially and at 8 and 52 wk. Ulcer healing and eradication rates were assessed; endpoints were ulcer relapse and ulcer rebleeding during 52 wk.RESULTS:Results after 8 and 52 wk were available for 211 and 179 patients, respectively. Eradication rate was 100% (95% CI = 96–100%) in the QT, 84% (95% CI = 74–91%) in the DT, and 4% (95% CI = 1–15%) in the OPl group. Ulcer healing rate was 95% (95% CI = 91–98%) in H. pylori negative and 8% (95% CI = 70–91%) in H. pylori positive patients. Ulcer relapses occurred in 2% (95% CI = 0.5–6%) of H. pylori negative and in 38% (95% CI = 24–54%) of H. pylori positive patients, and rebleeding occurred in five patients (three H. pylori positive and two negative).CONCLUSIONS:Eradication of H. pylori infection enhances healing of bleeding peptic ulcers after endoscopic therapy. H. pylori infection is an important independent risk factor for relapsing of nonbleeding ulcers in patients with bleeding peptic ulcer.

Self-Administration of Enzyme Substitution in the Treatment of Exocrine Pancreatic Insufficiency

The effect of self-administration (ad lib) of pancreatic enzyme substitution (Pancrease) in comparison with the dosage recommended by the manufacturer on abdominal symptoms and nutritional variables was studied in 10 patients with chronic pancreatitis. Both dosages were started in randomized order and they were continued for 4 weeks. Before and after each period of administration the patients were studied physically and weighed, and laboratory tests were performed. In addition, the patients kept daily records of pain (score, 0-3), bowel movements, amount of medication needed for maximum relief of symptoms and other remarks, if any. During self-administration, the number of capsules taken increased (5 +/- 1.3 to 11.4 +/- 2.4; p less than 0.001), the frequency of bowel movements decreased (3.6 +/- 1.4 to 1.6 +/- 0.7; p less than 0.05), and the pain was also relieved significantly (2.2 +/- 0.7 to 1.1 +/- 0.7; p less than 0.05) when compared with the regular dosage. Self-administration of the preparation did not have any significant effects on nutritional variables. Dryness of the mouth was the only complaint during self-administration of the drug in 4 of 10 patients. In conclusion, this study in selected patients with chronic pancreatitis indirectly supports the presence of a negative feedback regulation of exocrine pancreatic secretion in man. Thus, it may be beneficial to try self-administration of pancreatic enzyme substitution in selected patients to achieve maximum relief of symptoms in chronic pancreatitis.

Gastric cancers in finnish patients after cure of helicobacter pylori infection : a cohort study.

Helicobacter pylori infection is associated with gastric cancer. A total of 97% of the infected subjects have elevated levels of H. pylori antibodies. The antibody titers have been shown to decline rapidly (40–60% within 4–12 months) only after successful eradication therapy. We allocated 26,700 consecutive patients tested during 1986–1998 for H. pylori antibodies to 3 subcohorts: seropositive patients with rapidly falling antibody titers (Hp+CURED, n = 3,650), seropositive patients where no serological information indicating cure was obtained (Hp+NoInfo, n = 11,638) and seronegative patients (Hp–, n = 11,422). In the subcohorts, the standardised incidence ratios (SIRs) with 95% confidence intervals (CI) were defined for subsequent cancers of stomach, pancreas, colon, rectum, breast and prostate separately and for all cancers except stomach combined. The mean follow‐up time was 10.1 years and the number of gastric cancers was 72. For the Hp+CURED, the SIR for gastric cancers for the first 5 follow‐up years was 1.62 but decreased from the sixth follow‐up year thereon to 0.14 (CI: 0.00–0.75). Likewise, the risk ratio, defined in a Poisson regression analysis using the Hp+NoInfo group as the reference, decreased from 1.60 to 0.13 (CI: 0.02–1.00, p = 0.049). The SIR for Hp– was not significantly higher than that for Hp+NoInfo for any of the cancers analysed. To conclude, cured H. pylori infection led to a significantly decreased incidence of gastric cancers from the sixth follow‐up year. Advanced atrophic gastritis would be a plausible contributor to the elevated SIR in elderly Hp– patients.

Helicobacter pylori eradication as the sole treatment for gastric and duodenal ulcers.

Conclusions Eradication treatment for H. pylori-positive gastric or duodenal ulcer is sufficient, with no need to follow it with anti-secretory medication. Cure of the infection reduces ulcer relapses in patients who did not use NSAIDs or ASA.(95% CI, 73-100%) and 75% (95% CI, 19-99%) in H. pylori-negative (12 patients) and H. pylori-positive patients (four patients) (P = not significant). Ulcer relapses occurred in 5% (95% CI, 1-13%) of H. pylori-negative and in 36% (95% CI, 19-56%) of H. pylori-positive patients (P< 0.01). In H. pylori-negative patients who used NSAIDs or ASA the ulcer relapse rate was 30% (95% CI, 7-65%), whereas the ulcer relapse rate was 2% (95% CI, 0.4-10%) in patients who did not use NSAIDs or ASA (P< 0.05). No difference in ulcer relapse rate in H. pylori-positive patients who used or did not use NSAIDs or ASA was found. The eradication rate of H. pylori was 93% (95% CI, 76-99%) in the quadruple therapy group, 83% (95% CI, 64-94%) in the dual therapy group, 100% (95% CI, 87-100%) in the triple therapy group, and 0% (95% CI, 0-12%) in the lansoprazole and placebo group.

Helicobacter pylori eradication in the healing of atrophic gastritis: a one-year prospective study.

Objective. Whether gastric atrophy or intestinal metaplasia heals after successful treatment of Helicobacter pylori (H. pylori) infection is still a matter of controversy. The aim of this article was to clarify whether, after one year, H. pylori eradication is associated with healing in glandular atrophy and intestinal metaplasia in the corpus and antrum. Material and methods. Ninety-two H. pylori-positive peptic ulcer patients with atrophic gastritis (panatrophy, antral or corpus predominant) participated in the baseline study, 1-year prospective follow-up data being available from 76 patients. Mean age was 58±12.6 years (mean±SD) and the male/female ratio 2/1. The patients participated in an H. pylori eradication study in which they randomly received active eradication therapy. Endoscopy was performed before H. pylori eradication therapy and after 8 and 52 weeks, with specimens examined according to the Sydney system. Results. Of the 92 patients, 8 (9%) had panatrophy, 58 (63%) had antral- and 26 (28%) had corpus-predominant atrophic gastritis. After H. pylori eradication, the mean atrophy score declined in patients with antral-predominant atrophy from 1.5 (mean) to 0.7 (p<0.05), in corpus-predominant atrophy from 1.7 to 0.2 (p=NS) and in patients with panatrophy from 1.2 to 0.8 (p=NS). Atrophy healing was seen in 55% of antral-predominant atrophy patients who had successful H. pylori eradication.The mean antral atrophic score in one year declined in patients with duodenal ulcer (from 1.0 mean to 0.4) whereas it remained the same (1.3) in those with gastric ulcer (p<0.05). Conclusions. Atrophy can diminish or even disappear, especially in the antrum, during a 1-year follow-up after eradication of infection. Atrophy progression seems milder in patients with duodenal ulcer than in patients with gastric ulcer.

Size of the peptic ulcer in Helicobacter pylori-positive patients: association with the clinical and histological characteristics

Objective. Based on a large trial of Helicobacter pylori-positive peptic ulcer patients, we studied whether the size of the ulcer, along with other clinical and histological characteristics, has any effect on healing. We also studied the clinical and endoscopic characteristics associated with size of the peptic ulcer. Material and methods. A total of 333 consecutive patients with H. pylori infection and peptic ulcer were enrolled (mean age 54.8±12.7 years). Location of the ulcer was recorded by gastroscopy and the presence of H. pylori was assured by rapid urease test, histology and by serum H. pylori IgG and IgA antibody measurement. The diameter of the ulcer was measured by placing the opened biopsy forceps (7 mm) beside it. Biopsy specimens were examined in accordance with the Sydney system. Results. Mean size of the peptic ulcer was 13.2±8.3 in corpus, 11.3±5.3 in antrum, 13.8±7.8 in angulus, 9.5±5.3 in prepylorus and 9.2±4.7 mm in duodenum (duodenal versus gastric type; p<0.05). Average size of the ulcers was 9.4±5.3 mm in patients with Forrest III type and 11.5±6.8 in other types (p<0.05). Patients who were ≥50 years of age, currently smoking, or who had corpus-predominant chronic gastritis or atrophic gastritis, had larger ulcers than others. Size of index ulcers, successful eradication of H. pylori and the presence of atrophic gastritis were independent factors for healing. The odds ratio was 11.5 (95% CI 3.3–40.5; p<0.01) for eradication of H. pylori, 3.5 (95% CI 1.1–11.2; p<0.05) for size of the index ulcer (≤10 mm versus >10 mm) and 3.4 (95% CI 1.2–9.8; p<0.05) for atrophic gastritis versus no atrophy. Conclusions. Size of the peptic ulcer, successful H. pylori eradication and atrophic gastritis were independent factors for the healing of peptic ulcers. A number of clinical and endoscopic variables (age, current smoking, corpus-predominant gastritis, Forrest classification) were associated with size of the peptic ulcer in H. pylori-positive patients.

Cure of Helicobacter pylori infection in all compliant patients: report on 644 subjects

To the Editor: Treatment of Helicobacter pylori infection can result in therapeutic failure [1]. In the year 2000, in an open prospective follow-up study, we reported 120 patients with treatment fa...

New options in eradication of Helicobacter pylori

Better treatment options to eradicate Helicobacter pylori are needed, while we await a possible effective vaccine against the worlds most common infection. The goals of therapy for H. pylori infection should be an effective and low-cost therapy with a low frequency of side-effects. The currently available eradication regimens are cumbersome, which can lead to a reduction of compliance and a lower efficacy. More recent studies have shown, however, that the duration of antimicrobial treatment may be shortened, which also makes the treatment more cost-effective and more tolerable. At this point it seems relevant to treat H. pylori infection first with some antisecretory modification of triple therapy, while the therapeutic failures can be treated with other more relevant and suitable alternatives. Metronidazole is still a cornerstone of triple therapy and the more expensive clarithromycin is an alternative second-line treatment. Time will show the effectiveness and suitability of the latest topical 1-day treatments.

Clinical significance of widespread gastric metaplasia in the duodenal bulb

Background All the risk factors of peptic ulcer disease are not thoroughly understood. Goals To assess duodenal gastric metaplasia (DGM) in relation to Helicobacter pylori status and endoscopy findings with special reference to the effects of highly selective vagotomy. Study The study population consisted of 1056 adult patients and an additional 154 patients who had had a highly selective vagotomy. Their clinical and endoscopy records as well as the histology of gastric and duodenal biopsies were evaluated retrospectively. H. pylori infection had been determined by serology and culture. Results Widespread (more than 20%) DGM was strongly associated with H. pylori positive duodenal ulcer disease (in 59.7% of patients). The prevalence of DGM diminished progressively the more proximally the ulcer was located in the stomach, and was 2.5% in proximal gastric ulcers patients. In vagotomized patients, the prevalence of widespread DGM (8.4% of patients, median 14 years after operation and the majority still H. pylori positive) was close to that of patients with H. pylori gastritis without peptic ulcer disease (4.5%). Conclusions Widespread DGM is an indicator for an increased risk of duodenal ulcer among H. pylori positive patients and it could be used to select patients for eradication therapy.