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[15/48] Optimal Triple Therapy for H. pylon Eradication in an Area of High Resistance to Metronidazole. A Practical Approach Background: In 1997 we showed in a regional study that primary [...]

Background: The aim of our study was to test the feasibility of culturing Helicobacter pylori directly from biopsies aimed for rapid urease test in routine clinical practice., Materials and Methods: In 260 consecutive patients referred for gastroscopy because of dyspepsia one antral biopsy was routinely used for our "in house" rapid urease test (RUT). Positive biopsies were placed in a transport medium and sent to the laboratory. The biopsies were cultured and incubated at 37 degrees C for 5-7 days. H. pylori was identified and routinely tested for antimicrobial resistance by using the E-test., Results: In 118 out of 260 patients (45%) the urease test turned positive and the growth of H. pylori was sufficient to allow testing of antimicrobial resistance., Conclusion: H. pylori could be cultured from almost all positive RUT specimens. A liquid RUT is thus more suitable for culture, saving additional biopsies.

We have developed a PCR-based method to detect macrolide resistance and the virulence gene cagA in Helicobacter pylori within 24 h, thereby improving the lengthy process of culture-based approaches. Total DNA was prepared directly from stomach biopsy specimens. The procedure proved to be rapid and reliable and could be utilized for diagnostic purposes.

Aim: Primary resistance of H pylori strains to antimicrobials has direct therapeutical implications. For this reason we studied the prevalence of primary resistance of H pylori of Sweden, in a regional setting., Material and Methods: A total of 244 patients referred to our endoscopy unit have been evaluated prospectively for the occurrence of H pylori. Helicobacter pylori infection was established by a positive rapid urease test on an antral biopsy. If positive the biopsy specimen was transferred to a transportmedium for culture on a Skirrow medium. Antimicrobial resistance was evaluated by the E-test., Results: In 109 patients H pylori infection was seen and in all of them the culture was positive. No resistance was seen for amoxycillin and tetracycline. The resistance against metronidazole was 40.3% and and against clarithromycin it was 2.8%. For metronidazole there was a significantly higher resistance seen in women compared to men (53.3% vs 31.2%; p < 0.001)., Conclusions: Primary resistance to metronidazole was higher than expected and over average in Europe. The resistance for clarithromycin is still rare. Further monitoring is mandatory to detect changes in the community.

Background: This double-blind, randomized study evaluated the efficacy of dual and triple therapies including ranitidine for treatment of Helicobacter pylori infection., Materials and Methods: Dyspeptic patients (n = 105) with a positive rapid urease test formed the intention-to-treat population (ITT). All patients were assigned to 14 days treatment with ranitidine 300 mg b.i.d and clarithromycin 750 mg b.i.d. Group A (n = 53) also received a placebo twice daily, while group B (n = 52) received lymecycline 300 mg b.i.d. Treatment with ranitidine, 150 mg b.i.d, was continued for an additional 30 days. H. pylori infection was verified by culture. Twelve weeks after antibiotic treatment, H. pylori status was investigated by culture and 14C-urea breath test (UBT). The per-protocol (PP) group consisted of 73 patients (A, n = 38; B, n = 35)., Results: Cure rates were 87% (95% C.I. = 72% to 94%) vs. 72% (95% C.I. = 58% to 83%) in the ITT-group and 89% (95% C.I. = 73% to 97%) vs. 87% (95% C.I. = 72% to 96%) in the PP-population (culture and UBT) when triple and dual therapies were compared. In all patients who were not cured, clarithromycin resistance of H. pylori was acquired. Side effects were experienced by 54% of patients., Conclusions: The difference in efficacy between the two treatment regimens was not significant. However, the cure rates in this study are comparable to combination treatments with omeprazole. Treatment failures were due to acquired clarithromycin resistance.

Objectives: The aim of this study was to confirm the efficacy and tolerability of a new, low dose, short-term triple therapy for cure of Helicobacter pylori infection, as suggested by Bazzoli, in a larger population., Methods: On an "intention-to-treat" basis, 116 patients with active (n = 41) or healed (n = 47) peptic ulcer disease or ulcer-like dyspepsia (n = 28) and H. pylori infection received a 1-wk course of omeprazole 20 mg b.i.d., clarythromycin 250 mg b.i.d., and tinidazole 500 mg b.i.d.. Four weeks after treatment withdrawal, cure of H. pylori infection was evaluated by rapid urease test and histology., Results: One hundred and sixteen patients returned for follow-up. In 108 patients, H. pylori could not be identified 4 wk after cessation of therapy. The eradication rate was calculated to 93%. In addition, all patients with active peptic ulcers showed complete healing at follow-up despite no further treatment. Drug acceptance and compliance was excellent., Conclusion: Triple therapy as suggested by Bazzoli with omeprazole (in this study given b.i.d. for better compliance), clarythromycin, and tinidazole is indeed highly effective for both cure of H. pylori infection and for healing of peptic ulcers, is easy to perform, is cheap, and is without clinically significant side effects, even in a larger population.

In a double-blind randomised four-center trial 43 patients with gastric ulcer (20 men, 23 women; mean age 52.2 years) were treated with either pirenzepine (P) 50 mg b.i.d. (n = 24) or cimetidine (C) 400 mg b.i.d. (n = 19) during six weeks. In ten patients gastric juice was examined before and at the end of the treatment for concentration and type of the microbial flora, and for nitrite concentration. After six weeks 83% of the patients in both groups were either symptom-free or clearly improved. In 15/24 patients on P (62.6%) and in 13/18 on C (72.2%) the ulcer(s) were healed at the time of control endoscopy. In the ten patients investigated, intragastric concentrations of fungi, bacteria, and nitrite were not significantly changed by the treatment. In gastric ulcer, treatment with pirenzepine 50 mg b.i.d. or cimetidine 400 mg b.i.d. during six weeks does not result in significant microbial overgrowth or generation of nitrite.

The clinical features of primary sclerosing cholangitis were studied in 46 consecutive patients. Jaundice was the most common symptom (57%), followed by pruritus (28%), pain (24%), and fever (15%). Thirty-three per cent of the patients had no symptoms, merely laboratory changes. No significant relationship was observed between a numerical score of radiological bile duct changes at diagnosis and the clinical picture, or the clinical course during follow-up. If clinical deterioration occurred, this seemed to happen within the first eight years after the clinical presentation. Patients with only intra-hepatic bile duct changes (n = 10) did not differ clinically from those with extrahepatic changes as well. Forty-three out of 44 patients examined had inflammatory bowel disease, usually ulcerative colitis, with total colitis in 84%. Radiological bile duct changes had a significantly higher score in patients who had to be treated with a combination of sulfasalazine and steroids, suggesting a weak relationship between severity of bowel disease and bile duct disease.

It is known, that Pirenzepine inhibits basal, pentagastrin-, insulin- and peptone-stimulated gastric secretion. In this study the effect of three different doses of Pirenzepine was studied on acid secretion stimulated by modified shamfeeding (MSF). Each of eleven healthy volunteers underwent four secretion tests after pre-treatment for 4 days in random order by: no drug, tablets Pirenzepine 25 mg b.i.d., 50 mg b.i.d., or 50 mg t.d.s. Basal acid output 0-30' was reduced by 48%, 59% and 66% respectively and stimulated acid output 0-120' by 45%, 58% and 48% respectively. When acid secretion was calculated as volume corrected for duodeno-gastric reflux and pyloric losses the corresponding figures were 33.7%, 36.3% and 42.6%. Inhibition of MSF-stimulated acid secretion by a high dose of Pirenzepine was not complete. Pirenzepine 50 mg b.i.d. seems to be a suitable dose for clinical use, as acid reduction is as good as with 50 mg t.d.s. and side-effects are known to be less.

In a 25-year old woman with ulcerative colitis a lupus erythematosus syndrome occurred during treatment with salazosulfapyridine. The connection with medication was ascertained by reexposition. Some of the systemic complications of ulcerative colitis may possibly be due to the salazosulfapyridine medication.