Q. N. Karim

One week eradication regimen for Helicobacter pylori.

Although Helicobacter pylori is both a frequent cause of gastritis and an important factor in duodenal ulcer recurrence, no treatment regimen exists that is completely safe and effective. We have studied a short eradication regimen of tripotassium dicitrato bismuthate 120 mg four times daily and amoxycillin 500 mg four times daily for seven days with metronidazole 400 mg five times daily for three days (days 5-7). 106 patients with peptic ulceration and non-ulcer dyspepsia, who were also infected with H pylori, were entered into the study. H pylori was successfully eradicated in 76/106 (72%) patients (median follow-up 9.3 months). The rate of eradication was higher among patients with metronidazole-sensitive H pylori (40/43, 93%). In 17/30 patients in whom eradication failed, pretreatment metronidazole-resistant strains were subsequently isolated. Side-effects were mild, the commonest (24/106, 24%) being taste disturbance with metronidazole. A one-week eradication regimen is a safe, effective, cheap, and well-tolerated treatment for metronidazole-sensitive H pylori.

Lansoprazole, clarithromycin and metronidazole for seven days in Helicobacter pylori infection

Background: This study determines the efficacy and safety of a 1‐week triple therapy regimen of lansoprazole, clarithromycin and metronidazole in an area with a high prevalence of pre‐treatment metronidazole‐resistant strains of Helicobacter pylori.

Two-week eradication regimen for metronidazole-resistant Helicobacter pylori

At present there is no generally accepted treatment regimen for eradicating metronidazole‐resistant Helicobacter pylori. This study determines the eradication rate after treatment with 40 mg omeprazole o.m. and 500 mg amoxycillin q.d.s. for 14 days, with 120 mg tripotassium dicitrato bismuthate q.d.s. for the first week (Days 1–7) and 750 mg ciprofloxacin b.d. for the second week (Days 8–14). Thirty patients (16 male, mean age 45 years, range 16–80 years) with duodenal ulcers (n= 18) or non‐ulcer dyspepsia (n= 2) and metronidazole‐resistant H. pylori detected by histology, culture, in vitro sensitivity tests and a positive 13C‐urea breath test entered the study. Follow‐up was by 13C‐urea breath test at the end of treatment and at 1, 3, 6, and 12 months. Eradication was denned as a negative 13C‐urea breath test at least 1 month after finishing treatment. H. pylori was successfully eradicated in 21/30 (71%) patients (median follow‐up 10.2 months, range 4–12 months). A pre‐treatment ciprofloxacin‐resistant strain was isolated in 1/9 patients in whom eradication failed. Of 30 patients 29 completed the 2‐week regimen; one patient experienced dizziness after 3 days of treatment. The most common side‐effect was increased stool frequency (n= 6). This 2‐week treatment regimen for metronidazole‐resistant H. pylori is well tolerated and achieves an eradication rate of 70%.

Campylobacter pylori in esophagus, antrum, and duodenum

Two hundred forty-six patients with a wide range of upper gastrointestinal tract disorders were investigated for the presence of Campylobacter pyloriinfection in esophagus, gastric antrum, and duodenum. C. pyloriwas identified in 52% of patients in at least one site, and microbiological and histological techniques were used to exclude the presence of the organism. Esophageal infection was not significant and is probably due to reflux. Antrat C. pyloriwas significantly associated with active gastritis and active duodenitis and is possibly pathogenic.

Rapid diagnosis of Campylobacter pyloridis infection.

a day. At this time the platelet count was 256 x 109/l. Over the next nine days the cellulitis improved slightly, but on the ninth day a few purpuric lesions were seen on the lower limbs. These extended within 24 hours and the platelet count on the tenth day was 3 x 109/1 with a normal haemaglobin and white cell count. A bone marrow aspirate taken at this time showed hypercellularity and increased megakaryocytes, consistent with accelerated platelet destruction. Cephamandole was then stopped, four units of platelet concentrates were given, and cephalexin was started in an oral dose of Ig five times a day 12 hours later. The platelet count increased steadily thereafter and returned to normal within four days. Cephalexin was continued at the same doses during the subsequent three months and the platelet count remained normal throughout. Drug dependent platelet antibodies were shown using an immunofluorescence procedure4 with about 5 mg of cephamandole added to the incubation mixture of patients serum and platelets. Patients serum and the antibiotic solution were tested separately as controls. Other drugs given at the same time as cephamandole were frusemide, Slow K, sulindac, ibuprofen, panadeine, anginine, palfium, isosorbide dinitrate and rifampicin. All of these had been given for lengthy periods prior to the onset of thrombocytopenia, and with the exception of rifampicin, were continued subsequently without any adverse effects. The table shows the results of the platelet antibody immunofluorescence test (PIFT) performed in the presence of various cephalosporins and rifampicin, which was included as this was the only other drug discontinued at the same time as cephamandole. Platelet bound antibody was shown in the presence of cefaperazone and moxalactam, as well as cephamandole, but not in the presence of cefoxitin, cephalothin,